Architecture of Human Living Fascia 9781805012573, 9781805013082

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Dedication To the memory of Harold Kleinert, Claude Verdan and AJM Goumain who have inspired me during this work.

ARCHITECTURE of HUMAN LIVING FASCIA The extracellular matrix and cells revealed through endoscopy

Jean-Claude GUIMBERTEAU MD Surgeon. Bordeaux, France Member of the French Academy of Surgery Past-President 2012 of the French Society for Plastic and Reconstructive Surgery President of the Aquitany Stem Cell clinical and surgical group

Colin ARMSTRONG DO Osteopathic Practitioner, Grans, France

Forewords by Thomas W FINDLEY MD PhD, Professor, Physical Medicine, New Jersey Medical School, Newark, NJ, USA and

Adalbert I KAPANDJI MD, Surgeon, Longjumeau, France; Past President of the French Hand Surgery Society

First published in hardback in Great Britain in 2015 This paperback edition published in 2024 by Handspring Publishing, an imprint of Jessica Kingsley Publishers Part of John Murray Press 1 Copyright © Handspring Publishing Limited 2015, 2024 Illustrations and videos copyright © ENDOVIVO Productions srl 2015 Important notice: It is the responsibility of the practitioner, employing a range of sources of information, their personal experience, and their understanding of the particular needs of the patient, to determine the best approach to treatment. Neither the publishers nor the authors will be liable for any loss or damage of any nature occasioned to or suffered by any person or property in regard to product liability, negligence or otherwise, or through acting or refraining from acting as a result of adherence to the material contained in this book. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means without the prior written permission of the publisher, nor be otherwise circulated in any form of binding or cover other than that in which it is published and without a similar condition being imposed on the subsequent purchaser. A CIP catalogue record for this title is available from the British Library and the Library of Congress ISBN 978 1 80501 257 3 eISBN 978 1 80501 308 2 Jessica Kingsley Publishers’ policy is to use papers that are natural, renewable and recyclable products and made from wood grown in sustainable forests. The logging and manufacturing processes are expected to conform to the environmental regulations of the country of origin. Handspring Publishing Carmelite House 50 Victoria Embankment London EC4Y 0DZ www.jkp.com John Murray Press Part of Hodder & Stoughton Ltd An Hachette Company Commissioning Editors Mary Law and Andrew Stevenson, Handspring Publishing Limited Design by Bruce Hogarth, KinesisCreative Cover design by Bruce Hogarth, KinesisCreative Technical workup of illustrations and videos by Marc Bonnecaze, 16 ARTS production sarl

Language editing by Paula Moerland Copyediting by Kim Howell Typeset by DSM Soft

Contents

Dedications Foreword by Thomas Findley Foreword by Adalbert I. Kapandji Preface by Jean-Claude Guimberteau Preface and acknowledgements by Colin Armstrong List of Contributors How to use this book Glossary

Introduction History and architecture of living matter A surgeon’s observations The return of surgical exploration Intratissular endoscopy

1

Tissue continuity

Early theories of tissue elasticity Perioperative intratissular endoscopy leads to a new paradigm General anatomical conclusions Detailed anatomical conclusions Summary Red thread questions

2

Fibrillar continuity and form

The structuring role of the multimicrovacuolar network The fibrillar frame The concept of structured form Following the red thread

3

Mobility and adaptability

Maintaining tissue continuity during mobility Mechanical behavior of fibrils and fibers during mobility Global mechanical result Following the red thread

4

The relationship between the cells and the fibrillar architecture

Cell morphology and distribution The relationship between the fibers and the cells Following the red thread Conclusion

5

Spatial arrangement, tensegrity, and fractalization

Physical phenomena that influence living tissue Maximum coverage of a flat surface Filling the three-dimensional space The notion of equilibrium at rest and during movement How form can resist the force of gravity: tensegrity What is fractal organization? Following the red thread

6

Adaptations and modifications of the multifibrillar network

Scar tissue and adhesions Megavacuolar transformation Cellular overload The observable mechanical effects of manual therapy Following the red thread

7

Concept of connective tissue as the architectural constitutive tissue responsible for form

Form can be described Form is capable of mobility Forms can become more complex Afterword 1. Why does nature use spatially simple but irregular polyhedral forms to build a wide diversity of complex forms?

2. Are movements predetermined or random? 3. Why should there be an irregular, chaotic, fractal, nonlinear organization when order and linearity have proved to be so effective? 4. Does this multifibrillar system have the capacity to influence cellular genomic processes? Conclusion References and further reading Index

Forewords Thomas Findley

It was my honor to introduce Dr. Guimberteau to the first International Fascia Research Congress in 2007. The planning was well under way when he sent me a copy of his first DVD, Strolling Under the Skin. After watching it, I and other members of the planning committee had a ‘stop the press’ moment. We had to find a time for it to be shown, and an already packed schedule became yet fuller. Since then, he has produced new visual information for each Fascia Research Congress, based on many hundreds of video recordings he has made during endoscopic surgery, which allows a magnified view of living tissue. As a hand surgeon, Dr. Guimberteau knows that maintenance and restoration of gliding, controlling scar tissue, and directing or redirecting muscle forces are crucial to a good outcome. Over the past 40 years, he has regularly published descriptions of new surgical techniques. With improved surgical and imaging techniques, he was able to observe the tissues in motion as he was operating. He understood that tendons are not just ropes running in disconnected tubes or sheaths; rather, there are specific connections between them that allow for sliding of several centimeters or more. He informed his colleagues that a simple tendon transfer would not work as well as a transfer of both the tendon and the tendon sheath. Because our tendons do not protrude from our fingertips or forearm as we flex and extend our fingers, that motion which is greatest in the palm must perforce be zero at the extreme ends. And what kind of a structure will allow a variable amount of motion while still staying connected? As he looked at the tissues during surgery, he noted differences in tissue structure that seemed to vary with the amount of motion required in the tissue. These astute clinical observations led him to

describe a sliding system he termed the microvacuolar collagenic absorbing system. In this book, Dr. Guimberteau has placed his direct observations of tissue as a hand surgeon into the much larger context of the human body. His endoscopic observations encompassed those tissues he passed en route to the surgical site: epidermis, dermis, hypodermis, superficial fascia, subcutaneous tissue, deep fascia, muscle, tendons, periosteum, and bone. Nerves, blood vessels, and scar tissue were met along the way. He finds, when he looks closely, that this sliding structure is apparent in many other parts of the body besides the tendon sheath. Surgeons know from their daily experience that our bodies are a continuous structure that does not disintegrate into microscopic parts. Dr. Guimberteau points out that this continuity is not provided by cells lining up shoulder to shoulder (or more correctly, integrin to integrin) from front to back and side to side; rather, the extracellular fibers span the distances. These fibers not only connect individual cells but form extracellular three-dimensional spaces that are best appreciated by the live endoscopic techniques employed by Dr. Guimberteau rather than in fixed two-dimensional anatomic slides. As fascia anatomist Jaap van der Wal pointed out at the Fascia Research Congress in 2009, our perceptions of anatomy are limited by our conceptual understanding. He uses the example of the proposed separation between ligaments and muscles at a joint, which is displayed in most anatomy books; this is merely a product of the dissector’s knife in dead tissue, and it does not reflect the living anatomic situation. It is, in fact, physiologically impossible, because the ligaments must change length as the bones on either side of the joint move closer together or farther apart with changes in joint angle. On closer observation with fascia-sparing dissection techniques, van der Wal observed that the ligament and muscles fused into a single complex around the elbow joint. I have a lot of anatomic training, and I still struggle to understand Guimberteau’s beautiful photography, particularly the dynamic nature of his video recordings as we see fibers moving, dividing, and crossing, with consequent changes in the spaces these fibers define. My anatomically correct brain still resists the notion that these structures can change in front of

our eyes. But change of form is inherent in many parts of the body. Dr. Alan Grodzinsky showed at the Fascia Research Congress in 2007 that cartilage contains aggrecan, which looks very much like a brush. It can only be extruded in pieces from the cell, and must somehow assemble itself outside the cell into its final form. In the following lecture, Dr. Frederick Grinnell showed how the fibroblast changes shape from dendritic (round with long arms) to lamellar (polyhedral, very similar to the extracellular shapes seen by Dr. Guimberteau). Dr. Helene Langevin had just shown how this change of shape can be triggered by tissue stretch or rotation of an acupuncture needle. So if shape change is expected for proteins and other biological molecules as they are formed, and cells change shape depending on the surrounding forces, then why should the extracellular matrix be static? It is readily accepted that the extracellular matrix changes during wound healing, as the initial tissues remodel to their final form. I listened to the lecture by Dr. Rolf Reed at the Fascia Research Congress in 2012, in which he showed that swelling after acute injury is an active process. Under normal circumstances, the waterabsorbing proteins in the extracellular matrix are surrounded by fibers and not able to expand. With injury, these fibers relax, and the water flux from the capillary to the tissue can increase by 100-fold in minutes. But my brain still resists the idea that these fibers might be lengthening and contracting through our normal activities as well. After all, I learned my anatomy from a cadaver and a book, and neither one moved while I was studying! I invite both scientists and clinicians to peruse the following pages with an open mind, as Dr. Guimberteau shares the knowledge gleaned from many years of practice and study. Many years of study and thought are evident as he takes the reader through chapters covering: tissue continuity; specific forms of the fibrillar structure; mobility and adaptability; the relationship between cells and fibrillary architecture; spatial arrangement; and scars, inflammation, and other specific aspects including response to manual therapy; and the concept of fascia as the ‘constitutive’ tissue. While it is easy watching the accompanying pictures and videos, this is not easy reading, because it is material not covered in traditional medical training. However, Dr. Guimberteau’s findings will spawn future clinical and scientific advances as others seek to explore the ideas presented here. I would expect no less from the life work of such an accomplished surgeon.

Thomas Findley Newark, New Jersey, June 2015

Foreword Adalbert I. Kapandji

It is my pleasure, indeed an honour, to be invited to write the Foreword for this book - The Architecture of Living Fascia – written by my friend, JeanClaude Guimberteau, because he has transformed our way of seeing “connective tissue” with a great idea: to explore the subcutaneous tissue using an endoscope equipped with a high-definition camera allowing high magnification. It is truly amazing to see what he has discovered using this very simple approach. Of course, he first had to integrate this method of exploration into his routine surgical procedure. Then, once he had mastered this technique, what a pleasure, what joy to discover entirely new and hitherto unseen, structures and functions of living tissue. One should first take time to look at the images, and only then go on to read this wonderful book. I say “wonderful” because one can only marvel at the number and the beauty of the photographs and illustrations it contains. Jean-Claude Guimberteau’s key discovery is the structure of connective tissue as a “pre-stressed network”, which explains perfectly its role as an elastic link between the organs. This elasticity is due to the “filling of anatomical spaces” with polyhedral microvacuoles which contain a liquid that is under pressure. It explains how structures are able to return to their initial form as soon as mechanical constraint ceases. This is the observable evidence of tensegrity, another new science, which is found in many natural structures, but also in man-made structures such as reinforced concrete. The structure of the fibers in this network appear to be tubular as one can see bubbles moving inside them. As for the organization of this network, it is “fractal” and appears to be chaotic, but it is in fact perfectly structured, unlike true chaos. The connective tissue is the “great unifier” of our body – a huge meta-society of cells operating within our corporeal envelope. It establishes the flexible

and elastic connections between our organs, filling the spaces between different and incompatible forms. Their surgical cleavage is a disaster, because scar tissue replaces the connective tissue. It is this connective tissue which “orientates” and supports the microvessels which sustain life in our most delicate anatomical structures, particularly the tendons. It is this tissue that creates the connective pathways, the immense circulatory corridors, through which the neurovascular bundles pass, providing logistical support for the large organs – especially the brain, - and the limbs. It is this tissue that, according to Jean-Claude Guimberteau’s findings, explains the formation of the “sliding structures” that surround the tendons. The hitherto unrecognised role of connective tissue is to confer unity to our organism. This discovery raises our awareness of our inner world and its relationship with the rest of the universe. The role of connective tissue, previously neglected, I would even say treated with disdain, takes on renewed importance, thanks to the new concepts arising from the work of Jean-Claude Guimberteau. The elasticity of the subcutaneous connective tissue enables the epidermis, our body’s envelope, to clothe us with a suit of skin and to establish the borders between us and the outside world. By smoothing out the lumps of our anatomy, and by filling its hollows, connective tissue plays an essential esthetic role in the beauty of human beings, especially in women. The importance of this esthetic role becomes evident when it is lacking, for example when as a result of extreme deprivation, connective disappears completely. Without it there would be no beauty in painting or sculpture. Connective tissue is life: a flexible and taut skin is a sign of vitality and youth, for its healthy function depends on the underlying connective tissue. Christopher Columbus gave us access to new continents. Jean- Claude Guimberteau has discovered a new world in the connective tissue ... I invite you to explore it, as one would a symphony, with his new book! Adalbert I. Kapandji Paris, France, June 2015

Preface Jean-Claude Guimberteau

This book is the culmination of 20 years of intratissular endoscopic research carried out during more than 1000 surgical procedures. It is not a conventional anatomy text, systematically describing the various organs; there are countless such works. Rather, it takes a different view of the microanatomical structure and architecture of living tissue, showing how the fibrillar network extends throughout the entire body. I wrote it in a spirit of sharing. Firstly, to share the beauty of the images I was observing while exploring human tissues in my work as a surgeon. Although I had been working with these tissues for years, I had never really seen what I was looking at. This journey into living tissue was made possible by new video and digital technologies. I wanted others to see the colours, shapes, and forms that were revealed, and to appreciate the beauty of Nature and the structure of their bodies. I also wanted to share this newly acquired knowledge of the human body and how it functions. Our learned contemporaries have studied in great detail the habits of other living organisms such as red ants or Galapagos iguanas. They have gathered together a significant body of knowledge about such creatures, and yet they still know very little about the way the human body functions. I wanted to spread this knowledge so that everybody can benefit from it and better understand their own body from a new perspective The fibrillar network is one of total tissue continuity. Understanding this crucial insight enables us to visualise our body as a ‘global’ structure with a specific, three-dimensional architecture made up of elements that, while

fragile, have a stubborn capacity for adaptation. This suggests that there is an architectural system for all living organisms, whose role is far more important than simply connecting things. It is actually constitutive. I wanted to share my astonishment at the revelation that cells do not occupy the entire volume of the body, and are not responsible for form. The extracellular world, ignored during over half a century of research, is as important as the cellular world. And I needed to convey an understanding of the importance of the long neglected intracorporeal physical forces that impose their laws at all levels, and enable the growth of complexity in space and time. I experienced great difficulty in moving away from the tranquil certainty of rationality to enter a world of fractals and apparent chaos. I came to recognise that this seemingly chaotic fibrillar disorder, together with tissue continuity, ensures the efficiency of the living organism. The concept of order and proportionality suddenly seemed to lose ground to non-linearity and apparent disorder, which in fact permit creative adaptability and the tendency for life to auto-organise in the most efficient way. Finally I wanted to make others aware of the results of this exploration, which disturb our academic certainties and lead us into the realms of quantum physics, fractalisation and biotensegrity. Nature is certainly a symphony of fragility and complexity but it is gradually becoming more comprehensible. Perhaps after reading this book you will, like me, look at your body and life differently. This new appreciation of our living architecture should not be seen as a revolution, but rather as an evolution made possible by technological progress. Inevitably, observations using ever more effective optical procedures, as well as other new techniques, will bring about further changes in our perception of the world of living matter and shake up conventional beliefs. We are only at the beginning of this exploration! Jean-Claude Guimberteau

Pessac, May 2015

ACKNOWLEDGEMENTS Thanks first to my wife Danielle for her patience, tolerance and helpful criticism. Thanks to my anaesthetist colleagues for their acceptance of the extra time required for my investigations during surgery. Thanks to all the nurses and staff at the ‘Institut Aquitain de la Main’, Bordeaux. Thanks to the video technicians for their understanding and contribution and in particular Marc Bonnecaze http://www.mb-videos.com and Charline Courivault ([email protected])

Preface Colin Armstrong

It has been a privilege to work with Dr Guimberteau during the conception, translation and writing of this book. I first met Jean-Claude at the 2nd World Fascia Congress in Amsterdam in 2009. My main reason for attending the congress was to see him present his new film, The Skin Excursion. As a native English speaker and osteopath living and working in France I then started helping him with the translation of his films into English. In 2012 he asked me to collaborate with him on a project to write a book about his work. My involvement in this project began with the development of the structure of the book and the layout of the chapters. I worked closely with Jean-Claude during the translation, rewriting and editing of the text to ensure that the subtleties and nuances of his message were not lost in the process. Until recently research into anatomy has been carried out mainly on cadavers. By contrast, Dr Guimberteau’s investigations take place inside a living human body and this heralds the return of descriptive anatomy to the forefront of anatomical research. There are no boundaries between the macroscopic and microscopic fields of vision, the only boundaries being those imposed by the limitations of human understanding. Anatomical research has concentrated mainly on the macroscopic anatomical structures and, with the invention of the microscope, on cells. Jean-Claude Guimberteau has perfected a technique of intra-tissular endoscopy, which has enabled him to explore an intermediary level of observation – the mesoscopic level – which bridges the gap between the macroscopic and microscopic worlds. In so doing he has opened a window into the largely unexplored world of living human anatomy. He has discovered that within the extracellular matrix (ECM) there is a continuous,

bodywide, multifibrillar network of fibers and fibrils, extending from the surface of the skin to the periosteum, at all levels of organisation. Perhaps the most important message is that there are no distinct separate layers within the histological continuum of living matter. We discover that the whole body is structured by a vast single unitary tensional network that is composed of billions of interconnected multidirectional fibers and fibrils. The fibrils interweave and interconnect to create the three-dimensional microvolumes that Dr Guimberteau has named microvacuoles. These are the basic architectural units – fundamental building blocks of the body. He has also studied the behavior of these microvacuoles during movement – how they deal with constraint and how they adapt to specific functional demands in different areas of the body. This can be seen in what Dr Guimberteau calls the sliding systems, where the microvacuoles play an essential role in movement. The permanently hydrated multifibrillar, microvacuolar network is in fact the extracellular matrix, which has been described as a body-wide communication system essential to all living functions. The intimate relationships between the cells and the ECM are evident in the images presented in this book. Cells require a supporting framework, which is provided by the multifibrillar network. They are embedded within this fibrillar network, which extends throughout the body and provides structural support for cells and integrity for organs. Tension is distributed mechanically across the entire system. The links between the ECM and the cytoskeleton via the integrins are well documented. Every cell is thus connected to every other cell. James Oschman has described this as the ‘living matrix’. When the hand of a therapist touches a human body, it comes into contact with an intimately connected network of virtually all the molecules in that body.1 The tensegrity theory holds that a locally applied force will be transmitted throughout this network of pre-stressed fibers. We can see groups of cells moving together and being distorted by changes in tension in the fibrillar network, either as a result of direct traction on the tissues, or induced by manual traction of the skin. Cells are not only deformed, but they also move closer together or further apart. I believe these images of the intimate,

interdependent relationships between cells and the fibrillar framework to be of great significance to manual therapists. Dr Guimberteau’s extraordinary images reveal the complexity and intricacy of tissue mobility. The microvolumes formed by the interconnecting fibrils remind us of the three dimensional nature of the body. It is vital that manual therapists test all possible parameters of tissue mobility, and in all three dimensions, if we are to fully appreciate the complex patterns of somatic dysfunction. This book presents the work of a true ‘original thinker’ who has had the courage and perseverance to investigate human anatomy and movement from different perspectives. His innovative research confirms the concept of the global nature and continuity of living tissue, which is why it is of such relevance to manual therapists and movement teachers. The therapeutic implications of this research are wide-ranging, and difficult to qualify and quantify. Dr Guimberteau’s work challenges the traditional view of distinct, separate, stratified tissue layers and offers an alternative model to the reductionist view of anatomy that we learn from traditional medical textbooks. It is time to re-assemble the tissues that have been dis-assembled, separated, dissected and studied in minute detail. There is also a need to reappraise our understanding of the architecture, spatial configuration and morphodynamics of the human form. This book ultimately raises more questions than it answers, but hopefully it will serve as a foundation stone for further research in the exciting new field of living anatomy. Students of anatomy, whatever their calling, and therapists of all persuasions who work with living tissue, will find in these pages a wealth of new information on the architecture and organisation of living matter, and the concept of global dynamics put forward by Dr Guimberteau. 1. Oschman J. Energy medicine. Edinburgh: Churchill Livingstone; 2000. p.48. Colin Armstrong Grans, France May 2015

ACKNOWLEDGEMENTS I would like to thank my parents for teaching me to think independently, work intuitively and to follow my instincts. I would also like to thank my wife Catherine for her unfailing support and encouragement.

List of Contributors John F Barnes PT, LMT International lecturer and author on Myofascial Release; President and Chief Physical Therapist, John F Barnes Myofascial Release Treatment Centers & Seminars, Malvern PA, USA. Jean-Pierre Barral, DO, Diploma in Osteopathy, European School of Osteopathy, Maidstone, Kent, UK. Diplome d’Ostéopathie, Faculté de médecine de Paris-nord (département ostéopathie et médecine manuelle), Paris, France Founder and Director of the Barral Institute of Visceral Osteopathy; Osteopathy practitioner, teacher and author. Leon Chaitow ND, DO State Registered Osteopath (UK); Honorary Fellow, University of Westminster, UK. Editor-in-Chief, Journal of Bodywork and Movement Therapies Director, Ida P. Rolf Research Foundation (USA); Member, Standing Committees; Fascia Research Congress and Fascia Research Society, USA. Willem Fourie PT, MSc Physical Therapy Practitioner Roodeport, South Africa. Serge Gracovetsky PhD University of British Columbia, Canada; Emeritus Professor of Engineering, Concordia University, Montreal, Canada. Kenzo Kase DC Licensed chiropractor and acupuncturist; Founder Kinesio Taping Method, Japan. Stephen M Levin BS MD Ezekiel Biomechanics Group, McLean, Virginia, USA. Clinical Associate Professor, Michigan State University, College of Osteopathic Medicine,

Lansing, Michigan, USA (Retired) Clinical Assistant Professor, Howard University, College of Medicine, Washington, DC, USA (Retired). Torsten Liem DO, MSc Ost, MSc paed Ost Founder and Co-principal of Osteopathie Schule Deutschland; Member of the Osteopathic Research Institute Germany; Member of the managing board of the European Association of Pediatric Osteopathy and of the Institute for Integrative Morphology; Co-founder of Breathe Yoga. Thomas W. Myers LMT Author of Anatomy Trains, Walpole, Maine, USA. James L Oschman PhD President, Nature’s Own Research Association, Dover, New Hampshire, USA. Robert Schleip PhD, MA Director, Fascia Research Project, Institute of Applied Physiology Ulm University, Ulm; Research Director, European Rolfing Association eV, Munich, Germany.

How to use this book This publication is made up of a number of different parts and special design features. These are described and explained here in order to help the reader to obtain maximum value and enjoyment from using the material. The component parts are: • The book which includes 403 photographs and diagrams. • 90 video clips that can be accessed directly online using the voucher code printed in the book. To give the reader a better understanding of what they are looking at the following features have been incorporated into this publication.

THE BOOK Colour coding – A different colour is used for the headings and background design features in each chapter making it easier to find the beginning and end of the chapter. The key to the colours can be seen by referring to the Contents list. Glossary – Words which are likely to be unfamiliar to the reader are included in the Glossary. All the words defined in the Glossary are highlighted in blue the first time they are used in the text. Key statements – These highlight points which are of particular importance, particularly for the manual therapy practitioner. They are highlighted as shown here: Red Thread Questions – The author poses a number of key questions that are raised by his observations. These are listed at the end of Chapter 1. As the text progresses the questions are addressed individually chapter by chapter. These questions are highlighted as in the following example:

KEY STATEMENT The continuous, permanent link between all the components of the microvacuolar system provides the architectural organization and fibrillar framework that explains and confirms the concept of structured form.

Specialists’ commentaries – Some of today’s leading thinkers and practitioners in the fields of anatomy, body mechanics and manual therapy have been invited to add their comments on each chapter. These commentaries are found at the end of the chapter being commented on and highlight the relevance of the chapter content to the work of the specialist contributor. They are presented in boxes to distinguish them from the main text. The names of the authors appear at the start of each contribution. Their names and professional details are given in a List of Contributors at the start of the book. RED THREAD QUESTIONS 1. How is this tissue continuity structured, and how do these fibers ensure tissue cohesion? How do they come together to create a structured form?

Illustrations and their numbering – These are all referred to in the text. They are numbered according to their position in each chapter, so Figure 1.1; Figure 1.2 etc. The illustrations in the Introduction are prefixed by Int. so Figure Int.1; Figure Int.2 etc. The illustrations in the Afterword are prefixed by Aft. so Figure Aft.1; Figure Aft.2 etc. Video “stills” as illustrations – “Stills” from the videos are also included as illustrations in the text. They are numbered within chapters but are prefixed “Video”. So for example Video 1.1; Video 1.2 etc. Online videos – The video clips accompanying this text are organised by chapter and numbered sequentially by video number; the equivalent “still”

figure number is also shown. The video clips can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

Glossary Adaptational teleology Teleology refers to a line of thought that considers natural forces as being directed toward some sort of end goal or purpose. Darwin held that the value of any given adaptation within a species is relative to the survival and reproductive success of those members of that species which possess that particular adaptation to the environment. Adaptational teleology refers to teleology that is influenced by adaptation to the environment. Adipocytes Cells containing lipids. Arborescent In the form of a tree. Biotensegrity The application of tensegrity to biological organisms. Chaos In mathematics, this is the irregular, unpredictable behavior of deterministic, non-linear, dynamic systems. In this book, the term is used to describe complex systems that are apparently disordered but in which there is an underlying order in the apparently random patterns. Coevolution The process by which two or more interacting species evolve together, each changing as a result of changes in the other(s). Constitutive Having the power to give organized existence to something. In this book, this term refers to the multifibrillar network giving organized existence to the form. Decorin A small cellular or pericellular proteoglycan found in the extracellular matrix. This protein is a component of connective tissue that binds to type I collagen fibrils and plays a role in the assembly of the extracellular matrix. Deterministic A process whose resulting behavior is entirely determined by the constitutive features of its initial state, and which is not random. Dilaceration A splitting into smaller parts. Dynamic adaptation or adaptability The ability of the fibrillar network to adjust to the speed and nature of intrinsic movements, under changing conditions, to ensure the integrity of the network. Dynamic unpredictability

The dynamic unpredictability of a system refers to a type of behavior whose final result cannot be predicted despite a thorough knowledge of the basic components of the system and their interactions. This characteristic, which is the result of the large number of degrees of freedom of the system, appears to be inherent in the structural make-up of the system, and is universal. Emergence Emergence is a process whereby larger entities arise as a result of interactions between smaller or simpler entities, which themselves do not exhibit the same properties as the resulting larger entities. Endogenous Originating from within the body. Endomysium Meaning ‘within the muscle’, this is a traditional, artificial subdivision of part of the connective tissue that shapes each individual muscle fiber. Epimysium Meaning ‘around the muscle’, this is a traditional, artificial subdivision of the connective tissue that surrounds the entire muscle. Epineurium Meaning ‘around the nerve’, this is a traditional, artificial subdivision of the connective tissue surrounding a peripheral nerve. Extravasation A discharge or escape, as of blood, from a vessel into the tissues. Fascicle A term used to describe a bundle of nerve, muscle, or tendon fibers grouped together. Fractalization A natural phenomenon that exhibits a pattern that is repeated at every scale. If the replication is exactly the same at every scale, it is called a self-similar pattern (self-similarity). GAG chains Glycosaminoglycans (GAGs) or mucopolysaccharides are long, unbranched polysaccharides consisting of a repeating disaccharide unit. Global dynamics Forces and movements that relate to the whole body. Global Relating to the whole body. Glycosaminoglycans (GAGs) Linear polysaccharides consisting of repeating disaccharide units. Together with proteins, they form proteoglycans. Glycosylated proteins Glycosylation is the process by which a carbohydrate is covalently attached to a target protein. It refers to the enzymatic process that attaches glycans to proteins, lipids, or other organic molecules. Haversian system A concentric organization of compact bone tissue surrounding a central canal, the Haversian canal. The bone’s nerve and blood supplies pass through the Haversian canals. Histology The study of the microscopic anatomy of the cells and tissues of plants and animals. Hyaluronan (hyaluronic acid or hyaluronate) An anionic, non-sulfated glycosaminoglycan distributed widely throughout connective tissue.

Invagination The ensheathing, enfolding, or insertion of a structure within itself or another. Lamina densa A zone between the epidermis and the dermis of the skin. Macroscopic Observable using the naked eye. No magnification is required. Mechanotransduction The many mechanisms by which cells convert a mechanical stimulus into chemical activity. Mechanotransmission The physical transmission of mechanical stimuli to all parts of the organic structure—cells and fibers. Megavacuole The functional adaptive response of the multimicrovacuolar system to a repetitive mechanical constraint. Melanocytes Cells that pigment the skin, hair, and feathers of vertebrates. Mesoscopic Observable using the naked eye but requiring magnification (up to 3 ×) for better definition. In this book, the term is used to describe an intermediate level of observation between the macroscopic and the microscopic levels. Microscopic Too small to be seen by the naked eye but large enough to be observed under a standard microscope using magnification from 10 × up to 250 ×. Microvacuole A microvacuole is a volumetric unit that exists within a continuous architectural network of intersecting fibrils, creating microscopic spaces or microvolumes. Morphodynamic This term introduces the fundamental notion of the necessity to link form with the underlying mobile architecture. Morphostructure An interior architecture that structures the entire form. Multifibrillar Made up of many fibrils. Multimicrovacuolar Made up of many microvacuoles. Neovessel A tiny new blood vessel formed by neovascularization. Non-integrable A term used to describe systems that share a crucial common feature—an exponentially sensitive dependence on their initial condition. It is impossible to predict the future behavior of such systems. Organogenesis A term used to describe the development of the internal organs of an organism. Osmotic pressure The pressure which needs to be applied to a solution to prevent the inward flow of water across a semipermeable membrane. Parietal Relating to the walls of an anatomical cavity.

Pericellular Surrounding a cell. Perimysium A traditional, artificial subdivision meaning ‘surrounding the muscle fascicles’. In this book, the term is used to describe shaping the fascicles as well, not only surrounding them. Perineurium A traditional, artificial subdivision meaning ‘surrounding a bundle of nerve fibers’. Phylogenetic The study of evolutionary relationships among groups of organisms, species, and populations. Polyhedron (plural polyhedrons or polyhedra) In elementary geometry, this is a solid in three dimensions with flat faces, straight edges, and sharp corners or vertices. Proteoglycans Proteins that are heavily glycosylated. The basic proteoglycan unit consists of a ‘core protein‘ with one or more covalently attached glycosaminoglycan chains. Rheological Of or relating to rheology, which is the study of how matter flows and deforms, including its elasticity, plasticity, and viscosity. Stratum basale The deepest level of the epidermis. Structuring The manner in which the elements of anything are held, organized, interrelated, or put together in a particular way. Superficial fascia A fibrillar reinforcement lying in the hypodermis. Tensegrity Tensegrity structures are collections of stable struts and interconnected cables under tension. They maintain their integrity because their architecture involves isolated components in compression inside a net of continuous tension. Tropism The biological phenomenon of movement in a given direction in response to an environmental stimulus. van der Waals’ force (Named after Dutch scientist Johannes Diderik van der Waals). In physical chemistry, this is the sum of the attractive or repulsive forces between molecules, based on the property of solid surfaces to fix certain molecules by weak bonds. Vinculum (Pl. vincula) is a band of connective tissue containing tiny vessels which supply blood to the tendon. Virtual space An anatomical definition of a system of sliding that occurs without linkage and with total tissue discontinuity. The space between a bullet and the barrel of a gun is a good analogy.

Introduction History and architecture of living matter A surgeon’s observations The return of surgical exploration Intratissular endoscopy

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

Progress in digital endoscopic videophotography now allows us to see the living components of the human form. Observations made in vivo (Figure Int. 1) show structural elements that are difficult to identify from cadaveric dissection or from the study of preserved tissue samples (Figure Int. 2). Even the most sophisticated histological techniques fail to reveal these structures, but using digital videoendoscopy to observe living tissue, a profusion of fibers, fibrils, and microfibrils are revealed at both the mesoscopic and microscopic levels. This continuous network of fibers appears to extend throughout the body, suggesting that we need to rethink our understanding of the way in which living matter is organized. We can no longer view the body as a collection of cell-based organs held together by connective tissue. Instead, we must now see it as a constitutive fibrillar framework in which the organs are but local functional adaptations. Groups of cells with specific, specialized physiological functions are assembled within a multifibrillar network to form the organs. The cells are embedded in and supported by the fibrillar framework. This basic architectural pattern is the same for all the organs, as well as for the skin, fat, muscles, bones, tendons, nerves, and vessels.

Figure Int. 1 Perimuscular fibrillar mesh during surgical endoscopy of a living patient (in vivo – actual size)

Figure Int. 2 Perimuscular fibrillar mesh, dead and dissected, as observed through an electron microscope (in vitro – 10 x). (In collaboration with J.-P. Delage at INSERM, Université Bordeaux 2, France.)

KEY STATEMENT One of the aims of this book is to suggest a new model that describes the structural framework of the human body and the basic architecture of living matter—in other words, a new structural ontology.

HISTORY AND ARCHITECTURE OF LIVING MATTER Form through the ages Everything has a form. Human beings have a form. We are volumes of living matter surrounded by other natural forms, either living or inert. Throughout the ages, form has been considered from the perspective of appearance alone, without questioning the intimate organization of structured matter. This can be explained by the inability to observe living matter closely, as a result of technological limitations. The structuralist perception of living matter, which has evolved since the end of the 19th century, follows closely

the technological advances made in optical observation during the same period. Nevertheless, the organization of living matter has fascinated human beings since the beginning of time. For centuries, this debate had been the exclusive reserve of philosophers and theologists. However, the Age of Enlightenment in the 17th and 18th centuries marked the beginning of serious debate on the subject. Geoffroy Saint-Hilaire, a naturalist who established the principle of ‘unity of composition’, endeavored to clarify the nature of the connections that link the different parts of an organic entity, and that are responsible for the form of each particular entity. He attempted to provide a rational explanation of form by studying the contents. Renewed interest in scientific research and technological progress during the 19th and 20th centuries changed our perception of form, and its physical and spatial aspects were investigated further during this period. However, this was not a simple process, and several steps were necessary. Darwin introduced the concept of ‘adaptive finality’ but, perhaps more importantly, reaffirmed the notion that human beings are members of the animal world. The adaptational teleology proposed by Darwin had its detractors. The first was Sir D’Arcy Wentworth Thompson, a Scottish biologist and mathematician. His book On Growth and Form, published in 1917, pioneered the scientific explanation of morphogenesis, the process by which patterns are formed in plants and animals.1 He claimed that scientists were ignoring an essential factor, namely the physical forces responsible for form, and were overemphasizing the importance of evolution as the sole determinant of the form and structure of living organisms. The discovery of the cell and the mapping of the human genome in the late 20th century provided such a wealth of scientific evidence that it was difficult to consider form independently and without reference to the genetic code. Genes were thought to control and explain everything, including form and the development of form. According to this model, form should be simply the result of the spatial contiguity of the various structural elements of any given organic entity. This may be so, but it does not explain everything, nor does it provide a satisfactory explanation as to how form is created or how it is

maintained during movement. Our understanding of form was limited by the lack of consideration of its spatial and architectural aspects. Form exists and is structured, but how is it structured? Is the cell the only basic structural unit or is there another explanation? We need to steer a course between a philosophical vision, weighed down by the influence of ancient times, and a metaphysical model providing reassuring explanations. Thanks to modern technology, the observation of living tissue is once again a major method of scientific study, and its findings must be respected. It is important to avoid being seduced by theories that may be conceptually attractive but that in reality are inaccurate. Therefore we will first describe what we can observe through an endoscope, then we will try to make sense of what we have seen.

A SURGEON’S OBSERVATIONS Fundamental scientific research seems to have deserted operating theaters. In recent decades, surgeons have gradually become less involved in the fields of physiological and biological investigation. Modern surgeons tend to concentrate solely on their role as physicians and technicians, as surgical procedures now involve the use of sophisticated equipment. This was not always the case, and in the past the names of eminent surgeons have often been associated with important milestones in the quest for scientific knowledge. However, modern scientific research has shifted away from anatomical dissection and observation at the mesoscopic level in the operating theater toward the study of smaller and smaller structures, which can be seen only through microscopes in the laboratory. Published work has flourished, and a wealth of information is now easily accessible on the Internet. But this abundance of information is fragmented, and scientists can easily lose sight of the wider implications of this mass of knowledge. Research has become compartmentalized, and scientists working in unrelated fields may have difficulty understanding each other, because they follow such different educational paths. Accepted truths may seem contradictory, even though they may in fact refer to the same phenomenon but in a different context. We now need to put the pieces back together to appreciate the bigger picture.

