Phẫu Thuật Gân Bàn Tay (Tendon Surgery of the Hand)

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TENDON SURGERY
OF THE HAND
Editor-in-Chief
Jin Bo Tang, MD
Professor of Surgery, Founding Chair, Department of Hand Surgery,
Affiliated Hospital of Nantong University; Founding Chair, The Hand
Surgery Research Center, Nantong University, Nantong, Jiangsu, China
Editors
Peter C. Amadio, MD
Lloyd A. and Barbara A. Amundson Professor of Orthopedics, Consultant,
Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota, USA
Jean Claude Guimberteau, MD
Scientific Director, Aquitany Hand Institute, Pessac, France
James Chang, MD
Chief, Division of Plastic & Reconstructive Surgery, Professor of Surgery
(Plastic Surgery) and Orthopedic Surgery, Robert A. Chase Hand Center,
Stanford University Medical Center, Palo Alto, California, USA
Contributing Editors
David Elliot, MA, FRCS, BM, BCh
Hand Surgery Department, St Andrew’s Centre for Plastic Surgery, Broomfield
Hospital, Chelmsford, Essex, United Kingdom
Judy C. Colditz, OT/L, CHT, FAOTA
HandLab, Raleigh, North Carolina, USA

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TENDON SURGERY OF THE HAND
ISBN: 978-1-4377-2230-7
Copyright © 2012 by Saunders, an imprint of Elsevier Inc.
All Mayo drawings copyright © Mayo Foundation for Medical Education and Research.
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This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described herein. In
using such information or methods they should be mindful of their own safety and the safety of
others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method and duration
of administration, and contraindications. It is the responsibility of practitioners, relying on their
own experience and knowledge of their patients, to make diagnoses, to determine dosages and the
best treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Tendon surgery of the hand / editor-in-chief, Jin Bo Tang ; editors, Peter C. Amadio, Jean Claude
Guimberteau, James Chang ; contributing editors, David Elliot, Judy Colditz. – 1st ed.
    p. ; cm.
  Includes bibliographical references and index.
  ISBN 978-1-4377-2230-7 (hardcover : alk. paper)
  I. Tang, Jin Bo, 1963-
  [DNLM:  1.  Hand–surgery.  2.  Tendons–surgery. WE 830]
  617.5’75059–dc23

2012002534
Senior Content Strategist: Don Scholz
Manager, Content Development: Heather Krehling
Publishing Services Manager: Deborah Vogel
Project Manager: Brandilyn Tidwell
Designer: Louis Forgione
Printed in China
Last digit is the print number: 9  8  7  6  5  4  3  2  1

DEDICATION
I dedicate this book to my parents, Cheng Hua Tang and Xiou Feng
Zhao; my wife, Xiao Tian; and my daughter, Yu-Qing. Their support,
understanding, and sacrifice are the most fundamental to my past work
and completion of this book.
I also dedicate this book to my colleagues all past and present members of
the Research Center and the Department. In particular, it is dedicated to
an inspiring professor and tendon enthusiast: Seiichi Ishii, who mentored
me in my first work on tendons.
Jin Bo Tang, MD
This book is dedicated to my wife, Bari, for her continuous emotional
support and understanding; to my clinical colleagues at Mayo Clinic, for
their daily inspiration and for their generosity in accommodating the
many demands that the creation of this book has required; and to my
many mentors in tendon surgery over the years, especially James M.
Hunter, MD, whose high standards of tendon surgical skill and creativity
I can only hope to emulate.
Peter C. Amadio, MD
I would like to thank two illustrious colleagues, Harold Kleinert and
Claude Verdan, for influencing my way of thinking in tendon surgery
and for lighting the path for me to perform vascularized tendon grafts.
They never wavered in their support for my work, and they encouraged
me to continue investigations.
Jean Claude Guimberteau, MD
I wish to thank my family—James Sr., Lily, Anthony, Barbara, and
Cecilia Chang; Harriet Roeder; and Julia, Kathleen, and Cecilia Roeder
Chang—for their constant love and support. I also wish to honor all the
research fellows, residents, and hand fellows at Stanford who have worked
so tirelessly; and my surgical mentors, Vincent Hentz, Neil Jones, and Roy
Meals, who have taught me so much about the hand.
James Chang, MD

iv
PREFACE
investigators, surgeons, and therapists to author the text.
These chapters are contributed by respected surgeons/
investigators from renowned centers and innovative sur­
geons who offer unique and insightful techniques.
It is our essential goal to offer comprehensive cover­
age of international perspectives and techniques cur­
rently used in tendon surgery of the hand. In particular,
the section on primary flexor tendon repair and reha­
bilitation is a genuinely international collaboration,
highlighting methods and protocols of different units;
it is sure to provide readers with an abundance of infor­
mation, allowing them to judiciously plan their own
treatments based on the surgical and post-surgical care
principles described in the chapters. Extensor tendon
injuries are another topic with various treatment options.
Considering the variety of techniques and rehabilitation
protocols currently used, we have planned the related
surgical and rehabilitation chapters to reflect diverse
approaches to the injuries. Further, multiple therapy
protocols were contributed from the leading hand units
across the world; these protocols are published online
to provide the readers with rich and authoritative refer­
ences for deciding on treatment course for extensor
tendon injuries.
We are greatly indebted to the contributors from 15
countries spanning four continents; their high quality
contributions are the cornerstones of this book. Notably,
we should give our earnest gratitude to Dr. David Elliot
and Ms. Judy Colditz, our guest editors. Not only are
both eminent educators with vast experience on tendon
problems—as a surgeon and a therapist, respectively—
but they are also keen editors who have tirelessly devoted
their effort to this book. Dr. Elliot contributed his own
crystallized experience in seven chapters of this book
and also edited a portion of the primary and secondary
repair chapters. Ms. Colditz coordinated and helped edit
the chapters relating to rehabilitation. Furthermore, we
greatly appreciate the surgeons and therapists who con­
tributed therapy protocols in the online appendix and
video clips to enhance the contents of this book.
Finally, we feel obliged to express our appreciation to
the Elsevier staff and editors, especially Dan Pepper,
acquisition editor; Don Scholz, senior content strategist;
Mary Beth Murphy, developmental editor; Heather
This book, Tendon Surgery of the Hand, is intended to
address the lack of a comprehensive and up-to-date text­
book on the basic science and clinical practice of tendon
surgery in the hand.
Tendon surgery is one of the most important topics
in hand surgery; its importance to hand function and
its allure to hand surgeons are well-reflected in the vast
number of investigations and publications devoted to
this topic. Surprisingly, however, no comprehensive
book on tendon surgery of the hand (or of other parts
of the body) has been published in the last 25 years,
despite revolutionary changes in the treatment of tendon
injuries and disorders. The only landmark book on
tendons is Hunter’s Tendon Surgery in the Hand, from
1987. Therefore, we organized a group of international
experts in tendon surgery to produce a new volume. The
idea of compiling such a textbook was initiated during
a conference in Manchester, UK, in 2006 and was sub­
sequently reshaped, with updated media technology, by
Elsevier with publication of both print and online
versions.
Since the mid-1980s, the clinical practice of tendon
surgery has evolved considerably, and a great number of
innovative techniques have emerged. They include a
myriad of novel repair techniques, use of new suture
materials, novel tendon sheath and pulley treatments,
vascularized tendon grafts, and the development of
various postoperative rehabilitation methods. With
regard to the basic science, a wealth of new knowledge
has been accumulated. Our knowledge of tendon
biology and biomechanics has increased greatly, and a
number of new research fields—such as gene therapy,
tissue engineering, stem cell delivery, and gene silenc­
ing—have emerged. Advancements in updated clinical
techniques and cutting-edge technologies in the basic
science of tendon surgery are comprehensively summa­
rized in this book.
This book contains a total of 46 chapters (41 print
and online chapters and 5 web-only chapters), orga­
nized in five sections: basic science, primary flexor
tendon surgery, secondary flexor tendon surgery, exten­
sor tendon repair and reconstruction, rehabilitation
of tendon surgery, and the future of tendon surgery.
We have aimed to include a worldwide selection of

v
Preface
Krehling, content development manager; and Brandilyn
Tidwell, project manager. Without their advice on
content and careful copyediting, it would not have been
possible to accomplish this project. We also give our
great appreciation to the Elsevier art team for providing
superb color illustrations for this book, helping us
present our readers with a complex surgical topic in an
easily readable way.
We hope that this textbook helps practitioners,
fellows, residents, and medical students understand or
master key concepts and techniques of tendon surgery
of the hand and aids in treatment planning of the
often worrisome problems relating to the tendon of
the hand.
Jin Bo Tang, MD
Peter C. Amadio, MD
Jean Claude Guimberteau, MD
James Chang, MD

vi
CONTRIBUTORS
Philip E. Blazar, MD
Assistant Professor of Orthopaedic Surgery, Department
of Orthopaedic Surgery, Brigham and Women’s Hospital,
Harvard Medical School, Boston, Massachusetts
Lance M. Brunton, MD
Assistant Professor of Orthopaedic Surgery, Department
of Orthopaedic Surgery, University of Pittsburgh Medical
Center, Pittsburgh, Pennsylvania
Robert E. Bunata, MD
Assistant Professor, Department of Orthopaedic Surgery,
Bone and Joint Research Center, University of North Texas
Health Science Center, John Peter Smith Hospital, Fort
Worth, Texas
Yi Cao, MD
Fellow, The Hand Surgery Research Center, Nantong
University, Nantong, Jiangsu, China
Francesco Catalano, MD
Associate Professor, Hand Surgery Division, Department
of Orthopedics, Gemelli Hospital of Rome, Catholic
University, Rome, Italy
James Chang, MD
Chief, Division of Plastic & Reconstructive Surgery,
Professor of Surgery (Plastic Surgery) and Orthopedic
Surgery, Robert A. Chase Hand Center, Stanford
University Medical Center, Palo Alto, California
Chuan Hao Chen, PhD
Professor, Department of Anatomy, Bengbu Medical
College, Bengbu, Anhui, China
A. Bobby Chhabra, MD
Charles J. Frankel Professor and Vice Chair, Department
of Orthopaedic Surgery, University of Virginia Health
System, Charlottesville, Virginia
Roberto Adani, MD
Chief, Department of Hand Surgery, Azienda Ospedaliera
Universitaria Integrata Verona, Verona, Italy
Peter C. Amadio, MD
Lloyd A. and Barbara A. Amundson Professor of
Orthopedics, Consultant, Department of Orthopedic
Surgery, Mayo Clinic, Rochester, Minnesota
Kai Nan An, PhD
Professor of Biomedical Engineering, Department of
Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota
Rohit Arora, MD
Associate Professor of Trauma Surgery, Department of
Trauma Surgery and Sports Medicine, Medical University
Innsbruck, Innsbruck, Austria
Morad Askari, MD
Assistant Professor of Surgery, DeWitt Daughtry Family
Department of Surgery, University of Miami, Miami,
Florida
Joseph Bakhach, MD
Clinical Assistant Professor of Surgery, Plastic and
Reconstructive Surgery Department, Hand and
Microsurgery Department, American University of
Beirut Medical Center, Beirut, Lebanon
Pierre-Yves Barthel, MD
Department of Hand and Reconstructive Surgery,
Emile Galle Surgical Center, CHU Nancy, Nancy,
France
Alexandros E. Beris, MD
Professor in Orthopaedics, Department of Orthopaedic
Surgery, University of Ioannina School of Medicine,
Ioannina, Greece
Nada Berry, MD
Assistant Professor, Department of Plastic Surgery,
Southern Illinois University, Springfield, Illinois