Surgeons enjoy a privileged position compared with that of other scientists. They are artisans who know how to work with living matter, and who, over time during the practice of their art, have the opportunity to gain considerable insight into the behavior of this matter. They come into direct contact with living human tissue, and the knowledge gained through the manipulation and observation of this living matter is fundamental and very valuable. When you see the pulsing of an artery, the serpentine movements of an intestinal loop, or the dilation of pulmonary alveoli, you witness the expression of life in its many forms and begin to appreciate the tremendous diversity of the shape and form of living structures. This information is completely different to that gained by the study of tissue samples from rats or hamsters in the laboratory. It is neither more nor less important, but complementary, and it cannot be ignored.

THE RETURN OF SURGICAL EXPLORATION Recent technological progress and the ability to obtain high-definition digital video images allow surgeons to observe living matter more closely and in greater detail than hitherto. The surgeon can now obtain high-definition images at a magnification equal to that obtained using a normal microscope (40 ×). Crucially, these images can now be obtained in vivo and in situ. Of course, the electron microscope can explore structures at much greater magnification, but this can be used for the study of samples of dead tissue only. Such samples have been dehydrated and prepared using various mechanical procedures and chemical solvents. This is obviously not the same as in vivo observation of living tissue. Nevertheless, despite these limitations, both optic and electronic microscopic observation has considerably enhanced our knowledge of the cell, and important discoveries were made by scientists in the 19th century. These findings were extraordinary because humans discovered that they are composed of the same basic element as the rest of the living world: the cell. Cells may differ from one species to the next, but they share a common shape and form, and they function in a similar way. The cell is an essential building block, because it contains the magic book of genetic information: the genetic code. This enables reproduction, either of identical cells or of differentiated cells, depending on the functional requirements of the new cells. They can

repair themselves and divide to form new cells. Cells are found almost everywhere and meet all the functional requirements of the living body. Scientific research carried out by biologists during the 20th century focused almost exclusively on the cell. The quantity of this research into the cell and its components is colossal. It represents a truly international effort, because all nations around the world have participated in some way. As a result, the complex functional mechanisms of the cell are now well understood. However, intercellular exchange mechanisms still require further investigation, and the hypotheses that attempt to explain these processes are often contradictory. Surgeons are not in a position to give their opinion on these hypotheses, because such ideas are based on the findings of research done in laboratories under completely different conditions to those encountered during the observation of living tissue in the operating theater. However, when you place an endoscope with a camera inside the living tissue of a patient, your perception changes, and the underlying assumptions and ‘generally accepted truths’ underpinning these laboratory-based hypotheses no longer seem as reliable. Endoscopic technology enables surgeons to venture once again into this largely unexplored world and to extend their knowledge and understanding of living tissue. I believe that through sharing this knowledge we will learn more about how the body functions in both health and disease.

INTRATISSULAR ENDOSCOPY I began my investigation of living tissue in 1995, using a surgical microscope equipped with a mono CCD camera that permitted only low-resolution images. In 2001, I started using an endoscope designed for arthroscopy. Subsequently, in 2005, contact endoscopy with high-definition technology enabled us to transform blurred, indistinct photographs into sharp, clear images that provide evidence of the real architecture and behavior of living tissue (Figure Int. 3 and Video Int. 1).

Figure Int. 3 Use of the endoscope during surgery Video Int. 1

The photographs in this book were all taken during planned surgeries. Naturally, this type of perioperative endoscopy is carried out only with the patient’s consent. The time set aside for filming was limited to 30 minutes so that the work of the surgical team was not disturbed. These surgical interventions were performed either with or without a surgical tourniquet. The use of a tourniquet provides a clear, bloodless field, which allows detailed observation. However, the images obtained under these conditions are rather dull and do not reproduce the bright colors of living tissue. Filming in the absence of a tourniquet results in much more lively images, but the procedure is hampered by the extravasation of blood (Figures Int. 4A and B).

Figure Int. 4 A Cross-section of the skin during surgery with a tourniquet. There is no bleeding. (5 x)

B Cross-section of the skin showing extravasation of blood during surgery. (5 x)

The videos accompanying this book were filmed using an endoscope that combines a full high-definition camera with a flexible fiberoptic cable, a lens, and a cold light source (Figure Int. 5).

Figure Int. 5 A display of material used during surgical endoscopy: an endoscope with a full highdefinition camera, a flexible fiberoptic cable with a cold light source, and surgical instruments

I use either 2.5-mm or 4-mm lenses, with variable magnification and excellent focus, but the depth of field is extremely limited. The camera can be moved along surgical incisions, and the video can be viewed in real time on a screen in the operating theater (Figure Int. 6). Thanks to this new technology, it is now possible to obtain degrees of definition and detail never previously achieved.

Figure Int. 6 Viewing the video in real time on a screen in the operating theater during surgical endoscopy

The beauty of the images When I first saw these photographs, their beauty amazed me (Figure Int. 7 and Video Int. 2). This is what encouraged me to continue filming living tissue. Living matter is beautiful, and you can see a vast range of colors, such as bright reds, navy blues, pale or golden yellows, silvery or pearly whites, mauves, and purples.

Figure Int. 7 A world of fibers and colors. (10 x) Video Int. 2

Additional phenomena observed Another striking feature is the moistening of the tissues as soon as a surgical incision is made. Without a tourniquet, bleeding occurs immediately and hinders observation of the tissues. But even when a pneumatic tourniquet is applied so as to obtain a clear bloodless field, fluid exudes from the wound and trickles along the sides of the incision. This is evidence that the underlying tissues are permanently hydrated (Figure Int. 8 and Video Int. 3). This phenomenon can be seen when you cut through any structure containing liquid, for example when you cut through the skin of an orange with a knife. Such structures quickly dry up when exposed to atmospheric pressure or to the heat emitted by the lights in the operating theater. The tissue structures, no longer hydrated, adhere slightly to surgical instruments and need to be moistened regularly during any surgical procedure.

Figure Int. 8 A constant moistening of the structures occurs, even with a tourniquet applied. (130 x) Video Int. 3

In Figure Int. 9 and Video Int. 4, the edges of a surgical incision draw apart spontaneously and a phenomenon of distension and retractile invagination of the epidermis can be seen. This illustrates another phenomenon: the epidermis, like all our body structures, is under permanent endogenous tension.

Figure Int. 9 Cross-section of the skin, showing invagination of the edges of the skin incision and the emergence of the fatty lobules under the influence of intracorporeal pressure. (2 x) Video Int. 4

All available space is occupied by structures (Figure Int. 10 and Video Int. 5). There are no empty spaces. You can distinguish muscles, arteries, and veins, but moist, transparent veils of connective tissue surround them. This connective tissue fills the areas between the anatomical structures. You cannot distinguish areas of ‘virtual space’ between anatomical structures, nor can you see surgical planes as described in traditional anatomy textbooks. Even though living matter contains distinct anatomical structures, which can be separated by dissection, a living organism is not simply a conglomeration or assembly of separate parts. KEY STATEMENT The living matter of our bodies is a unified whole.

Figure Int. 10 There are no empty spaces in the body. All available space is occupied. (5 x) Video Int. 5

Surgeons observe the same gross anatomy in all human beings. Our bodies are constructed from the same blueprint, so we all have two arms and two legs, and our internal organs are disposed in the same manner. However, when you begin to observe anatomical structures close up and in detail, you find that we are all different. The individual make-up of each human being is unique. A journey toward discovery These observations of a questioning surgeon did not prepare me for what I am about to describe. I was simply trying to understand how tendons slide through neighboring tissues so that I could develop a technical procedure to reconstruct the flexor tendons of the fingers. My intellectual curiosity stopped there. I was aware of the existence of connective tissue that somehow enabled sliding of the tendon within the tendon sheath. I had learned about paratenons, peritenons, and virtual spaces with visceral and membranous sheaths. The description of these structures in the classic anatomy books provided a reassuring and logical theory of the movement of tendons within

their sheaths, but I found this to be completely inaccurate and hopelessly inadequate when I started observing living tissue through an endoscope. I therefore began to pay close attention to the study of this connective tissue, which has long been neglected by surgeons and anatomists. I was surprised to discover that it is composed of a network of collagen fibers, which are arranged in a completely disorderly fashion with no apparent logic (Figure Int. 11 and Video Int.6). I could have abandoned the task of trying to understand the complex organization of this tissue, but I was intrigued by the fact that it seemed to ensure the efficient, independent movement of adjacent structures with great precision and finesse. Could apparent chaos and efficiency coexist? I soon realized that this sliding system, which I then named the MicroVacuolar Collagenic Absorbing System (MVCAS), is found everywhere in the body and could be considered to constitute the primary framework of the body. I had noticed this during my early dissections. At the time, I did not understand what I was seeing. My logical, pragmatic, Cartesian mind was unprepared for this discovery. And yet what you are about to read is the result of many years of scientific observation of living tissue. Any surgeon who practices endoscopic surgery can verify the results. The sliding system, which enables movement between adjacent anatomical structures in living tissue, is organized in this chaotic way, so we must try to understand how it functions. Only then can we attempt to explain it.

Figure Int. 11 A typical fibrillar network, in which the fibers are arranged in a completely disorderly fashion. (130 x) Video Int. 6

1 Tissue Continuity Early theories of tissue elasticity Perioperative intratissular endoscopy leads to a new paradigm General anatomical conclusions Detailed anatomical conclusions Summary Red thread questions

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY The first observation of intratissular endoscopy is that everything seems to be linked and interconnected. It is important to emphasize that it is not the cell that provides the link but a profusion of fibers, fibrils, and microfibrils. One gradually realizes that the body is shaped by a fibrillar network at every level, from macroscopic to microscopic, and from superficial to deep. This fibrillar network plays a major role in shaping the substance of the body. It is not the cells alone that determine the form of the body; rather, they themselves are shaped and molded by the extracellular system in which they are embedded.

EARLY THEORIES OF TISSUE ELASTICITY When we massage, stretch, or pinch and lift the skin, we feel a little resistance to traction but the skin does not tear. When we let go, it returns to its initial position, as if from memory (Figure 1.1). The tissues respond instantly to the forces imposed on them by the manual therapist and then return to their initial state; the overall shape of the body is maintained. This ability of the body to restore form and maintain its integrity is important, but its significance often goes unnoticed.

Figure 1.1 A When you lift the skin, you feel progressive resistance to the traction until you reach a barrier B–D When you let it go, the skin returns slowly to its initial position as if by tissue memory

In the past, physicians described this phenomenon using the terms elasticity, flexibility, and plasticity, but without providing a satisfactory physiological explanation. In the 20th century, authors of anatomical texts tried to explain it from a strongly mechanistic point of view by alluding to notions of virtual space (Figure 1.2) and stratification of tissue. At the time, it was thought that the role of connective tissue was simply as packing or padding material filling the spaces between the organs, facilitating sliding between anatomical structures and providing a link between structures such as bones, muscles, and nerves.2, 3, 4, 5, 6 Descriptive anatomy all but stopped there. Then came the era of the microscope, using optical, electronic, slot, scanning, and transmission techniques to explore human tissue but at a very different level —that of the cell.

Figure 1.2 Virtual space A and B A simplistic model of a complex phenomenon that compares the sliding movement between anatomical structures with the movement of a bullet in the barrel of a gun

PERIOPERATIVE INTRATISSULAR ENDOSCOPY LEADS TO A NEW PARADIGM

Intratissular endoscopic surgery has changed our perception of human anatomy. It presents us with colorful images of moving living tissue. We can now study human tissue in life and motion, as opposed to in its static cadaveric form. Today, during surgery, we can study the living body at three different levels of magnification. • The macroscopic level: observable using the naked eye, as in this live dissection (Figure 1.3 and Video 1.1)

Figure 1.3 Dissection of the anterior aspect of the forearm at the macroscopic level (no magnification) Video 1.1

• The mesoscopic level: observable using the naked eye but requiring some magnification for better definition, as in this 2 × live dissection example (Figure 1.4) • The microscopic level: too small to be seen by the naked eye, but large enough to be observed under a standard microscope; here are a 10 × and a 40 × magnification of subcutaneous tissue (Figures 1.5 and 1.6).

KEY STATEMENT At the mesoscopic level, the first observation of note is the continuity of tissue (Figure 1.7).

Figure 1.4 Subcutaneous dissection of the anterior surface of the forearm at the mesoscopic level (2 ×)

Figure 1.5 Subcutaneous dissection of the anterior surface of the forearm at the microscopic level (10 ×)

Figure 1.6 Subcutaneous dissection of the anterior surface of the forearm at the microscopic level (40 ×)

Figure 1.7 Our first impression of the subcutaneous world is that there is no apparent order, but there is continuity (20 ×)

It might seem strange to have to discuss this concept of tissular continuity, but in the past, anatomists have tended to compartmentalize the body. However, as we shall see, connective tissue plays far more complex and important roles in the body than previously believed.

GENERAL ANATOMICAL CONCLUSIONS Tissue continuity: no layers, no empty spaces To the naked eye, connective tissue seems at first to be fairly uniform and unimportant, and of little interest to the anatomist. But as the camera slowly approaches the area between distinct muscle groups, a real entwining and interweaving of opalescent fibers strikes us, and we see that these fibers create links of total continuity. During surgical dissection, these images transform into displays of sparkling, scintillating mobile mirrors and ephemeral lights, disappearing almost immediately only to be replaced by others (Figure 1.8 and Video 1.2) What are these reflections? How and why are they produced? Why do they exist between muscular structures, and under the skin?

Figure 1.8 A world of fibers exists in every nook and cranny (65 ×) Video 1.2

During surgery, often without realizing it, the surgeon needs to separate, lacerate, and destroy this amalgam of structures that do not seem to be part of the organs and often hinder access to them. To expose the area that is to be worked on, the surgeon has to create a route of access and in the process must break through this mass of dense, heterogeneous fibers that appear to surround and wrap around all the internal organs, binding them together. This continuum of fibers, present in all spaces throughout the body, is what we commonly call connective tissue. It is important to emphasize that this socalled connective tissue is present everywhere within the body, linking separate structures from the muscular depths to the surface of the skin. KEY STATEMENT A connective tissue network exists throughout the body, from the macroscopic to the microscopic level, providing both fibrillar and histological continuity.

This continuity of a fibrillar network throughout the body is in accordance with the holistic view of many manual therapists. Contrary to conventional teaching, we now discover that there are no empty spaces, no separate layers of tissue sliding over each other. The global nature of connective tissue within the body is evident. But is this tissue solely connective? Is this really its only role? Fibrillar continuity: the existence of an extracellular world Cells are not found everywhere The recognition of the cell as the basic morphological unit and the understanding of its role in protein production were crucial discoveries. Shape is determined by the grouping together of cells, be they adipocytes, myoblasts, or osteocytes. The liver, thyroid gland, and bone are all examples

of dense cellular structures, each with its own specific function. However, the cellular elements that compose them, while certainly essential, are not entirely responsible for their form. Sometimes, cells are too scattered to influence the shape of anatomical structures. KEY STATEMENT Cells are not responsible for tissue continuity (Figure 1.9).

Figure 1.9 Cells are present here, but they are too scattered and their numbers and volume are insufficient to have any influence on shape and form (100 ×)

The cell is sensitive to external conditions and needs some kind of architectural support to live and function. It does not exist in isolation. The study of the cell has monopolized scientific attention and mobilized vast resources, but the extracellular world is still largely unexplored. It is, to all intents and purposes, a scientific desert. If we study only cells through the lens of a microscope, we are at risk of forgetting what surrounds them. Whereas areas of the body may be completely absent of cells, the same cannot be said of the fibrillar extracellular matter (Figure 1.10). For tissue of

such abundance, it is surprising that diagrams in most anatomy and histology textbooks represent it as simply a few lines of collagen or elastin fibers between the mast cells and fibroblasts (Figure 1.11). Why was it illustrated in such a simplistic way? If it is so simple, why are there several terms to describe it, such as connective tissue, extracellular matrix, ground substance, and interstitial spaces?

Figure 1.10 In some areas, cells are almost completely absent, as in this example. However, fibrillar matter is always present (65 ×)

Figure 1.11 A typical representation of the extracellular matrix, as found in most of today’s anatomy and histology textbooks

Our observations show that the extracellular fibrillar world—complex and all-encompassing—is of huge importance. It surrounds the cell and helps to provide and maintain shape and form, but it can only really be appreciated and fully understood in the living state. Therefore to study it we need to investigate living matter. It is for this reason that we have been using videoendoscopy to study living tissue in live patients. So what about this extracellular world? Observed in a living body, its ubiquitous nature is evident, therefore it is time to explore and understand its significance. Architectural continuity: fibrillar intertwining and microvolumes The concept of the microvacuole After cutting through the skin, if you apply light traction upward with small hooks on either side of the incision, structural elements that are initially stacked and piled up on each other will gradually unfold (Figure 1.12 and Video 1.3). Keep in mind that they are barely visible to the naked eye,

therefore they become apparent only on close observation through the endoscope using high magnification.

Figure 1.12 Watch the unfolding of subcutaneous fibers during light upward traction of the skin under high magnification. (20X) Video 1.3

These elements are flattened but create volume and participate in the creation of shape and form by their superposition on one another. The common assumption that the cells under the skin are arranged in a regular fashion is false. KEY STATEMENT There are numerous cell-free spaces, but they are not empty spaces.

In fact, they are filled with an apparently uniform tissue that exhibits a range of diverse colors and irregular geometric forms (Figure 1.13). The observation of living structures at magnifications between 10 × and 60 × reveals a mesh, a woven network, based on the repetition of a polyhedral unit that I have named the microvacuole. The microvacuole is the volume

created in the space between the intersections of fibrils. I chose the name ‘microvacuole’ to emphasize the concept of a space, a volume, unoccupied by the cell. I discarded the term ‘microalveolus‘, because it is too reminiscent of the structure of the lungs or of the honeycomb in a beehive, which are characterized by a very regular geometrical structure.

Figure 1.13 Diversity with uniformity shines here in a reflective sheet of colors and forms created by intertwining fibers with no apparent order (65 ×)

KEY STATEMENT Microvacuoles are volumetric units that exist within a continuous architectural network of intersecting fibrils enclosing microscopic spaces or microvolumes.

The shape of the microvacuole is polyhedral—completely irregular, yet simple (Figure 1.14). Each microvacuole has its own shape and form; no two are exactly the same. The fibrils run in all directions and, surprisingly, show no pre-established pattern; their arrangement has no apparent logic. They interconnect and interact with each other. The fibrils are a few microns in diameter, with extremely variable lengths and of irregular thickness, giving a disordered and chaotic appearance—a latticework of stems (Figure 1.15).

Figure 1.14 The microvacuole: the intersection of fibrils in three dimensions that form an irregular polyhedral unit of volume (130 ×)

Figure 1.15 Microvolumes are formed by the continuity of the microvacuoles, and they continue to show unending diversity in fibril length, thickness, color, and size (130 ×)

It is important to emphasize that everything in this extracellular world tends to be irregular and polyhedral. These polyhedrons are simple shapes but with sides that are mainly triangular, quadrilateral, pentagonal, or hexagonal. They are rarely more complicated. This is a constant, unvarying observation. Diversity is everywhere. We observe long or short fibrils, which are vertical, oblique, or transverse; close together or far apart; and of varying density. This formation, which some biophysicists call chaotic,7, 8, 9 displays another characteristic—the fractalization of this irregular network. This is, admittedly, somewhat surprising and can be confusing, because it contradicts what conventional teaching would lead us to expect. However, it is an undeniable fact and cannot be ignored. Smaller structures of similar design are found within large microvacuoles, and they fit together like Russian dolls. KEY STATEMENT The multifibrillar and multimicrovacuolar framework of connective tissue, which is found everywhere in the body, is essentially of an irregular and fractal organization (Figure 1.16).

Figure 1.16 Diversity is everywhere (130 ×)

Is the microvacuole the basic morphological unit of the body’s constitutive framework? This general impression requires supportive evidence that can be obtained only through detailed anatomical research.

DETAILED ANATOMICAL CONCLUSIONS For easy understanding, we have adopted the standard classification and arrangement of the tissue layers and anatomical structures from the epidermis down through the dermis, the hypodermis, and the subcutaneous tissues, to the deeper structures such as aponeuroses, tendons, muscles, and bones. The adjacent diagram is a simplified representation of the continuity of the intratissular fibrillar network that extends from the surface of the skin to the periosteum. In the body, there is no stratification of tissue and there are no separated layers. The skin

The outer limit of the body’s interior architecture is the skin. The skin separates two worlds. It is the border between others and ourselves, between the human form and the surrounding environment. We have already acquired a great deal of knowledge about the skin, through the work of anatomists, clinicians, and scientists. This recognition of the skin as the frontier between the self and the environment has inspired poets, artists, and philosophers. More recently, scientists, anatomists, and clinicians have studied its form and function in greater detail, so that its composition has been clearly defined. But although the structure and composition of the skin are well understood, the following questions remain. • How does the skin move? •

How do all its components adapt and link with each other during movement?

Our first observation is the wide variation in the morphology of the skin surface. It is fascinating to see that it displays many forms in the same person, all of which are variations of the same basic polyhedral pattern. This pattern is formed from the many visible outer surfaces of the threedimensional polyhedral structures that make up the epidermis, of which we will see more in the next section. The component surfaces may resemble squares, or they may appear as parallel cylinders with ridges that remind us of sand hills, or even as diamond-shaped panels that look like waves. Skin can glow with youth or sag with age, wrinkle with the weather or become thinner when people lose weight. We can see changes in response to the person’s activity, as in the palm of a manual worker or on the sole of the foot of a jogger. Changes also occur as a result of intrinsic influences, such the characteristic deep furrows seen in dermatosis, or stretch marks—the fractures of the dermis that occur during pregnancy (Figure 1.17). The morphology of the skin may vary significantly, but it is invariably woven into a framework of polyhedral shapes. They are simple, fundamental, and irregular, and yet are rarely described in anatomical literature. These observations raise more questions.

• Why is the surface of the skin composed of polyhedral shapes? • Why is the cutaneous surface not perfectly smooth?

Figure 1.17 Varying skin patterns from different parts of the body (5 ×) A The shoulder B The palm C Digital pulp D The abdomen (stretch marks) E The thigh F The sole G Young skin H Aging skin

The epidermis The epidermis has small polyhedrons imprinted into its surface, all of them irregular and different but limited to three, four, or five sides. Each side measures about 500 µ, with lines of about 50 µ wide between the polyhedrons. No one polyhedron looks like its neighbor, and their distribution is very irregular. These polyhedrons move in three dimensions (Figure 1.18 and Video 1.4), and as they move we can see changes, even at the surface, that indicate that their organization is probably fractal: one polyhedron fits inside another and each small polyhedron adjusts to its neighbor inside the bigger one. KEY STATEMENT The surface of the skin seems to be a complex mosaic pattern of irregular polyhedrons (Figure 1.19).

When the skin stretches and creases during everyday activities, these small polyhedrons move. Their shape and appearance change, and when the forces are removed they return to their initial state. Each movement performed during everyday life induces these imperceptible and generally unnoticed changes. Yet on closer observation we can see lines of force that change from vertical to horizontal, then become blurred and less distinct, and reappear, depending on the degree of pressure exerted on the skin.

Figure 1.18 The surface of the skin is malleable in all three dimensions (65 ×) Video 1.4

This diversity becomes more impressive as we draw the operating microscope closer. However, it is more difficult to take clear photographs close up, because the depth of field is reduced and fine movements within the patient, resulting from breathing and pulsations at rest, are amplified.

Figure 1.19 A Irregular polyhedrons on the surface of the skin (40 ×) B Zooming in, we see the same polyhedral irregularity inside the larger polyhedrons (65 ×)

Nevertheless, with careful observation we can see these changes on video recordings while playing the video in slow motion, especially at high magnification (Figure 1.20 and Video 1.5). The response to the constraint imposed by the applied physical force is obvious. Moreover, inside each polyhedron we can observe other subunits, with varying dimensions and forms, that remain inactive until the tension overwhelms the fibers and gives rise to their final shape. The furrows that mark the border between adjacent

polyhedrons align themselves in the direction of the applied stress, constituting lines of force.

Figure 1.20 Between their resting position and the end of the applied mechanical constraint, the polyhedrons at the surface of the skin change their shape, and new lines of force appear. (100 x) Video 1.5

If we look closely as traction is applied to the polyhedrons, we see the furrows that separate them spread apart as they adapt to their changing shape. These furrows between the polyhedrons can widen or shorten, and neighboring polyhedrons often overlap each other (Figure 1.21 and Video 1.6). This is evidence of a global system that is adaptable and capable of change. However, as soon as the constraint is removed the system returns to its original configuration, as if from memory and with unerring precision. Everything within the system is homogenous and coherent. It is probably fractalization that facilitates the dispersion of the mechanical constraint.

Figure 1.21 The cutaneous polyhedrons display individual movements. They bump into each other, move closer to one another, and disappear and reappear, and their boundaries shift and change (100 ×) Video 1.6

This dynamic behavior, based on fractal organization, is a fascinating phenomenon and will be described further in Chapter 5. It can be easily observed in heavily exposed skin, like the skin of the palm, where wrinkles are particularly visible (Figure 1.22).

Figure 1.22 Smaller polyhedrons move inside the large polyhedrons. This phenomenon is known as fractalization (65 ×)

The gymnastic agility of the polyhedrons, their apparent mechanical ability to change form and orientation, and the occurrence of unexpected lines of constraint suggest the existence of physical links between the surface of the skin and the depths of the epidermis. The photographs in Figure 1.23, taken through an endoscope in direct contact with the tissue, show a cross-section of living skin. The epidermis is structured as we would expect it to be, that is to say by fibers that form convergent lines of force along axes that run from the surface of the skin to the dermis in a more or less vertical direction. There is a close relationship between the floor of the interpolyhedral furrow in the epidermis and the depression in the surface of the basement membrane. When the furrows on the epidermal surface of the stratum corneum are not too pronounced, the underlying strata—the stratum granulosum, stratum spinosum, and stratum germaticum—are reshaped into non-prominent arches. When the epidermal surface of the stratum corneum is deeply furrowed, this reshaping of the underlying strata is more pronounced.

Figure 1.23 A The furrows between the polyhedrons correspond with irregular lines of force that are more or less vertical, and that originate in the epidermis and dermis (100 ×) B The architecture of the surface of the epidermis appears to be influenced by structures deep in the dermis. These lines of force can be seen in a cross-section of the epidermis (100 ×)

KEY STATEMENT The epidermis has an intimate, fibrillar morphodynamic architecture (Figure 1.24).

Figure 1.24 Representation of how the fibrillar network shapes and fashions the surface of the epidermis within which the epidermal cells are embedded (130 ×)

The surface of the epidermis is not like a smooth tiled floor, but more like a chaotic mosaic structure. This cutaneous architecture is not inert. It is living and under constraint, with fractal and irregular disposition of the fibers. It always returns to its original position, with perfect tissue memory.

The dermis Cutting through the epidermis and part of the dermis allows us to confirm our initial observations. Deep inside the dermis we find microfibrils that penetrate and infiltrate the matrix of the dermis, where they exert an influence on its shape. We call these structures microfibrils, because they are visible only at 10 × magnification (Figure 1.25).

Figure 1.25 These fibers arise from the subcutaneous area and penetrate deep into the reticular dermis (65 ×)

How do these microfibrils, rooted as they are in the depths of the subcutaneous tissue, give rise to irregular polyhedrons at the surface of the skin? KEY STATEMENT There are identifiable physical links between the skin surface and the deeper structures, which permit flexibility of the skin.

In certain cross-sections of the epidermis and dermis, you can see clearly the fibers that pass through the dermis, the basement membrane, and the epidermis, and extend into the furrows between the epidermal polyhedrons. Microfibrils cross the lamina densa and the stratum basale and shape the epidermis and its surface (Figure 1.26). This physical link can be clearly seen on photographs, but the interrelationships between the epidermis and the uppermost area of the dermis, the papillary dermis, are more complex than would be expected. A network of capillary vessels exists in the area between the deep portion of the epidermis and the papillary dermis.

Figure 1.26 A and B Cross-section of the dermis and the epidermis, showing fibers passing through the dermis and the epidermis in a vertical direction, further demonstrating continuity and suggesting complex interrelationships (100 × and 130 ×)

If we remove the epidermis, we find that the surface of the dermis is similar in appearance to that of the epidermis, with polyhedrons and furrows, but not identical. This is because they are both irregular, three-dimensional structures with oblique axes (Figure 1.27).

Figure 1.27 A Post-traumatic dermis fingertip surface, showing similarity to the epidermis pulp surface above (40 ×) B The surface of the dermis of an in vitro sample (40 ×). (Preparation by J.-P. Delage.)

Our observations show that the imprint of the furrows on the dermal surface does not exceed a depth of more than 2 mm. It seems that at greater depths than this, the extracellular matrix is shaped differently and is more irregular. Blood vessels and nerves are incorporated everywhere within this structure via a system of vertical, horizontal, and oblique networks ending with vascular loops called papillary ridges, which are also quite varied in shape (Figure 1.28).

Figure 1.28 A Papillary blood vessels, which comprise the vasculature of the dermis (100 ×)

What impresses us most in this world of great mobility is the general suppleness of the epidermis and the dermis, which can be folded and manipulated. There is no stratification and no separation between them (Figure 1.29A). The movement of the dermis is continuous with the movements of the epidermis and the hypodermis within this interwoven maze, where nerves and vessels coexist in harmony with the fibrillar network (Figure 1.29B and Video 1.7).

Figure 1.28 B The integration of epidermal cells and vascular loops within the fibrillar structure

Figure 1.29 A and B The suppleness of the epidermis and dermis is amazing, considering the dense, irregular fibrillar organization and connections within it that eliminate the idea of separate layers (100 ×). The presumed mobility of the dermis. (65 x) Video 1.7

Inlaid in the depths of the reticular dermis are fatty lobules that are in total physical continuity with each other within the fibrillar network. Note that there are no stratified or separate layers of tissue between the epidermis, the dermis, or the hypodermis. Let us continue our exploration.

The hypodermis Once the dermis and epidermis have been crossed, a greater mobility of structures within the hypodermis is evident. Fat lobules under tension rapidly bulge out between the superficial veins, emerging like bright yellow icebergs between the sectioned edges of the reticular dermis, under the influence of internal pressure (Figure 1.30 and Video 1.8).

Figure 1.30 As soon as an incision is made, fat lobules appear, like icebergs emerging from the sea (5 ×) Video 1.8

The vascularization is continuous between the reticular network and the papillary network (Figure 1.31). And contrary to what is often believed, the fibrillar continuity between the reticular dermis and the hypodermis is also total (Figure 1.32).

Figure 1.31 There is total fibrillar continuity between the reticular dermis and the hypodermis. The vascular supply is continuous and uninterrupted between the dermis and the hypodermis (10 ×)

Figure 1.32 There is no discontinuity between the dermis and the hypodermis. The dermis cannot be peeled away or separated from the hypodermis. There are no separate tissue layers (13 ×)

Fatty lobules look like little olive-shaped balloons (Figure 1.33). Their diameter varies from several millimeters to as much as 1 or even 2 centimeters. Although the size of the lobules varies considerably, they are consistently smooth in appearance and rounded in shape (Figure 1.34).

Figure 1.33 Fat lobules display a variety of sizes but maintain a similar shape (10 ×)

Figure 1.34 Fibers and fibrils frame and likely shape the fat lobules (20 ×) . There is complete tissue continuity.

The fibrils that leave the dermis are continuous with those that enter the fat lobules. These lobules are embedded deep in the reticular dermis and are in total physical continuity with each other within the fibrillar network. Fibrils surround the lobules (Figure 1.35). They ensure mobility between them, penetrating them and merging with the intercellular structures. In this way, the fibrils contribute to, and help to determine, the form of the lobules framing the adipocytes within them. The fibrils also extend toward the superficial fascia, which influences the functional and morphological properties of fatty tissue.

Figure 1.35 Fibers penetrate each lobule. They influence the arrangement of the adipocytes inside the lobules and determine their shapes (65 ×)

The mobility of the millions of adipocytes within each lobule during externally applied movement is fascinating. There is complete and total harmony between them as they flatten, dilate, turn, and twist within the spaces that contain them, without separating or dissociating from each other when external constraint is applied by the surgeon (Figure 1.36 and Video 1.9).

Figure 1.36 The adipocytes all move at the same time, supported by the fibrillar network. They are embedded in the fibrillar network (100 ×) Video 1.9

The adipocytes are not all exactly the same color (Figure 1.37). Adipose tissue can be white in certain areas in some patients. It also displays different shades of yellow, from pale yellow to bright buttercup to tawny. From our study of tissue samples under the scanning electron microscope, it would seem that the brown cells are in fact immature multifunctional cells with big nuclei, which are also capable of producing collagen. We are only at the dawn of our understanding of this cellular diversity.

Figure 1.37 Even fat lobules close to each other can be of different colors. The reason for the difference in color is unknown (40 ×)

Superficial fascia Situated within the hypodermis, and continuous with the fibrillar system extending from the dermis, we find the so-called superficial fascia. It is often difficult to distinguish the superficial fascia from the hypodermis, or to separate them surgically (Figure 1.38). Some 20th century authors observed this continuity and began to question the concept of separate tissue layers within the body.10 KEY STATEMENT The superficial fascia can be described as fibrillar reinforcement and a densification of the fibrillar network, but it should not be thought of as a sheet separated from other structures.

Figure 1.38 The superficial fascia can be described as a densification of the fibrillar network within the hypodermis. It contains few cells (10 ×)

Tissue continuity with adjacent structures is total. Cutting into the superficial fascia leads to a marked widening of the gap formed by an incision of the dermis. The role of the superficial fascia could therefore be to maintain stability of form by holding the rest of the hypodermis under tension.

Subcutaneous tissue Beyond the superficial fascia and the hypodermis, the tissues become increasingly supple with a greater capacity for sliding, because here the multimicrovacuolar system is composed of longer, less rigid fibers and the interfibrillar spaces are bigger. It is this relatively slack zone that contains the veins, arteries, and nerves. This is traditionally called the areolar connective tissue. Anatomists have long been aware of the existence of a gelatinous tissue beneath the hypodermis. This tissue appears to have no structure or form, and was initially called ‘honeycomb’ or ‘cribriform’ tissue, because it seems to be full of holes (known as Richet’s areolae; Figure 1.39).11 At the beginning of the 19th century, this tissue was found to contain small compartments, which were known as ‘logia’ or ‘cellula’, and for that reason it was also named ‘subcutaneous cellular tissue’.12 However, the structures found in this tissue are not cells containing a nucleus and cytoplasm, and this

erroneous nomenclature caused a great deal of confusion. Eventually, it was renamed ‘loose connective tissue’ or ‘areolar tissue’. The loose connective tissue is situated in the area beneath the hypodermis, just above the deep fascia that surrounds muscles, and it can also be found surrounding tendons, where it is known as the peritenon or paratenon. These are areas of great mobility within the body, and the role of loose connective tissue is to facilitate muscle contraction and the sliding movement of tendons (Figure 1.40 and Video 1.10). We can now enter the realm of active movement.

Figure 1.39 Richet areolae (5 x). (After exposure to atmospheric air in the operating theater.)

Figure 1.40 Fibrillar continuity between the depths of the hypodermis and the subcutaneous tissue surrounding the premuscular aponeurosis (2 ×) Video 1.10

Deep fascia The premuscular aponeuroses, or so-called deep fascia (fascia profunda), are found beneath the subcutaneous tissue (Figure 1.41 and Video 1.11). This is a different area of fibrillar densification, thicker and tougher than the superficial fascia. It is almost entirely composed of tightly woven fibers, as are the intermuscular septa. It surrounds and envelops the muscle, supporting and holding it in place when it contracts. The rigidity of the fascial envelope prevents the dispersion of energy as the muscle contracts, thereby ensuring optimal contraction of the muscle fibers. Energy loss is minimized, and the muscle contraction is more efficient, because the forces are directed longitudinally through the muscle to the tendon. This and other aponeuroses, as well as the deeper fascia, are completely continuous with surrounding structures. Notice that these fascial structures, be they aponeuroses or septa, are simply densified areas of the same fibrillar tissue, which confer strong internal tissue tension. The tension varies according to their functional role. They can be

identified as separate structures, but solely on the basis of varying fibrillar densification. They all arise from the same fibrillar system but are structurally organized in different ways, as well as comprising varying proportions of collagen and elastin fibrils (Figure 1.42).