vii
Contributors
Alphonsus K.S. Chong, MBBS, MRCS(Ed),
MMed(Orth), FAMS
Consultant Hand Surgeon, Assistant Professor,
Department of Orthopaedic Surgery, Yong Loo Lin School
of Medicine, National University of Singapore, National
University Hospital, Singapore
Sean P. Clancy, OTR/L, CHT
Program Coordinator, Hand Therapy, University of
Chicago Medicine, Chicago, Illinois
Judy C. Colditz, OT/L, CHT, FAOTA
HandLab, Raleigh, North Carolina
Monina Copuaco, OTC, CHT
Hand Therapist, Robert A. Chase Hand Center, Stanford
University Medical Center, Palo Alto, California
Massimo Corain, MD
Department of Hand Surgery, Azienda Ospedaliera
Universitaria Integrata Verona, Verona, Italy
Brandon E. Earp, MD
Department of Orthopedic Surgery, Brigham and
Women’s Hospital, Boston, Massachusetts
David Elliot, MA, FRCS, BM, BCh
Hand Surgery Department, St Andrew’s Centre for Plastic
Surgery, Broomfield Hospital, Chelmsford, Essex, United
Kingdom
Andrew E. Farber, DO
South Island Orthopaedic Group, Cedarhurst, New York
Felicity G.L. Fishman, MD
Department of Orthopaedic Surgery, Duke University,
Durham, North Carolina
Kristen E. Fleager, MD
Department of Orthopaedic Surgery, Stanford University
Hospital and Clinics, Stanford, California
Markus Gabl, MD
Department of Trauma Surgery and Sports Medicine,
Medical University Innsbruck, Innsbruck, Austria
Leesa M. Galatz, MD
Associate Professor, Shoulder and Elbow Service,
Washington University Orthopedics, Barnes-Jewish
Hospital, St. Louis, Missouri
Emily Grauel, MS
Virginia Commonwealth University School of Medicine,
Richmond, Virginia
Robert R.L. Gray, MD
Assistant Professor, Department of Orthopaedic Surgery,
Miller School of Medicine, University of Miami, Miami,
Florida
Heather Griffiths, mscot(regnb), CHT
Certified Hand Therapist, Horizon Health Network,
Moncton, New Brunswick, Canada
Jean Claude Guimberteau, MD
Plastic, Hand Surgeon, Aquitany Hand Institute, Pessac
France
Hiroyuki Kato, MD, PhD
Professor and Chairman, Department of Orthopaedic
Surgery, Shinshu University School of Medicine,
Matsumoto, Japan
Ioannis Kostas-Agnantis, MD
Department of Orthopaedic Surgery, University of
Ioannina School of Medicine, Ioannina, Greece
Armin Kraus, MD
Division of Plastic and Reconstructive Surgery, Stanford
University Medical Center, Palo Alto, California
Richard D. Lawson, MBBS, FRACS
Director of Hand Surgery Research, Department of Hand
Surgery and Peripheral Nerve Surgery, Royal North Shore
Hospital, University of Sydney, Sydney, Australia
Fraser J. Leversedge, MD
Assistant Professor, Co-Director, Duke Hand and Upper
Extremity Surgery Fellowship, Department of Orthopaedic
Surgery, Duke University, Durham, North Carolina
Beng-Hai Lim, MD
Center for Hand and Reconstructive Microsurgery
(CHARMS), Singapore
Paul Y. Liu, MD
Clinical Professor and Chair, Department of Plastic
Surgery, Brown University Alpert Medical School,
Providence, Rhode Island
Marios G. Lykissas, MD
Division of Orthopaedics, Cincinnati Children’s Hospital
Medical Center, Cincinnati, Ohio
Mollie O Manley, MD, MS
Department of Orthopedics, University of Pittsburgh
Medical Center, Pittsburgh, Pennsylvania

viii
Contributors
Michel Mansat, MD
Professor of Orthopedics and Traumatology, Department
of Orthopaedics and Traumatology, Toulouse University
Hospital, Toulouse, France
Pierre Mansat, MD, PhD
Professor of Orthopedics and Traumatology, Department
of Orthopaedics and Traumatology, Toulouse University
Hospital, Toulouse, France
Renzo Mantero, MD
Professor, Former Chief of Hand Surgery (Retired),
Ospedale San Paolo, Savona, Italy
Daniel P. Mass, MD
Professor of Surgery, Department of Orthopaedic Surgery,
University of Chicago, Chicago, Illinois
Antonio Merolli, MD, FBSE
Assistant Professor, Department of Orthopedics,
Universita Cattolica del Sacro Cuore, Rome, Italy
Arash Momeni, MD
Division of Plastic and Reconstructive Surgery, Stanford
University Medical Center, Palo Alto, California
Steven L. Moran, MD
Professor and Chair of Plastic Surgery, Professor of
Orthopedics, Division of Hand Surgery, Mayo Clinic,
Rochester, Minnesota
Nash H. Naam, MD, FACS
Clinical Professor, Plastic and Reconstructive Surgery,
Southern Illinois University and Southern Illinois Hand
Center, Effingham, Illinois
Lori Niemerg, OTR/L, CHT
Certified Hand Therapist, Department of Working Hands,
Southern Illinois Hand Center, Effingham, Illinois
Fiona H. Peck, MCSP
Burns and Plastic Surgery Department, Wythenshawe
Hospital, Manchester, Great Britain
Yeong-Pin Peng, FRCS
Department of Hand and Reconstructive Microsurgery,
National University Hospital, Singapore
Karen M. Pettengill, MS, OTR/L, CHT
Clinical Coordinator, NovaCare Hand and Upper
Extremity Rehabilitation, Springfield, Massachusetts
Brian C. Pridgen, BS
Department of Plastic and Reconstructive Surgery,
Stanford University Medical Center, Palo Alto, California
Mark A. Rider, MBChB, FRCS, FRACS
Department of Hand Surgery, SW Sydney Regional Hand
Institute, Sydney, Australia
Lorenzo Rocchi, MD
Hand Surgery Division, Department of Orthopedics,
Gemelli Hospital of Rome, Catholic University, Rome, Italy
Mario Igor Rossello, MD
Professor, Chief of Hand Surgery, Ospedale San Paolo,
Savona, Italy
Serge Rouzaud
Physiotherapist, Institut Aquitain de la Main, Bordeaux,
France
Michel Saint-Cyr, MD, FRCS(C)
Associate Professor, Department of Plastic Surgery,
University of Texas Southwestern Medical Center at
Dallas, Dallas, Texas
Robert Savage, MB, FRCS, FRCS Ed Orth, MS
Trauma and Orthopaedic Department, Royal Gwent
Hospital, Newport, Gwent, Great Britain
Ton A. R. Schreuders, PT, PhD
Rehabilitation Medicine, Erasmus University Medical
Center, Rotterdam, the Netherlands
Ombretta Spingardi, MD
Hand Surgery Department, Ospendale San Paolo,
Savona, Italy
Yu-Long Sun, PhD
Assistant Professor of Biomedical Engineering,
Department of Orthopedic Surgery, Mayo Clinic,
Rochester, Minnesota
Jun Tan, MD
Associate Professor of Surgery, Department of Hand
Surgery, Affiliated Hospital of Nantong University,
Nantong, Jiangsu, China
Jin Bo Tang, MD
Professor of Surgery, Founding Chair, Department of
Hand Surgery, Affiliated Hospital of Nantong University;
Founding Chair, The Hand Surgery Research Center,
Nantong University, Nantong, Jiangsu, China
Luigi Tarallo, MD
Department of Orthopaedic Surgery, Azienda Ospedaliera
Universitaria Policlinico Modena, Modena, Italy

ix
Contributors
Shian Chao Tay, PhD
Associate Professor, Department of Orthopaedic Surgery,
Associate Professor, Department of Biomedical
Engineering, Washington University, St. Louis, Missouri
Stavros Thomopoulos, PhD
Associate Professor, Department of Orthopaedic Surgery,
Washington University, St. Louis, Missouri
Michael A. Tonkin, MD, FRCS Ed Orth, FRACS
Professor of Hand Surgery, Head of Department,
Department of Hand Surgery and Peripheral Nerve
Surgery, Royal North Shore Hospital, Sydney Medical
School, University of Sydney, Sydney, Australia
Ghislaine Traber-Hoffmann, MD
Department of Ophthalmology, University Hospital
Zurich, Zurich, Switzerland
Shigeharu Uchiyama, MD
Associate Professor, Department of Orthopaedic Surgery,
Shinshu University School of Medicine, Matsumoto, Japan
Véronique van der Zypen, BSC PT
Certified Hand Therapist, Department of Orthopaedic,
Plastic and Hand Surgery, Division of Hand and
Peripheral Nerve Surgery, Inselspital, University of Bern,
Bern, Switzerland
Robert J. van Kampen, MD
Department of Plastic, Reconstructive and Hand Surgery,
University Medical Centre, Utrecht, the Netherlands
Gwendolyn Van Strien, LPT, MSc
Director, Hand Rehabilitation Consultancy, Den Haag,
The Netherlands, Director, Hand Therapy Unit, Lange
Land Hospital, Zoetermeer, the Netherlands
Esther Vögelin, MD, PhD
Chief and Codirector, Department of Orthopaedic, Plastic,
and Hand Surgery, Division of Hand and Peripheral
Nerve Surgery, Inselspital, University of Bern, Bern,
Switzerland
Xiao Tian Wang, MD
Assistant Professor, Department of Surgery, Brown
University Alpert Medical School, Providence, Rhode
Island
Ya Fang Wu, MD
Lecturer, The Hand Surgery Research Center, Nantong
University, Nantong, Jiangsu, China
Ren Guo Xie, MD
Associate Professor of Surgery, Vice Chair, Department of
Hand Surgery, Affiliated Hospital of Nantong University,
Nantong, Jiangsu, China
Hiroshi Yamazaki, MD, PhD
Chief, Department of Orthopaedic Surgery, Aizawa
Hospital, Matsumoto, Japan
Jeffrey Yao, MD
Assistant Professor, Department of Orthopaedic Surgery,
Stanford University Medical Center, Palo Alto, California
Chunfeng Zhao, MD
Associate Professor of Orthopedics and Biomedical
Engineering, Department of Orthopedic Surgery, Mayo
Clinic, Rochester, Minnesota