Figure 1.41 Premuscular aponeurosis: fascia profunda or deep fascia (also known as investing fascia) (2 ×) Video 1.11

Figure 1.42 Aponeuroses or septa are densified areas of the same fibrillar network. However, their structure differs because of their different functional roles A Premuscular aponeurosis (10 ×) B Intermuscular septum (10 ×). (Note the presence of several clusters of cells that are yellow.)

The architectural unity of this fibrillar system is total, but here we have an example of its capacity to diversify. Further examples of this diversification include ligaments and joint capsules. Below the premuscular aponeurosis, we find a looser microvacuolar system with bigger microvacuoles and fibers that are less rigid. This is the beginning

of the epimysium, which is found in the area immediately surrounding the muscle (Figure 1.43).

Figure 1.43 Beneath the premuscular aponeurosis you can see the epimysium, which is continuous with the perimysium. There is no discontinuity between them (10 ×)

Muscle Once we have cut through the skin, the muscle is not far below. It can be distinguished by its purple color and stringy texture, and it contracts as soon as we use the electrosurgical scalpel. Muscle is often viewed and therapeutically treated as though it is an entirely distinct and separate entity from neighboring anatomical structures. However, because it is surrounded by the connective tissue that we call epimysium, which are fibers that are continuous with those in the hypodermis, and therefore in continuity with the surface of the skin, muscle cannot be considered to be separately distinct. The epimysial fibers also enter, combine with, and penetrate deep into the perimysium, which separates, yet connects, the bundles of muscle fibers. Once again, we see that everything is connected and that there is no break in continuity (Figure 1.44).

Figure 1.44 The epimysial fibers are continuous with those extending into the hypodermis. They are therefore in continuity with the surface of the skin (5 ×)

To reach the muscular structures, you have to peel away the epimysium that ensheathes the muscle. On examination of the areas between distinct muscle groups, we observe again a continuous link between the muscles, created by the intertwining and interweaving of more of the same opalescent fibers (Figure 1.45). There are no sheets of tissue layers or sublayers. KEY STATEMENT The epimysium, perimysium, and endomysium together form one continuous structure. In contrast to the lengthened, longitudinal, and parallel aspect of the muscle cells, their architecture is neither parallel nor regular.

Figure 1.45 Perimysial fibers connecting muscle fascicles (13 ×)

Let us take a closer look at how the perimysial fibers surround, penetrate, and encircle the bundles of muscle cells (Figure 1.46). What is surprising is the impression of tissue fusion between the collagen fibers and the muscle cells within these bundles, while at the same time the muscle cells and the collagen fibers maintain an apparent anatomical independence. The muscle cells nestle within this fibrillar architecture in the same way that the adipocytes nestle within the fatty lobule. It would seem that the collagen fibers mold and shape muscle cells as a result of their intimate architectural relationship (Figure 1.47).

Figure 1.46 A closer look at the perimysial fibers where they penetrate the fascicles of muscle cells. (20 ×)

KEY STATEMENT Could it be that we have identified a fractal organization that provides a link between the muscle fibers, the epimysium, the perimysium, and the endomysium? If so, we would then be dealing with a coherent, global, functional tissue rather than with separate histological entities.

Figure 1.47 Muscle cells nestle within this fibrillar architecture (65 ×)

Sliding systems around tendons The sliding systems around tendons provide the ideal areas in which to study and understand fibrillar organization and behavior, because the fibrillar densification is low and there are relatively few cells. Two things are immediately evident: • the wide variety of vessels around the tendons, and •

the fact that, during movement of the tendon, the surrounding tissues remain stable and are not affected by the movement of the tendon, so there must be some kind of force absorption system.

One might think that, because all the structures are interconnected, the movement of any given structure would be directly transmitted to the surrounding tissues in a linear way. However, this is not the case, and we see that separate anatomical structures move at different speeds. For example, blood vessels accompany the sliding movement of tendons to ensure a constant blood supply to the tendon. Individual vessels within the same network move at different speeds, and can also move closer together or further apart. These different movements are dictated by the precise physiological requirements of each anatomical structure during movement. The multifibrillar network, which links these individual structures, allows them to move independently within the fibrillar framework (Figure 1.48 and Video 1.12).

Figure 1.48 Different speeds of progression exist within the same matter (area) and yet there is total vascular continuity (5 ×) Video 1.12

In the video, by looking at a Y-shaped blood vessel we were able to approach the problem more simply. The blood vessel had two branches, 1 and 2, with connections at the bottom at point A, and at the extremities B and C.

Analyzing the movement more closely, we observe that during flexion the two large vessels, 1 and 2, are indeed moving apart. However, compared with a smaller vessel, number 3, not only do they move faster but the two branches move at different speeds, because the distance between B and C has doubled. So several forms of speed and progression of distinct anatomical structures seem to coexist in homogeneous living matter. How can this be explained? It used to be thought that the only rational explanation is that several coaxial layers of connective tissue with progressively decreasing diameters are sliding between, tethering, and supporting the vascular structures. But this reductionist linear thinking no longer fits with what recent research has taught us about the human body. In vivo observation has rendered this supposition invalid, because it is surgically impossible to define a clear dissection plane between the paratenon and the tendon (Figure 1.49). There are no distinct laminated layers with stratified strips neatly stored next to each other. The traditional concept of several coaxial, conjoined layers with progressively decreasing diameters, which had long been used to explain the movement of tendons, relied on the theoretical concept of a virtual space between the layers. This mechanical phenomenon had been studied very little, because the problem had been considered by many to have been solved by the concept of the tendon sliding in its sheath, without touching the sides, like a bullet in a gun barrel. This theory of annular layers sliding together supposed the existence of a hierarchical histological distribution. We now know that no such hierarchical histological distribution exists, which means that we need a new way of thinking. We need to consider the problem in terms of global dynamics and continuous matter. If everything is connected, if everything moves at the same time in different ways, we must be able to explain how all the components connect and adapt to each other during movement.

Figure 1.49 During in vivo observations we are confronted with the fact that there is a microanatomical network of fibrils between the tendon and the surrounding tissues. This prevents a clear dissection between the tendon and the paratenon. The fibrils in this network surround and penetrate the tendon (5 ×)

KEY STATEMENT We must develop a theory that addresses the concept of a tissue continuum. This is in total contradiction to the traditional view of sliding structures.

How can we explain this ability of structures that are so close together to move in different planes and at different speeds? To answer this question, we needed to improve our knowledge of the tissue surrounding the tendons, its properties, and its different roles. In vivo video observations opened up this hitherto inaccessible microanatomical architecture to reveal a glossy, gel-like tissue surrounding the tendon (Figure 1.50 and Video 1.13). We can see that collagen fibers are disposed in random fashion within the glossy matter, criss-crossing the tendon and incorporating the blood vessels. We are faced with a new concept, that of global dynamics, with the presence of continuous matter between the

tendon and the surrounding tissue. The glossy matter referred to above is in fact loose connective tissue, situated between the tendon and neighboring anatomical structures.

Figure 1.50 This sliding tissue, often called the peritenon or paratenon, is in fact made up of fibers (10 ×) Video 1.13

When you look closer, you can see tissue containing pseudogeometrically shaped fibrillar structures or microfibrils surrounding tendons or aponeuroses (Figure 1.51 and Video 1.14). These microfibrils may be quite wide, with sharp edges, like knives, and with translucent surfaces, but they can also be narrow, long or short, swollen or cylindrical. Diversity is everywhere, and there is endless variety. We can see ropes, rigging, harnesses, transparent sails, and dewdrops, with rings that reinforce the solidity of some fibers like an articulated bamboo stem. Tissue continuity is total; the blend is homogeneous and the organization completely irregular, disordered, and fractal. Smaller fibrils are found between larger ones of a similar nature, and so on...

Figure 1.51 The sliding system is made up of fibers that penetrate the tendon. The fiber arrangement is polyhedral in appearance, and the fibers display a specific type of behavior. (5 X to 100 X) Video 1.14

This glossy tissue surrounding the tendons is composed of intertwining multidirectional filaments creating partitions that form microvacuolar volumes. We at one time named this the multimicrovacuolar collagenic absorbing system to emphasize its functional and architectural role. This three-dimensional tissue network is a continuous structure composed of billions of microvacuolar volumes. The basic unit of this sliding framework is the microvacuole (Figure 1.52 and Video 1.15).

Figure 1.52 Animated diagram of the peritendinous fibrillar organization of the multimicrovacuolar collagenous absorbing system Video 1.15

As we have already mentioned, the microvacuoles measure a few microns to a few hundred microns in diameter and are organized in a dispersed, branching, and fractal pattern. Apart from some adipocytes and fibroblasts, there are relatively few cells in this multifibrillar network. Our most extensive study of the mechanical behavior of fibrils within this network has been undertaken in the connective tissue around tendons. We will therefore describe the disposition and the dynamic behavior of these fibers within the sliding systems in Chapter 3. Tendons The anatomy of tendons varies and depends on the specific location and function of each tendon. An extensor tendon of a toe has almost the same form as a flexor tendon of a finger, but the size and shape are different. It is impossible to show the range of this diversity in a few illustrations, and we do not claim to do so in the following photographs. However, we would like to emphasize that such diversity exists. We also noted that cells are few in

number. If you remove the areolar tissue that constitutes the sliding system surrounding a tendon, the exposed tendon appears to be formed of white bundles, or fascicles. Fascicles are composed of bundles of fibers, which themselves are made up of fibrils, which seem to be arranged longitudinally and parallel to each other (Figure 1.53A). But we do not always find this longitudinal, parallel arrangement of fascicles inside the tendon; instead, intersection of fascicles occurs frequently. Between the fascicles, we find a fibrillar web linking them together. (Figure 1.53B). The vascularization of the tendon adapts to the density of the weave of the fibrillar web linking the fascicles and to the functional constraint that the tendon has to deal with. Therefore fibers in a tendon are not strictly parallel. Their arrangement is irregular, with cross-links, and their structure is more like that of a liana than that of a fiber-optic cable.

Figure 1.53 A The fascicles inside the tendon seem to be arranged in a longitudinal and parallel manner. However, this is not strictly true (20 ×)

Figure 1.53 B Tendons are composed of fascicles, which are bundles of fibers themselves composed of fibrils. All these components are linked (and interconnected) by a non-linear fibrillar network (40 ×)

Periosteum and bone Our in-depth general structural exploration now moves to the periosteum and bone. It is more difficult to approach the periosteum with an endoscope than to explore the sliding spaces. The periosteum is also composed of fibers, but they are thicker and more densely woven than those previously described. They are certainly more complex from a chemical point of view. KEY STATEMENT The periosteum and bone are an integral part of the body-wide fibrillar network (Figure 1.54).

Figure 1.54 The periosteum is composed of thicker, denser, more tightly woven fibers that penetrate the cortical bone (20 ×)

The transition between the periosteum and cortical bone is progressive with a gradual mineralization. At various points, there are strong connections known as Sharpey’s fibers. Cortical bone is an apparently lamellated structure composed of mineralized fibers arranged more or less parallel to each other (Figure 1.55).

Figure 1.55 The organisation of cortical bone tends to be lamellated, with mineralized fibers (40 ×)

Within cancellous bone, we discover an organization that is very like that of the dermis but with extreme densification of the fibrils and vascularization parallel to the cortex. Then, little by little, as you travel deeper into the bone, the fibrils become more loosely packed and the same multimicrovacuolar structures appear, often described as honeycomb-shaped (Figure 1.56).

Figure 1.56 The structural organization (architecture) of cancellous (spongy) bone is characterized by intertwining, intersecting fibrillar polyhedrons that form a polyhedral framework resembling a honeycomb (40 ×)

The acceptance of the notion of bone as part of a fibrillar system allows us to better understand this Haversian system of organization, composed of concentric lamellae that branch off in different directions and that are in total continuity with each other (Figure 1.57). The formation of concentric circles within the fibrillar chaos may be difficult to understand in terms of rational

reasoning, but we will see later in Chapter 7 that it is not only possible but also relatively simple.

Figure 1.57 Cross-section of bone, showing Haversian canals. The complex construction of the Haversian canals can be explained by (is the result of) a different type/kind of modeling of the fibrillar network (40 X)

Nerves The distribution of fibers around the peripheral nervous system is also surprising. It is similar to that of tendons because, although nerves play no active mechanical role in movement, they do move transversally and longitudinally during the movement of surrounding structures. Nerves are mobile! The length of the ulnar nerve increases by as much as 15 percent when the elbow is flexed compared with when it is in extension, and the median nerve can move as much as 1 centimeter laterally within the carpal tunnel. Surrounding the nerves, we find the epineurium (Figure 1.58)—the same system as that surrounding the tendons and with the same movement of fibrils. Within the nerves, the fibers spread out between the fascicles to form

the perineurium (Figure 1.59). This is continuous with the fibrillar network found at the periphery of the nerve.

Figure 1.58 The epineurium surrounding nerves shares the same fibrillar architecture as the paratenon (10 ×)

Figure 1.59 The perineurium divides and penetrates the nerve fascicles to form the endoneurium and is continuous with the network that forms the epineurium (40 ×)

These observations are already challenging the traditional view that structures such as axons and the perineurium have different embryological origins and grow and develop independently (i.e. axons from the ectoderm, and the perineurium from the mesoderm). Vessels We find among the arteries and veins more of the irregular and continuous disposition of fibrils, which allows us to better understand the eccentricity of the vascular patterns that we come across. KEY STATEMENT The microcirculation is an integral component of the multifibrillar network (Figure 1.60).

Figure 1.60 This vascular network is part of the microcirculation of this nerve (10 X)

During microsurgical dissection, careful separation of vascular structures is often required. We create a surgical plane separating the tissues, but this plane is not an anatomically natural one. The sliding system extends into the walls of the arteries and veins (Figure 1.61). The tissue layers—the tunica adventitia, the tunica media, and the tunica intima, are organized in roughly the same way as the epidermis, dermis, and hypodermis. Differences in densification and cellularization ensure that different roles can be performed, either resistance or the transmission of information.

Figure 1.61 The sliding system found at the tendon sheaths also shapes the tunica adventitia (outer layer) of the veins and the arteries A Fibers emerging from or merging into artery wall (20 ×) B Network of fibers penetrating vein wall (13 ×)

Lymphatics We started to explore the lymphatic system in vivo, but we discovered that it is not as simple as the system described in anatomy books. In the distal parts of the system, near the cells, it is not possible to clearly identify lymphatic structures, because any fibrillar structure we find is likely to be part of the lymphatic system. At more proximal sites, for example near the radial or ulnar vascular pedicles, we identified longitudinal structures that are apparently tubular and resemble ducts. They are neither arterial nor venous, and so they could be lymphatic structures. But their organization is not simple; they do not seem to be simple, hollow tubular structures like the lymph ducts described in anatomy books. They appear to be sponge-like structures. It is easy to identify the lymphatic system in the axilla, but as we move more distally it becomes more and more difficult to identify these increasingly delicate structures (Figure 1.62). Further research needs to be undertaken to enable us to understand how the extracellular system is drained.

Figure 1.62 Dissection of a lymphatic vessel around the ulnar artery, showing the flow of lymphatic fluid (5 ×)

Our impression is that the tubular, duct-like vessels in the proximal part of the lymphatic system are preceded more distally by structures that are not hollow tubes but actually sponge-like structures, and that the traditional images of neatly arranged tubular lymphatic vessels accompanying arteries and veins around the cells are highly questionable (Figure 1.63).

Figure 1.63 Microsurgical dissection of the distal lymphatic vessels reveals a spongy type of tissue, as opposed to any hollow, tubular structures. Further research is needed (65 ×)

Cells The majority of spaces are filled with cells with specific functions, but their distribution is not uniform. However, where cells are found we find the same fibrillar network around them. What seems clear is that the extracellular system serves, at a minimum, as a scaffolding for cells.

In later chapters, we will explain in more detail the physical links between the cells and the fibrillar network. But, for now, know that when we apply traction to the fibrils that surround a group of cells, we see that not only do the cells move but they also change shape: they flatten and lengthen. KEY STATEMENT The fibrillar network has an undeniable influence on the cytoskeleton within the cell.

SUMMARY Globality With only the evidence presented so far, we can already see that a tissue continuum extends into every area of the body, at every level. There is total fibrillar chaos, and this fibrillar chaos is found in every nook and cranny of our bodies (Figure 1.64).

Figure 1.64 This fibrillar tissue continuum extends into every area of the body at every level A The extensor tendons in the hand (10 ×) B The abdominal area near the rectus abdominis muscle (10 ×) C The dorsal area, beneath the latissimus dorsi muscle (10 ×) D Between the breast and the pectoralis major muscle (5 ×) E In the scalp (5 ×) F In the region of the hamstring muscles in the leg (5 ×)

Even structures that are not generally associated with movement, such as nerves, blood vessels, and the periosteum, are composed to a greater or lesser extent of these fibers. This fibrillar network seems to exist throughout the body. Is this fascia? In anatomy, the term fascia is defined as the physical connection that unites all parts of the body. This definition is very close to that of connective tissue, also called areolar or loose, which is said to support, connect, and separate different types of tissue and to be involved in the coordination of movement. But the understanding of what the definition of fascia comprises varies in different parts of the world. It ranges from a simple densification of tissue (such as the superficial fascia) to a solid, myotendinous structure (such as the tensor fascia lata). The term fascia is now very frequently used, but there is a lack of agreement on a precise, allencompassing definition of the term. This creates confusion from both the anatomical and the therapeutic perspectives. Traditionally, form has been used to describe the outward appearance of the body. Perioperative endoscopy enables us to study the internal architecture of the human form. The body’s internal architecture seems to be an ideal mesh made up of fibers, fibrils, and microfibrils, along with microvacuolar spaces that are colonized by cells to a greater or lesser degree (Figure 1.65 and Video 1.16).

Figure 1.65 Illustration of a continuous fibrillar architectural organization from superficial to deep Video 1.16

We believe fascia to be the continuous fibrillar network that extends from the surface of the skin to the nucleus of the cell. However, we will spare use of the term until all facets of this fabulous structure have been fully covered in the rest of this book.

RED THREAD QUESTIONS Endoscopic exploration has shown us that there is overall tissue continuity provided by a body-wide multifibrillar network in which there is no apparent order. This presents us with the following six key questions, which we address in the following chapters. We have called these ‘red thread’ questions; in the Greek legend of Theseus, Ariadne’s red thread enabled the former to find his way out of the labyrinth after slaying the Minotaur. RED THREAD QUESTIONS

1. How is this tissue continuity structured, and how do these fibers ensure tissue cohesion? How do they come together to create a structured form? 2. How can this fibrillar continuity permit two dynamically opposed roles, ensuring simultaneous mobility, absorption of forces, and sliding, while having no effect on surrounding tissues? 3. How do these fibers adapt to provide simultaneously mobility and uninterrupted energy supply during physical effort? 4. How do these fibers, which are under tension, preserve volume and maintain the shape of our bodies? 5. How can such an apparently chaotic fibrillar system, which contains such a diversity of shapes and combinations of fractal and chaotic patterns, result in coherent and efficient movement and ensure the return of tissues to their resting position after movement? 6. Can nature restore harmony to the multifibrillar network when it is subjected to forces that exceed normal physiological limits, as in pathology or as a result of trauma?

Any attempt to explain the morphological dynamics of living matter should be able to provide the answers to these questions. And finally, having by the end of the book answered these six key questions, they give rise to a major new overriding question. If the same multifibrillar architecture is found throughout the body, from the skin to the muscle and from the tendon to the periosteum, permitting constant intra- and interfibrillar movements and housing cells of different specifications, could the role of this fibrillar architecture be more important than has previously been supposed? Could it be that the connective tissue is not just inert packing tissue but the constitutive tissue from which the organs are developed? If we were to find this to be the case, it would be a significant paradigm shift.

Comment by Thomas W. Myers, LMT

The first glimpse of Dr. Jean-Claude Guimberteau’s unique imagery of living fascia at work in the body—mine was probably 10 years ago—strikes the viewer as unbelievable. There must be some trick or joke here—this cannot be the reality of tissue. But the unbelievable, when it is right in front of one’s eyes, requires a shift of fundamental premises. As a result of studying these films, my ideas have changed, my teaching has changed, and my touch—already honed from 30 years of manual therapy practice—was compelled to change as well. When I comprehended the fluidity and adaptive nature of what Guimberteau calls the sliding system, I stopped trying to ‘stretch’ fibrous tissue and was able to use my touch in a much more gentle manner along very precise planes to persuade adhesions to loosen and to promote healthy movement in the tissues. Structurally oriented therapists are not stretching mechanical ropes, wires, and fabric as if tuning the rigging of a sailing ship. In light of Guimberteau’s audacious exploration, we can now see that we are really altering the sol—gel state of the mucopolysaccharides, and thus the ‘flow’ of interstitial fluids, neural messages, and mechanical forces in the living matrix of tissue. To touch the surface is to stir the depths. We are in the midst of a fundamental rethinking of how we move—or, more fundamentally, ‘what moves’. We know body movement has to work biomechanically, thermodynamically, and hydrodynamically. We know it has to work cellularly, from the massive proliferation and diaspora in the embryo, through the short sharp shock of moving from the womb to the ‘air world’ at the moment of our first breath, to function in the adult as 70 trillion humming units surrounded, protected, and encased by the extracellular matrix. How? From the pia mater to the interosseous membranes, we have seen that matrix in books: tough and dry. We have seen that matrix in cadavers: unstretchable and adhered. Even in untreated cadavers, the fascia lies passive. To journey into the living body with Dr. Guimberteau is to wonder at a previously inert tissue come to dynamic life. Seeing the poetry of the dewy strings with shifting attachments and bubbly membranes is to understand anew how the body deals with movement—specifically with when to slide and when not to slide. The act of making any image illuminates one thing by excluding something else from view. Our traditional way of parsing the cadaver in anatomy has been tremendously useful, of course, but it has obscured our knowledge of what is between things, as ‘between things’ is exactly where we slipped our scalpel to reveal more defined structures. But between more durable structures is also precisely where the movement

happens, so our fundamental misunderstanding of movement has persisted until Guimberteau showed us the simple but startling reality. The idea of fascial continuity has been abroad in the world for some time. My own published work has been an attempt to map functional and stabilizing connections among the muscles, following the grain of the fabric through the parietal myofascia. Such maps as the Anatomy Trains—and there are a number—make predictions that lead to innovative strategies for chronic difficulties in posture and movement, a small part of a larger cultural movement to halt reductive parsing and look at the synergetic properties within systems as a whole. What Jean-Claude Guimberteau has done is far more profound: he has discovered what amounts to a ‘new’ system—which, once seen, becomes obvious—of how a colony of cells such as ourselves actually manages the ‘disruption’ of movement, a disruption between cells that must happen a million times a day in even the most sedentary person, without breaking cells, tearing tissue, or interrupting flow. We have for centuries contented ourselves that the ‘muscles fired by nerves move bones across joints limited by ligaments’ model explained human shape and stability. Osteopaths, Rolfers, and some others paid lip service to the idea of the body-wide fascial net but still explained therapeutic effects in terms of the biomechanics of levers and forces generated by individual muscles working from end to end via tough, identifiable connective tissue structures. By now, it is clear that this model is inadequate to the task, and that to progress beyond its current limitations biomechanics is going to need to include the implications of tensegrity engineering, fractal mathematics in fluid flow, and cybernetics in the play of individual neuromotor units. Guimberteau’s explorations reveal a highly adaptive system of fluids, gels, and fibers everywhere across the body that respond instantly and internally to the forces applied to them, mitigating any damage to the cells in the moving area and distributing strain efficiently into the tissues under the skin. We are very aware when we see the femoral artery that it is part of a larger circulatory system. Likewise, the brachial plexus can be identified as a structure, but it is also clearly part of the whole nervous system. But those of us who labor in biomechanics often work on the Achilles tendon, semispinalis, or thoracolumbar fascia as if they were independent structures, without the same awareness that these structures exist within a third body-wide effective system—the fascial web—equally dynamic and as autoregulatory as the other two. Through Guimberteau’s images and research, we now see a body-wide continuity of biomechanical response, far more fluid, chaotic, and self-organizing than we have previously conceived. Future generations will say ‘Of course’, dismiss our mechanical model as quaint, and build on his pioneering insights. But I am glad to have been of this generation, and to have been shocked, humbled, delighted, and finally changed by the arresting and important images Dr. Guimberteau brings back from his journey to see for himself.

2 Fibrillar Continuity and Form The structuring role of the multimicrovacuolar network The fibrillar frame The concept of structured form Following the red thread

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY In this chapter we will show how living matter is organised within a continuous fibrillar network. We will describe the structuring role of this network, which contributes to the construction and shape of the body and provides a framework for the cells. This implies an underlying organisation, an architecture, and a permanent, continuous link between the constituent structures. The architecture of this network is disconcerting, for the fibrils are not arranged reassuringly in an orderly, regular or predictable manner as we have been taught to expect. On the contrary everything seems to be in complete disorder but on closer observation we discover that the fibrils form volumetric units which I have named microvacuoles.

THE STRUCTURING ROLE OF THE MULTIMICROVACUOLAR NETWORK Microvolumes under pressure When the surgeon makes an incision in the skin and parts the tissues to gain deeper access, small bubbles appear at the surface of the exposed structures, be they muscle, tendon, or indeed any organ within the body (Figure 2.1 and Video 2.1). This occurs a few minutes after the incision has been made. These microbubbles, which can measure as much as 1 mm in diameter, are the manifestation of naturally existing volumes within the tissues—the microvacuoles. They are revealed because air at normal atmospheric pressure has entered them, either breaking through or diffusing across their walls. This is because the internal pressure of the microvacuoles is different from that of atmospheric pressure. This observation is fundamental, because it introduces the idea of a pressurized microvolume with clearly defined boundaries. We see this regularly during in vivo endoscopic exploration. It is central to all our observations.

Figure 2.1 A When the surgeon makes an incision in the skin and parts the tissues to gain deeper access, small bubbles appear at the surface of the exposed structures at atmospheric pressure. This occurs a few minutes after the incision has been made (5x) B This same action appears near muscle, tendon, or indeed any organ within the body Video 2.1

If we grasp with surgical forceps the tissue in which the microbubbles have formed, the traction creates strange movements brought about by the bursting of these bubbles at atmospheric pressure (Figure 2.2 and Video 2.2). This phenomenon indicates the existence of some kind of hydraulic system with pressure differences. We can see this hydraulic pressure phenomenon whenever traction is applied to the connective tissue surrounding the tendons. A froth of small bubbles appears immediately, which seems to constitute the

sliding tissue in its entirety. However, this happens only if traction is applied to these tissues in vivo. This phenomenon is not so readily observed in a cadaver, and not at all in preserved tissue.

Figure 2.2 A When the tissue, with its attendant microbubbles, is grasped using surgical forceps and then traction is applied, the traction puts the microbubbles under tension (2x) B A froth of small bubbles and fibers appears only if traction is applied. This provokes strange movements brought about by the bursting of the microbubbles at atmospheric pressure (20–100 x) Video 2.2

The examination of these microbubbles in Chapter 1 reveals a world constructed of interlacing fibrils—chaotically disposed. A real tangle of threads of different sizes, with no directional coherence (Figure 2.3). Total fibrillar chaos!

Figure 2.3 Microbubbles of many sizes and shapes A 2 × magnification B 10 × magnification C 40 × magnification

Figure 2.3 D A real tangle of fibrils of different sizes, with no directional coherence. (100 x)

Organized chaos We would like the stuff of our bodies to be orderly and well organized, but this is not what we found during our endoscopic exploration of living matter. The human mind will instinctively search for some semblance of order, and for a logical explanation as to how this chaotic system can function efficiently. However, we already know that this fibrillar chaos enables perfectly adequate sliding between adjacent structures, so efficiency and chaos go hand in hand! Is there an underlying order within the apparent disorder of these interlacing and interweaving fibers? As we move the endoscope closer to these multimicrovacuolar spaces, the light emitted by the endoscope is reflected from the glistening facets of the microvacuoles, which resemble a pile of mirrors dumped arbitrarily in a heap (Figure 2.4 and Video 2.3). On closer inspection, we see that they are made of the same interlaced, randomly disposed fibers, surrounded by liquid. It is a privilege for the surgeon to witness these structures that can be revealed only

by the observation of living tissue in situ. When we look at an isolated tissue sample, the fibrils within the tissue are no longer under tension, and so the underlying architecture cannot be seen.

Figure 2.4 As we move the endoscope closer to these multimicrovacuolar spaces, the light emitted by the endoscope is reflected from the glistening facets of the microvacuoles, which resemble a pile of mirrors dumped arbitrarily in a heap (40 ×) Video 2.3

So let us, like Alice in Wonderland, try to find a door into this heterogeneous matter so that we can begin to understand the strange world inside the human body. Microvolumes and diversity We may be tempted to abandon our search for any discernible regularity, not only because of the apparent chaos, but also because each microvacuole is unique. The first forms that we see are our microvolumes of irregular polyhedral shapes filled with liquid (Figure 2.5). Once exposed, the physical status of a

microvolume is unstable; contact with the endoscope causes it to break up, and only the frame remains. The two visible components of the microvolume —the fibrillar frame and the liquid contained within the frame—dissociate to reveal their simple, but irregular, polygonal structures with three or four, and sometimes five or six, sides (Figure 2.6). These polyhedral units, the microvacuoles, act as structuring elements or units within the tissue. They gather together and play an important role in the creation of shape and form. However, this two-dimensional representation of microvacuoles is misleading.

Figure 2.5 A and B The first forms we see are polyhedral, irregular microvolumes, but the physical status of a microvolume is itself unstable (60 ×)

Figure 2.6 A and B The microvolumes lose their content, either spontaneously or as a result of traction. Only the fibrillar frame remains (60 ×)

Microvacuoles are three-dimensional structures, predominantly polyhedral volumes, with no apparent order or regularity. The microvacuole is a threedimensional volume created in space by the intersection of fibrils. The term microvacuole was chosen to emphasise the notion of a volume that is unoccupied by cells. Here again, we must stress that everything in the extracellular world tends to be polyhedral and irregular. Diversity is the norm. The fibrils are long or short, vertical, horizontal or oblique. They can be close together or far apart, woven tightly or loosely. The fibrils interconnect and interact with each other. They branch off randomly in all

directions. We must therefore abandon our search for any discernible regularity. Through illustration, it is easier to show how the microvacuole is a threedimensional, structured volume (Figure 2.7A and B) created in space by the intersection of fibrils of near limitless differing lengths and densities (Figure 2.7C and D).

Figure 2.7 A–D The microvacuole is a three-dimensional volume created in space by the intersection of fibrils. The fibrils delimit the microvacuoles

It is also easier to find these sparkling, iridescent mirrors in areas of suppleness and flexibility where cells are scarce, such as the area just below the skin, or the area immediately surrounding tendons. Most of our examinations will be from these areas. In the next illustration, we attempt to show how the microvolumes are attached to each other and group together to create a larger structure of similar organization (Figure 2.8). A new form emerges that obeys rules very much like those of the basic unit. This observation is fundamental, because it provides a rational explanation of morphogenesis. We will expand on this in later chapters and in the Afterword (see page XXX).

Figure 2.8 The microvolumes are attached to each other, and they group together to create a larger structure of similar organization. A new form emerges which obeys rules very like those that govern the basic unit A 1 × multiplication B 5× multiplication C 25× multiplication D 1000× multiplication

The smallest microvacuolar volumes created in this way measure from a few microns to upward of 20−30 µm in diameter. This is about the same size as a cell. Some microvacuoles measure up to 200 µm in diameter. Smaller microvacuoles are frequently found surrounding tendons. Larger microvacuoles are found within the adipose tissue of the abdomen. This variation in size seems to depend on the nature of the mechanical and dynamic forces the microvacuoles have to deal with in specific areas of the body. We also see differences from one person to another. The microvacuolar network in some people is made of thinner, reedier fibers compared with that in others. This introduces the notion of specificity between individuals. We are all different, not only on the outside but also on the inside. Each individual is unique.

THE FIBRILLAR FRAME The fibrils that make up the framework of each microvacuole are in continuity with each other, but there are variations in the way in which the fibrils intersect. Some intersections are clearly defined, while others are less distinct, with the presence of veil-like intermediary zones between fibrils. Some fibrils are quite wide, with flat, reflective surfaces that resemble the steel blade of a knife. Others are similar in shape and appearance but with thin, translucent surfaces. They can also be narrow, or broad and swollen, short or long. Some are cylindrical, with many varying attributes (Figure 2.9). Others appear to be hollow, but at present we have no evidence to show that fluid flows through these fibrils. The question is the subject of ongoing research.

Figure 2.9 The shape of the fibrils themselves varies greatly. (200–400 x) A Smooth cylinders, like rods or shafts, with smooth edges B Cylinders that resemble bamboo stems, with annular rings reinforcing the fibrils at irregular intervals

C D E F

Cylinders with swellings that resemble buds on plant stems Cylinders with ‘diaphragms’ Some are olive-shaped Some appear to be hollow

Diversity is the norm, and the variety is endless (Figure 2.10 and Video 2.4). Here, the fibrils vary from 5 to 70 µm in diameter (Figure 2.11), with greatly variable lengths, giving the fibrillar network a chaotic, disordered appearance with a succession of threads, struts, cross-links, and stem-like shafts with nodular thickenings in places. The distance between intersections of these fibers ranges from about 10 to 100 µm; however because they form part of a continuous network, it is not possible to isolate individual fibers within this continuum. Nor can we measure the length of any given fiber, because they appear to always be in flux within that network.

Figure 2.10 The actual pattern of the weave can vary greatly, and can be more or less dense or irregular. The variety of the interfibrillar connections is endless. (100 ×) Video 2.4

Figure 2.11 The diameter of the fibrils varies between 5 and 70 mm (100 ×)

The wider surfaces, like steel blades, reflect light (Figure 2.12 and Video 2.5). Some form a more regular weave that looks like linear scaffolding (Figure 2.13), and others are more rounded, curving like cattle trails (Figure 2.14).

Figure 2.12 Wide surfaces reflect light like steel blades (100 ×) Video 2.5

Figure 2.13 Straight, more regular weave (100 ×)

Figure 2.14 Some fibrils are curved and the weave is less rectilinear (200 ×)

We can consider the microvacuole as a volume within a woven mesh of fibers in which the actual pattern of the weave can vary greatly. You can see tightly woven, close-knit fibers, like those in a silk veil (Figure 2.15 and Video 2.6), or loose, roughly woven fibers, similar to those found in coarse canvas (Figure 2.16 and Video 2.7).

Figure 2.15 Sometimes there is total fibrillar chaos! (100 ×) Video 2.6

Figure 2.16 At times, there is a more conventional weave (100 ×) Video 2.7

The fibril intersections are variable and may take the form of veil-like intermediary zones called ‘bourrelets de Plateau’ or ‘Gibbs rings’ (Figure 2.17 and Video 2.8).13, 14, 15, 16

Figure 2.17 Their intersections are sometimes changeable, and they may take the form of veil-like intermediate zones called ‘bourrelets de Plateau’ or ‘Gibbs rings’ (130 x) Video 2.8

Fibrillar dissociation The fibers of the fibrillar frame are made up of smaller fibrillar units (Figure 2.18). When subjected to mechanical stress within normal physiological limits, the fibrils within these fibers can separate and dissociate from each other while still maintaining tissular continuity. This shear-like separation is normal, physiological mechanical behavior and will be dealt with in more detail in Chapter 5, along with the fractalization characteristic of this chaotic network or morphostructure.

Figure 2.18 A and B These fibers are made up of smaller fibrils. The fibrils can dissociate when subjected to mechanical constraint within normal bounds. (200 ×)

Microvolume content diversity It is difficult to definitively identify the contents of the fibrillar frame separately from its filling. Additionally, the content ratios of each vary considerably, depending on their anatomical location and the function of the tissue in which they are found. We must not forget that the architecture may

also be partly, but to a very small extent, made up of nerve branches and lymphatic vessels, which closely resemble each other. In time, we may discover that the fibrillar frame and the content of each microvacuole are as integrated as tendon is integrated into muscle; they can be separated, but then they lose their functionality. However, we estimate the separate content as follows. The three-dimensional dynamic and fractalized fibrillar frame of the microvacuole (Figure 2.19) is primarily composed of collagen types I (about 70%), III, and IV, and elastin (about 20%). Microvacuoles contain a high percentage of lipids (about 4%). However, these proportions vary considerably, depending on their anatomical location and on the function of the tissue in which they are found.