x
CONTENTS
13 Clinical Primary Flexor Tendon Repair
and Rehabilitation
A The Bern Experience
116
Esther Vögelin, Ghislaine Traber-Hoffmann,
Véronique van der Zypen
B The Chelmsford Experience
125
David Elliot
C The Mayo Clinic Experience
133
Robert R.L. Gray, Peter C. Amadio
D The Nantong Experience
138
Jin Bo Tang, Jun Tan, Ren Guo Xie
E The Singapore Experience
153
Alphonsus K.S. Chong, Beng-Hai Lim,
Yeong-Pin Peng
F The Stanford Experience
157
Arash Momeni, Emily Grauel, James Chang
G The Australian Experience
161
Michael A. Tonkin, Richard D. Lawson
H The Wellington Experience
168
Mark A. Rider
14 Partial Tendon Lacerations
171
Morad Askari, Peter C. Amadio
15 Flexor Tendon Injuries in Children
179
Shian Chao Tay, Steven L. Moran
16 Primary Repair of the Flexor Pollicis
Longus Tendon
186
David Elliot
17 Treatment of Flexor Tendon Injuries
at or Proximal to the Wrist
A Zone 5 Flexor Tendon Repairs
194
David Elliot
B Methods and Outcomes of Zone
5 Flexor Tendon Repairs
198
Jun Tan, Jin Bo Tang
18 Flexor Tendon Repairs With Novel
Sutures and Devices
A Mantero’s Technique for Tendon
Repair
203
Ombretta Spingardi, Mario Igor Rossello,
Renzo Mantero
Section 1: BASIC SCIENCE
  1 Anatomy of the Tendon Systems in
the Hand
3
Robert J. van Kampen, Peter C. Amadio
  2 Tendon Nutrition and Healing
16
Peter C. Amadio
  3 Tendon Friction, Lubrication, and
Biomechanics of Motion
24
Chunfeng Zhao, Peter C. Amadio, Kai Nan An
  4 Biomechanics of Core and Peripheral
Tendon Repairs
35
Jin Bo Tang, Ren Guo Xie
  5 Biology and Biomechanics of the
Tendon-Bone Insertion
49
Stavros Thomopoulos, Leesa M. Galatz
  6 Gene Therapy for Tendon Healing
59
Jin Bo Tang, Ya Fang Wu, Yi Cao,
Chuan Hao Chen, Xiao Tian Wang,
Paul Y. Liu
  7 Tendon Tissue Engineering and
Bioactive Suture Repair
71
Brian C. Pridgen, Jeffrey Yao, James Chang
Section 2: PRIMARY FLEXOR TENDON
SURGERY
  8 Indications for Primary Flexor Tendon
Repair
81
Jin Bo Tang
  9 Treatment of the Flexor Tendon Sheath
and Pulleys
88
Jin Bo Tang
10 Venting of the Major Pulleys
98
David Elliot
11 The Omega “Ω” Flexor Pulley Plasty
104
Joseph Bakhach
12 Tendon Sheath and Pulley
Enlargement
111
Robert E. Bunata

xi
Contents
B Teno Fix for Tendon Repair
208
Antonio Merolli, Lorenzo Rocchi,
Francesco Catalano
19 Treatment of Rupture of Primary Flexor
Tendon Repairs
214
David Elliot
20 Closed Avulsion or Rupture of Flexor
Tendons
A Traumatic Avulsion of Flexor Tendons
219
Pierre Mansat, Michel Mansat
B Tendon Rupture After Fractures or
Carpal Disorders
228
Hiroshi Yamazaki, Hiroyuki Kato,
Shigeharu Uchiyama
C Rupture of the Pulleys
233
Rohit Arora, Markus Gabl
21 The Evolution of End-to-End Surgical
Tendon Repairs
239
Robert Savage
22 Outcomes of Flexor Tendon Repairs
and Methods of Evaluation
246
Jin Bo Tang
Section 3: SECONDARY FLEXOR TENDON
SURGERY
23 Tenolysis
261
Nada Berry, Peter C. Amadio
24 Single-Stage Free Tendon Grafting for
Flexor Tendon Injury in Fingers
266
Pierre-Yves Barthel, Pierre Mansat
25 A Historical Perspective on Flexor Tendon
Reconstruction and Surgical Procedures
274
Andrew E. Farber, Daniel P. Mass
26 Experience With Secondary Flexor
Tendon Repairs
279
Peter C. Amadio, Chunfeng Zhao
27 Secondary Reconstruction of the Flexor
Pollicis Longus Tendon
285
David Elliot
28 Staged Tendon Grafts and Soft Tissue
Coverage
297
David Elliot
29 Two-Stage Reconstruction With the
Modified Paneva-Holevich Technique
307
Alexandros E. Beris, Marios G. Lykissas,
Ioannis Kostas-Agnantis
30 Outcomes of the Modified Paneva-Holevich
Procedures and Early Postoperative
Mobilization
314
Nash H. Naam, Lori Niemerg
31 Vascularized Tendon Transfers for
Reconstruction
A Tendon Vascularity and Gliding, Island
and Free Vascularized Transfers
323
Jean Claude Guimberteau
B Physiotherapy After Vascularized
Tendon Transfers
340
Serge Rouzaud
Section 4: EXTENSOR TENDON REPAIR
AND RECONSTRUCTION
32 Extensor Tendon Injuries—Primary
Management
347
Brandon E. Earp, Philip E. Blazar
33 Sagittal Band Injuries—Primary and
Secondary Management
355
Kristen E. Fleager, Monina Copuaco, James Chang
34 Tendon Transfers for Extensor Tendon
Reconstruction
364
Lance M. Brunton, A. Bobby Chhabra,
Mollie O Manley
35 Soft Tissue Coverage for Extensor
Tendon Reconstruction
371
Michel Saint-Cyr
36 Treatment of Boutonnière and
Swan-Neck Deformities
383
Fraser J. Leversedge, Felicity G.L. Fishman
37 Vascularized Tendon Graft for Extensor
Tendon Reconstruction
394
Roberto Adani, Luigi Tarallo, Massimo Corain,
Jean Claude Guimberteau
Section 5: REHABILITATION OF TENDON
SURGERY
38 State of the Art Flexor Tendon
Rehabilitation
405
Karen M. Pettengill, Gwendolyn Van Strien
39 Customizing Flexor Rehabilitation
Based on Zone or Type of Injury
415
Fiona H. Peck
40 State of the Art of Extensor Tendon
Rehabilitation
427
Ton A.R. Schreuders, Gwendolyn Van Strien
Online-Only appendixes to 40:
Appendix 1 Therapy Protocols After Extensor Tendon
Repairs: St Andrew’s Centre for Plastic Surgery,
Broomfield Hospital, Chelmsford, Essex, UK
Appendix 2 Therapy Protocols After Extensor Tendon
Repair of the Thumb: St Andrew’s Centre for Plastic
Surgery, Broomfield Hospital, Chelmsford, Essex, UK

xii
Contents
Appendix 3 Therapy Protocols After Extensor
Tendon Repairs of Fingers: Mid Essex Hospital
Services, St Andrew’s Centre-Hand Therapy,
Essex, UK
Appendix 4 The Manchester Regimen for
Postoperative Rehabiliation After Finger Extensor
Tendon Repairs, Manchester, UK
Appendix 5 Protocols of Exercise After Repair
of Extensor Tendon Injuries, Queen Mary Hospital,
The University of Hong Kong, Hong Kong,
China
Appendix 6 Extensor Tendon Rehabilitation
Program, Queen Mary Hospital, The University of
Hong Kong, Hong Kong, China
Appendix 7 Therapy Protocols After Extensor Tendon
Repair, Springfield, Mass, USA
Appendix 8 Protocols of Sydney Hand Therapy &
Rehabilitation Centre, Sydney, Australia
Appendix 9 Therapy Protocols from Royal Free
Hamstead NHS Trust, London, UK
Section 6: CURRENT STATUS AND FUTURE
41 A Current Status and Future of Flexor


Tendon Surgery
441
Peter C. Amadio
41 B Current Status and Future
442
Robert Savage
41 C Future of Tendon Surgery of the Hand
443
Jin Bo Tang
APPENDIXES
1 Symposium Discussion 1
446
2 Symposium Discussion 2
447
3 A Postscript About Progression of
Thought on Primary Tendon Repair
450
Jin Bo Tang
ONLINE-ONLY CHAPTERS
42 Chemical Modification of Tendon
Gliding Surface
e17
Yu-Long Sun, Peter C. Amadio
43 Tendon Gliding: The Role and Mechanical
Behavior of Connective Tissues
e27
Jean-Claude Guimberteau
44 Molecular Biology of Tendon Healing
e42
Chuan Hao Chen, Ya Fang Wu, Jin Bo Tang
45 Molecular Methods to Prevent Adhesion
Formation
e50
Armin Kraus, James Chang
46 Tendon Repairs in Replantation Surgery
e58
Ren Guo Xie, Jun Tan, Jin Bo Tang
ONLINE VIDEOS
Visit to view exclusive proce­
dural videos and to see the full list of expert video
contributors.
Full printed book contents are also available at