Figure 2.19 A and B Three-dimensional diagrams to illustrate the fibers and fractalized fibrils, which are the frame for a gel content (75 ×)

The microvacuolar filling, being aqueous, is primarily composed of the following. • Highly hydrated proteoglycan gel (Figure 2.20): 72% • Collagen type I: 23% • Lipids: 3% • Collagen types III, IV, and VI: 2%

Figure 2.20 A and B The microvacuoles are filled with a proteoglycan gel. The morphology of the intravacuolar content is poorly defined and varies in different parts of the body. (130 ×)

Lipids are hydrophilic, and probably play a role in the exchange of fluids between neighboring microvacuoles and between the microvacuoles and the circulatory system. This would explain the relatively high lipid content of the microvacuoles. Each microvacuole can change shape during movement while its volume remains constant. Even though the intravacuolar volume appears to be globally incompressible, the internal pressure varies locally, depending on the movement required by the tissue in which the microvacuoles are found. This

ensures the transmission of pressure throughout the microvacuolar network. The greater the movement required, the smaller and more densely packed are the microvacuoles within the tissue. The attraction power of hydration is mediated by glycosylated proteins called proteoglycans. The basic proteoglycan unit consists of a core protein with one or more covalently attached glycosaminoglycan (GAG) chains.16 Glycosaminoglycans are long unbranched polysaccharides consisting of a repeating disaccharide unit (Figure 2.21). The strong negative charge of the GAGs attracts water molecules and facilitates their passage across the microvacuolar membrane, ensuring hydration (the process of absorbing and retaining water) of the microvacuoles. This, in turn, ensures the maintenance of intravacuolar pressure and resistance to compression, which explains the ability of the microvacuoles to adapt to changes in shape. The links between the collagen fibers and the proteoglycans in the microvacuolar gel may be provided by collagen type IV filaments that resemble pearl necklaces. Direct links between the collagen type I fibers and small proteoglycans such as decorin can also be found. These links also exist between collagen type I fibers and larger molecules such as hyaluronan (hyaluronic acid or hyaluronate).

Figure 2.21

Arrangement of glycosaminoglycans. Glycosaminoglycans are long, unbranched polysaccharides. The bonds between the collagen fibers and the proteoglycans of the microvacuolar gel may be provided by collagen type IV. There are no empty spaces. (400 ×)

Water is a major constituent, present at every level, sensitive to its environment, responsive under pressure, simultaneously independent and interconnected, and often overlooked by researchers. Its presence is an undeniable reality, clearly evident during intratissular observation (Figure 2.22A and Video 2.9). The moistened appearance of anatomical structures immediately after a surgical incision is proof that our body spaces are essentially water-filled (Figure 2.22B and C, and Videos 2.10 and 2.11). But rapid dehydration of these tissues after a few minutes of surgery is also a well-known phenomenon, giving rise to the need to moisten the tissues, which tend to dry out even more quickly under the operating light (Figure 2.23). Despite differing microanatomical architectures and functions, the water-filled microvacuoles are under pressure, albeit lower, as is the blood in the circulatory system, and their haemodynamic status (the flow of fluids within each network) is interconnected.

Figure 2.22 A A cutaneous incision showing the importance of fluids in the body (10 ×) B Fluids and fibers are closely linked but easily dissociated (130 ×) C Fluid seeps into the entire operating field in certain patients (130 ×) Video 2.9, 10 and 11

Figure 2.23 The rapid dehydration of the tissues during surgery is a well-known phenomenon. (40 ×)

It is obvious that a satisfactory biomechanical explanation of the sliding of the subcutaneous structures must take account of the basic principles of fluid dynamics, such as osmotic pressure, superficial tension, and van der Waals forces (Pr Herbage, INSERM Laboratories, Lyon, France, November 2004 personal communication). Intratissular bubbles We often find microbubbles inside large fibrillar structures (Figure 2.24). Their size varies widely. Colleagues have suggested that these bubbles are, in fact, atmospheric air that has become trapped after being accidentally introduced during surgery, and that they are not a natural phenomenon. However, we see them too frequently for this to be the case. Of course, we need to carry out further studies to measure the gaseous proportions of the air contained in these bubbles. Gaseous exchange is a possible explanation, and it is likely that certain fibers allow the passage of fluids that we call lymph but that are, in fact, interstitial fluids. Endoscopy will enable us to better describe and understand this world of fluids and fibrils in the future.

Figure 2.24 Inside large fibrillar structures, we frequently see microbubbles of different sizes. This could be explained by gaseous diffusion, but we do not fully understand this phenomenon A 200 × magnification B 200 × magnification C 400 × magnification

Within this microvacuolar network, the fibers resist tension, and the intramicrovacuolar liquid resists compression. The residual volume of intramicrovacuolar liquid remains constant. This enables us to provide an

explanation of water distribution within the body. Naturally, any attempt to explain water distribution within the body needs to satisfy all other requirements of living matter.

THE CONCEPT OF STRUCTURED FORM In Chapter 1, we asked, ‘How is this tissue continuity structured, and how do these fibers ensure tissue cohesion? How do they come together to create a structured form?’ KEY STATEMENT The continuous, permanent link between all the components of the microvacuolar system provides the architectural organization and fibrillar framework that explains and confirms the concept of structured form (Figure 2.25).

Figure 2.25 The notion of a structured form is the result of an architectural organization and a continuous, permanent link between all the components. The influence of various physical forces plays a crucial role in the creation and maintenance of a structured form.

By intertwining in an irregular, fractal manner, the fibers determine the volume of the microvacuole, which is filled with a GAG gel, and by accumulation and superposition, these multimicrovacuolar polyhedral units build elaborate forms. The resulting fibrillar framework fulfils this structuring role within the body. KEY STATEMENT A living form has to be structured, but it also needs to be mobile, supple, adaptable, and self-sufficient.

• Mobile. This means that the structures move together harmoniously to perform required tasks without influencing neighboring and peripheral structures. The mobile structures are endowed with a form of tissue memory, enabling them to always return to their original state once they have carried out a required movement, unless they are injured during the mechanical constraint. • Supple. Structures must be able to bend easily without damage or rupture, responding readily to the constraint and facilitating the functional interdependence of the components. • Adaptable. An adaptable structure is capable of responding instantly to any unexpected mechanical constraint that requires it to change its form, such as sudden local traction. • Self-sufficient. Self-sufficiency means that the essential requirements of life, such as electrical energy, oxygen, and metabolic factors, are diffused constantly throughout living tissue, no matter what constraint is imposed on it, or what physical effort is required of it. This can be achieved only if the pathways of energy supply are integrated into the structural organization of the tissue.

FOLLOWING THE RED THREAD To meet the other specifications of living matter (mobility, suppleness, adaptability, and self-sufficiency), we can now answer the first question from

our list at the end of Chapter 1 (page 56). RED THREAD QUESTIONS 1. How is this tissue continuity structured, and how do these fibers ensure tissue cohesion? How do they come together to create a structured form?

We have seen in this chapter how the fibrils intertwine to create microvolumes—the ‘microvacuoles’—that create tissue continuity and cohesion, and hence structured form.

Comment by Robert Schleip, MA, PhD

One should probably ask the patients rather than their manual therapists about whether and how the quality of a practitioner’s touch changes after being exposed to the impressive imagery and descriptions about fascia in this chapter. I would not be surprised if the patients then reported experiencing a more connected or slower but deeper touch to their bodies. There are times in my professional life as a scientific researcher and manual therapist at which I notice that, after having spent several days in the science laboratory, the ability of my hands, heart, and brain to meet the tissues of my clients tends to be less refined and less skilful than it could be. Usually this is the case after I have spent several days being hypnotized by the conventional anatomical textbook pictures of muscles and fascia, or have been working with formalin-preserved bodies in the anatomical dissection halls. As helpful as these studies are for my intellectual understanding, they can also be partially ‘poisoning’ for the tactile sensitivity of my hands during treatment sessions. The deceptive delusion of the usual anatomical images arises not only from their artificially fragmented arrangement, but also from their inability to show the semiliquid quality of the tissues in their natural condition. Under the spell of these textbook images, it is tempting to assume that the fasciae and muscles would be rather dry organs, as they appear in the illustrations in those books or in anatomical exhibitions. In fact, as the beautiful images and descriptions of Dr. Guimberteau reveal, the quality of living fasciae has as little in common with those dry tissue images as does the quality of dry prunes, raisins, or dried oranges with those of juicy plums, grapes, and other fresh fruit. As a part-time teacher for other bodywork practitioners, I frequently have the privilege of showing some of Dr. Guimberteau’s impressive video documentaries about living fascia to my students. I always observe a different working quality in the hands of the students afterward. It also happens to me, in what is now a predictable manner, that whenever I subsequently touch fascia again as a therapist, I feel a drastic change in the quality of my working hands. When encountering a seemingly hard and unyielding place in the tissue, I no longer push with a demanding quality against the perceived resistance, as would make sense when working with solid and dry materials, like working with entangled ropes. Instead, when remembering the liquid and complex nature of the fibrous fascial network, as shown and described in this chapter, it makes more sense to work in a less force-oriented manner. Rather than tearing stuck and adhered fibers apart from each other, it becomes more convincing to explore, in a multidirectional manner, how the semiliquid fibers might be seduced to ‘untangle’ by a gentle shift of their nodal points, by a lengthening of their trunks (similar to stretching glue), or by a gradual bifurcation, as shown in some of the pictures in this chapter.

One could say to myofascial therapists, ‘What you see (in your mind’s eye when you touch) is what you get (in terms of the working dynamics under your hands)’. If you want to continue working with a forceful technique, then there is no need to replace the textbook images of dry muscles and fascial tissues in your mind. However, if you are open to a shift toward a more listening, more exploratory, and more gentle quality of your manual touch, then I highly recommend you to deeply dive into the imagery and descriptions in this chapter before translating your newfound knowledge into the fascinating interaction between your hands and the liquid juicy fascia under the skin.

3 Mobility and Adaptability Maintaining tissue continuity during mobility Mechanical behavior of fibrils and fibers during mobility Global mechanical result Following the red thread

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY Through our observations, we see how this elaborate microfibrillar construction, composed of microvacuoles filled with collagen and glycosaminoglycans or with cells, is capable of adapting to all types of constraint in three dimensions, thanks to its mobility and other inherent properties.

MAINTAINING TISSUE CONTINUITY DURING MOBILITY At no time does the fibrillar network of the connective tissue and fascia system move spontaneously. An applied force is needed, whether it be external, such as during massage, or internal, as a result of muscle contraction or the movement of tendons. The mobility of these fibrillar structures can be seen during videoendoscopy, but the limited depth of field of the camera makes it difficult to focus accurately on specific structures. This renders video analysis difficult and time-consuming. Some images were obtained by miracle alone! When a tendon slides through the surrounding connective tissue, the fibrils divide and intertwine. This is shown clearly in video sequences over a period of about 3 seconds (Figure 3.1 and Video 3.1). The film provides reliable evidence of the movement of fibers and fibrils in the vicinity of the tendon as it slides through the surrounding connective tissue. First, the fibers react immediately to the slightest mechanical constraint by quivering intensely, then the larger fibers move and lengthen. Both fibrils and fibers are capable of movement. Insofar as the microvacuoles are formed by fibers and fibrils, they also adapt to movement by stretching, widening, and shortening, while being able to return to their original shape (Figure 3.2 and Video 3.2). To achieve this, all the components must possess certain inherent qualities, such as elasticity and intrinsic cohesion. Let us take a closer look at the way these fibers and fibrils move, by examining fibrillar movement below the skin during traction of the skin.

Figure 3.1 A tendon slides through the surrounding tissue, where the fibrils divide and intertwine to accommodate it. In the video, this is shown in sequences of about 3 seconds, with the fibers highlighted in yellow for clarity. First, the fibers react immediately to the slightest mechanical constraint by quivering intensely, then the larger fibers move and lengthen (60 ×) Video 3.1

Figure 3.2 A microvacuole can change shape (adapt) by stretching, widening, or shortening, and still be able to return to its initial shape. These changes occur simultaneously and in synchrony with the movements of the fibrillar system to return to its initial shape. (60 ×) Video 3.2

MECHANICAL BEHAVIOR OF FIBRILS AND FIBERS DURING MOBILITY Orientation of the fibers occurs in the main direction of the force We applied gradually progressive traction to the tissue, to a maximum of 3 Newtons per cm2. We identified five phases of movement of the sliding system over a period of 2 seconds (Figure 3.3 and Video 3.3). • Sequence A (duration 0.15 seconds) shows that the fibrils react immediately and begin to quiver as soon as traction is applied to the tissue. • Sequence B (duration 0.35 seconds). Here we see that some fibers are not completely aligned in the direction of the force. • Sequence C (duration 0.45 seconds) shows that some fibrils adopt certain movements that gradually permit their mechanical participation and submission to the constraint. • Sequence D (duration 0.55 seconds) allows us to see that, as the traction increases, the fibrils then align themselves in the direction of the force. • The final sequence E (duration 0.45 seconds) towards the end of the applied traction shows that even distantly related fibrils gradually orient themselves in the same direction.

Figure 3.3 Fibrillar movement below the skin in response to traction applied to the skin, showing how orientation of fibers during movement occurs in the main direction of the force. The five phases of movement of the sliding system have been selected over a period of 2 seconds (see text). At the first pause in the video, we highlight the fibers to identify them. The video is paused at each phase thereafter (20 ×) Video 3.3

Notice that all the fibrils participate in the local tissue response to thetraction: the microvacuoles change shape in response to the constraint, and their volumes are compressed (which also alters the internal pressure.) The fibrils stiffen as strain is put on their collagen structure, and the number of fibers involved increases as the traction increases, which likely explains the tissular resistance that is felt as more traction is applied. This suggests a correlation between the increased number of fibers under tension and the resistance felt by surgeons during traction, and by manual therapists during soft tissue manipulation. KEY Statement The alignment of the fibrils always occurs in the direction of the applied force, and under normal physiological conditions it is accomplished without damage or rupture of the fibrils.

Some fibrils move more than others, and they do not all react with the same intensity; in other words, we do not see a global linear shift of fibrils. Nevertheless, tissue continuity is maintained at all times. The force is transmitted, distributed, and finally absorbed, but the way this is achieved appears to be non-linear, because the variety and intensity of the fibrillar movements seem to be unpredictable and subject to change. This will be exploredfurther in Chapter 5. Maximal efficiency and force absorption As we have seen in Chapter 1 and as a constant observation in vivo, the fibrillar architecture allows maximum mobility without influencing the surrounding tissues. Therefore the fibers must be able to absorb the forces associated with constraint, because they have to deal with them without breaking or rupturing. The physiological limits of the elasticity of the fibrils are thus respected, and no rupture of the tissue is allowed to occur under normal physiological conditions. Any such disruption would lead to the destruction of vessels and nerves, and to the subsequent interruption of information and energy supplies. The rheological relationship, that is the local relationship between restraint and distension, cannot be unlimited and linear, as it would be in an elastic system, because that is not what we observe. When the collagen fibrils reach their maximum stretching potential, they are unable to perform further movement. There are two solutions: • either the fibers fracture or rupture, which is an unacceptable physiological solution, or • it could be that there is another mechanical solution that involves a more general fibrillar response. Each fiber, before it reaches its maximal stretching point, recruits the adjacent fiber, which is then put under tension, but this tension is now slightly decreased. The second fiber will behave in the same way, and before it reaches its own maximum stretching point it will recruit another adjacent fiber, and so on. This would explain the dispersion of the force—a dilution that avoids the risk of fibrillar rupture. The closest fibers are fully distended,

and the fibers furthest away are only slightly involved. This system is reminiscent of a suspension system. We can now explain how it is possible to accommodate two apparently contradictory roles simultaneously—efficient optimal movement in full contact with the vector, and energy absorption at the periphery—without disturbing the surrounding tissues in a continuous, mobile crisscross of fibrils. If this mechanical hypothesis, which is based on careful observation, is proved to be generally correct, then it constitutes a surprising and elegant solution to the requirements of living matter for optimal movement. Interfibrillar movements between individual fibrils A variety of complex interfibrillar movements ensure that the contradictory roles of movement and energy absorption are carried out simultaneously. Fibrils lengthen It seems that as soon as movement begins, the fibrils are able to stretch out, thereby increasing their length. This ability of the fibrils to lengthen is the first property we see (Figure 3.4A and Video 3.4, and Figure 3.4B and C). The fibers can increase their length by as much as 15−20 per cent. This is the initial fibrillar response and the most commonly observed, whether light or heavy traction is used. During the lengthening of certain fibrils, we can sometimes see small annular bulges inside the fibrils that stretch out during traction. This is similar to the behavior of an earthworm or of a spring (Figure 3.5 and Video 3.5). It implies that molecules, perhaps ofelastin, are prearranged so as to allow for distension and retraction in that area of the fibril, permitting the fibril to return to its initial position.However, these bulging rings are not always found, and the fibrils often lengthen without revealing any hint of their internal architecture.

Figure 3.4 A Animated diagram to illustrate the lengthening of fibers (60 ×) Video 3.4

Figure 3.4 B–E As soon as movement begins, the fibrils respond by stretching out and lengthening. Note the change in length of the central, horizontal fiber between

B and C, and again between D and E (100 ×)

Figure 3.5 During the lengthening of certain fibrils, we can sometimes see small, annular bulges inside the fibrils that stretch out during traction. This is similar to the behavior of an earthworm or of a spring (150 ×) Video 3.5

Fibrils migrate The migration of fibrils along other fibrils is another commonly seen phenomenon (Figure 3.6, and Videos 3.6 and 3.7). It is the existence of mobile junctions that enables one fibril to slide along another. In this way, energy is dispersed and absorbed throughout the fibrillar network. This ensures efficient distribution of the constraint as it is applied to the tissue.

Figure 3.6 A The common migration of a fiber along other fibers by the way of mobile junctions . In this way energy is dispersed and absorbed throughout the fibrillar network (100 ×) B Animated diagram to illustrate the migration of fibers (60 ×) Video 3.6 and 7

Fibrils divide During stronger traction, we see that the fibril is capable of dividing into two, three, or four smaller fibrils (Figure 3.7 and Videos 3.8 and 3.9). This means that the distribution of energy is spread across several fibrils simultaneously, and is thus absorbed more efficiently.

Fibrillar division and the sliding of fibrils along each other seem to occur in distinct ‘separation zones’, which suggests morphological determinism(Figure 3.8 and Video 3.10).

Figure 3.7A The fibril has the capacity to divide into two, three, or four smaller fibrils, thus facilitating the dispersion of energy in three dimensions (150 ×) Video 3.8

Figure 3.7B Animated diagram to illustrate the dividing of fibers (60 ×)

Video 3.9

Figure 3.8 It would seem that these movements of division and sliding only occur in distinct ‘separation zones’. This raises the question of morphological determinism (i.e. could these zones be predetermined?) (400 ×) Video 3.10

Fibrils are also linked and fixed Sometimes interfibrillar crossings, or links, are stable and do not seem to be dynamically involved. This real and distinct stability explains the overall permanence of the form during movement, and suggests a structure with a predetermined architecture and behavior that are not entirely random (​Figure 3.9 and Video 3.11). Other links are not visible but reveal that they must exist when new fibers appear mid-sequence (Figure 3.10 and Video 3.12).

Figure 3.9 The link between the two fibers we can see in the video is clearly a stable link. This also introduces the idea of a predetermined architecture and behavior, which are not entirely random (200 ×) Video 3.11

Figure 3.10 Sometimes new fibers appear that were not visible at the start of a sequence. They are in continuity with another fiber, although at first there is nothing to

indicate this continuity. In this video, a new fiber appears toward the end of the sequence and plays a mechanical role in the movement (100 ×) Video 3.12

These observations are difficult to record, and it was possible to make them only with fibrils that were 10 microns or more in diameter. Interfibrillar movements within the microvacuole Movement also occurs between the fibrils within the microvacuole. It is impossible to ignore the mechanical role of the other types of collagen, such as collagen types III and IV, and the glycosaminoglycans, duringmovement within the microvacuole. It is difficult to see the collagen types III and IV fibrils inside the microvacuoles, but observation at high levels ofmagnification reveals a network of interwoven fibrils that are themselves made up of smaller fibrils. These fibrils are wave-like in appearance when they are not under tension (Figure 3.11). This is further evidence of the fractal nature of the fibrillar architecture.

Figure 3.11 Observation of the spaces between the fibrils at high magnification reveals an interweaving of the fibrils, which are themselves made up of smaller fibrils. These small fibrils are wave-like in appearance when they are not under

tension (150 ×)

These interfibrillar movements imply that certain fibrillar intersections have the ability to fuse or separate, instantaneously. This could occur by polymerization and depolymerization at the molecular level, and probably involves collagen or elastin. Further research is needed in this area.

GLOBAL MECHANICAL RESULT A veritable firework display of fibrillar movement explains the global dynamic behavior of the fibrillar network (Figure 3.12 and Video 3.13). The fibrils intertwine, intersect, and overlap each other, but behave in a harmonious manner when traction is applied to the tissue. The fibrils align themselves in the direction of the force imposed on the tissue. The lengthening seems to be the primary response in dealing with the mechanical constraint, and appears to play a leading role in facilitating movement. The combined of division, sliding, and the fractal organization of the fibrillar network ensures that the force is diffused throughout the network.

Figure 3.12 The mobility, flexibility, and elasticity of the fibrillar structures create a gigantic firework display of fibrillar movement (60 ×)

Video 3.13

The combination of lengthening, division, and sliding also permits mobility of the tissue in any direction and in three dimensions, and in particular during movement. These phenomena also explain how the applied force dissipates and loses its strength beyond a certain distance. The fact that these forces have no effect on the surrounding tissues demonstrates the energy-​absorbing capacity of the fibrillar system. KEY STATEMENT The combined action of these three distinct, yet closely related, types of fibrillar behavior enables the fibrillar network to adapt to the constraint in three dimensions, while at the same time dispersing and reducing the force of the constraint and also preserving the capacity of the structures to return to their resting positions (Figure 3.13 and Video 3.14).

Figure 3.13 The combined action of these three distinct, yet closely related, types of fibrillar behavior enables the fibrillar network to adapt to the constraint in three dimensions (100 ×) Video 3.14

This astonishing fibrillar behavior involves the simultaneous movement of billions of fibrils. The dynamic potential of the combination of these three movements is incalculable (Figure 3.14, and Videos 3.15 and 3.16).

Figure 3.14 A The dynamic potential of the combination of these three mechanical solutions is incalculable (60 ×) Video 3.15

Figure 3.14 B Animated diagram to illustrate the dynamic potential of fibers (60 ×)

Video 3.16

FOLLOWING THE RED THREAD RED THREAD QUESTIONS 2. How can this fibrillar continuity permit two dynamically opposed roles, ensuring simultaneous mobility, absorption of forces, and sliding, while having no effect on surrounding tissues?

This combination of movements provides us with some of the answers and we can now explain fibrillar mobility, the capacity to accommodate apparently contradictory roles (efficient mobility, energy absorption and the interdependence of these movements). We now know that fibrillar continuity is provided by the multimicrovacuolar and multifibrillar network. The structures are able to move together harmoniously to perform required tasks without influencing neighboring and peripheral structures. The mobile structures are also endowed with a form of tissue memory, enabling them to always return to their original state once they have carried out a required movement, unless they are injured during movement.

Comment by Jean-Pierre Barral, DO

Osteopaths are mechanics who do their best to restore good mobility to the bodies of their patients. They trust their hands but very often do not know exactly how the body is reacting to their treatment. Dr. Jean-Claude Guimberteau’s research is fundamental to us. It helps us on our way to a better understanding of the human organism. Generally in medicine, we speak about two kinds of mobility. 1. visible movements produced by external forces applied to a structure 2. a combination of small movements, very often difficult or impossible to see, such as peristalsis, the wave-like muscular contractions of the intestine. Osteopaths refer to motility, which is different. This is an invisible, subtle movement produced by the organ itself—an inherent movement specific to each organ. It is as if the cells of each organ, when they are functioning well, transform part of their energy into tiny, harmonious movements. Dr. Jean-Claude Guimberteau’s work shows that when youapply a force to a tissue there is, initially, a simple movement in reaction to the applied force, but also, a little later, other smaller, more complex movements. The orientation of thesesubsequent movements is less predictable. This is veryimportant for us. Each practitioner works on the tissues following their own, individual, logical approach, but we are not able tototally control thereactions of the body. We mustremain modest and acknowledge that our role is to send a ‘good message’ to the body, but having received our‘message’, it will react in its own way. This is one of the basic principles of Andrew Taylor Still, founder of osteopathy, in explaining what we do with our manual treatment. When speaking of a restriction of mobility in a part of the body, Still frequently said, ‘Find it, fix it, and leave it alone.’ Another concept, reinforced by Dr. Guimberteau’s research, is also fundamental to us: the notion of tension and pressure. To put it simply, by acting on the tissues, we try to influence the direction of the fibers as well as the pressure in different body cavities and canals, such as within the skull, the thorax, the inguinal canal, and the carpal tunnel. Any kind of abnormal tissue tension will have an effect on the pressure inside a cavity. Let us take the example of the thorax. To permit theexpansion of the lungs, it needs to maintain negative pressure. A mechanical problem involving a rib or the pleura will alter this pressure, which will then affect the oxygen, carbon dioxide, and pH levels in the blood.

Finally, Dr. Guimberteau explains that the body reacts in all three dimensions. This is a key point for us. In the body, nothing is absolutely flat. Our hands must test for restricted mobility of fibers in all possible directions. If you miss one direction, the results will never be entirely satisfactory. We must help to support the adaptationcompensation system within the body.

4 The Relationship Between the Cells and the Fibrillar Architecture Cell morphology and distribution The relationship between the fibers and the cells Following the red thread Conclusion

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY Blood vessels on the arterial side of the microcirculation ensure that the essential energy requirements of life, such as oxygen and metabolic nutrients, are continuously distributed throughout living tissue. Nerves ensure the distribution of the various information components. Distribution is maintained no matter what constraint is imposed on it, or what physical effort is required of it. This can be achieved only if the pathways of information and energy supply are integrated into the structural organization of living tissue in such a way as to ensure maximum efficiency without obstruction or impediment. Whether blood, nerves, or lymph vessels, they must accompany physiological movement while continuing to function correctly at all times. We therefore need to know more about the nature of the relationship between blood vessels, nerves, lymph, and the fibrillar architecture. We also need to know how the cells are distributed under the skin, and if this fibrillar architecture is the route by which energy and information are distributed to the cell. How does the cell fit into the tangle of fibers that we have seen in earlier chapters?

CELL MORPHOLOGY AND DISTRIBUTION Cells display a wide variety of shapes. They can be square, round, or oval, or resemble simple polyhedrons with four or five faces, but they are all different. Our in vivo observation of cells in situ also reveals a wide variety of colors and sizes of cells and their disposition. It is not easy to observe at the cellular level during perioperative endoscopy, because of the small size of most cells and the difficulty of identifying specific cell types. The cells in the epidermis and the dermis are particularly difficult to see, as are the muscle cells. Melanocytes, however, can on occasion be seen deep inside the epidermis and are easily identified by their brown color. They are located at the junction between the epidermis and the dermis, just above the papillary ridges (Figure 4.1).

Figure 4.1 A cross-section of the skin, showing the brown melanocytes on the edge of the papillary dermis, which is the uppermost area of the dermis. The papillary loops appear to extend beyond the area known as the Malpighian layer, which is the deepest area of the epidermis (60 ×).

It is in the hypodermis that the cells become easier to see, the most obvious being the adipocytes within the fat lobules. Adipocytes can also be easily observed in the sliding areas around the tendons, where the tissue is more supple and less dense; the fibers are woven more loosely, and clusters of cells can be identified between or on the fibers. Cells are sometimes spread over the surface of tendons, nerves, veins, or muscles (Figure 4.2). Distinguishing features of different cells • Adipocytes that are found in the fat lobules of the hypodermis are usually canary yellow. They vary from 60 to 120 microns in diameter. They are grouped together in the lobules, which have smooth, rounded contours. Some of these adipocytes have a good blood supply, but in other areas the capillary vessels are sparse and the adipocytes appear to be poorly vascularized (Figure 4.2A−C).

Figure 4.2 The adipocytes vary in color from pale yellow to bright yellow or amber. Sometimes they are almost white in color (100 x) A Some appear to have no blood vessel nearby. B Sometimes there are a few blood vessels. C Sometimes they are highly vascularised.

• The cells are different in the areas between the fatty lobules and the muscular aponeuroses and around tendons in the sliding spaces. Here, they vary from 30 to 100 microns in diameter and are amber yellow. Sometimes, however, they may be very pale yellow or even transparent (Figure 4.3).

Figure 4.3 A Fibers with groups of cells between them can be observed in the areas where the tissue is less dense and more supple. These areas are found below the hypodermis and above the muscular aponeurosis (10 ×).

Figure 4.3 B These groups of cells are called clusters; they contain several millions cells (30 ×).

• They are found in clusters of varying shapes around and along blood vessels. Their distribution is similar to the positioning of houses built along a road running through a small town or village, with a greater density at the centre of the village and thinning out on either side. These clusters of cells resemble bunches of grapes or fish spawn, but their shape is often oblong and their size seems to be larger in vivo than in vitro. The number of the cells within each cluster depends on its length. Clusters of 2 mm in length contain at least 5 million cells. We analyzed these cells, and many of them (20%) are immature cells. These may be fibroblasts, preadipocytes, or pluripotent cells. They have a large nucleus with plenty of mitochondria, and an apparently huge production of collagen. • These cells are sometimes spread over the surface of muscles, tendons, nerves, or veins. They cover the surface of these structures, rather like wild flowers growing in a meadow. However, in certain areas (Figure 4.4) I have not been able to identify any discernible logic regarding their distribution, except in the case of vascular tropism.

Figure 4.4 In some areas cells are spread over the surface of: A Tendons (10 ×). B Nerves (40 x). C Veins (40 x) D Muscles (40 x) They cover the surface of these structures rather like a tablecloth, or a carpet of wild flowers growing in a meadow.

THE RELATIONSHIP BETWEEN THE FIBERS AND THE CELLS Here again, we must emphasize that these groups of cells are completely enfolded and surrounded by the fibrillar network. They are embedded within

this framework. Cellular organization is supported, maintained, and probably shaped by this interwoven latticework of fibrils (Figure 4.5 and Video 4.1). KEY STATEMENT There is total continuity between the cells and the intercellular spaces.

Figure 4.5 A There is no doubt that the position of cells in space is determined by this interwoven latticework of intersecting fibrils (60 ×). B There is total continuity between the cells and the intercellular spaces (200 ×). Video 4.1

There are several interesting observations to note concerning the relationships between cells, vessels, and fibers. • As mentioned previously, cells are found in large clusters along microcapillaries (Figure 4.6), and just as frequently strung out along the vessel in small numbers.

Figure 4.6 Very often, cells are found in clusters along microcapillaries (130 ×)

• Along the fibers, cells are found either in pairs, like ladybirds on a blade of grass, or in small groups, like families (Figure 4.7).

Figure 4.7 A and B Sometimes we see just a few cells strung out along the fiber at a distance from the main group of cells (200 ×)

• We sometimes see groups of cells, arranged in several layers, that seem to completely colonize a fiber. On other occasions, groups of cells appear to engulf and swallow the fiber (Figure 4.8).

Figure 4.8 Sometimes you come across groups of cells that seem to completely colonize a fiber. A Arranged in several layers like insulation (20 ×). B These climb on like a caterpillar (60 ×). C Hanging off a fibrillar connection (130 ×). D Sometimes groups of cells appear to swallow the fiber (200 ×).

• At times, we see a few cells, often only two or three, that are situated at intervals and completely isolated at a distance from the main group of cells (Figure 4.9A). What are they doing there? Are they in the process of migrating somewhere else, or are they there on a permanent basis? • The adhesion between cells is not permanent. Sometimes they are in groups with strong intercellular cohesion, and the cell shapes are more angular or polyhedral (Figure 4.9B). On other occasions, the intercellular cohesion is weaker, and in this case the shape of the cells is more spherical (Figure 4.9C).

Figure 4.9 A Sometimes, at a distance from a dense cluster of cells, we encounter individual cells with no visible vascular supply (60 ×). B In some areas, we see strong intercellular cohesion (200 ×). C In other areas, the intercellular cohesion is weaker, and in this case the shape of the cells is more spherical (150 ×).

Mechanotransmission and mechanotransduction Cells are mechanically dependent on the fibers to which they are attached: the slightest traction along a fiber brings about a change in the orientation and position of the cells, and can even cause the cells to change shape. The mobility and flexibility of these groups of cells is surprising considering the complexity of their arrangement (Figure 4.10 and Video 4.2). This phenomenon is clearly visible and could be an example of mechanostimulation inducing mechanotransduction 17, 18, 19 (Figure 4.11 and Video 4.3).

Figure 4.10 The mobility and flexibility of these groups of cells is surprising considering the complexity of their arrangement (60 ×). Video 4.2

Figure 4.11 The mechanical dependence of the cells on the fibrillar network is total and can be observed when traction is applied to the fibrils. The slightest traction on the fibrils modifies the orientation and position of the cells. The shape of the cells is also modified as a result of traction on the fibrils. This could be an example of mechanostimulation inducing mechanotransduction (130 ×). Video 4.3

The consequences of this are unclear, but the cytoskeleton must be influenced in some way. Strong traction on the fibrils provokes a decrease in diameter and a lengthening of the cells. Release of the traction allows the cells to return to their initial shape and position (Figure 4.12 and Video 4.4).

Figure 4.12 Strong traction on the fibrils provokes a decrease in diameter and a lengthening of the cells. Release of the traction allows the cells to return to their initial shape and position (130 ×). Video 4.4

The interconnection between the extracellular matrix and the cytoskeleton, via the integrins, has been amply demonstrated by others in vitro. The nucleus of a cell appears transparent under microscopic endoscopy, but the mechanical influence of the cytoskeleton on the nucleus and other organelles within the cell has also been well demonstrated by others. Current research into cell membranes suggests close links between the intracellular and extracellular environments. It is possible to imagine that some form of mechanostimulation of the fibrillar network may have an effect on cellular production. How does the microvacuolar system ensure cell survival? The vascular supply channel has many shapes (Figure 4.13). Again, there seems to be no apparent order or logic. Major blood vessels are arranged in fairly straight lines, rather like the trunks of trees, with smaller vessels branching off them. The shape of the capillary network is astonishing,

however. Like the fibrillar network, on the surface there seems to be no apparent order or logic. Capillaries follow irregular, sometimes rather sinuous paths, winding like country lanes.

Figure 4.13 The shape of the capillary network is astonishing. There is no apparent order or logic. A Large vessels are arranged in fairly straight lines (10 ×). B Medium vessels branch and curve around (60 ×).

C Smaller vessels often follow irregular, sometimes sinuous paths, like winding country lanes (130 ×).

All the nerves, arteries, veins, and lymphatics make use of and rely on the scaffold of the multifibrillar and multimicrovacuolar structures, which appears to account for the pattern of their distribution (Figure 4.14).

Figure 4.14 Arterioles, capillaries, venules, and nerves all make use of the multimicrovacuolar system for support. This accounts for their seemingly random pattern of distribution (130 ×).

At the cellular level, we sometimes see a pericellular capillary network. Each cell is surrounded by a tiny capillary vessel of around 10 microns in diameter. Surprisingly, in some areas this applies to all cells, but in other areas only a few cells are encircled in this way (Figures 4.15 and 4.16, and Video 4.5). Nevertheless, often one has the impression that some cells are not directly vascularized, because they are not in direct contact with a capillary.

Figure 4.15 Observation of the blood vessels reveals variations in their pericellular distribution. It is astonishing to see that in some areas a capillary of 10 or less microns in diameter encircles each cell (200 ×). Video 4.5

Figure 4.16 A Sometimes several cells are encircled very closely (100 ×) B Sometimes only a few cells are encircled in this way (100 ×)

The flow of information and energy follows the path of the multimicrovacuolar structures, which in turn ensures efficient distribution. The enormous advantage of this arrangement is that the cellular and extracellular elements receive a continuous, uninterrupted supply of energy and information, even during movement, because when the fibrillar scaffolding moves, the vessels move with it. There is no rupture in the supply line.

KEY STATEMENT We could say that energy supply is dependent on the architecture of the microvacuole as well as on the support of the microvacuolar framework.

Future generations of anatomists will probably smile at these discoveries. We are at the dawn of this type of exploration, and as technology advances new physiological explanations will doubtless be formulated.

FOLLOWING THE RED THREAD We have now answered Red Thread Question 3 from the end of Chapter 1: RED THREAD QUESTIONS 3. How do these fibers adapt to provide simultaneously mobility and uninterrupted energy supply during physical effort? The circulatory and nervous systems are an integral part of this fibrillar mesh

CONCLUSION In Chapters 1 through 4, we have described our observations of living matter during perioperative endoscopy. Let us now attempt to interpret these observations and try to make sense of what we are seeing. To help us with this, we can draw a number of conclusions. • A continuous fibrillar network provides tissue continuity throughout the body. • This fibrillar network encloses microvolumes that we have called microvacuoles, which are filled either with cells or with collagen and glycosaminoglycans. • The theory of the microvacuole permits a better understanding of the notion of form and volume, and the organization of living matter. • The multimicrovacuolar system ensures the uninterrupted transmission and exchange of energy and information, even when it is subject to constraint, by maintaining the functional independence of specific anatomical structures.

• The concept of the microvacuole meets the necessary requirements for a definition of a living organism, because it provides an explanation as to how the tissues adapt to constraint while preserving their initial form. This is possible because the tissues are already under tension. Perioperative endoscopy has provided a wealth of information. However, many questions remain and they cannot be answered by observation alone. • How does this multimicrovacuolar system deal with gravity? • Why is the architecture of this fibrillar network fractal, and why does it appear to be chaotic?

Comment by James L. Oschman, PhD

It might seem that the anatomy of the human body is well established. Countless anatomy books testify to our incredibly detailed knowledge of the structural design of the living organism, worked out by centuries of careful anatomical observation, to the point at which we might suspect that there is little remaining to be discovered. This book totally shatters that myth. Dr. Guimberteau is taking us on an unbelievably exciting voyage into a new and uncharted world. His exploration is an adventure as thrilling as any experienced by the great explorers of new continents, the depths of oceans, or other territories never seen before by humans. In this book, new worlds are being discovered—worlds never visited before and never even dreamt of. Dr. Guimberteau’s new world is nothing like that seen in cells and tissues dissected from the body, interesting and valuable though they may be. Instead, it is a very close look at what is actually happening under the skin of living, breathing human beings. The word ‘holistic’ recognizes that our bodies have continuity in structure and function —something that has been obvious for a very long time. Various concepts relate to this continuity and its physiological and medical significance. One is the thesis developed in the classic book The Extracellular Matrix and Ground Regulation: Basis for a Holistic Biological Medicine by the distinguished Austrian histologist Alfred Pischinger, in collaboration with his German colleague Hartmut Heine.1 They stressed this as a ‘system of systems’, because it is the one system that touches all the other systems in the body. Their functional descriptions followed on from those of A.T. Still, the founder of osteopathy, who stated that the fascia is the place to look for the causes of diseases and the place to begin treatments.2 Pienta and Coffey referred to the same network as a ‘tissue tensegrity matrix’.3 We described the same system as a ‘living matrix’.4 This was based on the discovery of the integrins that span the cell membranes, connecting the extracellular matrix with the cytoskeletons, as well as the links across the nuclear envelope that tie the nuclear matrix and DNA into a continuous fabric reaching into every part of the organism. Never before has this profound discovery been so beautifully documented. For those of us who work with living tissue, as scientists or therapists, Dr. Guimberteau has provided with a rich and exciting expedition of discovery, filled with new information for us to absorb and evaluate and to use to redefine our previously limited pictures of what is happening within us. What leaps from these pages is his cautious excitement about the new world he has discovered and that he wants to share with us. It is an inspired description, virtually poetic in its tone. His videos blend science and art in a way that reinforces the idea that truth is beauty and beauty is truth.

REFERENCES

1. Pischinger A. The extracellular matrix and ground regulation: basis for a holistic biological medicine. Berkeley, CA: North Atlantic Books; 2007. 2. Still AT. Philosophy of osteopathy. Kirksville, MO: AT Still; 1899. 3. Pienta KJ, Coffey D. Cellular harmonic information transfer through a tissue tensegrity-matrix system. Med Hypotheses. 1991;34:88–95. 4. Oschman JL, Oschman NH. Matter, energy, and the living matrix. Rolf Lines. 1993;21:55–64.

Comment by Leon Chaitow, ND, DO

Among the main tenets that guide osteopathic practice is an appreciation that the human body possesses, and depends on, self-regulatory mechanisms that in turn involve intimate inter-relationships between structure and function. Osteopaths therefore frequently focus clinical attention on identification and normalization of biomechanical (and other) obstacles to self-regulation, with the aim of enhancing or restoring functionality through manually applied manipulation, mobilization, and rehabilitation methods. Emerging awareness of the remarkable characteristics of mechanotransduction supports these therapeutic concepts and practices, offering insights into some of the mechanisms involved. Mechanotransduction describes processes by which cells and tissues respond to alterations in their architectural features, with consequent changes in their shape being mirrored by modification of biological function. As the structural form of cells alters in response to applied load—for example involving forces such as torsion, tension, shear, compression, stretch, bending, and friction—processes are triggered involving chemical signaling that profoundly influence cellular behavior and development, including gene expression. Dr. Guimberteau’s films of living tissue reveal the intimate relationships between the cells and the continuous, body-wide multifibrillar network that is a major component of the extracellular matrix. In this chapter, we see that cells are embedded within microvolumes (microvacuoles) formed by the intertwining of collagen fibers within this network. In Chapter 6, we see how manually applied traction to the skin is transmitted to the prestressed fibers in the multifibrillar network. These films show how the cells change their shape and spatial relationships in response to externally applied mechanical constraint. It is therefore reasonable to conclude that the mechanical stimuli produced by manual therapy techniques affect cell function through force transmission and mechanotransduction. A number of in vitro studies that have modeled osteopathic treatment methods lend support to this hypothesis. They have provided evidence of cellular responses that may explain beneficial clinical outcomes. These in vitro results mirror observed clinical outcomes in the treatment of somatic dysfunction, such as plantar fasciitis.6 Standley et al. summarize the potential clinical importance of modulated application of manual load from an osteopathic perspective as follows: ‘It is clear that strain direction, frequency and duration, impact important fibroblast physiological functions known to mediate pain, inflammation and range of motion. Clinical translation of these studies is important to definitively identify cause and effect of manual medicine treatments.’1

Kumka and Bonar explain that mechanotransduction occurs ‘as cells convert a diversity of mechanical stimuli, transmitted throughout the extracellular matrix, into chemical activity to regulate morphology and function of tissues.’2 Wipff and Hinz give the example of myofibroblasts—connective tissue cells that help to reconstruct injured tissue by secreting new extracellular matrix and by exerting high contractile force.3 They note that deregulation of these activities leads to tissue contracture and fibrosis, and that two principle factors drive the development of myofibroblasts: particular levels of mechanical stress that are sensed by these cells, using specialized matrix adhesions, and transforming growth factor-β. In their words, ‘myofibroblasts work best under stress.’ For example, osteopathic methods such as Myofascial Release4 and Strain Counterstrain5 have been applied to ‘distressed’ human fibroblasts. In both cases, sheets of fibroblasts were repetitively stressed for 8 hours, resulting in morphological changes as well as the presence of inflammatory products. These were then ‘treated’ by modeled osteopathic soft tissue methods for 60 seconds. Results included enhanced morphological appearance and, more importantly, the markedly reduced production of inflammatory cytokines. In another study, cellular changes resulting from load application automatically influenced tissue behavior. For example, when subjected to mechanical strain, fibroblasts in fascia secreted interleukin-6, which induced myoblast differentiation, increasing myotube numbers by up to 78%—a process essential for muscle repair.7 The multiple features identified by researchers, such as those listed above, involve applied load, which modifies cellular architecture and physiological behavior via the unique attributes of biotensegrity—as discussed in Chapter 5. Biotensegrity comprises homeokinetic structures that are stabilized by a combination of continuous tension and discontinuous compression, which converts ‘dynamic mechanical information into biochemical changes’.8 The resulting self-organizing biological processes therefore take place in a fluid-based, accommodating environment, in which—in healthy tissues —load is absorbed, transmitted, communicated, and responded to, resiliently, by the specialized cells of living matter. From a personal perspective, the insights that emerge from Guimberteau’s filming of living tissues makes the way that application of manual therapy influences the body infinitely more comprehensible—while simultaneously providing clinical challenges. The ways in which subdermal tissues and structures are able to adapt to compression and other forms of applied load by modification of shape, orientation, and arrangement, while simultaneously altering their biochemical status, represent the clinical puzzle that all manual therapists face. What degree, duration, and direction of load (compression, torsion, stretch, shear force, etc.)—in other words, what dosage—will have the optimal effects in the tissues being addressed?

REFERENCES

1. Standley PR, Meltzer K. In vitro modeling of repetitive motion strain and manual medicine treatments: potential roles for pro- and anti-inflammatory cytokines. J Bodyw Mov Ther. 2008;12:201–3. 2. Kumka M, Bonar J. Fascia: a morphological description and classification system based on a literature review. J Can Chiropr Assoc. 2012;56:179–91. 3. Wipff PJ, Hinz B. Myofibroblasts work best under stress. J Bodyw Mov Ther. 2009;13:121–7. 4. Meltzer KR, Cao TV, Schad JF, King H, Stoll ST, Standley PR. In vitro modeling of repetitive motion injury and myofascial release. J Bodyw Mov Ther. 2010;14:162– 71. 5. Eagan TS, Meltzer KR, Standley PR. Importance of strain direction in regulating human fibroblast proliferation and cytokine secretion: a useful in vitro model for soft tissue injury and manual medicine treatments. J Manipulative Physiol Ther. 2007;30:584–92. 6. Wynne MM, Burns JM, Eland DC, Conatser RR, Howell JN. Effect of counterstrain on stretch reflexes, Hoffmann reflexes, and clinical outcomes in subjects with plantar fasciitis. J Am Osteopath Assoc. 2006;106:547–56. 7. Hicks MR, Cao TV, Campbell DH, Standley PR. Mechanical strain applied to human fibroblasts differentially regulates skeletal myoblast differentiation. J Appl Physiol. 2012;113:465–72. 8. Swanson RL 2nd. Biotensegrity: a unifying theory of biological architecture with applications to osteopathic practice, education, and research—a review and analysis. J Am Osteopath Assoc. 2013;113:34–52.

5 Spatial Arrangement, Tensegrity, and Fractalization Physical phenomena that influence living tissue Maximum coverage of a flat surface Filling the three-dimensional space The notion of equilibrium at rest and during movement How form can resist the force of gravity: tensegrity What is fractal organization? Following the red thread

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY In this chapter, we will begin to interpret our findings relating to the organization of living matter and to try and make sense of them. We will show that the framework of fibrillar structures obeys conventional physical rules, but that these structures also exhibit nonlinear behavior. This opens the door to a world where nonNewtonian and fractal physics have a role to play.

PHYSICAL PHENOMENA THAT INFLUENCE LIVING TISSUE Living tissue is under the influence of fundamental physical phenomena. The following is a non-exhaustive list of these: • tissue continuity • tissue tension • the permanent presence of fluid in the tissues • capillary pressure • electrical potentials • constant temperature • gaseous exchange • varying pressure and concentration gradients • forces between fibrils and cells • the existence of intratissular bubbles • the bursting of microvacuoles, caused by pressure differentials and surface tension • emission of water droplets and vapor during endoscopy

Crucial as these physical characteristics are, we must remember that the main force that living tissue has to deal with is gravity. Although we might initially expect that the fibrillar architecture would obey the laws of classic Newtonian physics, in practice we also encounter non-linear behavior at all levels, which can be explained only by non-Newtonian physics and fractal geometry. Nothing is regular, but there must be an underlying logic to the irregular arrangement of these anatomical structures, and so we are faced with difficult but essential questions about how living matter is organized.20, 21, 22, 23

• How are microvacuoles assembled to create a form? • What rules govern their spatial arrangement? The microvacuole is a microscopic space framed by the intertwining of fibrils. This morphological unit is revealed when we lift and apply traction to anatomical structures inside a living body. However, under normal physiological conditions microvacuoles are in fact flattened and piled up together. The volume contained within each microvacuole is unstable, because a microvacuole is not a hermetically sealed polyhedron (Figure 5.1). However, it does exist; it is not a virtual volume. Intravacuolar pressure fluctuates, but the volume remains constant. There is a permanent diffusion of molecules in and out of the microvacuole along a concentration gradient. The microscopic spaces contained within the microvacuoles resemble soap bubbles. This raises questions that have long intrigued philosophers and scientists: • How do three-dimensional structures most efficiently fill a given volume? • How are they best arranged?

Figure 5.1 Microvacuoles in the preaponeurotic area (100 ×). The microvacuole is not a hermetically sealed polyhedron, but it is a real morphological entity

MAXIMUM COVERAGE OF A FLAT SURFACE: FILLING THE TWO-DIMENSIONAL SPACE Maximum coverage of a surface to leave no gaps can be achieved by the use of geometrical or non-geometrical shapes (Figure 5.2). Regular polygons of equal size and shape, such as equilateral triangles, squares, or hexagons, can be fitted together perfectly to completely cover the surface. Non-geometrical shapes can also fit together perfectly. We see this in complex mosaic patterns. This polygon solution is also employed at the skin surface of many animal species, as well as on plant surfaces (Figure 5.3).

Figure 5.2 A Regular polygons of equal size and shape, such as equilateral triangles, squares or hexagons, can be fitted together perfectly to completely cover the surface B Non-geometrical shapes can also fit together, as in complex mosaic patterns

Figure 5.3 Polygons are also found at the skin surface of many animal species. This is also true of many plant surfaces A Human skin B Surface of a mushroom C Sardine scales D The surface of the foot of a guinea fowl

FILLING THE THREE-DIMENSIONAL SPACE The rule of the minimal surface area contained within a boundary refers to the minimum space into which you can put the maximum number of volumes. The occupation of space in all three dimensions is a problem that has been studied since ancient times. A solution was proposed that made use of polyhedrons. These can be either regular or irregular, equal or unequal. The possibilities provided by this solution are numerous. Pythagoras, followed by Plato, defined five regular polyhedrons.24

1. The tetrahedron is the simplest. It is a polyhedron composed of four triangular faces. This geometric surface encloses the minimum volume within the maximum surface area. This is the complete opposite to a sphere, which encloses the maximum volume within the minimum surface area. 2. The hexahedron, commonly known as a cube. 3. The octahedron, which is a polyhedron with eight faces. 4. The icosahedron is a regular polyhedron with 20 identical equilateral triangular faces (Figure 5.4A). 5. The dodecahedron (Figure 5.4B) is composed of 12 equal and regular pentagonal faces. It is capable of filling space optimally by forming a network of dodecahedrons that is both regular and isotropic (which means that its structure is identical in all directions in space).

Figure 5.4 A Icosahedron B Dodecahedron

One must begin by asking how elements are arranged within living matter. Joseph Plateau (1801–1883), a Belgian physicist, formulated Plateau’s laws, which describe the structures formed by soap films. The mathematical problem of the existence of a minimal surface within a given boundary is named after him.13, 25The arrangement of the structures formed by soap films (bubbles) and their occupation of space, as described in Plateau’s laws, help us to understand how structural elements could be organized in living matter.

Soap bubbles are a polyhedral network, because they contain small, unequal, polyhedral volumes with a variable number of faces that form partitions within the network. They fill space optimally and are arranged in a state of maximal contraction, with the surface area reduced to its minimum. Their structure is random and has no fixed orientation. There is no external constraint, so their occupation of space can be described as static. However, the surface tension produces internal constraint. When a partition disappears, rearrangement of the whole network occurs immediately. The shape and the orientation of the partitions are modified until a new equilibrium is achieved. This new equilibrium is maintained until the next partition breaks up and disappears, and so on. But Plateau’s laws in relation to soap bubbles do not explain the differences in tissue density between, for example, a fat lobule under tension and the sliding spaces where cells are absent (except for a few fibroblasts). Moreover, the resulting forms, even if they are homogenous, display a great variety of shapes and sizes. Despite their apparent regularity, neighboring fat lobules do not resemble each other. The overall appearance of living matter is chaotic, as we have seen, and there is no regularity. Nevertheless, Plateau’s law of minimal arrangement makes use of polygonal, triangular, pentagonal, hexagonal, and icosahedral forms. These forms are similar to microvacuolar shapes found in the body, and are also a perfect match with the basic forms of tensegrity. We will discuss tensegrity in more detail later in this chapter. The similarity between these microvacuolar systems, Plateau’s laws of physics, and the architectural concept of tensegrity is disconcerting (Figure 5.5), and is a line of research that we should follow even if we know that the comparison is not valid and that the behavior of soap bubbles cannot be equated with the behavior of living tissue.

Figure 5.5 Plateau’s law of minimal arrangement makes use of polygonal, triangular, pentagonal, hexagonal, and icosahedral forms A A network of icosahedrons B These forms are similar to microvacuolar forms found in the body. (10 x) C Neighboring fat lobules do not resemble each other. Diversity exists within the apparent regularity. (2 x) D Soap bubbles are a good example of a polyhedral network. The network is chaotic in appearance, and there is no apparent regularity. (10 x)

KEY STATEMENT It could be argued that the organization of fibrils into microvacuolar volumes, by making use of minimal surface areas, reduces the quantity of materials used and enables the system to deal with physical constraint more efficiently.

The behavior of the microvacuole seems to obey the ‘principle of economy’, a methodological principle of efficient reasoning proposed by William of Ockham in the 14th century, which came to be known as Occam’s (sic) razor. William of Ockham (1287−1347) was an English Franciscan friar and philosopher who argued that one should always opt for an explanation in terms of the fewest possible causes, factors, or variables. In other words, all that is superfluous is useless and must be eliminated. This principle can be

used to explain many natural phenomena. If we apply Ockham’s principle to the microvacuolar system, it reveals the following insight: the elaboration of the final form does not use any fiber or microvacuole more than is strictly necessary. This highlights the economy and efficiency of the microvacuolar system. A single factor, and an important one, disrupts this relative harmony and prevents easy understanding: all the forms are irregular and appear to be arranged in a disorderly fashion. They certainly appear to be polyhedrons, but they are totally different from one another and completely irregular. However, it is undeniable that microvacuoles are very similar to icosahedral forms, which, in mathematical terms, are the most suited to the role of spatial arrangement and mobility. KEY STATEMENT The use of the irregular polyhedron as the fundamental unit of form seems to be a necessary consequence of the basic physical forces acting on living organisms.

If we now accept this concept regarding the arrangement of the multimicrovacuolar structures, we must address the following three questions. • How do the multimicrovacuolar structures, formed in this way, arrange themselves? • How do they maintain their equilibrium? • Are they capable of adapting to movement by changing their shape and form? As a first step in trying to answer these questions, we should look again at tissue tension. Tissue tension is an everyday observation during surgery. The edges of the skin spontaneously draw apart a few millimeters as soon as the surgeon makes an incision. Cutting through an aponeurosis is like cutting an elastic band. Stitching together the two ends of a ruptured tendon requires considerable traction by the surgeon to overcome the resistance of the retracted fibers of the injured muscle and to bring the two ends together, so that the tendon can be repaired.

Pre-existing endogenous tensions These observations confirm the existence of a permanent state of tissue tension within the body (Figure 5.6 and Video 5.1). There is an intrinsic, preexisting constraint. The fibers and fibrils in the multifibrillar network are prestressed. They form a continuous tensional network throughout the body. The importance of this will become clear later in this chapter, when we discuss the concepts of tensegrity and biotensegrity. KEY STATEMENT The structural components of our tissues are in a permanent state of preexisting endogenous tension.

Figure 5.6 Endogenous tissue tension. There is a permanent state of tissue tension within the body, which means that the fibers and fibrils in the multifibrillar network are prestressed. Here are examples from four different areas of the body A The edges of the skin spontaneously draw apart a few millimeters as soon as the surgeon makes an incision. (5 x) B Cutting through an aponeurosis is like cutting an elastic band. (5 x) C Section cut of a tendon causes the edges to draw apart strongly. (5 x) D Several minutes after the surgeon exposes the subcutaneous area just below the hypodermis, tiny bubbles with distended walls appear at the surface. They resemble soap bubbles. (5 x) Video 5.1

As described in Chapter 2, when the surgeon exposes the subcutaneous area just below the hypodermis, to reveal a network of woven fibrous tissue, tiny bubbles appear at the surface of this tissue. They resemble soap bubbles with distended walls about to burst, but they are not flattened, despite the force of gravity. When we apply traction to this tissue with forceps, these small bubbles appear to explode. This is evidence of the existence of microvolumes under internal pressure, which is different from atmospheric pressure. The pressure exerted by the circulatory system also influences tissue tension within the living body. Our tissues are under tension, but this tension is the result of many physical forces, including electrical potential. The existence of electrical activity within the body is confirmed by simple diagnostic procedures, such as electrocardiograms, electromyograms, and electroencephalograms. This electrical tension must play a role in the maintenance of form, because the severance of a nerve leads to the collapse of muscle tissue and to atrophy of the skin in the area supplied by the nerve. The irregular multifibrillar network of interweaving fibrils, composed of multiple forms and volumes, can be torn, just like any woven fabric. However, this structured tissue, which looks very delicate, is in fact perfectly capable of maintaining its integrity, even in areas of considerable tissue tension. What are the mechanisms that enable the tissues to maintain their form while dealing simultaneously with external forces, such as gravity, and with internal forces, as we have already seen? In a resting state, there must be equilibrium between the different forces acting on the tissues. The idea of a relationship between differing forces and pressures is not new. We are used to measuring respiratory, cardiac, arterial, and intracranial pressure, but these are pressures within cavities filled with liquid or air. However, we now also have evidence of pressure differences within homogenous matter. Our bodies are under tension, and they manage to develop sufficient force to oppose gravity and preserve form. How does intracorporeal

tension achieve this? Traditional biomechanical theories fail to provide satisfactory answers to these questions. We must therefore leave the beaten track and search for new explanations, breaking out of the confines of traditional thought processes to pursue different modes of scientific thinking. But any new theory must be compatible with observations made during endoscopy and comply with strict specifications. These include endogenous tissue tension, tissue architecture, volume, dynamic adaptability, transmissible energy, and resistance to the gravitational force. Observation and the basic laws of classical Newtonian physics teach us that resistance to gravity could be achieved in two ways. 1. The pre-existing microvacuolar tension provokes a structural reaction to the gravitational force. 2. The biomechanical properties of the fibers and the organizational capacity of the fibrillar network facilitate the dispersion of the force.

THE NOTION OF EQUILIBRIUM AT REST AND DURING MOVEMENT How is form maintained at rest? The microvacuole is maintained in one of two ways. 1. The microvacuole is filled with cells; it constitutes a cluster of cells whose size and number are variable, but the volume of the microvacuole is maintained by the resident cells. 2. The microvacuole is filled with collagen and glycosaminoglycans, as in the sliding systems; this is where the search for an explanation of the ability of the microvacuole to maintain its volume is interesting, because even if the microvacuole is a microvolume, it is the cumulative nature of the system that gives rise to the form. A microvacuole cannot exist in isolation. Its existence depends on its association with other microvacuoles. Its natural tendency, driven by the strong cohesion between water molecules, would be to assume a spherical

shape. However, this is not the case, because many other factors are involved that determine its polyhedral shape. First, surface tension, which is a localized increase in energy at the surface of a liquid and depends on the cohesive force between identical molecules, is proportional to the strength of the intermolecular cohesion of the liquid in question. Strong cohesive bonds exist between water molecules. Surface tension, or surface energy as it is also known, may then cause internal constraint, because there is a pressure difference between the inside of the vacuole and the stiffer fibrillar frame. Furthermore, water adheres to the surface of the membrane and may be transported by capillarity, a phenomenon in which surface tension is an important factor. Capillarity enables sap to travel upward inside the trunks and branches of trees despite the force of gravity. Other factors involved certainly include osmotic pressure and the phenomenon of adsorption—the adhesion of molecules to solid surfaces. Weak, reversible bonds are created by van der Waals’ forces. And it seems likely that intravascular pressure and body temperature will also influence the extracellular environment in some way. Gravity balances this interplay of internal forces, but the intravacuolar pressure—in a state of equilibrium within fixed boundaries—remains greater than the external pressure (Figure 5.7). This positive pressure difference is explained by the Young−Laplace equation.26 The pressure is positive because of energy loss consequent on the creation and maintenance of the interface. Three main factors—the external tension, the behavior of the fibers, and the intravacuolar environment—all have a bearing on the pressure gradient. The result is that the structures remain under tension and are therefore subjected to internal constraint, and the volumes are maintained.

Figure 5.7 At rest, the structures remain under tension and internal constraint because of the difference between the internal pressure of the microvacuole and the relatively rigid fibrillar frame A Intratissular microvacuoles. (130 ×) B Schematic diagram

We cannot expand our explanation of the mechanics of non-homogeneous environments and fluids any further, because of our lack of expert knowledge in this field. The incompressible intravacuolar volume may be subjected to localized areas of compression that immediately cause an increase in the distension of the fibers, which in turn produces a global tension−compression effect in the surrounding microvacuoles. This alternation of tension−compression is repeated in a decreasing manner toward the periphery (Figure 5.8).

Figure 5.8 The incompressible intravacuolar volume is subject to localized areas of compression, which immediately result in an increase in the distension of the fibers that make up the fibrillar frame of the microvacuole. This, in turn, causes compression of the surrounding microvacuoles and increases the tension of the fibers that constitute their fibrillar frames. As a result, or in other words, the microvacuole changes shape but the volume remains stable A State of equilibrium B Generalized increase in pressure C Raised intravacuolar pressure. This increase in pressure is then transmitted to the next adjacent microvacuole, and so on

These microvolumes are permeable and leaky, and in a stable state permeability is ensured by the drainage of the extracellular environment,

known as lymphatic drainage—but this is probably not the only mechanism at play. There is equilibrium between all the microvacuoles, which possess the same relative dynamic force relationship with one another. Their volume, pressure, quality, architecture, and resistance to the force of gravity can therefore be maintained under normal physiological conditions. KEY STATEMENT We must not forget that this complex state of equilibrium is maintained in the absence of hermetically sealed membranes. We are dealing with a space that is at once both open and partitioned.

How is form maintained during movement? During normal, physiological, voluntary movement, the multimicrovacuolar system continues to play its role. It is vital that equilibrium is maintained. (In Chapter 6, we will see what happens when tissues are forced beyond their physiological limits.) Movement is brought about by the behavior of the fibrils. Individual microvacuoles are globally incompressible, like a balloon, so when external pressure is applied to them they are forced to change shape, thus exerting pressure on adjacent microvacuoles, which in turn must change shape as pressure is applied to them, and so on. In this way, local compression spreads throughout the system (Figure 5.9 and Video 5.2). At the same time, the fibrils are required to deal with the constraint and they orient themselves in the direction of the imposed force. Distension of the fibrils enables the microvacuoles to lengthen. Their ability to slide over each other enables them to rearrange themselves to adapt to the imposed constraint. The force of the imposed constraint weakens progressively as it spreads out towards the periphery, and is absorbed in all three dimensions. The system functions in the same way as a shock absorber.

Figure 5.9 Now we apply our model of equilibrium to living tissue. Movement is carried out by the fibers. The microvacuoles are deformed, but because their volume is incompressible, the resulting deformation affects the adjacent microvacuole, which in turn is subjected to a local increase in pressure. This increase in pressure is then transmitted to the next adjacent microvacuole, and so on. (130 ×) Video 5.2

In this way, the three dynamic properties of the fibrils act together to maintain internal equilibrium during movement. 1. They lengthen to deal with traction. 2. They move independently in relation to each other to spread the local increase in pressure throughout the system. 3. They are able to divide to create new volumes to absorb the force acting on the multimicrovacuolar system. KEY STATEMENT This network of collagen fibrils undergoes constant rearrangement, which brings about displacement of their bifurcation points, enabling the network to deal with the mechanical demands imposed on it while at the same time ensuring progressive absorption of the force at the periphery (Figure 5.10).

Figure 5.10 A and B This network of collagen fibrils undergoes constant rearrangement, which entails displacement of their bifurcation points, enabling the network to deal with the mechanical demands imposed on it while at the same time ensuring progressive absorption of the force toward the periphery of the network C and D Even in distension (C) or compression (D), forces are transmitted but volume is relatively preserved, maintaining the global shape or form

The pre-existing constraint in the fibrillar network confers a degree of elasticity to the system, allowing it to return to its original configuration as soon as any exogenous constraint is removed. Tissue memory can be influenced by other factors, such as the glycosaminoglycan composition and the hydrophilic quality of the intravacuolar liquid, the quality of the fibers, and the type and density of the collagen. This working model aims to remain true to our observations but is certainly imperfect (Figure 5.11). It attempts to account for the basic physical features of living tissue in vivo. Nonetheless, it provides us with an explanation of the method of building a living form.

Figure 5.11 This working model provides us with an explanation of the method of building a living form, whose architecture consists of multiple, water-filled microvolumes Volumes seem to change but remain stable, although local shapes alter A Rest position B Compression C Distension

This raises a question that is often forgotten: how can this living matter, which we consider to be in a state of mechanical equilibrium, maintain its shape and form while at the same time resisting gravity and even overcoming it during periods of growth?

HOW FORM CAN RESIST THE FORCE OF GRAVITY: TENSEGRITY The concept of tensegrity was developed by Buckminster Fuller (1895– 1983), an American architect and systems theorist. He introduced the element of tension into construction. This was quite revolutionary, because man-made constructions had always been solid structures that made use of the forces of gravity and the compressions they are subjected to. Relevance and implications Tensegrity is very useful in helping us to understand our relationship with gravity. Buckminster Fuller 27set out to create an energy-efficient structure that would require the least possible energy to fulfill its purpose. He discovered that the tetrahedron meets these requirements. As already mentioned, the tetrahedron (a polyhedron composed of four triangular faces) has a high surface area to volume ratio. It combines a large surface area with a minimal volume. The advantage of this configuration is that it can shift

from one form to another without requiring more space. This confers real stability during movement. Tensegrity structures are different to traditionally conceived structures. They maintain their integrity because their architecture associates global tension with local compression, and because they are in a state of permanent, preexisting tension (Figure 5.12). Buckminster Fuller was the first architect to design structures employing this approach.

Figure 5.12 Tensegrity structures combine global tension with local compression and are in a state of permanent, pre-existing tension A Compression struts (orange) float in a tensional network of prestressed cables (yellow) B Polyhedral microvacuoles are defined by an intertwining of fibers enclosing liquids under tension. (200 x) C Schematic diagram: anteroposterior view D Schematic diagram: lateral view

From the architectural point of view, a tensegrity structure is a collection of stable struts and interconnected cables under tension, which rearrange themselves when subjected to external constraint, and which return to their initial form and equilibrium as soon as the constraint is removed. The organization of interlinked elements that make up the structure is able to

disperse and absorb the forces of compression by diffusing them throughout its continuous tensional network. This concept is closely related to the principle of synergy and antagonism (or negative synergy), which is an all-pervading characteristic of biomechanics. Synergy is the interaction of multiple elements within a system to produce an effect greater or different from the sum of their individual effects. Synergia is a Greek word that means ‘working together’. Buckminster Fuller studied the implications of synergy in great detail, and proposed a new term, synergetics. This refers to the behavior of dynamic systems in which combined action is favored over the actions of individual components.27 KEY STATEMENT A tensegrity structure provides a global response to a local mechanical stress. The result is a degree of independence from the force of gravity (Figure 5.13 and Video 5.3).

Figure 5.13 A Without a tensegrity model, our fibrillar structure would collapse under gravitational force B With the tensegrity model, our structure absorbs and disperses the compression by spreading the load throughout the entire network, including the structures at the periphery C The video shows the global response to local mechanical constraint Video 5.3

These phenomena are ubiquitous in biomechanics, and there are many examples of tensegrity in the natural world. One example is the intervertebral disk. In the microscopic domain, Donald Ingber applied this concept to the intracellular cytoskeleton.28 It is difficult not to draw a parallel between the icosahedron or tetrahedron and the microvacuole. We must admit that within the fibrillar network we sometimes see forms that resemble those in Euclidian geometry, but very rarely. There is, however, a direct relationship between the observable and indisputable existence of microvacuoles and the theory of tensegrity (Figure 5.14). I do not know of any other biomechanical theory that provides such a clear and rational explanation of what I observe during my endoscopic explorations. As we have seen, the fibrils slide along each other, sometimes dividing into two, three, or four subfibrils, thereby immediately spreading the constraint into newly formed spaces. This provides a simple explanation, not only of the distribution of the force of gravity, but also of the ability to allow movement, which decreases at the periphery with little impact on surrounding structures (Figure 5.15 and Video 5.4).

Figure 5.14 The behavior of microvacuoles and the fibrillar network is well explained by the theory of biotensegrity. There is some relationship between the observable existence of microvacuoles and the theory of tensegrity. This cannot be underestimated A Parallel arrangement of fibrils. (200 x) B Opposing triangles. (200 x)

C Superimposed triangles. (200 x) D A succession of triangles. (200 x)

Figure 5.15 Trifurcation (division into three branches) of a fibril. This mechanism diffuses and absorbs force through the fibrillar network. (200 x) Video 5.4

BIOTENSEGRITY Biotensegrity, a term formulated by Stephen Levin, is the application of the principles of tensegrity to living matter. It introduces the element of tension and the concept of equilibrium between the structures, and represents a major advance in our understanding of the organization of the anatomical structures. Biotensegrity can be applied to biological organisms at all levels, from the molecule to the vertebral column.29, 30 Just as tensegrity involves the concept of elements under tension and compression, so biotensegrity is a model of the organization of living matter conceived as a network of intersecting cables and struts that are either under tension or compression.

This organization would ensure perfect equilibrium between the constituent structures, and the ability to resist the force of gravity. If this model is applicable to living matter, it would explain how such basic structures could take part in the construction of the human body at all levels, from individual molecules to the entire form. The biotensegrity model involves geometric shapes—similar to Plato’s icosahedrons—but these icosahedrons are idealized force transmitters, not actual physical structures that can be clearly visualized in the body. The stick and string models are representations of dynamical forces within a constantly changing milieu. These forces are present concurrently at the subcellular, cellular, regional, and organism level, hence they may span the macroscale, Newtonian scale, and that at which quantum principles operate. However, this theoretical model, unique as an attempt to articulate the influence of gravity on human architecture, is not fully applicable to living matter. Biology imposes its laws, its forms, and various other features, which can be readily observed in vivo. This adds another dimension to the equation —at once singular and more complex. • The living matter that constitutes the architecture of the human form is composed of cells and fibers that form three-dimensional microvolumes. These basic architectural units are both polyhedral and irregular and are in total continuity and under tension. Their distribution and arrangement do not display any apparent order, and are not in accordance with Euclidean geometry or linear mathematics. Instead, there appears to be a non-linear and chaotic, but efficient, organization. Efficiency is a feature of all complex systems. • There are no empty spaces in living matter. The microvolumes between the fibers are filled either with cells, with their own cytoskeletons, or with pressurized fluids. Their components are hydrophilic. They provide form by the accumulation of their volumes, which remain constant. The pressurized intravacuolar contents are localized areas of compression within the continuous tensional network of fibers. • Mobility of the fibrils is permitted by their ability to distend and dissociate. Dynamic fractalization is the term I use to describe this dissociation. This

allows an imposed constraint to be absorbed at all levels of living matter, which explains its ability to resist gravity or any other imposed constraint. • Dynamic fractalization involves non-linear behavior, with unpredictable as well as deterministic characteristics. The polyhedral frame of the microvacuole is never stable, and is likely to change at any given moment. This element of randomness and unpredictability is characteristic of microvacuolar movement (Figure 5.16). The shape of the intramicrovacuolar volume is never constant, and the inherent potential for changing shape is considerable. • My observations show that there is no hierarchy in the manner in which the fibrillar structures are arranged in the body. They are not organized as tensed cables and rigid struts. In the biotensegrity model, movement takes place at the junction between those cables and struts, but my observations show that fibrils can move in many different ways—they can lengthen, shorten, move along each other, and divide (Figure 5.17). • Furthermore, biotensegrity does not take account of differences in the quality of the fibrils. The fibrillar framework can resist and adapt to increased tension by strengthening the fibrils with extra collagen. I have seen that in response to repetitive constraint there is an increase in the resistance of the fibrils, implying that the quality of the fibrils can change. The quantity of the fibrils also increases in response to mechanical demand (Figure 5.18 and Video 5.5).