1
SECTION
1
BASIC SCIENCE

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3
CHAPTER
1 
ANATOMY OF THE TENDON
SYSTEMS IN THE HAND
Robert J. van Kampen, MD, and Peter C. Amadio, MD
reinforced by the pisiform-hamate ligament. On the
radial side, the retinaculum firmly inserts into the volar
ridge of the trapezium (trapezial tuberosity) and the
tubercle of the scaphoid. Occasionally an insertion into
the styloid process of the radius can be seen.1,2
Controversial terminology surrounds this strong,
fibrous band that crosses the volar side of the carpus.
According to the Terminologia Anatomica, the term flexor
retinaculum carpi should be used. However, in textbooks,
the terms flexor retinaculum, transverse carpal ligament and
anterior/volar annular ligament are used for the same
structure.3
In hand surgery, it is often preferred to distinguish
between the different parts of the flexor retinaculum.
Stecco et al3 investigated its histological and anatomical
features. Continuous with the antebrachial fascia, a
fibrous reinforcement was identified at the volar side of
the wrist. After removal of this layer, another fibrous
layer was found, with strong lamina and histological
similarities to those of a ligament. According to Stecco’s
group,3 “ligament derives from Latin ligare (to bind) and
means a sheet or band of tough fibrous tissue connecting
bones.” They stated that “the role of the pulley for the
tendons of the flexor muscles is assumed above all” for
this deeper layer covering the carpal tunnel, and there­
fore the term transverse carpal ligament was suggested to
be the most appropriate.
In addition to the thickened continuation of the
antebrachial fascia and the transverse carpal ligament,
Cobb et al4 described a third, more distal segment com­
posed of an aponeurosis between the thenar and hypo­
thenar muscles. Based on their anatomical findings,
they advocate a more extensive release when dividing
the carpal ligament.
Tanabe and Okutsu5 endoscopically released the
flexor retinaculum in management of carpal tunnel syn­
drome and found that the mean distance between the
ends of the retinaculum increased from 1.3 mm to 6.6
mm if the distal fibers were also divided. They therefore
concluded that sectioning of the distal fibers is essential
for endoscopic carpal tunnel release.
OUTLINE
This chapter describes the anatomy of the flexor and
extensor apparatus in the hand and wrist, supple­
mented with relevant clinical and biomechanical
features. It emphasizes the key importance of the reti­
nacular structures of the wrist and fingers and reviews
both normal anatomy and common variations of the
flexor and extensor tendons in the hand. Special atten­
tion is given to the vincula tendinea and pulleys sup­
porting the flexor tendons in the digital flexor
sheaths—in particular, the structure and biomechanics
of the pulley system. The key role of the A2 and A4
pulleys is emphasized. Finally, a closer look is taken
at the tendons and bands contributing to the extensor
mechanism, and their action on the metacarpophalan­
geal and interphalangeal joints is discussed.
The hand, with the carpus, is the most complex collec­
tion of interconnected joints in the human body, and a
large assembly of tendons carries out its extensive range
of motion. Distinctive groups of muscles execute the
actions of these tendons on the hand. Together with
numerous aiding structures, the tendons form an inge­
nious biomechanical system that gave humans the
ability to perform complicated tasks and develop dex­
terous professions that require sophisticated hand and
finger movement, like hand surgery. Treatment of hand
disorders is similarly delicate and complex; therefore, a
thorough understanding is essential to provide adequate
treatment.
FLEXOR RETINACULUM
On the volar aspect of the wrist, the carpal bones form
a deep excavation over which the flexor retinaculum
arches, creating the carpal tunnel. The tendons of the
flexor digitorum superficialis (FDS) and profundus
(FDP) and the flexor pollicis longus (FPL) pass through
this tunnel together with the median nerve.
This retinaculum inserts on the ulnar side into the
pisiform bone and the hook of the hamate and is

4
Section 1:  Basic Science
different populations all over the world.9 In humans,
this tendon is seen as rudimentary, and for that reason,
and its easy accessibility, the palmaris longus is often
used as a tendon graft.
To the radial side of the median nerve, the FPL tendon
can be found; to the ulnar side, the superficial flexor
tendons. When coursing through the carpal tunnel the
superficial flexor tendons are arranged in pairs, the
tendons to the middle and ring finger form the superfi­
cial pair, and the little and index finger tendons form
the deep pair. Dorsal to the superficial tendons lie the
flexor profundus tendons.2,8
In the case that the palmaris longus tendon is absent,
the tendon of the flexor superficialis indicis can some­
times be found between the superficial flexor tendon to
the middle finger and the median nerve. In other varia­
tions, the palmaris longus tendon can separate into two
or three tendons, the muscle can be doubled, the muscle
can be reversed or inverted, and partial or complete
insertion in the antebrachial fascia can be seen. Addi­
tionally, insertion into the pisiform bone, scaphoid,
flexor carpi ulnaris tendon, and muscles of the thenar
has been observed.8
Accessory slips for the FDS and FDP are frequently
observed, especially to the index finger. Slips arise from
the ulnar tuberosity to the superficialis tendon of the
index and middle finger, and from the annular ligament
to the superficialis tendon of the little finger. The super­
ficialis tendon to the little and index finger can be absent
and the index finger’s deep flexor tendon can divide into
two tendons or have a shared origin with the FPL.8
The flexor carpi radialis (FCR) tendon courses through
its own synovial sheath that forms a narrow osteofi­
brous tunnel when passing the trapezium. The radial
side of the tunnel is formed by the body of the trape­
zium and the volar side by the trapezial tuberosity. On
the ulnar side, the tunnel is separated from the carpal
tunnel by a thick septum. Distally, the FPL tendon pivots
around this septum. At the floor of the tunnel, the
tendon sheath lies in contact with the volar capsule of
the scaphotrapeziotrapezoid (STT) joint. The narrow
tunnel induces a higher risk of primary stenosing teno­
synovitis; however, because of the close relationship
with surrounding structures, tenosynovitis can also
occur secondary to traumatic or degenerative changes.
Tenosynovitis of the FCR tendon is not an uncommon
finding in arthritis of the STT joint, which can cause
additional pain to the baseline osteoarthritic pain.10,11
The FCR tendon is also suggested to play a role in
stabilizing the scapholunate joint through its close rela­
tionship between the FCR tendon sheath and the liga­
ments attached to the tuberosity of the scaphoid. The
tendon was thought to use the distal pole of the scaph­
oid as a pulley to increase its mechanical advantage and
prevent the scaphoid from rotating into flexion. Unlike
in previous hypotheses, Salvà-Coll et al12 found that
EXTENSOR RETINACULUM
On the dorsal side of the wrist, a thickened part of the
deep antebrachial fascia is found, holding the tendons
of the extensor muscles in place. It works in continuity
with the volar carpal ligament and for the previous
stated reasons the term dorsal carpal ligament or posterior
annular ligament could also be suggested. However, the
term extensor retinaculum is most commonly used.
As studied by Taleisnik et al,6 the deep antebrachial
fascia begins to thicken proximal to the radiocarpal
joint and becomes the dorsal annular ligament, a compo­
nent of the extensor retinaculum of the wrist. Distally,
this supratendinous layer is continuous with the pretendi­
nous fascia of the hand. On the ulnar side, it inserts in
three distinct places: proximal around the flexor carpi
ulnaris tendon, the middle part into the triquetrum and
pisiform bone, and distally onto the fascia of the abduc­
tor digiti quinti and base of the fifth metacarpal.
The retinaculum attaches to ridges on the radius,
forming septa that divide the space below the extensor
retinaculum in six compartments through which the
extensor tendons pass. The six compartments are further
described in the section about extensor tendons.
Within the supratendinous layer, at the floor of the
fourth and fifth compartment, lies the infratendinous
layer, from which circular fibers form a tube around the
tendons within the compartments. In the sixth compart­
ment, a duplication of the infratendinous layer forms a
tube around the extensor carpi ulnaris (ECU) tendon
from the ulnar styloid to the triquetrum. This subsheath
stabilizes the tendon along the groove in the distal ulna
and contributes to the stability of the distal radioulnar
joint. Proximally, longitudinal fibers form the linea
jugata that reinforces the tendon to prevent subluxation
during full supination. The ECU subsheath is frequently
injured, typically in young athletes who play racket or
stick sports, which can result in recurrent subluxation of
the ECU tendon.7
FLEXOR TENDONS IN THE HAND
The tendons in the wrist have a relatively constant
arrangement with the median nerve. This arrangement
varies mainly when muscle or tendon anomalies are
present. It is important to keep these variations in mind,
because it can be confusing even for the experienced
surgeon. Usually, the median nerve can be found directly
under the tendon of the palmaris longus. Sometimes,
the nerve lies more superficial, next to the palmaris
longus tendon. The median nerve is also frequently
observed to split in the forearm.8
The palmaris longus tendon lies completely enclosed
in the deep fascia of the forearm between the superficial
veins and cutaneous nerves. The presence of this tendon
is highly variable, as its absence has been reported from
0.6% to 63.9% (either bilateral or unilateral) among