Figure 5.16 There is an element of apparent randomness and unpredictability that is characteristic of microvacuolar movement A A stretch-inducing force enters the fibrillar network B The fibrils stretch under the duress C The microvacuoles adapt to the constraint and change shape

Figure 5.17 Continuing from Figure 5.16 and exhibiting the distension, division, and sliding capacities A the constraint is gradually diffused... B dispersed.... C and absorbed by the fibrillar network

Figure 5.18 The fibrillar framework can be reinforced to deal with repeated strain by strengthening the fibrils with extra collagen so that they can resist and retain tension, like the steel bars in reinforced concrete. This video (2 x) is a comparison of the thickness of an annular ligament (also known as the flexor retinaculum or transverse carpal ligament) in a manual worker and a younger subject. The ligament can be thickened and reinforced or not, depending on the manual activity of the person A The younger subject B Our older laborer Video 5.5

Differences can also be explained by variations in the water content, which can fluctuate because of factors such as fibrillar density and osmolarity. Very few in vivo studies have been carried out, especially concerning the spatial arrangement of water molecules inside the microvacuoles and their relationship with the proteoglycans. Similarly, there have been very few in vivo studies into the exact nature of the fibrils. Much research is still required in this field. In conclusion, biotensegrity is a good working model for understanding living structure, provided that the reader does not think that the body

comprises hierarchies of icosahedrons!. Biotensegrity can be conceived as a model on which we must build in the light of what we observe in vivo. It explains many of the phenomena that we observe, especially the ability to resist gravity, but it needs to be developed and refined if it is to account for the full complexity of organic structure and function. Moreover, we need to consider a new factor: fractalization (Figure 5.19).

Figure 5.19 A–D Four different examples of fractalized fibrillar networks with their differing similarities. Fractalization is an essential feature of living organisms. The structural elements are fractalized from the beginning of development, but the process of fractalization can occur on demand, as necessary. (130 x)

WHAT IS FRACTAL ORGANIZATION? Constitutive fractalization Constitutive fractalization is fractalization of the components or constituent elements in organized structures. Benoit Mandelbrot (1924−2010), a Polishborn French and American mathematician, was the first person to use the term ‘fractal’, from the Latin fractus, which means broken or fractured. In 1967 he proposed a definition of fractal organization: ‘A fractal organization

is any pattern that is reproduced in a regular or irregular fashion at different scales, which can vary from small to large.31, 32 Fractal structures are frequently encountered in living organisms. If you zoom in on a fractal pattern, it will look very similar to the original shape. This property is called self-similarity. One only has to look at a tree and its leaves to see that the basic pattern of the tree is repeated in a similar, but not identical, fashion on a decreasing scale as the main branches, smaller branches, and twigs follow the same basic but irregular pattern, which differentiates one type of tree from another. The same phenomenon can be seen when looking at the leaves. KEY STATEMENT Fractalization adds another dimension to the chaotic aspect of living matter. Fractal structures lack regularity, but this irregularity is neither random nor arbitrary. There is regularity in the irregularity.

Fractal objects display ‘scale invariance’. A fractal structure looks the same whether close to or from a distance. Whatever the magnification, they show the same basic pattern of organization. Some authors have suggested that fractal structures represent the underlying geometry of nature (Figure 5.20).33, 34, 35

Figure 5.20 Many structures are fractal, for example the following A The skin B The bronchial tree C Intestinal villi D Tree E Leaf

Why is fractalization so important in living matter? Many living structures are fractal. Examples include the cerebral cortex, the pulmonary alveoli, the intestinal villi, and the skin. The fractal dimension enables these structures to increase the surfaces that separate two different environments, thus providing a greater surface area for exchange (Figure 5.21). The fractal organization of the lungs, with successively smaller divisions of the bronchi, provides the advantage of increasing the surface area of the alveoli, thus facilitating efficient gaseous exchange between blood and air. If we were able to unfold the lungs, their surface area would be similar to that of a tennis court. Fractalization allows this surface area to be compacted into several cubic centimeters inside the body. In other words, fractalization increases not only the surface area of fractal structures but also the volumes contained within them. This behavior has been retained by nature because it increases metabolic efficiency and maximises the exploitation of space.

Figure 5.21 Fractalization enables anatomical structures to increase the surfaces that separate two different environments, thus providing a greater surface area for exchange A With regular fractalization B Fractalization can be irregular. It is not necessarily symmetrical C Fractal organization of a rectilinear surface

Dynamic fractalization Dynamic fractalization is the ability to react and adapt to mechanical constraint in three dimensions, through the repeated fractal division of the component fibrils. This both prevents the rupture of collagen molecules and preserves the integrity of the microvacuoles (Figure 5.22 and Video 5.6). The skin and the fibrillar network are good examples.

Figure 5.22 These structures have been retained by natural selection, because they increase metabolic efficiency and maximize the exploitation of space. Collagen fibrils possess certain intrinsic properties that enable them to react and adapt to dynamic mechanical constraint in three dimensions. (200 x) Video 5.6

However, the capacity for instantaneous adaptation is not the only advantage of dynamic fractalization. First and foremost, it has a mechanical influence on the slow growth and development of a form (Figure 5.23 and Video 5.7). Fractalization enables self-assembly and growth. This is a process in which, without external direction, a disordered system of pre-existing components forms an organized structure or pattern as a consequence of specific, local interactions between the components themselves. Fractalization enables the

transition from one stable form to another when there is a sufficient energy available.

Figure 5.23 Growth and increase in volume are achieved without rupture or loss of continuity of the collagen fibrils that constitute the fibrillar network Video 5.7

The process of slow dynamic fractalization of the fibrillar framework provides an ideal environment for cell multiplication and the development of specific volumes, such as adipocytes (Figure 5.24 and Video 5.8). Adipocytes store energy reserves, and while fat deposits can be found almost anywhere, my observations confirm that they are found most frequently in the more supple, expansile, and flexible areas of the subcutaneous sliding systems.

Figure 5.24 A The process of slow, dynamic fractalization provides an ideal environment for cell multiplication and the development of specific volumes, such as adipocytes, which form fat lobules .(10 X) B Colonization of microvacuolar spaces by adipocytes Video 5.8

The capacity of the fibrils to replicate the basic polyhedral shape, combined with the phenomenon of dynamic fractalization, enables us to understand how all the possible forms that we observe in the human body may be created. As we have already pointed out, these are all simple shapes. KEY STATEMENT Furthermore, the ability of the fibrils to deal with both extrinsic and intrinsic mechanical constraint, and to align themselves in the direction of the imposed force, suggests that the basic structural framework of all the organs may be organized in this way.

Any shape or form can be produced by this mechanical behavior of the fibrillar network, including complex, chaotic, and irregular forms. However, nature uses surprisingly simple and relatively regular forms in the human body. Examples of cylindrical or round structures include blood vessels, the bronchial tree, intestines, and the excretory canals (Figure 5.25 and Video 5.9). Tendons are examples of longitudinal structures. Intermuscular septa and some joint ligaments are also longitudinal, but their fibers are differently arranged (Figure 5.26 and Video 5.10).

Figure 5.25 Construction with a dynamic functional purpose; all forms can be created, yet the simplest are chosen. Let us examine the simple, round form A Round shapes can form during dilacerations when forces are uniform. (100 x) B Animated diagram showing the capacity of the fibrillar framework to produce a round shape C We also see round structures, such as the tubular form for the vessels, nerves, and excretory ducts. (10 x) Video 5.9

Figure 5.26 A quick look at the longitudinal form and purpose-oriented construction A Tendons. (20 x) B Intermuscular septa and many joint ligaments, albeit with differently arranged fibers. (20 x) C Animated diagram of a type of construction with a dynamic functional purpose Video 5.10

Dynamic fractalization enables us to consider morphogenesis, organogenesis, and phylogenesis from a new perspective.

FOLLOWING THE RED THREAD We have now answered red thread questions 4 and 5. RED THREAD QUESTIONS

4. How do these fibers, which are under tension, preserve volume and maintain the shape of our bodies? 5. How can such an apparently chaotic fibrillar system, which contains such a diversity of shapes and combinations of fractal and chaotic patterns, result in coherent and efficient movement and ensure the return of tissues to their resting position after movement?

Now we can try to answer a very frequently asked practical question: can nature restore harmony to this multifibrillar network when it is subjected to forces that exceed normal physiological limits, as in pathology or through trauma?

Comment by Stephen M.Levin, BS, MD

Dr. Guimberteau has no greater admirer of his work than I. As a fellow surgeon, I appreciate the technical skill involved, and the intellectual fortitude it takes to step outside the box and think of other ways of comprehending what we are experiencing. I was in the same place some 40 years ago as I started my work in applying the principles of tensegrity to biologic structures, coining the term biotensegrity. In biotensegrity, as I define it, tensegrity icosahedrons are used to model biologic organisms from viruses to vertebrates, and their cells, systems, and subsystems, in self-organizing, hierarchical, load distributing, low energy—consuming structures. I have found that for biologic structures only the definition that includes the closed system concept of Snelson and Fuller succeeds. In biotensegrity, tensegrity icosahedrons are used to model the structure and mechanics of biologic organisms from viruses to vertebrates: their cells, systems, and subsystems.1,2 Ever since Dr. Guimberteau first sent me his photographs, when he was looking for an explanation of the seemingly random structure he observed in living tissue, I have been in awe of his truly remarkable work. Dr. Guimberteau perceived an architectural pattern at the connective tissue level that I first recognized at the spinal column and musculoskeletal level. I wrote to him, ‘Of course I see [in your photographs of connective tissue] nothing but tensegrities’ (personal communication, 2002). The tensegrity icosahedrons in biotensegrity are force diagrams, not actual physical structures that can be seen in the body. They define the structural and mechanical relationship within cells and between cells, organs, regions and, ultimately, the structural and mechanical integrity of the organism and how it responds to external forces. Biologic tensegrity icosahedrons represent forces within an instant of time and in a constantly changing milieu, simultaneously, at every organizational level, and they may cross several scales of organization. Consistent with Dr. Guimberteau’s observations, they are in a continuous flux, so that what applies at one instant does not exist in the next. This is the very heart of fractal dimensions and chaos theory. When looking at a fractal representation, there is an underlying organization that is often obscured. Formulae generate highly organized, infinite, repeating multiscale patterns that may appear chaotic. In chaos theory, these formulae are the ‘strange attractors’. For a fractal to be more than a representation, it must have structural stability. In biotensegrity theory, the strange attractor is the tensegrity icosahedron. This generates a tangible physical structure on which to hang your hat.

The cytoskeleton of a cell reconfigures according to the stresses on the cell, and I feel certain that the entire musculoskeletal system is doing the same thing as it goes through its various contortions. Dr. Guimberteau has beautifully substantiated that the connective tissue does likewise, albeit on a different timescale (the cell does it in milliseconds; bones do it in weeks). The fibrillar network and the cells within it coalesce to form a structural continuum of continuous tension and discontinuous compression that defines a tensegrity: ‘Tensegrity describes a closed structural system composed of a set of three or more elongate compression struts within a network of tension tendons, the combined parts mutually supportive in such a way that the struts do not touch one another, but press outwardly against nodal points in the tension network to form a firm, triangulated, prestressed, tension and compression unit.’3 As tensegrity icosahedrons may have fractal dimensions, and an icosahedron may span several partial subunits (and shift back and forth) (personal communication to J.C. Guimberteau, 2002), we have a model for the extensibility, contraction, and changing direction of the sliding mechanism, as well as its ability to stretch, divide, fuse, and even move. What Dr. Guimberteau is showing us are, in my view, fractal patterns that are self-similar and hierarchical (personal communication to J.-C. Guimberteau, 2002). The organization of the tissues of the body follows minimal energy, self- organizing, physical laws related to the soft, condensed matter that is the very stuff of biologic material and foam formation. The changing structures Dr. Guimberteau demonstrates are closely related to foam patterns, and the same laws create tensegrities. Apparent deviations are merely ‘coarsening’ of the structure, much as the bubbles of foam in beer coarsen, but the triangular support is then found (in systems science terms) in the metasystem, the next level of structure (personal communication to J.-C. Guimberteau, 2006). Pour yourself a beer with a big head and watch what happens. Notice how it mimics the patterns and sliding mechanisms Dr. Guimberteau has discovered in subcutaneous tissue. emulsions that are in a fluid state but are integrated within the fibrillar network. With mechanical behaviors quite different from water, they adhere to a set of rules that are inviolate—as inviolate as the rules of physics that pertain to motion, gravity, and the geometry of space filling. What may appear as ‘random’ or ‘irregular’ may be a perceptual paradox. Clouds look irregular and random to us, but their structure is rigidly governed by physics. ‘There are no two snowflakes alike’ and ‘All snowflakes are hexagons’ are an obvious contradiction that shows us that it is all about perception. The irregularities we perceive may be finely ordered when viewed from another perspective. What Dr. Guimberteau describes in the constantly changing microvacuoles and microfibers is entirely consistent with the biotensegrity model, and is occurring at every level of organization, at every scale and across scales. It may be difficult, even impossible, to ascertain the true structural organization at any one scale, because we are usually stuck with being able to visualize only one scale at a time. As a plastic surgeon, Dr. Guimberteau naturally focuses on the elastic soft tissue; as an orthopedic surgeon, I was taught to focus on the compression resisting bone. I came to realize that tension begets compression, and vice versa. They are interdependent and must mutually coexist. When dealing with the tension components, we must recognize

that we are at the same time engaging the compression components at both the macro and micro scales. We must always be aware of both. Even today, I see nothing but tensegrities in Dr. Guimberteau’s marvelous endoscopic demonstrations; he has breathed life into a theoretical model.

REFERENCES 1. Levin SM. The icosahedron as a biologic support system. In: Proceedings of the 34th Annual Conference on Engineering in Medicine and Biology, Volume 23; 1981 Sep 21–23; Huston, TX. Bethesda: Alliance for Engineering in Medicine and Biology; 1981. 2. Levin SM. The icosahedron as the three-dimensional finite element in biomechanical support. In: Dillon JA, editor. Proceedings of the International Conference on Mental Images, Values, and Reality; 1986 ; Philadelphia: PA. Salinas, CA: Intersystems Publications; 1986. 3. kennethsnelson.net [Internet]. Available from: http://www.kennethsnelson.net/faqs/faq.htm.

6 Adaptations and Modifications of the Multifibrillar Network Scar tissue and adhesions Megavacuolar transformation Cellular overload The observable mechanical effects of manual therapy Following the red thread

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY The harmonious balance of this morphodynamic system in perpetual search of equilibrium will eventually be disrupted. Over the course of a lifetime, this irregular, multifibrillar, chaotic, fractal system will undergo many changes. It may be subjected to brutal external aggression, such as that experienced in an accident; or deteriorate through overuse, leading to repetitive strain; or be modified by muscular hypertrophy or excess adipose tissue. The network’s components will also eventually suffer the inexorable effects of time, leading to their inevitable degradation. There are a wealth of biochemical data on the nature of these modifications, but they are too numerous and varied to cover within the scope of this book, which is concerned with the observation of living matter. And several strange and unexpected anatomical observations have encouraged us to consider tissue response from a phylogenetic perspective and in the context of dynamic adaptation.

SCAR TISSUE AND ADHESIONS Let us clear up a common misconception: adhesions are often referred to as scar tissue, but in reality adhesions are a complication of scarring, which is a result of a wound, such as a surgical incision in the skin. Adhesions may also form in the presence of inflammatory disease, or conditions such as complex regional pain syndrome. Adhesions are also more amenable to change, for instance by manual therapy. Therefore the external appearance of a scar can be misleading, because it does not always indicate the extent of the underlying tissue destruction. A breach in the cutaneous barrier and the subsequent brutal exposure of the subcutaneous world to the external environment upsets the fibrillar harmony. Fortunately, physiological mechanisms stand in readiness to deal with the trauma, and the wound is sealed quickly and efficiently. If the injury is not fatal, the damaged tissue will be repaired, but not always to its exact former state, and usually with variations in the quality of the scar tissue (Figure 6.1 and Video 6.1).

Figure 6.1 After injury, the fibrillar harmony is disrupted. The damaged tissue will be repaired, but not always exactly to its former state, and with variations in the quality of the scar tissue Video 6.1

Even though the biological repair process is one of the primary survival mechanisms, and the potential for satisfactory repair exists, it is not always completely successful. This can be because of metabolic or mechanical factors, or a combination of the two. The repair process involves well-known chemical reactions; however, we now know that the morphodynamic organization of the fibrillar collagen network creates tensional forces that influence the attempt to repair the damaged tissue. • What do we discover beneath the scar a few weeks or months following the trauma? • Will we find the same fibrillar harmony that existed before the injury? • Will dynamic equilibrium have been restored to the fibrillar network? Or will we find a makeshift repair job? Let us explore this world that has been destroyed and then repaired. Two principles govern the body’s attempts to repair tissue damage.

• Everything depends on the nature of the initial trauma. The greater the tissue destruction, the less successful will be the repair, especially if different types of tissue are involved. • Scar tissue formation is not selective. Scar tissue forms at the site of tissue damage, and the repair process encompasses and incorporates any type of injured tissue into the same scar. This applies to all types of tissue, including the dermis, muscles, tendons, and bone. Initially, the same repair process applies to all tissue components and the scar tissue remains undifferentiated for several weeks. Subsequently, over time, a specific movement or function may be restored. KEY STATEMENT Because scar tissue formation is a non-specific process, nature does not repair and reshape living matter exactly as it was before injury, and the results are often disappointing (Figure 6.2).

Figure 6.2 Nature does not repair and reshape living matter exactly as it was before injury, and the results are often disappointing. This photograph shows an internal scar 1 year after the injury. (2 x)

Consider the case of a simple post-surgical scar (Figure 6.3 and Video 6.2). The surface of the epidermis has been reconstituted with polyhedrons that move in a way that closely resembles the normal mobility of the epidermis. Lines of force act across the scar and shape it. The constraint has influenced the remodeling of the epidermal surface. Sporadically, beneath the dermis, long adhesions appear that are supple, mobile, and slightly retractable, but they do not interfere much with the general flexibility. Forces still act normally through the tissue.

Figure 6.3 A simple post-surgical scar A The surface of the epidermis has been reconstituted with polyhedrons that move in a way that closely resembles the normal mobility of the epidermis. (5 x)

B Long adhesions (by-products of scars) can be seen below the dermis. These are supple, mobile, and slightly retractable but do not interfere much with the general flexibility of the area surrounding the scar. (5 x) Video 6.2

This is not the case with the next scar shown (Figure 6.4 and Video 6.3). Even though it also appears to be well integrated into the surface of the skin and the polyhedral forms at the surface of the epidermis have been reconstituted to closely resemble those in the rest of the epidermis, the area beneath this scar is completely different. Traction on this scar reveals adhesions between the dermis and the sliding surfaces below. The dermis is hard and lacking in mobility, and has obviously lost its ability to function properly. The arborescent configuration of the microcirculation has been replaced by a disorderly collection of neovessels arranged in bush-like formation. Where the adhesions between the dermis and the underlying sliding surfaces are, the fibers are wide and bunched tightly together. Hardly any microvacuoles or blood vessels remain. At the periphery of the scar, we see normal adipocytes, microvacuoles, and correctly vascularized tissue.

Figure 6.4 A This scar appears to be well integrated into the surface of the skin, and the polyhedral forms at the surface of the epidermis have been reconstituted to closely resemble those in the rest of the epidermis. However, the area beneath the scar is completely different to that seen in Figure 6.3 and Video 6.2. (2 x) B Here, we can clearly see that traction on the scar reveals adhesions between the dermis and the sliding surfaces below. The dermis is hard and lacking in mobility, and has obviously lost its ability to function properly. (5 x) C Here, the fibers are wide and bunched tightly together. They lack the mobility of the original tissue. The microcirculation in the dermis is disorganized, and we can see adhesions between the dermis and the underlying sliding surfaces. (100 x) Video 6.3

But the adhesions do not stop here. They extend deeper toward an area where a tendon has been sectioned in the past (Figure 6.5A) and we see what can only be described as a fibrillar apocalypse, with distended fibrils, interwoven like the broken masts and rigging of a ship after a shipwreck, with thickened

ropes composed of collagen type I fibers scattered all over the place. They are arranged in an irregular fashion, and have lost their intrinsic mobility. The area resembles a forest that has been ravaged by a hurricane. The underlying order of the original fibrillar chaos has been lost. Suppleness and flexibility have been replaced by the stiffness of the adhesions.

Figure 6.5 An adhesion is an area in the multifibrillar network where dynamic fibrillar harmony has been lost A Tendinous adhesions. (5 x) B Adhesions surrounding an osteosynthesis plate. (5 x)

Some scars are not able to reach maturity (Figure 6.5B). This is always the result of irritation of the scar tissue, which may be due to the presence of a foreign body, the section of a nerve, or functional tension. The scar shown in Figure 6.6A and Video 6.4 is a good example. It is inflamed and purple, and the scab has not yet healed. It is still painful 3 months after the injury. An incision reveals the chaotic appearance of the dermal vessels. The tissues are fragile and can easily be peeled away. It is evident that the healing process has not been completed. This could be caused by the continued presence of collagen type III fibers. At the base of the scar, we discover a reddish area lined with small bunches of blood vessels—evidence of inflammation (Figure 6.6B). The persistence of inflammation here can be explained by the presence of strange, humid adhesions with small bubbles in their midst, which are attached to a muscular aponeurosis, restricting movement and perpetuating the inflammatory process.

Figure 6.6 A Immature scar 3 months after injury. (2 x) Video 6.4

Figure 6.6 B In these scars, we find reddish areas lined with small bunches of blood vessels, which are evidence of inflammation. Adhesions form between the scar and underlying aponeuroses. (5 x)

Sometimes the functional impairment is evident, as in the next case, shown in Figure 6.7 and Video 6.5. This scar invaginates with each movement of flexion of the anterior surface of the forearm. The harmonious arrangement of the cutaneous polyhedrons has not been restored. During surgical exploration of the scar, we discover tissue that is thickened, swollen, edematous, and covered with the small blood vessels characteristic of neovascularization. This is evidence of the persistence of the inflammatory phase. The tissues are fragile, and they need to be dissected carefully. It is difficult to distinguish different tissue types; the differences between the various types are not clear. Gradually, the surgeon manages to isolate the adhesion and free the tendon, restoring its mobility. The functional improvement will rapidly optimize the quality of the scar. During surgical exploration of scar tissue, it is surprising to discover how tough and resistant these adhesions are.

Figure 6.7 This scar invaginates with each movement of flexion of the anterior surface of the forearm. The harmonious arrangement of the cutaneous polyhedrons has not been restored. The tissues are fragile, and they need to be dissected carefully. It is difficult to distinguish different tissues; the differences between the various types are not clear. (2 x) Video 6.5

KEY STATEMENT A scar does not have any functional use. Its sole purpose is to plug the gap in the damaged tissue (Figure 6.8).

Figure 6.8 A Scar tissue (the whiter tissue) and its attendant adhesions are an aborted attempt at tissue reconstruction and are a poor imitation of the original tissue. (2 x) B Non-specific scar tissue is laid down at the injury site. (2 x)

A scar remains an area of somatic dysfunction and real structural chaos, with no functional purpose, as opposed to the normal fibrillar organization, which can be described as a chaotic system with functional determinism. The formation of scar tissue introduces disorder into the fibrillar chaos. Adhesions are responsible for the disappearance of dynamic fibrillar harmony. The repair process therefore does exist, but it is very basic and non-specific. Injured tissues are not restored to their original configuration if the structures

are destroyed or badly damaged. Scar tissue and its attendant adhesions are an aborted attempt at tissue reconstruction, and are a poor imitation of the original tissue (Figure 6.8). Children sometimes exhibit a surprising ability to reconstruct damaged tissues. Their tissues possess a powerful capacity for healing that is progressively lost during adulthood and is almost completely absent in the elderly. Why is it that, as we get older, tissues are unable to perform correctly the work that they were able to undertake before? Perhaps in the future it will be possible to restore cell selectivity so that damaged tissue can be reconstructed instead of the formation of non-specific scar tissue at the injury site. This ability to reconstruct the original collagen arrangement is a promising avenue for future generations to explore. Edema Edema is the simplest pathological state. Post-traumatic or post-operative edema is a sudden expansion of the microvacuoles resulting from increased intravacuolar pressure with mechanical distension of the fibrillar structures. Extravasation also occurs (Figure 6.9 and Video 6.6). The swollen, distended fibers are unable to unfold, lengthen, or perform their role in the distribution of tension, and this interferes with the sliding mechanisms. However, intrinsic changes affecting both the fibrils and intravacuolar liquid are usually limited, and conditions are eventually restored to normal.

Figure 6.9 Post-traumatic or post-operative edema is a sudden expansion of the microvacuoles. This is caused by increased intravacuolar pressure, with mechanical distension of the fibrillar structures. Extravasation also occurs. (2 x) Video 6.6

In some cases, edema is followed by intrinsic changes. This can occur even in the absence of any tissue destruction or any obvious wound. These changes are similar to those found in scars. This explains the surprising phenomenon of excessive adhesion formation, which is possibly a consequence of limited extravasation of red blood cells and plasma and of changes in the fibrillar and vacuolar contents. These adhesions could delay recovery. This inability to restore the tissues to their initial state can be further hindered by circulatory diseases such as arteritis, seen in diabetics and smokers. Ecchymosis This is the same phenomenon as edema but with the addition of extravasation of red blood cells and plasma into the interstitial area (Figure 6.10 and Video 6.7). The extracellular milieu is filled with red blood cells, usually of venous origin because veins are more superficial and more vulnerable to injury. Their walls are thinner and more fragile than those of other blood vessels. This extravasation is usually of traumatic origin, but the cause can sometimes be intrinsic, such as in the presence of varicose veins.

Figure 6.10 Ecchymosis is the same phenomenon as edema, but with the addition of extravasation of red blood cells and plasma into the interstitial area. (2 x) Video 6.7

All the structures of the skin are affected: the epidermis is dilated, which gives it an ‘orange peel’ appearance; the fibers are distended, as are the microvacuoles; and the chemical composition of the intravacuolar gel is probably altered, but not damaged nor destroyed, therefore morphodynamic recovery is still possible. Although all the tissue structures are affected, the outcome is usually favorable, with little or no long-term after-effects. The resulting tissue hypertension and changes in skin color decrease with time, and the characteristic purple-blue color of the bruise changes to green and then to yellow, before disappearing completely. Hematoma This follows the extravasation stage of ecchymosis. The elevated plasma pressure, the raised fluid volume, and the presence of red blood cells disturbs or destroys the local fibrillar framework by pushing the fibrils apart or tearing them, thereby creating a cavity. A limited area of expansion exists, and fluids collect in this area under the force of gravity, which results in a gradual

increase in local tension (Figure 6.11 and Video 6.8). Degradation of the debris and reabsorption of the fluids takes place slowly, and the capacity for dynamic recovery may be disrupted. In addition, the skin can be affected, becoming thinner. Fatty tissue at the periphery of the hematoma often hardens. As a result, local tissue suppleness and flexibility may be reduced. Sometimes the effects of tissue retraction can be seen at the skin surface.

Figure 6.11 A hematoma is characterized by the presence of blood in the extravascular space. The elevated plasma pressure, raised fluid volume, and presence of red blood cells disturbs or destroys the local fibrillar framework by pushing the fibrils apart or tearing them, thereby creating a cavity. Fluids also collect in this area under the force of gravity. (2 x) Video 6.8

Inflammation Inflammation can be destructive and occur anywhere, but the sliding systems are most sensitive to the inflammatory process. Changes in transparency, density, and color within the fibrillar system are easily seen: fibrils thicken; transparency is lost; and bright colors fade becoming dull and usually slight brown (Figure 6.12). Inflammation is also characterized by an excessive fluid reaction, with dilation of fibers and microvacuoles and proliferation and

dilation of microvessels responsible for the redness that often accompanies inflammation (Figure 6.13 and Video 6.9). The swelling is clinically visible (Figure 6.14).

Figure 6.12 A The fibrillar system in inflamed tissue loses its transparency. (5 x) B The fibrils themselves become thicker and opaque. They change color, and are usually brown or grey. (5 x)

Figure 6.13 Inflammation is characterized by an excessive fluid reaction with dilation of fibers (microvacuoles), and proliferation and dilation of microvessels (blood and lymph) Video 6.9

Figure 6.14 A This vasodilation and edema explain the clinically visible swelling B You can also see the efflorescence of the microvessels, which are responsible for the redness associated with inflammation. This can be localized (as seen here). (5 x) C generalized, (5 x) or D can even develop within tendinous structures. (10 x)

Intrinsic changes affect both the fibrils and the intravacuolar liquid. Restoration to the original state is not the rule (Figure 6.15). Fibrils swell, are shortened, and may even retract. Small intratissular bubbles form inside the microvacuoles. These bubbles are not artifacts; that is to say, they have not been introduced by the endoscopic observation of the tissues. They are a natural feature of the inflammatory process, but in healthy tissue they are not present in such numbers. They may be evidence of the difficulty faced by the tissues in dealing with gaseous exchange. The presence of these bubbles and the increased opacity of the extracellular environment indicate changes in the quality of the intravacuolar gel. Combined with the thickening of the fibrils, this creates stiffness and loss of mobility, and interferes with the ability of the fibrils to slide over each other. The cellular reaction is very real but does not seem to be prolific.

Figure 6.15 A–D Small intratissular bubbles inside the microvacuoles. These bubbles are not artifacts; that is to say, they have not been introduced by the endoscopic observation of the tissues. They are a natural feature of the inflammatory process, and are not present in such numbers in healthy tissue. They may be evidence of the difficulty faced by the tissues in dealing with gaseous exchange. (5 x, 10 x, 20 x)

Sometimes you find localized edema with foci of hypervascularization, but on other occasions the vascular proliferation is invasive, like ivy growing on an aging tree (Figure 6.16).

Figure 6.16 Hypervascularization

A Sometimes you find localized edema with foci of hypervascularization, like confetti. (20 x) B On other occasions, the vascular proliferation is invasive, like ivy growing on an aging tree. (20 x)

The difference between inflammation and scar tissue is that in inflammation the tissue components have not been destroyed. The tissues retain a capacity to recover once the cause has been treated. However, if the inflammation is neglected or badly managed, tissue destruction eventually occurs, and the process always progresses in the same way: there is enlargement of the microvacuoles, increasing scarcity of fibrils, and the creation of multiple enlarged areas filled with fluid. The increasing scarcity of fibrils is a result of destruction of the fibers, which explains the persistence of local changes in shape without a systematic return to the original form (Figure 6.17). In this case, the process is irreparable and will result in impaired function. Sometimes, the multifibrillar system disappears locally, and is replaced by a cyst-like megavacuole. But Megavacuoles can also occur in other circumstances.

Figure 6.17 If the inflammation is neglected or badly managed, tissue destruction occurs. The process always progresses in the same way A There is enlargement of the microvacuoles, increasing scarcity of fibrils, and the creation of multiple enlarged areas filled with fluid. At the same time, destruction of the fibers occurs. This process is irreparable and will result in impaired function. (10 x) B Sometimes the multifibrillar system will disappear, replaced by a cyst-like megavacuole. (20 x)

MEGAVACUOLAR TRANSFORMATION This development is present, as we have previously observed, in inflammation, in tendinitis, in old bruises, and especially in olecranon bursitis. Olecranon bursitis is a pathology that occurs at the proximal end of the ulna and involves the secretion of an abnormal amount of fluid between the skin and the bone. This secretion is a reaction to activities that involve repeated leaning of the elbow on hard surfaces, such as a desk or table. This area is vulnerable, because the skin at the tip of the elbow is relatively thin. Repetitive pressure on the olecranon process degrades the sliding system that allows the anatomical structures to slide over each other. Olecranon bursitis is often discovered unexpectedly during surgery in the absence of clinical signs and symptoms (Figure 6.18).

Figure 6.18 A Olecranon bursitis is a pathology that occurs at the proximal end of the ulna. Repetitive pressure on the olecranon process degrades the sliding system that allows the anatomical structures to slide over each other. A cavity is formed, in which randomly arranged crossbeam-like structures can sometimes be seen. (5 x)

Figure 6.18 B Olecranon bursitis is a pathology that occurs at the proximal end of the ulna. Repetitive pressure on the olecranon process degrades the sliding

system that allows the anatomical structures to slide over each other. A cavity is formed, in which randomly arranged crossbeam-like structures can sometimes be seen. (5 x)

Any external constraint, such as repetitive stretching or pressure, may modify the fibrils and their architectural arrangement and result in the formation of a megavacuole. This involves progressive destruction (dilaceration) of the fibers, which eventually rupture, resulting in the creation of a larger space or cavity with different physiological characteristics (Figure 6.19 and Video 6.10). Therefore the multifibrillar, microvacuolar system is transformed into a megavacuole.

Figure 6.19 External constraint, such as repetitive stretching or pressure, may modify the fibrils themselves and their architectural arrangement. This involves progressive destruction (dilaceration) of the fibers, which eventually rupture, resulting in the creation of a larger space, or cavity, with different physiological characteristics. The multifibrillar, microvacuolar system is transformed into a megavacuole. (20 X) Video 6.10

Megavacuolar transformation begins with an edematous phase characterized by the enlargement of the microvacuoles and the fibrils, and with the presence of numerous bubbles inside the fibrils. Gradually, the fibrils rupture and non-fibrillar spaces are created. Fluid coming from the opened intravacuolar spaces collects in these larger non-fibrillar spaces, in which the only structures which remain unchanged are some blood vessels. It is interesting to note the surprising morphological similarity between a digital tendon sheath and its vincula and the inside of an olecranon bursitis. Olecranon bursitis is an example of functional adaptation that occurs gradually over a lifetime, often in the absence of clinical symptoms, but with distinct changes in physiological and metabolic behavior as a result of the tissue being subjected to repeated mechanical stress (Figures 6.20, and Video 6.11).

Figure 6.20 Areas subjected to repeated mechanical stress usually react the same way, with edema (caused by the impaired reabsorption of fluids), vasodilation, thickening, and extracellular exudation. The rupture of fibrils leads to the creation of non-fibrillar spaces in which fluids collect. (5 x) Video 6.11

• Could this megavacuolar reaction, which occurs over the course of a lifetime, provide an explanation, for example, of the multiform nature of the different anatomical descriptions of the sliding of the flexor tendons inside the carpal and digital sheaths? • Could there be a relationship between the transformation of the fibrillar system and the mechanical constraint? • In a broader context, if we consider the human phylogenetic chain, could this relationship between the transformation of the fibrillar system and the mechanical constraint provide an explanation for the emergence of the ability to grasp? During flexion of the wrist, the pulley that reinforces the anterior wall of the carpal tunnel stabilizes the tendons and ensures the transmission of the muscle contraction to them with minimal energy loss. The tendons within the carpal tunnel are subjected simultaneously to both longitudinal and lateral forces. This provokes a megavacuolar reaction similar to that seen at the elbow. We can clearly identify the transition zone between the multifibrillar and megavacuolar systems called the common carpal sheath (Figure 6.21A and B).

Figure 6.21 A and B It is interesting to note the surprising morphological similarity between a digital tendon sheath (A) (5 x) and the inner surface of an olecranon bursitis (B) (5 x). Even the arrangement of the blood supply is similar

In the fingers, these megavacuoles surround the entire circumference of the tendons as soon as other pulleys appear (Figure 6.22 A,B,C and D). Wherever mobility is associated with parietal—referring to the wall of a

body cavity or membrane, such as parietal pericardium or parietal peritoneum (the membrane lining the abdominal cavity as opposed to the visceral peritoneum that envelops the abdominal organs)—constraint we see a megavacuolar reaction. This type of reaction is also seen in the pleura and the pericardium.

Figure 6.22 The tendons within the carpal tunnel are subjected simultaneously to both longitudinal and lateral forces. This provokes a megavacuolar reaction similar to that seen at the elbow We can clearly identify the transition zone between A the multifibrillar system (2 x) and B the beginning of megavacuolar reaction. (10 x) C When the carpal canal (5 x) and D the digital canal (10 x) are subjected to excessive forces, they behave in the same way

CELLULAR OVERLOAD In the hypodermis, the microvacuoles are normally filled with adipocytes. However, in the case of lipid overload the number and size of the adipocytes increases, and there is a corresponding increase in the size of the microvacuoles. As a result, the hypodermis becomes thicker and heavier and the skin is stretched (Figure 6.23 and Video 6.12).

Figure 6.23 In the hypodermis, the microvacuoles are normally filled with adipocytes. However, in the case of lipid overload the number and size of the adipocytes increases, and there is a corresponding increase in the size of the microvacuoles. As a result, the hypodermis becomes thicker and heavier and the skin is stretched. (5 x) Video 6.12

Obesity occurs in two distinct stages (Figure 6.24).

Figure 6.24 Obesity occurs in two distinct stages. A and B Weight loss at an early stage allows a return to the initial form, because gravity has not yet damaged the fibrillar framework. The internal tension resists the gravitational force C and D The second stage of obesity is characterized by extreme dilatation of the microvacuoles. Volume and weight increase steadily. This leads to distension of the fibrils, with loss of elasticity, so that they are unable to resist the force of gravity and return to their original configuration. Form is modified and the contours collapse

• Initially, the microvacuoles are dilated by the adipocytes, which replace the proteoglycans. The intravacuolar tension increases but the fibrillar framework, although distended, retains its inherent properties. Weight loss at this stage allows a return to the initial form, because gravity has not yet damaged the fibrillar framework. The internal tension resists the gravitational force. • The second stage of obesity is characterized by extreme dilation of the microvacuoles. Volume and weight increase steadily. This leads to distension of the fibrils, with loss of elasticity, so that they are unable to resist the force of gravity or return to their original configuration. Form is modified, and the contours collapse.