5
Chapter 1:  Anatomy of the Tendon Systems in the Hand
loading the FCR tendon rotated the scaphoid in flexion
and supination, while rotating the triquetrum in flexion
and pronation. These opposite rotations are attributed
to relax the dorsal scapholunate ligament.
The FCR tendon inserts into the base of the second
metacarpal and gives off a strong, tendinous slip to the
third metacarpal. Frequently a small slip to the trapezial
tuberosity can be seen. Other variations are insertions
in both the trapezium and scaphoid and in the base
of the second, third, and fourth metacarpals. The FCR
muscle can even be absent. Insertion in the transverse
carpal ligament can also be seen and may cause confu­
sion with the palmaris longus tendon.8
The flexor carpi ulnaris (FCU) encloses the pisiform
bone, which can be seen as a sesamoid bone for this
tendon. The FCU attaches to the base of the fifth meta­
carpal and hamate, via the pisohamate and pisometa­
carpal ligaments. The pisohamate ligament creates an
additional tunnel, Guyon’s canal, between the hook of
the hamate and pisiform bone through which the ulnar
artery and nerve pass. Occasionally, the FCU tendon
doubles before inserting in the pisiform bone. The FCU
can also merge with the flexor superficialis or profundus
tendon.8
The FPL tendon passes through its own osseo-
aponeurotic canal and inserts at the distal phalanx of
the thumb. Sometimes an additional tendon to the
index finger is found. The FPL tendon can be absent, in
combination with a significant smaller thumb. Another
variation is splitting of the tendon into two or three slips
that insert into the scaphoid or flexor retinaculum.8
FLEXOR TENDON SHEATHS
Structure of the Sheath at Wrist and Palm
In the wrist, synovial sheaths allow the flexor tendons
to glide through the carpal tunnel. The sheaths begin
approximately 2.5 cm proximal to the transverse carpal
ligament and extend distally to the neck of the metacar­
pals. In the fingers, the flexor tendons are also sur­
rounded by sheaths. A considerable level of variation in
communicating patterns between these sheaths and the
digital flexor sheaths is observed.13
As reported by Fussey et al,13 the most common
pattern shows one common flexor tendon sheath or ulnar
bursa surrounding the tendons of the FDS and FDP. A
second sheath, forming the radial bursa, envelopes the
FPL tendon.
In most cases the little finger flexor sheath works in
continuity with the tendons along the phalanges. Like­
wise, the FPL tendon sheath accompanies the tendon
along the thumb as far as its insertion.13
Occasionally communications between the common
flexor tendon sheath and the second, third, and fourth
digital tendon sheaths are observed in the palm. Fur­
thermore, the ulnar and radial bursa can be found to be
Figure 1-1  Nutritional microenvironment of the flexor
tendon. In zone 2 the tendons are intrasynovial within the
digital flexor sheath. Zone 3, in the palm of the hand, is
extrasynovial tendon. In the carpal tunnel, zone 4, the
tendon is surrounded by a hybrid of both intrasynovial and
extrasynovial tissue. SM, Synovial membrane; SF, synovial
fluid; PT, paratenon; SSCT, subsynovial connective tissue.
Tendon
Intrasynovial
Tendon
Zone 2
Zone 3
SM
SF
SM
SF
SSCT
PT
Zone 4
Extrasynovial
Tendon
?
connected. In case of an infection within the sheath, the
communication between the ulnar and radial bursa can
result in the “horseshoe abscess.”
In the carpal tunnel, the subsynovial connective
tissue (SSCT) connects the flexor tendons with the syno­
vial membrane of the ulnar bursa. It consists of fibrous
bundles parallel to the tendons, which in turn are inter­
connected by smaller microfibrillar fibers. By acting as
a sliding unit, the SSCT reduces friction and maintains
the integrity of the vascularity around the tendons. Non­
inflammatory fibrosis of the SSCT is the most common
histological finding in carpal tunnel syndrome, which
suggests injury to the SSCT to be an important etiologic
factor14 (Figures 1-1 to 1-4).
Structure of the Digital Flexor Sheath
The tendons of the FDP and FDS lie deep in the palm
of the hand, beneath the superficial palmar arch and the
superficial branches of the median and ulnar nerve.
There, the tendons are surrounded by several layers of
loose connective tissue. Vessels emerging from the
palmar arches traverse through this tissue toward the
tendons, forming the paratenon.
In a histological study of the flexor tendon sheath by
Cohen and Kaplan,15 two vascular systems are observed
to become organized in the paratenon; one adjacent to
the tendons, the other more peripheral. The develop­
ment of a “synovial-lined cleft” between these systems
creates a separation into a visceral and a parietal
synovium.
The parietal layer lines the wall of the tunnel through
which the tendon glides. As the layer continues distally,
the layer was found to be uninterrupted and reinforced
externally by dense bands of collagen. By maintaining
the tendons close to the bone and joint surface, these
bands act as a system of pulleys, facilitating efficient
finger movement. Between these reinforcements, the
thickness of the parietal synovium is greatest and is
called the membranous part of the tendon sheath.

6
Section 1:  Basic Science
The visceral layer or epitenon adheres to the tendon,
creating a synovial space between the two layers. It was
found to be supported by a thin cover of laminated col­
lagen. All structures entering the tendons are surrounded
by epitenon. In the opposite direction along these struc­
tures, the visceral layer works in continuity with the
parietal layer. The synovial layers extend distally to the
insertion of the FDP tendon, where they become
confluent.
VINCULA TENDINEA
On the palmar osseous side of the tunnel, vessels pro­
trude through the synovial layers, forming mesenterial
folds or mesotenon. These vascular bands connect the
dorsal side of the flexor tendons with the palmar side
of the flexor sheath. In consideration of their tendinous
structure, these bands are named vincula tendinea (vin­
culum derives from Latin and means “bond or link”).
Figure 1-3  Sliding unit in the carpal tunnel region has
both structures (i.e., paratenon and synovial sliding
mechanism). All layers from the flexor retinaculum to the
tendon are shown. The tendons in the carpal canal have a
subsynovial connective tissue and a bursa, containing
synovial fluid between the parietal and visceral synovium
(hematoxylin-eosin; original magnification, ×400). (From
Ettema AM, Amadio PC, Zhao C, et al: Changes in the
functional structure of the tenosynovium in idiopathic carpal
tunnel syndrome: a scanning electron microscope study,
Plast Reconstr Surg 118:1413-1422, 2006.)
Flexor
retinaculum
Parietal synovium
Visceral synovium
Subsynovial
connective tissue
Tendon
Figure 1-2  Flexor tendon zones. The zones are numbered
from distal to proximal. Zone 1 contains a single tendon, the
flexor digitorum profundus tendon. Zone 2 is the critical area
of the digital flexor sheath. It contains both the profundus
and superficialis tendons, and the area where the profundus
tendon penetrates the superficialis at the chiasm of Camper.
In the extrasynovial zone 3 the lumbrical muscles arise. Zone
4, the carpal tunnel, contains mixed intra/extrasynovial
tissue. Zone 5 is also extrasynovial, without the lumbrical
muscles. In the thumb, although we have marked zones 1 to
5, one may consider that zones 2 and 3 do not exist,
because there is only a single tendon, and no lumbrical.
II
II
III
III
IV
IV
V
I
I
I
I
I
Several variations in the vincula tendinea have been
observed. Ochiai et al16 studied the distribution patterns
of the vincula in the fingers of 35 human hands. Their
study showed that four transverse communicating
branches arising from the digital arteries enter the flexor
tendon sheath through openings in the pulleys, travel­
ing toward the vincula. The sites of entry are at the base
of the proximal phalanx, the neck of the proximal
phalanx, the base of the middle phalanx, and the neck
of the middle phalanx (Figure 1-5).
Two kinds of vincula were found within each digital
flexor tendon sheath: vessels arising from the transverse
communicating arteries protrude through the meso­
tenon forming short, triangle-shaped folds (vincula
brevia) and long, slender vincula longa (Figure 1-6).
The vincula brevia were found consistently in all dis­
sected fingers. The vinculum brevis superficialis (VBS)
arises from the volar plate of the proximal interphalan­
geal (PIP) joint and attaches to the decussation of the
superficialis tendon. The thin, triangle-shaped meso­
tenon of the vinculum brevis profundus (VBP) arises at the
distal third of the middle phalanx and attaches near the
insertion of the profundus tendon.
In contrast, several variations in the long vincula can
be found. Ochiai et al16 found the vinculum longum
superficialis (VLS) to have a radial, ulnar, or two-sided
origin at the base of the proximal phalanx. Absence of
the VLS was also observed, mainly in the middle and
ring fingers. They also mentioned that the vascularity of

7
Chapter 1:  Anatomy of the Tendon Systems in the Hand
Figure 1-4  Top, Loose vertical fibers join adjacent layers
in the subsynovial connective tissue (scanning electron
microscopy; original magnification, ×1100). Bottom, The
loose vertical fibers between adjacent layers are stretched
during flexor tendon movements (scanning electron
microscopy; original magnification, ×1000). (From Ettema
AM, Amadio PC, Zhao C, et al: Changes in the functional
structure of the tenosynovium in idiopathic carpal tunnel
syndrome: a scanning electron microscope study, Plast
Reconstr Surg 118:1413-1422, 2006.)
Figure 1-5  The tendon sheath contains the annular
pulleys A1 to A5 and the cruciate pulleys C1 to C3.
A5
A4
A3
A2
A1
C1
Common
digital artery
Branch to
vincular longum
superficialis (VLS)
Proximal
transverse
digital artery
Intermediate
transverse
digital artery
Distal
transverse
digital artery
C3
C2
Figure 1-6  The blood vessels enter the flexor tendons through the vincular system.
Vinculum
longum
superficialis
(VLS)
Dorsal
Flexor digitorum
superficialis
Vinculum
brevis
superficialis
(VBS)
Vinculum longum
profundus (VLP)
Flexor digitorum
profundus
Vinculum brevis
profundus (VBP)
the profundus tendon is less in adults than in fetuses.
These findings can be a possible explanation for the
higher incidence of triggering in the middle and ring
fingers and in older patients.
For the vinculum longum profundus (VLP), Ochiai
et al16 found five types, named distal, middle, mixed,