WEIGHT LOSS Weight loss diminishes the volume of the fatty tissue and the vacuolar tension, but the fibrils are permanently altered. In adults, they do not regain their original properties (Figure 6.25). However, children possess a much greater capacity for remodeling of the fibrillar network, because the growth process is still present and active.

Figure 6.25 Weight loss diminishes the volume of the fatty tissue and the vacuolar tension, but the fibrils are permanently altered. In older adults, they do not regain their original properties, and ptosis, or drooping, results. Aging-related ptosis occurs in the abdomen, breasts, and arms A Abdominal ptosis B Ptosis of the breast

AGING Aging could be considered as the revenge of gravity on endogenous tension. The sagging of structures like the skin can be explained by the distension of fibers that have lost their intrinsic qualities (Figure 6.26A and Video 6.13): there is a decrease in the volume, number, and quality of the fibers; the microvacuoles are larger; and the reabsorption of fluids is less efficient. The endogenous intratissular pre-tension, which was able to resist gravity during growth and then peaked during adulthood, begins its slow decline with the onset of old age. During the aging process, the fibrils become gradually less resistant to tension and lose their dynamic capacity to return to the original form. The intrafibrillar tension decreases. Ptosis occurs in the abdomen, breasts, and arms. Gravity can no longer be resisted. The weight of the remaining mammary glands or fatty tissue drags the aging, distended cutaneous and subcutaneous structures downward.

There is a close connection between the skin of the face and the facial muscles of expression (Figure 6.26B). The fibrillar connections are more intimate here, and they are undoubtedly more efficient and are designed to last longer to facilitate facial expression. However, the aging process is accelerated by excessive exposure to the sun and other external factors.

Figure 6.26 A Aging can be considered as the revenge of gravity on endogenous tension. There is a decrease in the quality of the fibers and the intravacuolar contents. During the aging process, the intrafibrillar tension decreases and the fibrils become gradually less resistant to tension. (2 x) B The sagging of the cutaneous and subcutaneous structures of the face affects some areas more than others, especially the lower part of the face (and neck) Video 6.13

THE OBSERVABLE MECHANICAL EFFECTS OF MANUAL THERAPY I have recorded several video sequences that illustrate the effects of different techniques on the subcutaneous multifibrillar network (Figure 6.27 and Video 6.14).

Figure 6.27 Our endoscopic observations confirm that traction applied directly to the skin has a direct effect on the subcutaneous fibrillar network. The mobility of the subcutaneous fibers, adipocytes, blood vessels, and cells can be clearly seen Video 6.14

• What are the observable mechanical effects of manual therapy? • How do manual techniques influence the multifibrillar mechanism? It is no longer possible to argue that manual therapy has no effect on the subcutaneous tissues. Our endoscopic observations confirm that traction applied directly to the skin has a direct effect on the subcutaneous fibrillar network, and that mechanotransmission is likely in play. It is also evident that manipulation in three dimensions seems to be the best way to deal with the mechanical potentialities of the fibrillar structures.

It is not our role to say that any one given manual therapy technique is more or less efficient or gives better results than any other. Each manual therapist will find an explanation for the mechanism of action of his or her particular therapy, but, increasingly, science should be able to explain the basis of such interventions. This book provides a starting point for further research into these mechanisms.

FOLLOWING THE RED THREAD We can now answer the last red thread question. In answer, to summarize, the mobile, adaptable fibrillar network with its intersecting fibers develops a mechanical harmony that is lost when healthy tissue is damaged. The body’s repair mechanisms are unable to restore the fibrillar network in the damaged area to its original condition. The replacement tissue is of poor quality, but this can be improved by early mobilization of the injured area by manual therapy to enhance the flexibility of the scar tissue. RED THREAD QUESTIONS 6. Can nature restore harmony to the multifibrillar network when it is subjected to forces that exceed normal physiological limits, as in pathology or as a result of trauma?

Comment by John F. Barnes, PT, LMT, NCTMB

When I was studying physical therapy at the University of Pennsylvania decades ago, I clearly remember my anatomy professor telling us to cut through the fascia and throw it away. Too many people still view fascia as unimportant packing material. After my own trauma and personal investigation into the fascial system through my experiences with treating patients from around the world, I realized that to release the fascia requires very different principles. Almost all past research was performed on cadavers and focused entirely on the fibrous network of the fascial system. Although the fibrous network is very important, it is equally important to address the fluidity of the ground substance of the fascial system. Understanding this involves unique principles based on fluid dynamics. The continuity of the ground substance is shown in Dr. Guimberteau’s high-definition digital video images. Every human being has different fascial strain patterns. Engaging a fascial restriction with gentle but firm pressure for 5 minutes in our Myofascial Release technique will elicit the phenomena of piezoelectricity, mechanotransduction, and phase transition, and ultimately lead to release. Such sustained mechanical pressure results in fibrillar mobility and the other changes in fibrillar behavior that are seen in Dr. Guimberteau’s work. This, in turn, leads to mechanotransductive effects in the cell, and probably occasions the production of interleukin-8, the body’s natural anti-inflammatory. A picture is worth a thousand words. Dr. Guimberteau’s important discoveries in the living human being have been extremely helpful to therapists and physicians in their understanding of fascia, and confirm what they have been feeling under their hands. The beautiful liquid crystalline nature of fascia in Dr. Guimberteau’ s images represents the true nature of the fascial system and provides some explanation for the effectiveness of Myofascial Release for the reduction of pain and increasing range of motion. Dr. Guimberteau’ s series of DVDs and this book beautifully illustrate and describe the structure, fluidity, and importance of the fascinating network of fibrils and microtubules that make up the fascia system. His timely contributions have enhanced our therapeutic artistry and ability as Myofascial Release therapists to locate and release myofascial restrictions, and illuminate the role that fascia plays in one’s overall health.

Comment by Kenzo Kase, DC

Years ago, I remember taking students from my chiropractic school in Japan to view cadavers in a dissection laboratory. I was instructing them on the anatomy, physiology, and pathology of the human body. But as I looked at the exposed tissue, I always wondered, ‘How does this really work in a living person?’ I knew the names of the body structures, and I knew their function. I had the knowledge of what we thought was happening in a living person, but I always felt there was a big piece missing. As I looked at the exposed cadaver tissues, I saw muscle, bone, organs, and fat. But, of course, I never saw fluid or fluid movement. I could never see how the muscles and fascia actually moved when someone ran or jumped. How could I fully comprehend the processes happening in a living body when I could not see what was actually happening? So for 40 years I have created pictures in my head of the inside of the body. I told my students when they viewed the cadavers, ‘This is not everything. You can look at this body, but what you see is hard and not the reality of what a living person looks like. You need to imagine how this looks with fluid circulating and lubricating the tissues.’ There should be constant movement of the tissues. When I saw the endoscopic images from Dr. Jean-Claude Guimberteau’s videos, I said to myself, ‘This is it! This is what I have been imagining all these years.’ I was so surprised that the images looked so much like what I had pictured. It was amazing to see the fluid moving along all the fibers of the fascial areas and making all the sliding movements possible. I was able to meet Dr. Guimberteau when he was the keynote speaker at the 2013 Kinesio® Taping Association International Research Symposium at Stanford University. I discussed with him my techniques of using Kinesio® Tex Tape and applying it to the skin to lift the epidermis and dermis. As the top layers of skin are lifted, more space is created in the tissues underneath. As this space is created, compression of the tissues is alleviated, fluid begins circulating more freely, and body tissues can cool as stagnated blood and lymph are dispersed. Space, movement, and cooling. Dr. Guimberteau’s description of tissue structure and function provides wonderful insights into how these therapeutic benefits may actually come about. I was fascinated by his drive to continually search for new knowledge and new understanding of the body and its functions. His passion for his work is inspiring. At Stanford, we discussed possible collaborative research that would investigate how the Kinesio® Taping Method works. What happens under the skin as we apply tape to the surface layers? He and I have very similar philosophies. We are always looking for more information, more knowledge about living mechanisms. We both believe that you

must continue studying and learning. We want to understand everything we can about the human body. I am excited about the possibilities of what we can learn by working together. Dr. Guimberteau’s work has revolutionized the way we look at the human body, and has provided the world with a fascinating image of what is truly under the skin!

Comment by Willem Fourie, PT, MSc

Over the past 40 years of my career as a physiotherapist, my profession has undergone subtle evolutionary changes in treatment approaches in response to the increasing evidence base of the profession. Developing as a manual therapy to assist with the recovery of patients from trauma, surgery, or disease, movement has always been the mainstay of our treatment approaches. This includes massage therapy, graded passive movements, and exercises. We all knew that the manual movement and manipulation of tissue improved the quality of the tissue flexibility and ultimately the quality of movement of the patient. However, we always suffered from a paucity of evidence for what we did intuitively in our treatment sessions. This left me personally often doubting my ability in the face of the lack of scientific proof. Over time, the medical world insisted on proof in the form of outcome-based evidence for our treatment modalities to produce best practice protocols. In physiotherapy, this resulted in a slow retreat from using manual and massage therapies, when only anecdotal evidence existed for what we were doing. In the past decade, a resurgence of interest in the understanding of the human connective tissue and fascial systems has rekindled the old spirit of manual and massage therapy that used to be the mainstay of treatment selection for the older generation of physiotherapists. In this respect, the work of Dr. Guimberteau has been pivotal in my own new understanding of how tissues and systems respond to injury and trauma. He has further augmented the knowledge base of observed dysfunction resulting from tissue scarring and adhesions. The simplicity of his approach and the clarity of his images give me, the therapist, new confidence in approaching my referring surgeon to explain what I am aiming to achieve in my treatment protocol. Dr. Guimberteau’s endoscopic observations confirm what I have been feeling under my fingers and hands as restricted gliding of tissue layers under the skin after surgery and trauma. They further confirm my own dissection observations of how the sophisticated collagen and areolar connective tissue layers create intricate relationships between all the anatomical structures within the living body. The value of this chapter on scars, inflammation, adaptation, and modification to the multifibrillar network cannot be overemphasized. Complications and dysfunction caused by scar tissue and adhesions are costing the medical world millions of dollars annually. Any contribution toward understanding the hidden world of the scar below the observed dermal layer must therefore be welcomed and applauded. As the result of the insights of Dr. Guimberteau, which are given in this chapter, the clinical reasoning of the therapist is greatly enhanced and can now provide a more controlled therapeutic

intervention, with the benefit of improved functionality for the patient after trauma or surgery. This chapter gives me, the physiotherapist, the confidence to approach my referring surgeon with a treatment plan based on objectivity, rather than giving intuition as the reasoning behind my treatment selection.

7 Concept of Connective Tissue as the Architectural Constitutive Tissue Responsible for Form Form can be described Form is capable of mobility Forms can become more complex

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

SUMMARY Now that we have presented our observations of the structure of living matter, we can say that ‘form’ is the morphological result of the fractal, chaotic mesh of intertwined fibrils that plays the key architectural and structuring role within living tissue.

FORM CAN BE DESCRIBED What scientific observation has revealed As we have seen in the Introduction, the organization of living matter has been a subject of discussion since ancient times. The language and concepts used to describe such organization has been influenced by various sometimes metaphysical - underlying presumptions about form and its constituents. But now, technological advances have enabled us to examine living matter microanatomically and to move toward a more objective, more scientific synthesis of form and function, abandoning the received ideas of the past. Objective scientific observation is the only way forward, the only point of reference (Figure 7.1 and Video 7.1).

Figure 7.1 Endoscopic observations confirm the continuity of the architecture of living matter. A continuous global network of interconnected fibrils in three dimensions links all the constituents to form an organic entity. (10 x) Video 7.1

The multifibrillar architecture of the extracellular environment One of the privileges of the microsurgical transplant and plastic surgeon is the opportunity to operate in different areas of the body, and thus to build up an extensive knowledge of human anatomy. Any surgeon who undertakes such microsurgery can confirm that fibrillar tissue is found everywhere in the body. Endoscopic observation reveals it in every corner of our anatomy. It is found in muscles, in and around tendons and blood vessels, surrounding nerves, and in the periosteum. All the organs of the body seem to share the same basic fibrillar framework—of course with different architectural features. And the fibrils not only pervade the entire body, but also—at the microscopic level—link the cells to the intercellular matrix. Therefore it is logical to see a relationship between this continuous fibrillar network and the resulting form of the body, and to search for a new architectural model (Figure 7.2).

Figure 7.2 It is not easy to provide irrefutable evidence of the relationship between the collagen fibers and the contours of the body. Here, at the elbow of an obese subject, this relationship can be clearly seen A Depression in the tissue beneath the epicondyle B A surgical incision in the depression reveals taut underlying fibers C Distended fat lobules caused by adipocyte overload have put these fibers under tension. This fibrillar tension extends into the depths of the underlying tissue. (5 x)

This fibrillar tissue thus constitutes a global system. It is a system of total continuity. The concept of tissue layers, neatly arranged in separate strata, compartments, and sheaths, although useful as a means of teaching and learning anatomy, is ultimately false.

The fundamental architectural unit of the body: the concept of the microvacuole Our observations show that this all-pervasive tissue is built up from fibrillar connections, in three dimensions, that link all the parts of the body together, and in so doing create an organic entity. The networks of ubiquitous fibrils intertwine to create three-dimensional polyhedral microspaces—the microvacuoles—which may be seen as the fundamental architectural unit of the body. They are filled with glycosaminoglycans, which in turn are framed, or occupied by cells of different shapes, sizes, and functions (Figure 7.3, and Videos 7.2 and 7.3).

Figure 7.3 The concept of the microvacuole enables us to explain the following A The shape, volume, and mobility of the structural elements, as well as their multiplication and growth B The location of cells Video 7.2 and 3

These units are not arranged in stratified, hierarchical layers, but instead apparently randomly and chaotically. Form can also be understood as the consequence of the conglomeration and accumulation of these microvacuoles, microvolumes, and the mesh of intertwined fibrils. Thanks to the information we have obtained using videoendoscopy, we can now also understand how these anatomical structures move and return to their resting state, and how they receive energy and information and maintain their integrity without loss of tissue continuity, except in the few instances when this is a functional necessity.

We now understand the fibrillar organization and morphodynamic potentiality of the collagen and elastin network that extends from the surface of the skin to the cell, and we also understand the links between the fibrillar network and the cell via the integrins, and the intercellular cohesion provided by the collagen fibrils. The network has the capacity to adapt to fill a space, to build all possible forms, and therefore to enable the growth of complex forms and to permit the changes incurred under the influence of physical forces alone. The multimicrovacuolar mesh, with its pseudogeometrical configuration that provides the basic architecture of living matter, gives rise to questions of importance and common interest for mathematicians, biochemists, and physicists. For the first time, we now have an elegant and simple architectural concept and model of the microanatomical organization of living matter that originates from observation of living tissue. It is not just theoretical—it can be readily observed by any surgeon and provides the necessary clarification to continue this line of research, without the development of complex theoretical models. It is now possible to sketch the outlines of an interpretation that is at once structural and functional, and to consider the human body as a mesh of intertwined fibrils and cells that extends throughout the body, with variations in fibrillar and cellular density. All the constituent elements are linked together and are capable of movement, energy distribution and the removal of metabolic waste. This is a new way of looking at the human body. The body, its external appearance and its internal organization, has an architecture that is radically different from conventional models. The role of the extracellular matrix—a global network responsible for form The body can no longer be considered as machine-like, made up of separate parts with the organs joined together by connective tissue. If there is total continuity between the surface of the skin and the nucleus of the cell (Figure 7.4 and Video 7.4), and if that continuity extends throughout

the global form and that of the body organs, then it is only logical to conclude that there is a relationship between tissue continuity and form, and to propose a new paradigm.

Figure 7.4 This fibrillar architecture is responsible for the body framework in its entirety, from the surface of the skin to the periosteum and the structure of bone. It is a veritable continuum. This is far more than simple connective tissue —it is our constitutive tissue Video 7.4

KEY STATEMENT Connective tissue is, in fact, the constitutive tissue. It does not only link the different parts together—it is the frame in which the parts are developed.

Redefining fascia The moment has now come to propose a personal definition of this term. It must be in accordance with what we have observed. The definition must also be capable of being adapted to the semantic usage that we encounter among the various schools of thought and research in this field. Cells, as we have seen, cannot be responsible for the continuity and the

integrity of the living form. Their existence requires a support system and an architectural framework. Several anatomical terms are used to describe the tissue between cells: the extracellular matrix, interstitial tissue, the multimicrovacuolar collagenous absorbing system, loose or areolar tissue, and the tissue known as connective tissue, which is often referred to as fascia —but all this leads to confusion. In anatomical terms, fascia is defined as the material link that connects and unites all parts of the body. In fact, it is very similar to the connective tissue that is described as being involved in support and in linking movement. But this definition is often interpreted differently, depending on schools and continents, ranging from simple densification of tissue, such as the superficial fascia to a solid myotendinous structure such as the tensor fasciae latae and the iliotibial band. The term ‘fascia’ is often overused, misused, and used indiscriminately, which creates confusion from both the anatomical and therapeutic perspectives. For example, what exactly is fasciitis? What does the commonly used phrase ‘We are going to treat the fascia’ mean? But fascia has become too universal a term to be removed from the medical or paramedical vocabulary. However, it needs to be—indeed must be— redefined, precisely because of its universal character. I propose the following definition. KEY STATEMENT Fascia is the tensional, continuous fibrillar network within the body, extending from the surface of the skin to the nucleus of the cell. This global network is mobile, adaptable, fractal, and irregular; it constitutes the basic structural architecture of the human body.

Fascia, thus defined, can modify its fibrillar characteristics depending on the functional demands—but it would still be the same system. Everybody might then work with it in their own specific manner, but when fascia was spoken of, its meaning would be clear to everyone.

FORM IS CAPABLE OF MOBILITY

Morphodynamics: the fibrillar network facilitates mobility We have defined the structure of fascia’s fibrillar network in Chapter 2. In Chapter 3, we saw how the fibrillar network moves, and how in turn this intrinsic movement enables mobility in the organism. We can observe how structures deform and return to their resting state. Knowledge of fascia’s fibrillar architecture permits us to understand: • how structures receive information, • how they maintain their integrity while moving relative to one another, and • how they are capable of energy distribution, even during effort, without loss of tissue continuity and rupture (except in those few cases where such loss is a functional necessity). Fascia’s fibrillar matrix constitutes a physicochemical continuum that moves, lives, and metabolizes. The structuring elements participate in all of these functions. To do this, there must be complete tissue continuity, from the biggest macroscopic anatomical structures down to the smallest microanatomical structures. Moreover, this fibrillar architecture provides complete physical continuity within the fibrillar framework, which extends to and includes microscopic structures such as, for example, the helicoidal protein of elastin, collagen, and water molecules. But to explain our observation of the microfibrils stretching and splitting, we need to imagine that the collagen molecules also move in a certain way (Figure 7.5 and Video 7.5).

Figure 7.5 A The entire spectrum of possible fibrillar movements is set in motion within this highly mobile network. Everything moves, even inside the molecules. (15 x) B Morphodynamics must associate form and movement at all levels of living matter, including intramolecular mobility Video 7.5 and 6

KEY STATEMENT The relationship between the shape and the mobility of the anatomical structures is absolute, and this applies both to the external appearance of the form and to its internal molecular organization. Any attempt to explain the organization of living matter and to define morphodynamics must take account of this statement.

Morphodynamics can be considered as the science of the form and of its movement (Figure 7.5B and Video 7.6). It is derived from scientific observation and refers to the distribution of the constituent elements at all levels within living matter. Their spatial configuration determines the dynamic form, beginning with the cellular origins of an organism. Traditional chemical definitions do not describe the mobility of molecules, and the forms that are represented in diagrams are at best inaccurate and often insignificant from a morphodynamic perspective. And yet the morphodynamic configuration of the molecules not only helps us to understand how they function but is necessary to ensure mechanical coherence. Biotensegrity In Chapter 5, we saw how the fibrillar network and its cellular content may constitute a tensegrity structure. Tensegrity is an architectural concept. Extending this concept to the realm of biology—‘biotensegrity’—may throw light on how living structures deal with stress and movement. Biotensegrity provides a very helpful working model that can aid understanding. However, the biotensegrity concept has huge implications for energy transmission within the living form, and for the ability to deal with both intentional and unintentional stress and movement. The ability of a tensegrity structure to ‘share’ loading across the entire form, as opposed to responding only close to the point of load, explains some otherwise puzzling aspects of anatomical performance. As Donald Ingber has shown, this wide-scale communication of movement and force works not only at the mesoscopic level but also with and within the cell.1 The effects of mechanotransduction in one location may hence be caused by stimuli remote from the cells concerned. The complexity of the balance of tensions and compressions within the body is so great that certainly other biomechanical hypotheses will enhance this concept, but for the moment it remains the only one able to explain our capacity to resist the force of gravity. Dispersed pattern and fractalization

A key conclusion from observation of the fascia’s fibrillar network is that it is irregular and fractal in nature (see Chapter 5). There is no discernible regularity of form, but patterns detectable at one magnification reproduce themselves repeatedly at higher magnification—the classic irregular fractal and polyhedric picture. This fibrillar network constitutes a complex system. Complex systems must adapt to a constantly shifting set of parameters. There is no fixed point of equilibrium. These systems are constantly moving from one state to another in an attempt to achieve equilibrium, but they always remain in a state of instability. This permanent state of instability enables the system to explore the fields of possible physicochemical solutions in the most efficient way. Fractalization is superimposed on the chaotic nature of the multifibrillar system, introducing a type of regularity into the irregularity of chaos. As we have seen, fractal objects are found in many areas of biology, including the ramifications of the vascular network, the alveoli, the bile duct, and the nervous system. A fundamental question arises from this finding. Why do living organisms appear to adopt this form, when we might have thought that order and linear relationships would be more effective? Western culture tends—to a greater extent than other cultures—to cleave to order and equilibrium, and to linear, deterministic relationships between components of a system. But here in the fascia we see an irregular, fractal, chaotic, non-linear system. From the outset, research into the existence of disorderly systems has tended to be dismissed as being of little or no importance. These phenomena cannot be explained by mathematical formulae, and they do not adhere strictly to the laws of Newtonian physics. In the course of our constant search for knowledge, we have had to gradually accept that nature does not function in straight lines, and that the law of proportionality of cause and effect, which refers to the relationship of two variables whose ratio is constant, could in fact be based on non-linear rules. Nevertheless, these complex systems, in constant search of equilibrium, can be described using rigorous scientific methods and can be shown to manifest a clear and definite underlying order within the apparent disorder.

FORMS CAN BECOME MORE COMPLEX Organogenesis As explained in Chapter 4, cells cannot of themselves be responsible for the continuity and integrity of living form. Cells cannot explain the shape of the body. Only the extracellular fascia’s fibrillar network can do this (Figure 7.6 and Video 7.7). The existence of cells requires a support system and an architectural framework.

Figure 7.6 Scissiparity—the division of individual fibrils—is frequently observed within the fibrillar network. Fractalization and the intrinsic properties of the fibrillar network are factors that facilitate this phenomenon. This allows us to better explain growth, the construction of an organic volume, and its resistance to gravity Video 7.7

The body is a global fibrillar system in which specialized cells have evolved to carry out specific functions by forming organs. Although there are specific differences, driven by differing functional needs, it seems that all organs share the same general fibrillar framework.

The organization of the skin into epidermis, dermis, and hypodermis perfectly illustrates the adaptation of this framework to cellular functional requirements. The density of the fibrillar tissue and the abundance or scarcity of cells, depending on their role, are the factors that determine and differentiate what we traditionally think of as separate skin layers. The same basic arrangement of cells within the fibrillar framework can be seen in the thyroid, in muscles and tendons, and in other anatomical structures with specific functions. The theory of emergence may also be of relevance in this context. The capacity of the fibrillar network to develop in density, quantity, and quality permits the emergence of a variety of forms with the same underlying architectural rules. This is organogenesis. The morphological and physicochemical equilibrium that ensures continuous metabolic exchange must be respected, but the transition to a higher level in morphological terms cannot be similar to the lower level, because it will be subject to new constraints and different intrinsic obligations. It will therefore be endowed with new capabilities, but the primary layout will remain. A multifibrillar framework can be transformed easily under the influence of diverse forces to produce morphological forms (Figure 7.7).

Figure 7.7 Computer modelling of the three-dimensional fibrillar network can easily produce a multitude of morphological forms, including the simple forms of life. A Undifferentiated, with no distinguishing features B Crown-shaped, with a space in the center C Spiral D Cylindrical

As discussed in Chapter 5, living matter is able to produce three-dimensional forms such as squares, lozenges, rounded cylinders, and coiled or tubular forms, but these forms are always simple (Figure 7.8). The completely random organization of the network allows this because it is found at all levels throughout the body, from the simple forms that make up the DNA to the microtubules of the cytoskeleton and the molecules. This firework display of diverse forms is already present and will continue to flourish. Certain lines of development will deviate from existing ones while remaining within the same developmental axes.

Figure 7.8 Life has retained only the simple forms of which we are composed. A Longitudinal aspect of a tendon B Rounded aspect of fat lobules C Coronal organization of a vein with a central canal D Squares on the surface of the skin E Oval shape of the Pacinian corpuscle F Elliptic organization of the skin of the fingertip

We will see an efflorescence of different structures—deterministic chaos, ready to explore all avenues (Figure 7.9). This is where coevolution intervenes, but always in accordance with the basic specifications of life.

Figure 7.9 In general, the organization of living tissue does not make use of the classic Euclidean forms. Instead, it uses irregular forms A The irregular pattern of the fibrillar framework B The irregular pattern of the surface of the epidermis

A new structural ontology We have seen that all the components of fascia’s multifibrillar system with its fractal, chaotic configuration work together to determine the behavior of the system as a whole. The system comprises a network of interacting agents, but no single agent directly influences the others. There is no one, allencompassing rule that dictates the global dynamic behavior of the system. We have also seen that there is total fibrillar continuity between the surface of the skin and the nucleus of the cell—a continuity that extends throughout the entire form, and indeed creates that form. This concept represents a radical departure from conventional models. The resulting structural rationalism envisages living matter as a dynamic, gravity-resistant system in perpetual search for equilibrium (Figure 7.10 and Video 7.8).

Figure 7.10 From now on, the body can be considered differently, and a new structuring ontology can be proposed. Everything is linked, and everything can move Video 7.8

At the beginning of this book, we stated that, traditionally, ‘form’ had been viewed from the perspective of appearance alone - the outward form. But now the perspective has changed, revolutionized by a new understanding of the nature of the connective tissue - the fascial multifibrillar network - that constitutes the architecture of living organisms. Key to this understanding has been observation of the tissue in vivo. In vitro studies cannot fully explain the living world. In future, with increasing miniaturisation of endoscopic instruments, it will certainly be possible to undertake more detailed exploration of living matter in situ, and to expand on the knowledge already obtained through in vivo endoscopic observation. Understanding the nature of the fascia’s fibrillar network provides us with a new language with which to describe form, and in turn throws light on what we do when we work therapeutically with a living body. This structural vision of living matter allows us to bring together molecular and physicochemical biodynamics and quantum physics, uniting scientific

disciplines. It should help to build bridges as the links between the different research communities become clearer. KEY STATEMENT These observations give rise to a new paradigm: Connective tissue, the fascia’s fibrillar network, is in fact the constitutive tissue. No longer is it seen as the passive padding or linkage between the main organs of the body. It - the constitutive tissue - creates the architecture. It is the frame within which all the body’s components develop, exist, and have their being. This change in the view of what constitutes living form creates a new ‘structural ontology’—a new way of categorizing and talking about what makes an organism.

In the Afterword, I will discuss the implications of such a radical change of view and give some personal interpretations and hypotheses relating to this paradigm shift.

Comment by Serge Gracovetsky, PhD

In an earlier life, I was trying to resolve the contradictions created by Bartelink’s representation of spinal mechanics. Bartelink believed that the back muscles are responsible for lifting the trunk, and that in so doing, the role of the lumbodorsal fascia become central to providing a physiological solution for the weight lifter undertaking a 200-kg lift without destroying his spine in the process. But the mathematical model required a very specific and precise description of the insertion points of the fascia and the muscles to the bone. A direct consequence is that any small change in the local attachments of the fascia to the tips of the spinous processes would bring about noticeable differences to the way in which the forces generated by the hip extensors would be transmitted all the way up to the upper extremities. Moreover, this effect is compounded by the very non-linear and viscoelastic properties of the collagen. The resulting sensitivity of the response of the loaded spine to minute anatomical changes was unreasonable, because a minor injury could potentially destabilize the entire musculoskeletal system. But this is not our everyday experience. I was unable to find a good explanation for this paradox, until one morning in October 2007, in Boston, where I listened for the first time to the representation of tissue arrangement proposed by Dr. Guimberteau. That was quite an eye-opener for me. This elegant concept, the smoothness and the continuity between the various tissues, wonderfully illustrated by in vivo images of the collagen being stretched, switched on a light in my mind. Now, finally, the interaction between fascia, bone, and muscles made sense. I could visualize the forces flowing through the body and the dynamic reconfiguration of the transmission pathways. This summarizes for me what this book is all about. It is wonderfully written and illustrated and represents a fresh approach to the rigid mathematical formulation of biomechanical models that for too long relied on the fixed vector attachments of the various components of the spine. Dr. Guimberteau’s model permits a quick and easy reconfiguration of the local anatomy as it responds to the applied forces. The infinity of solutions it offers is bound to optimize the use of resources. As such, Dr. Guimberteau’s concept goes beyond being a simple anatomical description and touches on the potential mechanisms needed to accomplish the changes necessary for the survival of the species in accordance with the evolutionary principles so brilliantly laid out by Darwin.

Afterword Why does nature use spatially simple but irregular polyhedral forms to build a wide diversity of complex forms? Are movements predetermined or random? Why should there be an irregular, chaotic, fractal, non-linear organization when order and linearity have proved to be so effective? Does this multifibrillar system have the capacity to influence cellular genomic processes? Conclusion

The video clips mentioned in the sidebars can be accessed at https://library.singingdragon.com/redeem using the code GACERGM.

In this final section of the book, I will expand the scope of my reflection into areas that are rarely addressed during medical or paramedical studies. It was only through 30 years of working as a surgeon that I developed the critical mind that enabled me to investigate the subjects I am about to discuss. I am pleased that my learning developed little by little, in this order, because it has given me greater freedom, and the curiosity to address the problems I encountered along the way. I was surprised to discover that things were far more complicated than I had anticipated.36 Discussion of my work inevitably gives rise to the following four questions, which in my view are fundamental. Although I have no firm answers to these questions, I believe it is productive to discuss them. 1. Why does nature use spatially simple but irregular polyhedral forms to build a wide diversity of complex forms? 2. Are movements predetermined or random? 3. Why should there be an irregular, chaotic, fractal, non-linear organization when order and linearity have proved to be so effective? 4. Does this multifibrillar system have the capacity to influence cellular genomic processes?

WHY DOES NATURE USE SPATIALLY SIMPLE BUT IRREGULAR POLYHEDRAL FORMS TO BUILD A WIDE DIVERSITY OF COMPLEX FORMS? Our observations have revealed that the forms encountered in living tissue, whether microvacuoles or cells, all have a polyhedral, irregular frame (Figure Aft.1). We have seen that this can be explained by the interweaving of fibers in three dimensions. These forms are the result of the construction of molecular elements, but these elements are themselves also constructions with their own distinctive forms. These basic, elementary forms are very often tubular, helicoidal, or spheroidal, as seen for example in the cytoskeleton. Collagen fibers and the double helix structure of chromosomes (DNA molecules) are other examples.37

Figure Aft.1 A Polyhedral vascular pattern B Polyhedrons at the surface of the skin C Polygonal cells D Polygonal microvacuoles

Figure Aft.1 E Cabbage leaf F Sponge G Part of a butterfly wing

The more complex structures that make up living organisms employ the same simple, basic forms. There is little variation in these forms, which are limited mainly to polyhedrons, cylinders, oval and helical shapes, and, less frequently, squares, rectangles, and elliptical and star-shaped forms. These forms exhibit different types of dynamic behavior, such as winding and unwinding, elongation, invagination, and densification, but always making

use of the same basic shapes. It is interesting to note that all members of the animal and plant kingdoms seem to be organized in the same way. 38, 39 This gives rise to further questions. • Why does this morphological limitation exist? • Why is there such similarity in shape? I suggest that the answers to these questions may relate to the fact that microvacuolar spaces, the cells, and the multifibrillar network are all subject to the same physical forces and to the laws that govern them (Figure Aft.2).

Figure Aft.2 A An electrocardiograph B Pressurized blood in an artery C Droplets on the lens of an endoscope D Fluid inside the body

The permanent presence of fluids, the changes in the opacity of the tissues, the evaporation of droplets, the bursting of the microvacuolar bubbles, body temperature, the presence of electrical potentials, and perioperative vascular pressure are all observable and measurable physical phenomena. In addition to these directly observable and often palpable phenomena, we must remember that there are also less evident physical forces present in the body,

including atmospheric and osmotic pressure, electromagnetic polarity, gravity, and nuclear forces. The polyhedral structure, with its fractal nature and the positional arrangement of its elements, is not just a simple juxtaposition of adjacent structures. It is the result of the combined influences of all the physical forces that we have just described. These forces have imposed forms that will persist in the evolutionary chain. There is nothing random or haphazard about the disposition of microanatomical elements, the variety of shapes, forms and volumes, or the colors, because they are the basic building blocks of life. This may seem to be a minor point, but it is a fundamental conclusion that leads to many more unanswered questions about the organization of living matter. All these factors enable us to better understand the organization of the human form, and this also applies to other living species, both plant and animal. The neo-Darwinists assert that shape and structure are the epigenetic expression of the genetic program and the primacy of the functional. However, my observations lead me to conclude that this view is insufficient to explain what I see, and I am directed back to the work of D’Arcy Thomson, 100 years ago.He believed that the shape and form of living things are also a consequence of natural forces. He was convinced that neither chance nor the laws of evolution can account for the genesis of shape, the harmonious growth, the limited number of living shapes, the similarity of their forms, and the undeniable unity of living organisms. He questioned whether adaptive forces alone, through Darwin’s natural selection process, could account for the development of form, and wondered whether they might be complemented by physical and mechanical forces. In attempting to answer the first question and those arising from it, a possible conclusion is that, to build morphological structures, the architecture of life obeys the fundamental physical forces that result in the selection of initial forms, permitting evolution within the same structural pattern, as well as diversity, and ensuring its permanence over time.

ARE MOVEMENTS PREDETERMINED OR RANDOM?

We introduced the concept of fibrillar chaos in Chapter 2, the intrinsic ability of the fibrils to permit movement in Chapter 3, and fractalization in Chapter 5. However, we can now add another phenomenon to these observations: dynamic unpredictability. This takes us into an unexpected domain. Watching these fibrils of different diameters sliding along other fibrils, dividing and lengthening in a fraction of a second, is disturbing when you think about the mobility of molecules necessary to enable that movement. It is also challenging to understand how these phenomena can occur simultaneously in millions of fibrils, thus permitting movement, either voluntary or involuntary, throughout the entire body. Our filmed observations contain sequences that are unexpected. During very brief periods of time—about 1 second—you can see the fibrils ‘hesitating’ about whether to move up or down another fibril (Figure Aft.3A and Video Aft.1A).

Figure Aft.3 A This sequence shows what appears to be a fibril hesitating about whether to move up or down another fibril (100 x) Video Aft.1A

This indeterminacy is a fundamental observation. All movements, and all combinations and sequences of movements, seem possible. This is also the

case when division into two, three, or four fibrils occurs. Nothing can predict this behavior. There are no warning signs or indications of when or where fibrils will divide in this way. This uncertainty seems to be of structural origin. Some fibrils appear to be capable of moving randomly in response to external constraints; however, others clearly have strong, stable links to each other, and as a result their mobility is inevitably restricted (Figure Aft.3B and Video Aft.1B).

Figure Aft.3 B This sequence shows, on the contrary, a strong, stable physical link—predetermined structural continuity (130 x) Video Aft.1B

Sometimes a particular movement will appear to be unpredictable but is in fact predetermined. A fibril that was previously hidden suddenly appears and turns out to be in continuity with another fibril, thus demonstrating the predetermined character of that movement (Figure Aft.3C and Video Aft.1C). Only the specific movement carried out in exactly that way could have occurred.