8
Section 1:  Basic Science
pulleys (termed annular proximal and annular distal)
and two cruciate ligaments (cruciate proximal and
distal). The first annular proximal (AP1) pulley origi­
nates just proximal to the metacarpophalangeal (MCP)
joint and ends at the middle of the proximal phalanx.
There it is overlapped by the proximal cruciate ligament,
which extends over the distal third of the same phalanx.
The second annular proximal (AP2) pulley is positioned
at the PIP joint; the third annular distal (AD1) pulley is
over the proximal third of the middle phalanx, where it
was overlapped by the distal cruciate ligament. At the
distal interphalangeal (DIP) joint is the second annular
distal (AD2) pulley; the third annular distal (AD3)
pulley is at the base of the distal phalanx.
A more commonly accepted description was given by
Doyle.20 After dissecting 80 digits, Doyle concluded
there are five annular (termed A1 to A5, from proximal
to distal) and three cruciate (C1 to C3, from proximal
to distal) pulleys (see Figure 1-5). The A2 pulley is the
largest pulley in the fingers, approximately 1.5 to 1.7 cm
long, which are located in the proximal part of the
proximal phalanx. This pulley has a distinct semilunar
and thick leading edge and the annular fibers are over­
laid with circular fibers. The second largest annular
pulleys are A4 pulley at the middle of the middle
phalanx and A1 pulley (at the level of the MCP joint);
the A3 pulley (at the PIP joint level) is rather narrow,
about 3 mm in length. The A5 pulley at the DIP joint
level is very small and sometimes indistinguishable.
Strauch’s most distal annular structure (AD3), a
pulley distal to the DIP joint, is not described by other
investigators, including Doyle.20 The second and fourth
annular pulleys were found to be always present—A3
and A5, respectively—in 80% and 90% of the speci­
mens. The cruciate pulleys sometimes are single oblique
bands or Y-shaped.
Lin et al21 further differentiated between pulleys that
attach to the bony floor of the digital canal formed by
the phalanges and pulleys that insert into the volar
plates covering the joints. The two annular bony pulleys
over the shaft of the proximal (A2) and middle phalanx
(A4) are the longest and strongest. These pulleys remain
nearly constant to the joint axis and shorten the least in
finger flexion.
In contrast, the distance between the volar plate
pulleys (A1, A3, and A5) and the joint axis showed a
significant increase in flexion of the fingers. The volar
plate pulleys also tend to have a greater shortening com­
pared to the bony pulleys. The cruciate pulleys attach at
one end to bone and at the other end to the palmar
plate. They show the most anatomical variation and
shortening.
Due to the concave shape of the volar shaft of the
phalanges, absence of the bony pulleys leads to bow­
stringing of the flexor tendon over this curvature. A
second form of bowstringing occurs over the joint, when
proximal, and absent to refer to the site of insertion at
the profundus tendon.
The distal type was found to be very rare; the middle
type was most commonly found and travels through the
decussation. The proximal type arises between the two
slips of the superficialis tendon and passes through the
bifurcation. The mixed type is similar to the proximal,
but no VLS is found.
The index finger most often had a radial or two-sided
VLS, and the middle type of VLP. In the long finger, no
predominant type was found. Most long fingers had the
middle type of VLP combined with the radial type of
VLS or a middle and proximal type of VLP in combina­
tion with two-sided VLP.
In the ring finger, the VLS was most commonly
absent, often in combination with mixed type VLP or
both mixed and middle types. The predominant type
for the little finger is the middle type of VLP and a broad
ulnar-sided mesotenon forming the VLS.
The area in which the vincula can be found is often
referred to as “no-man’s land” as surgical treatment of
flexor injuries often have poor outcome (see Figure
1-2). One possible explanation for these poor results
could be the disruption of the vincula, and thus blood
supply to the tendons. Amadio et al17 investigated the
relationship of the vincular status on final total active
motion after primary tendon repair and early mobiliza­
tion. This study showed a statistically significant decrease
in total active motion when the vincular system was
injured. Disruption (or absence) of vincula could there­
fore be an important prognostic factor of the outcome
of flexor tendon repair.
In the thumb, the vinculum breve forms a continuous
band with the FPL tendon proximal to its insertion. After
complete laceration of the FPL tendon at the interpha­
langeal joint, the intact vinculum produces some flexion
of the joint by its connection with the volar plate.18
THE PULLEY SYSTEM
The strengthening elements of the digital flexor sheaths,
called pulley, are condensation of dense connective
tissue and segmentally distributed along the digital
sheath. They serve to restrain the tendons from bow­
stringing and to accommodate maximum mechanical
efficiency of tendon excursion.
Several descriptions of these pulleys have been
reported.19-21 The popularly used nomenclature is based
on Doyle’s classic anatomical work.20
Strauch and de Moura19 investigated the pulleys in 72
fingers and found that a “complex synovial lined tube”
surrounds the flexor tendons to the central three rays.
At either edge two main “cul-de-sacs” enclose the
tendons. Between the pulleys are smaller cul-de-sacs,
which tend to flatten in extension, allowing for adjust­
ment in length of the sheaths in finger motion. Strauch
and de Moura19 described two sets of three annular

9
Chapter 1:  Anatomy of the Tendon Systems in the Hand
single pulley, loss of function increased significantly
when this pulley was the final pulley to be cut.
INTRINSIC MUSCLES: THE LUMBRICALS
AND INTEROSSEI
An unusual muscle originates in the palm of the hand.
Instead of attaching to bone, the lumbrical muscle arises
from a movable medium, namely the FDP tendon and
inserts distally, after crossing the MCP joint, into the
extensor expansion.26 Although their origin is at the
profundus tendon, the lumbrical muscle covers a great
part of the superficialis tendon. The first and the second
lumbrical muscles are unipennate muscles and arise
from the palmar surface and radial sides of the tendons
of the index and middle fingers, respectively. The third
and the fourth are bipennate muscles that originate at
the contiguous side of the profundus tendons of the
middle and ring fingers and the ring and little fingers,
respectively. All pass at the radial side of the finger in
which they insert at the dorsal side of the MCP joint.26
The lumbricales are found to vary in number between
two and five. The most frequent variation can be seen
in the third lumbrical, as two tendons originate and
insert in the middle and ring fingers. Another variation
shows only one tendon from the third lumbrical to the
ulnar side of the middle finger.26
The main action of the lumbrical muscles is to keep
the fingers stretched as the MCP joint flexes. They act as
a moderator band between flexor and extensor mecha­
nism in the finger. When the flexor tendon is pulled, the
origin of the lumbrical muscle moves proximally, this
way the muscle is stretched. With the MCP joint in
flexion the lumbrical muscle pulls the interphalangeal
joints into extension, by moving the extensor mecha­
nism proximally.27
The interosseous muscles are numbered from radial to
the ulnar side of the hand. According to their relative
position to the intermetacarpal spaces, three palmar
and four dorsal interossei arise between the metacarpal
shafts. The palmar interossei are unipennate muscles that
arise on the opposite side relative to the middle finger
metacarpal and insert on the same side into the proximal
phalanx; therefore, the palmar interossei produce adduc­
tion of the fingers relative to the third ray.26
The dorsal interossei are composed of two muscle
bellies arising from the adjacent metacarpals. The
tendons on the ulnar side of the axis of the third ray
insert on the ulnar side of the proximal phalanx; on the
radial side of the middle finger, the tendon inserts on
the radial side of the proximal phalanx. In this way, the
action of the dorsal interossei is abduction of the fingers
relative to the middle finger.26
Variations in the interossei are seen in the number of
muscle bellies and insertions of the tendons. The palmar
interossei can be bipennate with two tendons inserting
in each corresponding side. One or even all palmar
in flexion. The A2 and A4 are not at an equal distance
on both sides from the PIP joint; the reason for this may
be to optimally control a combination of both joint and
bony bowstringing.21
The volar plate pulleys only restrain bowstringing
over the joint, and the cruciate pulleys seem to mainly
modulate force transmission, by increasing the moment
arm in flexion beyond 45 degrees. Absence of the A2
and A4 pulleys has the greatest effect on joint motion,
even when only the bony type of bowstringing is per­
mitted, by preserving the other pulleys that keep the
tendons close to the joint axis. The absence of the A3
pulley alone has minimal effect on joint motion.21
By remaining in close contact with the tendons that
glide through them, the pulleys generate friction. Zhao
et al22 found that the A3 pulley contributes to reducing
the gliding resistance of the tendons against the A2 and
A4 pulleys. By keeping the tendons close to the PIP joint
axis, the A3 pulley reduces the angle between the edges
of the pulleys and the tendons, which reduces gliding
resistance. This occurs mainly in greater angles of PIP
flexion. The presence of this pulley may prevent a
tendon repair site from buckling under the A2 pulley.
Two other structures also contribute to the pulley
system of the flexor tendons: the transverse carpal liga­
ment and the palmar aponeurosis.
The transverse carpal ligament arches over the flexor
tendons as they traverse toward the palm of the hand
and performs a pulley function by keeping the flexor
tendons in proximity of the wrist. After transsection of
the transverse carpal ligament in fresh-frozen cadavers,
Kline and Moore23 demonstrated that flexor tendons
move an additional 5.5 mm forward from the joint axis,
when flexing the wrist. The motion of the wrist required
a 25% increase of excursion for the FDP tendons and a
20% increase for the FDS tendons. As Kline and Moore
stated, this increase in excursion could clinically result
in decreased grip strength by reducing the remaining
tendon excursion over the other joints. Consequently,
the total active finger motion could decrease if maximal
muscle contraction is reached.
At the level of the MCP joints, the fibers of the palmar
aponeurosis and intertendinous septa form an archway
over the flexor tendons. By anchoring in the deep trans­
verse carpal ligament, this archway keeps the tendons
near the axis of the MCP joint and can therefore be seen
as an additional pulley—palmar aponeurosis (PA)
pulley.24 Manske and Lesker25 sequentially cut the PA
and the first and second annular pulleys in various orders
and studied the influence on joint motion. Cutting only
one of these pulleys resulted in minimal loss of function.
Increased loss of flexion was observed when one of the
annular pulleys was cut in combination with the PA
pulley. The A2 pulley was found to be the most impor­
tant as a single pulley, followed closely by the A1 pulley.
Although the PA pulley was the least important as a

10
Section 1:  Basic Science
dorsal side of the distal radius in six compartments
formed by the extensor retinaculum (Figure 1-7).
Most radial in position, the abductor pollicis longus
(APL) tendon passes through the first compartment,
together with the extensor pollicis brevis (EPB) tendon.
It inserts on the radial side of the first metacarpal and
thereby induces abduction of the first ray of the hand.
Usually the APL has multiple slips. Common insertions
of these slips are the trapezium and the origin of the
abductor pollicis brevis or opponens muscle. In 71% of
100 dissections, Brunelli and Brunelli29 found that one
or two extra tendons in the first compartment belong
to a musculotendinous unit. By inserting in the trape­
zium, the main function of this unit is abduction of
the carpus and it was therefore named the “abductor
carpi” muscle. Brunelli and Brunelli consider that the
absence of this muscle, which was seen as abnormal,
leads to a higher risk of instability and arthritis of the
trapeziometacarpal (TM) joint, because of the loss of a
interossei can be absent. The dorsal interossei are some­
times found to originate more proximal at the base of
the metacarpals or even at the carpalia. The insertion of
the tendon of the second dorsal interossei can be on the
ulnar side of the second metacarpal so that the abduc­
tion of the fingers is relative to the axis of the second
ray, instead of the third.26
CHIASMA TENDINUM OF CAMPER
After leaving the carpal tunnel, the flexor digitorum
tendons diverge and spread out to the fingers. As in
logical accordance with their names, the superficialis
tendon lies on top of the profundus. However, after
the tendons pass distal to the MCP joint, the profundus
tendon starts to penetrate through the bifurcated super­
ficialis tendon. At the middle part of the proximal
phalanx, the superficialis tendon divides into two slips
that rotate laterally.27 The most dorsal fibers of the
rotated slips emerge to the other side and, after crossing
each other, they finally insert at the lateral volar crest of
the middle phalanx. The other fibers of the lateral slips
continue on the lateral side and insert on the lateral
crest on the volar surface of the middle phalanx, where
they unite with the crossed fibers. The superficialis
tendon has a long insertion from the base of the middle
phalanx toward the neck.27
The profundus tendon passes through the tunnel
formed by the superficialis tendon at the level of the
proximal phalanx. The tunnel is narrowed by the vincu­
lum breve superficialis. The FDP tendon passes the volar
capsule of the DIP joint, to which it is firmly connected.
More distally, the tendon spreads out to insert widely
into the volar base and fat pad of the distal phalanx.27
This intersection of fibers of the FDS tendon forms a
plate beneath the flexor profundus and is called the
chiasma tendinum of Camper, named after the Dutch phy­
sician Petrus Camper, who gave a detailed description
of this structure in his book on the anatomy of the arm
and hand. The chiasma tendinum is an essential biome­
chanical element of the gripping function of the hand.
When longitudinal tension is applied to the deep flexor
tendon, the volar surface of the superficial tendon is
pushed against the A2 pulley. As grip is sustained, the
profundus tendon is compressed by the two slips of the
superficialis tendon. These mechanisms provide stabili­
zation of the interphalangeal joint, which aids in obtain­
ing grip on an object.28
EXTENSOR TENDONS AT THE WRIST
A detailed description of the extensor tendons and its
variations can be found in the anatomical textbooks
of Standring2 and Kaplan1 and Hunter.26 By passing
the wrist joint, the extensor tendons assist in extending
the wrist and, depending on their position toward the
median axis, provide radial or ulnar deviation. From
radial to ulnar, the tendons pass through grooves on the
Figure 1-7  The extensor retinaculum and extensor
tendons. Extensor tendons gain entrance in the hand from
the forearm through a series of six canals. The extensor
tendons are covered with a synovial sheath. APL, Abductor
pollicis longus; EPB, extensor pollicis brevis; EPL, extensor
pollicis longus; ECRL and ECRB, extensor carpi radialis longus
and brevis, respectively; EIP, extensor indicis proprius; EDC,
extensor digitorum communis; EDM, extensor digiti minimi.
Note the junctura tendinea (JT) connecting to the extensor
tendon of the ring fingers.
JT
EIP
ECRL ECRB
EDC
EDM
APL
EPL
EPB
Lister’s
tubercle
I II
III
IV
V VI
Retinaculum