Figure Aft.3 C This sequence shows the beginning of an apparently unpredictable action. The fibril that was previously hidden suddenly appears and turns out to be in continuity with the other fibrils. This demonstrates the predetermined character of that particular movement (100 x) Video Aft.1C

This mixture of random and predetermined movements involving millions and millions of fibers and fibrils allows us to state that when you take a spoon and start eating, for example, you will never repeat this gesture in exactly the same way. And when you put the spoon back on the table, the prestressed fibers in the multifibrillar network will return to their original position but not necessarily in exactly the same way as after the first spoonful. The introduction of an element of non-deterministic mobility to the movement of the fibers allows us to think that any given movement at a specific time is unique and will never be repeated. Each action is unique (Figure Aft.3D and Video Aft.1D).

Figure Aft.3 D This sequence shows two separate fibrillar movements filmed 10 seconds apart, one after the other, in the same area and under the same constraint. These two movements do not resemble each other. The initiation of the mobility of the fibrils differs in each case because of the simultaneous occurrence of seemingly nondeterministic and predetermined fibrillar behavior. Each action is unique (100 x) Video Aft.1D

The mobility of the fibrillar architecture is not the result of a single predetermined mechanism. On the contrary, it seems to come about in a random manner from a range of different potential movements. One particular movement is chosen at a given time to carry out a specific, nonreproducible action. This indeterminacy is surprisingly reminiscent of the uncertainty principle of quantum physics.40

WHY SHOULD THERE BE AN IRREGULAR, CHAOTIC, FRACTAL, NON-LINEAR ORGANIZATION WHEN ORDER AND LINEARITY HAVE PROVED TO BE SO EFFECTIVE? Western culture tends to accord more importance than other cultures to order. We find it reassuring. The principle of causality, which can be traced back to the ancient Greek philosophers, is the foundation stone of this line of thought.

Causality is the relation between causes and effects, when the effect is understood to be a consequence of the cause. It is difficult to leave the shores of predictable and reassuring order and to approach those of chaotic unpredictability. I found this to be a very challenging step to take from a scientific point of view, and made this conceptual leap only with difficulty. From the outset, research into the existence of disorderly systems has tended to be dismissed as being of little or no importance. These phenomena cannot be explained by simple mathematical formulae, and they do not adhere strictly to the laws of Newtonian physics.41, 42 In the course of our constant search for knowledge, we have had to gradually accept that nature does not function in straight lines, and that the law of proportionality of cause and effect, which refers to the relationship of two variables whose ratio is constant, could in fact be based on non-linear rules. Nevertheless, these complex systems, in constant search of equilibrium, can be described using rigorous scientific methods and can be shown to manifest a clear and definite underlying order within apparent disorder.43 Evidence of non-linearity Wherever you look beneath the skin, the distribution and general layout of the structures display no sign of regularity or pure symmetry. Sometimes groups of cells are arranged parallel to each other, or resemble familiar, reassuringly geometrical shapes. However, on closer inspection we discover that their distribution is not as regular as it appears to be, and that the pattern is not repeated elsewhere. Minds that have been shaped by the logic of the principle of linear causality find it difficult to accept the idea that the architecture of the sliding system, which is responsible for harmonious movement in the body, is completely irregular and apparently chaotic. And yet our observations confirm the existence and efficiency of this irregular, chaotic, and fractal system. The organization of living matter is therefore far more complex than we have hitherto imagined, and is completely different to what we were taught. If we are to fully understand how living matter is organized, we must abandon any

preconceived ideas. We need to look further than simple explanations that are accessible or reassuring because they fit in with our traditionally rational way of thinking. This requires a different scientific approach based on in vivo observations. We must accept the fact that in vivo observations may call into question certain in vitro observations. This is because in vitro studies are carried out on dead, chemically prepared tissue samples that do not replicate the dynamic properties of living tissue in situ, because they are no longer subject to endogenous tension. Now that we are confronted with the proposition that irregular, chaotic, and fractal systems can be efficient, we will try to discover more. Chaotic systems in biology: appearance and underlying order44 The issue of the apparent contradiction of order and efficiency within chaotic systems (Figure Aft.4) was first raised in 1795 by Laplace, the master of determinism, in his essay entitled Essai Philosophique sur les Probabilités.45 Laplace states that order is created by random events. He said that, ‘in a series of events occurring over an indefinite period of time, the effect of regular and constant causes will, in the long term, outweigh the effect of irregular causes.’ This assertion was confirmed by Andreï Kolmogorov (1903–1987), one of the greatest mathematicians of the 20th century.46 He provided mathematical proof that ‘the large scale, collective actions of random phenomena create non-random regularity.’ We must try to proceed, but step by step. Chaos in biology does not refer to a situation in which ‘anything goes’. Dynamic chaos is the hallmark of dynamic systems that do not conform to the rules of classical Newtonian physics, and that are characterized by behavior that is neither periodic nor ‘quasiperiodic,’ because of the inherent non-linear nature of the system. It is not the result of haphazard or random actions.

Figure Aft.4 A The natural architectural fibrillar organization is structural chaos with functional determinism B A fractal is a geometric pattern that is repeated at every scale. If you zoom in on a fractal pattern, it will look similar or exactly the same as the original shape. This property is called self-similarity

Chaos in the macroscopic domain of biological science can be qualified as deterministic chaos, because both unpredictability and non-randomness are present at the same time. How is this possible? How and for what purpose can two seemingly contradictory phenomena operate in the same system at the same time?

The ability to search for higher solutions, afforded by deterministic chaos, provides the necessary conditions for an efficient system, if not a perfect one. It also facilitates the deployment of the dynamic solutions that exist in the natural world and that are likely to play a role in the emergence of new structures with specific dynamic configurations. In other words, a complex system searching for equilibrium will always be found to be in a state somewhere between stability and change. Such a system is therefore capable of adopting a wide variety of configurations, all the more so because it can make use of other intrinsic characteristics, such as fractalization. This means that a chaotic system is able to explore a large portion of the available space to facilitate whatever movement is required. KEY STATEMENT Deterministic chaotic behavior is one of nature’s potential dynamic capabilities. It broadens the field of possible solutions, allows them to be explored more efficiently, and permits greater complexity (Figure Aft.5).

Figure Aft.5 A Fibrils in a rabbit B Fibrils in a marrow

C Fibrils in seaweed D Human fibrils

Fractalization is superimposed on the chaotic nature of the multifibrillar system, and it further complicates matters. We believe that the irregular fractalization of the fibrillar structures inevitably results in the chaotic appearance of the fibrillar network. As we have seen in Chapter 5, fractal objects lack regularity. But this irregularity is not random. There is an underlying regularity in the apparent irregularity. Fractal objects display scale invariance in the sense that, regardless of magnification, they express the same general pattern of organization. Fractal objects are found in many areas of biology. The inherent dynamic properties: dynamic and irregular fractalization, and morphological chaos, cannot be considered separately. We must take account of their combined influence. The ability to explore all possible solutions (exploratory feasibility), which is a feature of chaotic systems, provides a wide range of dynamic behavior that can lead to complexity. These complex systems are in a permanent state of flux and are never at rest. The search for equilibrium is constant and ever changing. Equilibrium is not a fixed point in the system but a constantly shifting set of parameters, rather like Plateau’s soap bubbles. This state of a system in search of equilibrium (which demonstrates instability within previously acquired stability) favors the growth of complexity. It leads to biological evolution by adding unexpected constraints to the emergence of life. We can describe these systems as being non-integrable. They must be defined by non-predictable equations. We must not forget that this chaotic organization, which we have observed, creates new possibilities because of the basic, polyhedral, architectural framework that has probably always been present in living matter. The distinctive feature of this type of system is the holistic nature of its behavior. In other words, it is the result of the sum of the interactions between its constituent components. It is impossible to isolate the independent behavior of individual elements. All the components of this entire multifibrillar system, with its chaotic configuration, work together simultaneously to dictate the behavior of the

system as a whole. The system must be studied in its entirety. It is made up of a network of interacting agents, but no single agent directly influences the others. There is no one all-encompassing rule which dictates the global dynamic behavior of the system. The term coevolution, normally applied to the interaction between evolving species, could be used to describe the multiple interactions of the elements in a complex living system. These dynamic capabilities present a coherent way of exploring movement, and they are indispensable factors in the evolutionary process. We are now in a position to provide a rational explanation for the chaotic and irregular aspect of these biological systems. These insights also throw light on the underlying universal mechanisms of evolutionary systems and the ways in which complexity permits the growth and development of living organisms.

DOES THIS MULTIFIBRILLAR SYSTEM HAVE THE CAPACITY TO INFLUENCE CELLULAR GENOMIC PROCESSES? We have seen that this fractal, chaotic fibrillar architecture generates complexity and paves the way to change. However, this architecture does not come from nothing. It is the result of cellular activity, and is therefore theoretically controlled by the genetic programme. The genome contains the entirety of an organism’s hereditary information, including the genetic blueprint responsible for building its form.47, 48, 49, 50, 51, 52 And yet, even though our genetic heritage is immutable, the form of the finished adult structure is capable of change. How is this possible? Normally, unless a mutation occurs, change is very slow for the highly specialized genomic structures, which are incapable of rapid optimal adaptation to the surrounding environment. But in apparent contradiction to this principle, I have encountered clinical cases that seem to exhibit changes that cannot be accounted for by genomic mutation. Loss of function and growth

This photograph (below, left) shows the hand of a 7-year-old patient, in which only the flexor tendons of the third digit were sectioned by glass in early childhood (Figure Aft.6A). They were not repaired surgically. 4 years later, the injured finger was similar to the other fingers but was smaller and shorter than the corresponding finger on the other hand. Nevertheless, its shape is normal. The growth of the finger was slowed by the simple fact that the tendons responsible for flexion and regular use of the finger were not surgically repaired. Why are all the structures of the finger affected, while only some of the tendons were sectioned? Why does a small local injury have a global effect on the growth of the finger? Why does the lack of function lead to a reduction in the size of the finger? In this case, growth hormones, which travel via the intact blood vessels, played their role, but the morphological outcome was incomplete. In this particular case, the growth potential of the cells seems to have been slowed down by the absence of mechanical stimulation. But, as we have seen in Chapter 4, the cells are influenced directly—mechanically—by the fibrils that form the framework of the extracellular fibrillar system. Increased use leading to hypertrophy of the form In this case, the index, middle, and ring fingers of an employee at a printing works were amputated (Figure Aft.6B). Only the little finger remained to carry out pincer movements with the thumb. The little finger grew slowly, and all its structures increased in volume in a regular manner. There was a global, harmonious change in shape as a result of the increased use of the finger. Functional overuse was responsible for increased mechanical demand on the cells, which responded with greater-than-normal growth of all the structural elements, again in a harmonious fashion.

Figure Aft.6 A The third digit (of a 7-year-old patient) is similar to the other fingers, but it is smaller and shorter than the corresponding finger on the other hand B The final form of the little finger, which was subject to functional overuse and developed beyond normal limits, both in length and width and in size and volume

How is it possible for the growth of the entire finger to change while the global form of the finger remains unaltered? Does the degree of function influence the development of the final form? What limits the increase in growth? Olecranon bursitis Olecranon bursitis is an example of functional adaptation that develops gradually over the years as a result of the tissue being subjected to repeated mechanical stress (Figure Aft.7A). Clinical symptoms may be absent, but there are distinct changes in physiological and metabolic behavior. It is a megavacuolar response to a repetitive parietal constraint. We have seen in Chapter 6 that wherever mobility is associated with repetitive parietal constraint, there will be a megavacuolar response. This capacity to develop an olecranon bursitis is not transmissible from one generation to the next, but it can last a lifetime. The persistence of this condition must therefore involve cellular renewal. These local mechanical changes have certainly influenced the peripheral cells in the area of the bursitis and have also modified their behavior, and perhaps their DNA, in a progressive manner. Could this megavacuolar reaction provide an explanation for the widely varying anatomical characteristics of the carpal and digital sheaths, where pressure during flexion is very high? For example, for the multiform nature of the different anatomical descriptions of the sliding of the flexor tendons inside the carpal and digital sheaths, where pressure in flexion is very high (Figure Aft.7B and C)? In a broader context, if we consider the human phylogenetic chain, could this development of the relationship between the transformation of the fibrillar system at the wrist and fingers under the mechanical constraint have occurred simultaneously with the emergence of the ability to grasp?

Figure Aft.7 A Olecranon bursitis develops during the course of a lifetime. It is an example of an adaptive behavior. It is not transmissible B The carpal tunnel is a mechanical adaptation to repetitive flexion C In the fingers, megavacuoles surround the entire circumference of each tendon as soon as other pulleys appear

The inherent properties of the digital and carpal sliding sheaths are transmissible. They are a defining component of human anatomy. They exhibit variation of tissue architecture from fibrillar to megavacuolar; the creation of this diversity has required a number of gradual changes during the process of phylogeny, the first stage of which could have been bursitis. These changes must have come about very slowly as the ability to grasp developed. Could this transformation of the tissue architecture, adapted to the needs of repetitive flexion, have been maintained and transmitted over time? In the light of my cellular observations, I do not think that we can completely reject

the suggestion that mechanical factors may have some influence on our genetic transmission. Hypothesis Finally, bringing together all these thoughts based on the observations made in this book. 1. We have seen before that fibrillar structural elements are under the direct influence of fundamental physical forces. These elements link directly, via integrins and the cell membrane, through the cytoskeleton, to the nucleus; this is made possible by mechanotransmission (Figure Aft.8A). 2. We have seen that external and internal factors exert a reciprocal influence on one another. Everything is subject to the same basic physicochemical laws, and optimal structure and function can be achieved only within the limitations of such physicochemical factors. 3. We cannot rule out the possibility of a mechanical influence on the quantity and quality of cell production. Neither can we rule out the concept of adaptive cell multiplication (as in olecranon bursitis), but not all cells are involved. The modification is local. Only the local extracellular links seem to be capable of transmitting and modulating this mechanical influence 53(Figure Aft.8B). 4. The changes in cell behavior cannot be explained by distribution of information via the blood, because not all the cells seem to be directly connected to the blood supply (Figure Aft.8C). 5. Moreover, these local morphological changes are not time-limited. This contrasts with what happens during the formation of scar tissue, when, over time, normal cellular behavior is resumed. On the contrary, these changes in cell behavior, discussed above, continue over time and involve the inevitable renewal of local cells reproducing the acquired modifications. The genome of these cells has therefore been influenced in a sustainable and transmissible way.

Figure Aft.8 A Mechanotransmission and mechanotransduction are fundamental, because changes in fibrillar tension have a mechanical effect on the cells. Changes in fibrillar tension distort the cells and cause them to change shape

Figure Aft.8 contd B Animation of mechanotransmission between cells and the fibrillar frame C The relationship between the fibers and cells is so close that we sometimes see ‘fibers of cells’ D The vascular network does not distribute blood directly to each and every cell Video Aft.2

This raises the following question: does the extracellular environment influence stem cell function and the genotype (Figure Aft.9)? The answer could be that the influence of the extracellular environment causes a slow transformation of the genetic heritage.

CONCLUSION The importance of the role of the extracellular matrix must be reconsidered, and this will provide new, more coherent theories, particularly in the fields of embryology, morphogenesis, and phylogenetics.55, 57 This challenges the concept of the supremacy of the all-powerful genome, while revealing its submission to basic universal forces and demonstrating the crucial role of non-genomic factors. Finally, the link between efficiency and chaos, which differs substantially from the Western thinking of classical Greek and Cartesian philosophy, is rather disconcerting. It also underlines the architectural similarity of the human form to other living organisms in the animal and plant kingdom. It emphasizes the fact that humans are no different from other living forms. At the end of this chapter, we come to a central realization—the complexity of the organization required to create life. This revelation is not new; since ancient times, mankind, in an attempt to make sense of this complexity, has turned to metaphysics. However, as technology advanced, science increasingly became capable of offering other ways of understanding this complexity and the reasons for it. But the momentum of biological research in the laboratory must not be allowed to divert us too far from the essential purpose of science. The new knowledge resulting from research must be used for the service of humanity. The knowledge of man in the service of man. I believe that surgical exploration must be a cornerstone of this modern research, and an essential point of reference, because it is the only way to provide a clear and precise description of the anatomy of human living matter as it really is. Matter, a hackneyed and overused term, which is often used dismissively, needs to regain its place at the center of scientific debate, because matter is

the key to everything.

Figure Aft.9 In conclusion, the importance of the role of the extracellular matrix must be re-evaluated

Comment by Torsten Liem, DO, MSc (Ost.), MSc (Paed. Ost.)

In 1543, Andreas Vesalius published the first large modern textbook of anatomy: De Humani Corporis Fabrica. To this day, its approach to the analytical presentation of isolated cadaveric structures is everywhere to be found in anatomical atlases. We have become used to seeing matter presented as separate components, as it is in traditional anatomical teaching; the experience and structural patterns we have known so far lead us to see this as a fact to be taken for granted. But this is only one of many possible ways of seeing things. It depends on a conditioned perception of reality, and does not have any real, tangible material basis. We are, in fact, constantly and simultaneously dealing with the dynamics of relationships, change, attachment, and potentiality. Their imprint characterizes our life in the world. We do not see elements of color; we see a red rose. We do not hear sound waves; we hear the patter of raindrops. Nor do patients sense the nerve receptors of their skin being stimulated; they feel a kiss. And we, as practitioners of manual therapies, do not palpate anatomy in isolation but, in the words of Guimberteau, in ‘irregular, chaotic, fractal, non-linear’ patterns of organization. Textbooks of anatomy and the anatomy of dead, disconnected fragments of the body simply create the illusion of separation. When we instead take the more complex view described by Jean-Claude Guimberteau, we see that we are not just treating material substance or fragmented pieces of matter and anatomy. This is relevant therapeutically. The essential question in treatment is not ‘What is there?’ but ‘What is happening?’ Guimberteau uniquely demonstrates this. He lifts the veil of the failure to see, to reveal, the living dynamics of tissue not seen before. He shows us the dynamics ‘...of a multilayered and ubiquitous tissue that changes its fibrillar features according to its functional demand ... but it would be always the same system’. At the beginning of the 19th century, Bichat demystified symptoms and diseases, relating them to pathological anatomy. Broussais confuted the idea of disease as antinature, by showing it to be an organic reaction to internal or external agents, in the course of which the functioning and the anatomy of the body become disturbed. Guimberteau’s book and videos open up to us a similar fundamental paradigm shift. By lifting the veil over the hitherto unseen world beneath our skin, he provides a fresh dimension in which, in a remarkable way, we are able to see and experience the

interwoven nature of fascial structures. These images, and the stories that Guimberteau tells, demystify the anatomy of individual structures in isolation, and place the anatomy books that have been written so far in a fresh and less unquestioned context, giving us direct experience of living anatomy. Do these affect palpation? Do they change anything? Absolutely. They free us from the dead anatomy of the dissection laboratory and the atlas of anatomy, whose images are branded on our minds and have distorted the perception and interpretation of our palpatory findings. Guimberteau provides us with a new context in which we can share the experiencing of living tissue. Here it is not static, isolated individual images that occupy the foreground, but the continuity of tissue, a dynamic process of interactions and processes of chaotic change in the tissue. In this chapter (and this is not to ignore the hypothetical answers he formulates), Guimberteau dares to go far beyond established knowledge of anatomical structures. Yet we can still let ourselves be moved and enchanted by such living anatomy—and through our hands pass on that enchantment.

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Index Illustrations are comprehensively referred to from the text. Therefore, significant items in illustrations (figures and tables) have usually only been given a page reference in the absence of their concomitant mention in the text referring to that illustration.

A adaptation/adaptability 78 dynamic 123, 135, 143 adaptational teleology 3 adhesion (intercellular) 104 adhesion (pathological) see scar tissue and adhesions adipocytes 19, 36, 37, 42, 97, 98, 136, 145 lipid overload 158, 159 aging 160 air (atmospheric) pressure and microvolumes 61–3 anatomy 18–54, 111 endoscopic 10, 164 mechanics 139 scientific/surgeon’s observations 10, 169 arborescent configuration of the microcirculation 145 areolar (loose connective) tissue 28–9, 45, 55 arteries 51–2, 108 atmospheric pressure and microvolumes 61–3

B Barnes, John F., contribution by 163 Bartelink’s representation of spinal mechanics 180 basal stratum (stratum basale) 31 Bichat, Marie François Xavier 198 biomechanics see mechanics biotensegrity and tensegrity 112, 121, 130–2, 139–40, 175 blood, extravasation 6, 151 blood vessels (vascular circulatory/system) 51–2, 107–8

dermal 32 fiber and cell relationships with 102 pressure in 122 scars and 147 see also neovessels bone 48–50 bourrelets de Plateau 71 Broussais, François-Joseph-Victor 198 bubbles and microbubbles 61–3, 119–22 in adhesions 147 intratissular 61–3, 75–7, 153 hematoma and 153–4 surgical incisions and 8, 122 microvacuolar, bursting 62, 117, 185 soap 119–20, 122 bursitis, olecranon 155–7, 193–4

C cancellous bone 49 capillaries 102 network (pericellular) 107, 108 carpal tunnel 50, 157, 158, 193 cells 5, 54, 97–109 cytoskeleton 54, 106, 111 fiber relationships with 101–9 genomic processes, multifibrillar system influences on 192–7 historical perspectives 3 morphology and distribution 97–100 overload 157–8 survival, microvacuoles and 107–9 world outside see extracellular environment chaos 11, 64, 65, 139, 146, 188–90 deterministic 178, 189, 190 efficiency and 197 fibrillar 23, 50, 54, 63, 64, 71, 146, 149, 175, 185 organized 64 children, repair and healing processes 150 circulatory system see blood vessels clusters of cells 97, 99, 100 coevolution 178, 191 collagen (and collagen fibers/fibrils) 10, 42, 43, 45, 85, 90–1, 125, 126, 135, 144, 171, 173 microvacuolar 72, 73, 74, 135 multimicrovacuolar collagenous absorbing system (MVCAS) 11, 46, 172 complex patterns and forms 176–9, 183–5 building a wide diversity of 183–4

equilibrium in see equilibrium fibrillar network as 175 polyhedrons and 183–5 connective tissue 19, 20, 172, 179 loose 38–9, 45, 55 constitutive fractalization 133–4 constitutive tissue/framework 24, 172, 179 fibrils 2 continuity (tissue) 2, 13–80, 83 fibrillar 19–24, 36, 39–40, 56, 58–80 form and 172 maintenance during mobility 83 cortical bone 49 cylindrical (round) forms/structures 68, 136, 137 cytoskeleton 54, 106, 111

D Darwin, Charles 3 see also neo-Darwinists decorin 74 deep fascia 39–41 dermis 30–4, 97, 176 scars/adhesions and 145, 146 determinism chaotic determinism 178, 189, 190 morphological determinism 89 movements and randomness vs. 185–7 digital tendon sheath 156, 158, 194 dilaceration 156 dispersed pattern and fractalization 175–6 dodecahedron 119 dynamics 198 dynamic adaptability 123, 135, 143 dynamic chaos 189 dynamic fractalization 130, 131–2, 135, 136, 137, 191 dynamic unpredictability 185 of fibrils 125 global 44, 45, 91–2, 178, 191 see also morphodynamics

E ecchymosis 151 economy of microvacuolar system 120–1

edema 150–1 efficiency chaos and 197 of microvacuolar system 120–1 of movement, maximum 85–6 elasticity early theories 15 loss in obesity 159 emergence (in life of new structures) 177, 190 grasping ability 157–8, 194 empty spaces, filling of see spaces endogenous tissue tension 9, 121–3, 160, 188 endomysium 42, 43 endoscopy (observations in) 5 anatomy in see anatomy intratissular see intratissular endoscopy videoendoscopy (endoscopic videophotography) 2, 21, 83, 171 energy 78, 97, 110 microvacuoles and 109, 123 muscle contraction and 39, 157 tensegrity/biotensegrity and 127, 175 epidermis 26–30, 97, 144, 145, 176 tension 9 epigenetics 185 epimysium 41, 42 epineurium 50 equilibrium 190 morphological 177 physicochemical 177 at rest and in movement 123–6 evolution 3, 185, 191 see also coevolution exploratory surgery 5 extracellular environment/milieu/world/system (in general) 19–21, 23, 54, 196 ecchymosis and 151 multifibrillar architecture 169–70 extracellular matrix 20, 171–2, 197, 198 cytoskeleton and 106 form and 171–2 extravasation 150 blood 6, 151

F fascia, definitions 55–6, 172–3 fascicles, tendon 47

fat(ty) lobules 9, 34, 35–6, 37, 97, 98, 120 distended 170 fibers cells relationships with 101–9 intertwining/interweaving/intersecting fibrils and 18, 21–4, 22, 42, 46, 65–6, 68, 71, 78, 83, 91, 122, 162, 170, 171, 183 mechanical properties see mechanics fibrils 58–80 aging and 160 biotensegrity and 130, 132 fibrils (Continued) chaos 23, 50, 54, 63, 64, 71, 143, 149, 175, 185 collagen see collagen constitutive framework 2 continuity 19–24, 36, 39–40, 56, 58–80 dissociation/division 72, 88, 92, 129, 130, 185 diversity/variety 68 frame 68–77 inflammation and 153 intertwining/interweaving/intersecting fibers and 18, 21–4, 22, 42, 46, 65–6, 68, 71, 78, 83, 91, 122, 162, 170, 171, 183 lengthening 86, 92, 185 linked and fixed 90 mechanical properties see mechanics migration 87 movement/mobility 83–91, 125–6, 130, 173–4 mechanical behaviour during 84–91 network see multifibrillar networks weight loss and 160 see also microfibrils fibroblasts 27, 47, 100, 112 flat surface, maximum coverage 118 flexibility and suppleness 15, 78, 146 forces on fibers/fibrils absorption 85–6 orientation of fibers in main direction of 84–5 form and 122 of gravity see gravity form and shape 167–80 continuity and 172 describing 169–73 epigenetic factors 185 extracellular matrix in maintenance of 171–2 fractalization in growth and development of 135, 136 geometrical vs. non-geometrical 118 historical perspectives 3–4 hypertrophy of 192–3

mechanisms in maintenance of 122 mobility/movement and 125–6, 173–5 morphodynamics as science of 174 at rest, maintenance 123–4 structured 77–8 see also morphology Fourie, Willem, contribution by 165 fractalization 23, 28, 72, 133–7, 175–6, 185, 191 constitutive 133–4 dispersed pattern and 175–6 dynamic 130, 131–2, 135, 136, 137, 191 irregular 78, 175, 191 Fuller, Buckminster 126, 127 functional loss 192

G GAGs (glycosaminoglycans) 74, 83, 90, 110, 123, 126, 170 genetics and genes historical perspectives 3 multifibrillar system and 192–5, 192–7 see also epigenetics geometrical shapes biotensegrity and 130 non-geometrical shapes vs., 118 Gibbs rings 71 globality 54–5 connective tissue 19 extracellular matrix 171–2 fibrillar network 91–2, 170, 176 global dynamics 44, 45, 91–2, 178, 191 glycosaminoglycans (GAGs) 74, 83, 90, 110, 123, 126, 170 glycosylated proteins 74 Graceovetsky, Serge, contribution by 180 granular layer (stratum corneum) 29 grasping ability, emergence 157–8, 194 gravity (and resistance to it) 117, 123, 124, 126–9 aging and 160, 161 biotensegrity and 130, 132 form and 122 obesity and 159 ground substance 20 growth fractalization enabling 135 loss 192

H Haversian system 50 healing see repair and healing hematoma 151 hexahedron 119 histology 2, 19, 20, 44 history of living matter 3–4 holism 19, 111, 191 hyaluronan (hyaluronic acid; hyaluronate) 74 hydration (moistening) of tissues 8, 74, 132 hypertrophy of form 192–3 hypodermis 34–7, 41, 97, 98, 158, 176

I icosahedron 119, 120, 121, 129, 130, 132, 139 inflammation 147, 152–4 Ingber, Donald 129, 175 injury (traumatic) repair processes see repair scarring see scar tissue and adhesions integrins 106, 111, 171, 194 interfibrillar movements between individual fibrils 86–90 within microvacuole 90–1 interstitial spaces 20 intertwining/interweaving/intersecting fibers and fibrils 18, 21–4, 22, 42, 46, 65–6, 68, 71, 78, 83, 91, 122, 162, 170, 171, 183 intratissular bubbles see bubbles intratissular endoscopy 6–11, 15 perioperative 6, 16–18 invagination 9, 184 scar 148

K Kase, Kenze, contribution by 164 Kinesio® Taping 164 Kolmogorov, Andreï, 189

L

lamina densa 31 Laplace, Pierre-Simon 189 layers absence of 18–19 several, cells arranged in 104 lengthening, fibril 86, 92, 185 linear vs. non-linear organization 188–9 lipids adipocytes, overload 158, 159 microvacuolar 73 living matter/tissues fractalization and its importance in 134 history 3–4 physical phenomena influencing 117 spaces in see spaces longitudinal forms/structures 47, 52, 136 loose connective tissue 38–9, 45, 55 lungs, fractalization 134 lymphatics 52–3, 108

M macroscopic level/domain 16, 19, 173, 190 Mandelbrot, Benoit 133 manual therapy, mechanical effects 161–2 mechanics/biomechanics (incl. mechanical properties/behaviour) (bio)tensegrity and 128, 129, 132 dynamic fractalization and 136, 139 endoscopic anatomy 139 fibers and fibrils 123 in mobility 84–91 manual therapy 161–2 spinal, Bartelink’s representation 180 mechanotransduction 105–6, 175, 194 osteopathy and 112 mechanotransmission 105–6, 194 subcutaneous tissue 162 megavacuole 154, 155–8 olecranon bursitis 155–7, 193, 194 melanocytes 97 membranes, cell 106, 111, 194 mesoscopic level 2, 16, 175 microbubbles see bubbles and microbubbles microfibrils 2, 30–1, 46, 173 microscopic level/domain 2, 16, 19, 129, 169

microvacuoles 21–4, 46–7, 62, 64–7, 68, 70, 72–4, 83, 109, 110, 117, 118, 153, 154, 155, 158–9, 170–1, 183 aging and 160 bursting (of bubbles) 62, 117, 185 cell survival and 107–9 economy and efficiency 120–1 enlargement/dilatation in megavacuolar transformation 156 in obesity 159 form and its maintenance in movement 125 at rest 123–4 fractalization and 135 interfibrillar movements within 90–1 in movement 131 form and its maintenance 125 pressure in 74, 117, 124, 150 tensegrity and 129, 131, 132 volumes see microvolumes see also multimicrovacuolar systems/networks microvolumes (microvacuolar volumes) 21–4, 46, 120 diversity and 65–8 content 72–5 pressure and 61–3 migration, fibril 87 minimal arrangement, Plateau’s law 120 mobility see movement moistening (hydration; water content) of tissues 8, 74, 132 morphodynamics 143, 171, 173–4 epidermis 30 morphology 177 cells 97–100 deterministic 89 skin 24, 25 see also form morphostructure 72 motility (rather than mobility) osteopaths referring to 94 movement/mobility (of structures) 78, 94 continuity and its maintenance during 83–90 equilibrium and 125–6 fibrils see fibrils form and 125–6, 173–5 microvacuolar see microvacuoles predetermined vs. random 185–7 sliding systems see sliding systems two kinds of 94 see also motility multifibrillar (fibrillar) networks and structures 2, 15, 19, 43, 47, 54, 56, 92, 93, 108, 110, 121,

122, 129, 141–65, 169–70, 175, 177, 178, 184 cellular genomic processes and 192–5, 192–7 as complex system 175 dynamic fractalization and 135, 136 extracellular environment 169–70 fascia as 173, 176, 179 globality 91–2, 170, 176 microcirculation in 51 mobility/movement and 83–90, 125–6, 173–4 multimicrovacuolar systems/networks 23, 38, 49, 61–8, 93, 108, 109, 110, 121, 171 collagenous absorbing system (MVCAS) 11, 46, 172 muscle 41–2 contraction 39, 83, 157 Myers, Thomas W., contribution by 57 myofibroblasts 112

N neo-Darwinists 185 neovessels and neovascularization 145, 148 nerves 50–1, 108 dermal 32 non-geometrical vs. geometrical shapes 118 non-integrable systems 191 non-linear vs. linear organization 188–9

O obesity 159 observations (scientific incl. surgeon’s) 5, 169 anatomy 10, 169 bubbles appearing with incisions 8, 122 endoscopic see endoscopy Occam’s razor 120–1 octahedron 119 olecranon bursitis 155–7, 193–4 ontology, structural 178–9 order 188–90 organogenesis 137, 176–7 Oschman, James L., contribution by 111 osmotic pressure 75, 123, 185 osteopathy 94 mechanotransduction and 112

P parietal structures 158, 193 pericellular capillary network 107, 108 perimysium 41, 42, 43 perineurium 50, 51 periosteum 48–50 phylogeny/phylogenesis/phylogenetics 137, 143, 157, 193–4 physical phenomena influencing tissues 117 physicochemical equilibrium 177 plasticity 15 Plateau, Joseph 119–20 see also bourrelets de Plateau polygons 65, 120, 183 irregular 65 regular 118 polyhedrons 22–3, 119, 121, 127, 136, 144 cells 97, 104 complex forms and 183–5 irregular 22, 26, 27, 31, 65, 121, 183–5 microvacuolar 65, 66, 117, 118, 131, 170 regular 119 skin 24, 25, 26, 28, 29, 31 premuscular aponeuroses (deep fascia) 39–41 pressure circulatory system 122 intravacuolar 74, 117, 124, 150 microvolumes and 61–3 osmotic 75, 123, 185 proteins, glycosylated 74 proteoglycans 73, 74, 132 obesity and 159 ptosis 160

R repair and healing processes (injury) 144, 149, 162 children 150 rheological relationship 85 round (cylindrical) forms/structures 68, 136, 137

S

Saint-Hilaire, Geoffroy 3 scale invariance pf fractal objects 133, 191 scar tissue and adhesions 143–50, 165 edema and 150 inflammation and 154 Schleip, Robert, contribution by 79 scientific observations see observations self-assembly, fractalization enabling 135 self-sufficiency 78 shape see form and shape skin 24–41, 176 cells 97 ecchymosis 151 fibrillar movement with traction of 83–90 polygons 118 see also subcutaneous tissue sliding systems 11, 57, 92 blood vessels 52 inflammation and 152 phases of movement of 84–5 scars/adhesions and 145 tendons and 10, 43–7, 52, 83, 194 soap bubbles 119–20, 122 spaces, filling of all (lack of empty space) 9, 18–19, 21, 130 nature’s use of spatially simple forms 183–5 three-dimensional space 119–23 two-dimensional space 118 spinal mechanics, Bartelink’s representation 180 spongy (cancellous) bone 49 stem cells and extracellular matrix 197 stratum basale 31 stratum corneum 29 stratum germaticum 29 stratum granulosum 29 stratum spinosum 29 stretching point, maximum 85–6 structuring of form 77–8 epigenetic factors 185 multimicrovacuolar network role in 61–8 ontological 178–9 subcutaneous tissue 16, 38–9 manual therapy and its mechanical effects 161–2 superficial fascia 36, 37–8, 172 suppleness and flexibility 15, 78, 146 surface, flat, maximum coverage 118 surface tension 119, 123 surgery

bubbles appearing with incisions 8, 122 edema after 150 exploratory 5 intratissular endoscopic 6, 16–18 observations in see observations scar from 144–5 synergy and synergetics 127

T teleology, adaptational 3 tendon(s) 47 scar tissue/adhesions 146, 148 tendon sheath digital 156, 158, 194 sliding system 10, 43–7, 52, 83, 195 tensegrity and biotensegrity 112, 120, 121, 127–32, 139–40, 175 tension endogenous/intracorporeal 9, 121–3, 160, 188 surface 119, 123 tetrahedron 119, 127 Thompson, Sir D’Arcy Wentworth 3 three dimensions (living matter/body/tissues in) 177 filling the 3D space 119–23 reacting or moving in three dimensions 92, 94 tissue continuity/elasticity etc. see continuity; elasticity etc. traction on skin, fibrillar movement with 83–90 trauma see injury tunica adventitia and media and intima 52 two-dimensional space, filling 118

V van der Waals’ forces 75, 123 vascular system see blood vessels veins 51–2, 108 Vesalius 198 vessels see blood vessels; lymphatics videoendoscopy (endoscopic videophotography) 2, 21, 83, 171 vincula 156 virtual space 9, 15, 44

W

water status (hydration/moistening) of tissues 8, 74, 132 weight excess (obesity) 159 loss 160 in obesity 159 wrist and grasping ability 157–8, 194

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