11
Chapter 1:  Anatomy of the Tendon Systems in the Hand
The sixth compartment contains the ECU tendon,
which runs through a groove between the head and
styloid process of the ulna; after “encapsulating” the
pisiform bone, it attaches to the base of the fifth meta­
carpal. Frequently, a slip extends from the insertion to
the capsule of the MCP joint or the proximal phalanx
of the fifth digit.
VARIATIONS IN EXTENSOR TENDONS
TO THE FINGERS
Numerous variations exist in the extensor tendons to
the fingers. Zilber and Oberlin33 studied the pattern of
extensor tendons of 50 hands to determine the statisti­
cal distribution, combined with the results of previous
studies. In the most frequently encountered pattern, the
EDC provided one tendon to the index and middle
finger, two to the ring finger, and none to the little finger.
In this pattern there is a single extensor indicis tendon
and a double extensor digiti minimi tendon. A septum
is seen between the extensor digiti minimi tendon and
the EDC after they have emerged from the extensor reti­
naculum. Always observed is the extensor indicis tendon
lacking a junctura tendinum.
After reviewing the literature on variations in the
fingers extensor tendons, Zilber and Oberlin33 stated
that the different descriptions have certain contraindica­
tions, especially regarding the ring finger. A large varia­
tion was seen in the number of EDC tendons, ranging
from 5 to 12 tendons. The absence of a tendon to the
index finger is exceptional. The EDC tendon to the little
finger is often replaced by a structure arising from the
ring finger that joins the tendon of the extensor digiti
minimi at the level of the MCP joint. Some authors
describe this structure as a tendon and others as a junc­
tura tendinum. This may lead to differences in results
reported with respect to the EDC tendons to the fourth
and fifth fingers.33
The absence of the extensor indicis tendon is a rare
finding. An extensor medii digiti or extensor medii pro­
prius has been reported as a tendon for the middle
finger arising from the extensor indicis. The extensor
digiti minimi tendon can be absent with or without
substitution of a tendon from the EDC or ECU to the
little finger. The EDM can also be formed by two distinct
muscles or by one muscle with up to three tendons. The
two-tendon pattern is seen as the normal pattern. The
EDM can be identified by two tendons running in
the same sheath on the ulnar aspect of the wrist in 60%
to 90% of cases. This is important to know because this
extra tendon is useful for tendon transfers.33
Asymmetry is often seen between the right and the left
hand. Especially with respect to the EDM, this shows one
tendon favoring one hand more than the other in 20%
of cases. It is necessary to have thorough understanding
of these arrangements of the multiple extensor tendons
when performing tendon surgery33 (see Figure 1-7).
force to balance the other abducting forces that pull the
base of the first metacarpal and cause a shearing effect
on the TM joint.
Other studies did not show a significant relationship
between supernumerary tendon insertions and TM joint
arthritis. However, the presence of a septum within the
first extensor compartment does seem to play a role in
the pathogenesis of TM arthritis.30
The EPB inserts into the base of the proximal phalanx
of the thumb. The tendon can be fused with the extensor
pollicis longus (EPL) or absent. It often has its own
subsheath within the first compartment. This may be an
important factor in de Quervain disease. The tendons of
the extensor carpi radialis longus (ECRL) and brevis
(ECRB) pass under the muscle bellies of the abductor
pollicis longus (APL) and EPB before passing under­
neath the dorsal carpal ligament, in the second com­
partment. Repetitive resisted extension of the wrist can
cause inflammation of the tenosynovium at this inter­
section, which is therefore called “intersection syn­
drome.” It was thought to be caused by friction of the
muscle bellies at the intersection; however, Grundberg
and Reagan31 demonstrated this inflammation is based
on stenosing tenosynovitis of the sheath of the radial
wrist extensors within the second compartment. The
radial wrist extensor tendons attach at the dorsal radial
aspect of the base of the second and third metacarpal,
respectively. Variations exist in the number of tendons
arising from the muscle bellies and cross slips between
these tendons. Occasionally, an extensor carpi radialis
accessorius can be seen with insertion into the bones or
muscles in the thenar region.
In the third compartment, EPL obliquely crosses the
long and short extensor carpi radialis tendons and
inserts into the base of the distal phalanx of the thumb.
The tendons to the thumb form a triangular interval
(anatomical snuffbox), wherein the radial artery can be
found. The EPL tendon goes around Lister’s tubercle,
which is a frequent site of chronic tenosynovitis. This
could eventually lead to “drummer boy’s palsy,” when
the EPL tendon ruptures.
The extensor indicis proprius passes through the
fourth compartment together with the extensor digito­
rum communis (EDC) tendons and joins the common
extensor tendon to the index finger, on the ulnar side.
Occasionally an extensor digitorum brevis manus
(EDBM) muscle can be found in the fourth compart­
ment, which can be confused with a ganglion. The
EDBM has the same insertion as the extensor indicis
proprius and could therefore be seen as variant of that
muscle.32
Through the fifth compartment, distally to the distal
radioulnar joint, runs the tendon of the extensor digiti
quinti proprius or extensor digiti minimi. It merges at
the proximal phalanx with the little fingers extensor
expansion.

12
Section 1:  Basic Science
At the base of the proximal phalanx the extensor
tendon infiltrates the dorsal lamina; the tendon trifur­
cates and spreads out over the PIP joint. At the distal
end of the proximal phalanx, fibers from the lateral
bands join the middle band or central slip. After cross­
ing the PIP joint, the central slip is fused with the
capsule and inserts at the base of the middle phalanx26,36
(Figure 1-9).
The central slip particularly extends the middle
phalanx, unless the MCP joint is in hyperextension.
When the PIP joint is flexed, the central slip contributes
to the extension of the proximal phalanx by dorsal dis­
placement of the middle phalanx on the head of the
proximal phalanx.36
A narrow, tendinous band arises at the volar aspect
of the distal end of the proximal phalanx. This oblique
retinacular ligament (ORL) courses obliquely to the
dorsal side of the middle phalanx, where it joins the
lateral bands to the distal phalanx. It helps stabilizing
the lateral bands and is also attributed to extend the DIP
joint in harmony with the extension of the PIP joint;
however, biomechanical investigations have refuted
this. This “link” ligament passes volar to the PIP joint
axis only when the joint is flexed; the same applies, in
greater extend, to the DIP joint. The oblique retinacular
ligament was observed only to aid in extension when
the DIP joint was flexed more than 70 degrees.37,38
At the PIP joint a homologue to the sagittal bands
originates from the volar aspect of the PIP joint. The
transverse retinacular ligament maintains the extensor
mechanism in position and pulls the lateral bands
volarly, in flexion of the PIP joint.26
Distal to the insertion of the central slip the dorsal
hood continues toward the distal phalanx as a thin
membrane between the lateral bands. This area covering
On the dorsum of the hand, the extensor tendons are
interconnected by tendinous bands called junctura ten­
dinea. The presentation of the juncturae shows several
variations. Most often an oblique slip branches off the
tendon of the ring finger to insert distally in the tendon
of the little and middle fingers. A thin transverse band
can be found between the middle and index fingers.
There are three types of juncturae: a filamentous trans­
verse or oblique band, a much thicker and well-defined
junctura, and a “y”- or “r”-shaped tendon slip.34
With the fingers in flexion, the juncturae restrict the
neighboring fingers from extending independently. This
especially accounts for the ring finger as the juncturae
originate at the tendon of the ring finger and course
distally35 (see Figure 1-7).
EXTENSOR MECHANISM OF THE FINGERS
Kaplan and Hunter26 and Smith35 thoroughly describe
the extensor mechanism of the fingers. As the common
digital extensor tendons approach the distal end of the
metacarpals, they spread out to form an aponeurosis
over the MCP joint and proximal phalanx, the extensor
expansion or dorsal hood. The tendon is fixed at the
midline of the MCP joint by a band of sagittal fibers
that arises volarly at the deep transverse metacarpal liga­
ment and the volar plate of the MCP joint. These sagittal
bands aid in the extension of the proximal phalanx and
restrict the tendon from moving proximally.26
Between the sagittal bands and the MCP joints run
the tendons of the interosseus muscles that insert at the
lateral tubercles on the base of the proximal phalanx.
These tendons allow for lateral deviation of the fingers.
By its connection with the extensor expansion, the inter­
ossei can flex the MCP joint. Fibers between the lateral
ligaments and the extensor expansion prevent the inter­
osseus tendons from luxating dorsally in extension. The
radial side of the proximal phalanx, slightly distal to the
lateral tubercles, normally also receives the insertion of
the lumbrical tendon.26
Distally, lateral bands formed by a continuation of
the interossei and lumbricales course to the sides of
the PIP joint and the middle phalanx (Figure 1-8).
Oblique slips attach to the base of the middle phalanx
and merge with the central tendon. The remaining
portion of the lateral bands continues at the sides of
the middle phalanx and turns dorsally near its head.
There the bands unite and continue as a wide band over
the DIP joint that inserts at the base of the distal
phalanx.36
Between the lateral bands of the interossei, distal to
the sagittal bands, transverse fibers arch over the dorsal
side of the proximal phalanx. The fibers of this interten­
dinous lamina gradually change from horizontal to
oblique from distal to proximal. The lamina courses
from the extensor tendon to the volar plate of the MCP
joint and acts as a flexor of the proximal phalanx.35
Figure 1-8  Extensor mechanism lateral view. ORL, Oblique
retinacular ligament; TRL, transverse retinacular ligament.
Sagittal band locates dorsal and lateral to the MCP joint of
the finger. The tendons of the interosseus and lumbrical
muscles insert in the proximal phalanx and form the lateral
bands, which is interconnected with the central slip by the
sagittal band at the MCP joint.
ORL
TRL
Lateral
band
Lumbrical
Interosseus
Sagittal band
Central slip

13
Chapter 1:  Anatomy of the Tendon Systems in the Hand
of the FPB as one of the palmar interossei.2,39 The oppo­
nens pollicis inserts along the entire length of the lateral
side of the metacarpal bone of the thumb. It flexes the
metacarpal at the CMC joint and therefore contributes
to opposition of the thumb; a combination of actions
that brings the tip of the thumb and the other fingers
together. The abductor pollicis brevis, FPB, and oppo­
nens pollicis form the thenar muscles.2,39
The adductor pollicis tendon inserts in the first
annular pulley and the ulnar sesamoid at the MCP joint.
The volar plate is firmly attached to the proximal
phalanx, what gives the adductor pollicis the ability to
directly act on the phalanx. The adductor pollicis also
has an extension to the ulnar lateral tubercle and the
dorsal aponeurosis of the thumb. Its actions are adduc­
tion of the thumb and flexion of the MCP joint2,39
(Figure 1-10).
Some controversy exists about the pulleys of the
thumb. An annular pulley arises from the volar plate of
the MCP and interphalangeal joint. At the level of the
shaft of the proximal phalanx an oblique pulley can be
found. The proximal part of the oblique pulley shows
variation and is suggested to be seen as a separate trans­
verse pulley. These pulleys arising from the proximal
phalanx are most important in preventing bowstringing
of the FPL tendon. However, the oblique part alone does
not prevent bowstringing.40
the middle phalanx is called the triangular ligament (or
triangular lamina). It retains the lateral bands close to
each other by bonding them over the dorsum of the
middle phalanx (see Figure 1-8).
TENDONS IN THE THUMB
The FPL tendon courses through a groove on the volar
side of the first metacarpal, in its own flexor sheath. In
the volar capsule of the MCP joint, two sesamoid bones
are embedded, which firmly wedge the FPL tendon.
Distally the tendon inserts widely in a deep excavation
in the volar surface of the distal phalanx. It flexes the
interphalangeal joint of the thumb, as well as the MCP
and carpometacarpal (CMC) joint.2,39
The abductor pollicis brevis is inserted by a thin, flat
tendon into the lateral aspect of the MCP joint capsule
and unites with the fibers of the flexor pollicis brevis
(FPB) to the radial sesamoid. It moves the thumb ante­
riorly (abduction) and also contributes to opposition
and extension of the thumb.2,39 The FPB forms a tendon
near the MCP joint, to which it adheres, and inserts into
the lateral sesamoid bone and the lateral tubercle of the
proximal phalanx. It flexes the thumb towards the palm
of the hand. Some anatomists describe the medial part
Figure 1-9  Extensor mechanism dorsal view. LB, Lateral
band. The connections between the central slip and lateral
band are illustrated. The triangular ligament connects the
lateral bands over the dorsum of the middle phalanx.
LB
Central
slip
Triangular
ligament
Figure 1-10  The flexor pollicis longus (FPL) pulley system
differs from the finger pulley system in that there is a strong
fibrous oblique pulley between the A1 and A2 pulleys. There
are no cruciate pulleys in the thumb.
A2
A1
Oblique pulley
Adductor pollicis
Flexor pollicis brevis, deep head
Synovial sheath

14
Section 1:  Basic Science
base of the proximal phalanx. Frequently an insertion
in the distal phalanx is observed. By acting on the CMC
and MCP joints the extensor pollicis brevis extends and
abducts the thumb.2,39 The extensor mechanism of the
thumb shows similarities with the expansion over the
fingers MCP joints. It is formed by EPL and EPB, and
the extensions of the abductor brevis on the radial side
and adductor on the ulnar side.2,39
On the dorsal side of the thumb the EPL tendon
courses over the ulnar side of the MCP joint. From there
it broadens, crosses the interphalangeal joint and inserts
widely into the base of the distal phalanx. It extends the
distal phalanx of the thumb and contributes to abduc­
tion and extension of the wrist.2,39
The EPB tendon is concealed by the dorsal aponeu­
rosis as it crosses the MCP joint and inserts in the dorsal
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19. Strauch B, de Moura W: Digital flexor tendon sheath: An
anatomic study, J Hand Surg (Am) 10:785–789, 1985.
20. Doyle JR: Anatomy of the finger flexor tendon sheath and
pulley system, J Hand Surg (Am) 13:473–484, 1988.
21. Lin GT, Amadio PC, An KN, et al: Functional anatomy of the
human digital flexor pulley system, J Hand Surg (Am) 14:949–
956, 1989.
22. Zhao CF, Amadio PC, Berglund L, et al: The A3 pulley, J Hand
Surg (Am) 25:270–276, 2000.
23. Kline SC, Moore JR: The transverse carpal ligament. An
important component of the digital flexor pulley system,
J Bone Joint Surg (Am) 74:1478–1485, 1992.
24. Doyle JR: Anatomy and function of the palmar aponeurosis
pulley, J Hand Surg (Am) 15:78–82, 1990.
25. Manske PR, Lesker PA: Palmar aponeurosis pulley, J Hand
Surg (Am) 8:259–263, 1983.
26. Kaplan EB, Hunter JM: Extrinsic muscles of the fingers. In
Spinner M, editor: Kaplan’s Functional and Surgical Anatomy
of the Hand, ed 3, Philadelphia, 1984, JB Lippincott,
pp 98–102.
27. Kaplan EB, Hunter JM: Functional anatomy of the flexor
tendon system: The muscles and tendon systems of the
fingers. In Hunter JM, Schneider LH, Mackin EJ, editors:
Tendon and Nerve Surgery in the Hand, A Third Decade, St.
Louis, 1997, Mosby, pp 240–252.
28. Ijpma FF, van de Graaf RC, van Gulik TM: Petrus Camper’s
work on the anatomy and pathology of the arm and hand in
the 18th century, J Hand Surg (Am) 35:1382–1387, 2010.
29. Brunelli GA, Brunelli GR: Anatomical study of distal insertion
of the abductor pollicis longus. Concept of a new musculo-
tendinous unit: the abductor carpi muscle. Ann Chir Main
Memb Super 10:569–576, 1991.
30. Opreanu RC, Wechter J, Tabbaa H, et al: Anatomic variations
of the first extensor compartment and abductor pollicis
longus tendon in trapeziometacarpal arthritis, Hand (NY)
5:184–189, 2010.
31. Grundberg AB, Reagan DS: Pathologic anatomy of the
forearm: intersection syndrome, J Hand Surg (Am) 10:299–
302, 1985.
32. Ogura T, Inoue H, Tanabe G: Anatomic and clinical studies
of the extensor digitorum brevis manus, J Hand Surg (Am)
12:100–107, 1987.
33. Zilber S, Oberlin C: Anatomical variations of the extensor
tendons to the fingers over the dorsum of the hand: A study
of 50 hands and a review of the literature, Plast Reconstr Surg
113:214–221, 2004.
34. Von Schroeder HP, Botte MJ, Gellman H: Anatomy of the
juncturae tendinum of the hand, J Hand Surg (Am) 15:595–
602, 1990.
35. Smith RJ: Balance and kinetics of the fingers under normal
and pathological conditions, Clin Orthop Relat Res 104:92–
111, 1974.
36. Ubiana R: Anatomy of the extensor tendon system of the
fingers. In Hunter JM, Schneider LH, Mackin EJ, editors:
Tendon and Nerve Surgery in the Hand: A Third Decade, St.
Louis, 1997, Mosby, pp 547–550.

15
Chapter 1:  Anatomy of the Tendon Systems in the Hand
39. Kaplan EB, Riordan DC: The thumb. In Spinner M, editor:
Kaplan’s Functional and Surgical Anatomy of the Hand, ed 3,
Philadelphia, 1984, JB Lippincott, pp 124–142.
40. Bayat A, Shaaban H, Giakas G, et al: The pulley system of
the thumb: Anatomic and biomechanical study, J Hand Surg
(Am) 27:628–635, 2002.
37. Harris C Jr, Rutledge GL Jr: The functional anatomy of the
extensor mechanism of the finger, J Bone Joint Surg (Am)
54:713–726, 1972.
38. el-Gammal TA, Steyers CM, Blair WF, et al: Anatomy of the
oblique retinacular Ligament of the index finger, J Hand Surg
(Am) 18:717–721, 1993.

16
CHAPTER
2 
TENDON NUTRITION
AND HEALING
Peter C. Amadio, MD
TENDON NUTRITION
Vascular Sources
Tendons have two sources of vascular nutrition. Extra­
synovial tendons are supplied by circumferential vessels
in the paratenon, a multilayered system elegantly
described by Giumberteau7 and illustrated in Chapter
31. Intrasynovial tendons, such as those in zone 2 in
the hand, are supplied through the segmental vincular
system.8-10 This segmental system results in predictable
watershed zones within the flexor tendon (Figure 2-1),
with intercalated regions on the palmar aspect of the
tendon with little in the way of blood supply. The
number and location of these zones also varies by digit,
with the ring finger generally having the fewest vincula.10
Synovial Fluid
Intrasynovial tendons have a second source of nutrition,
of course—synovial fluid. This mechanism is especially
important in avascular and hypovascular regions of the
tendon3,11-14 and is dependent on the pumping effect of
digital motion. Tendons whose vincula are absent or
damaged and that do not move are therefore deprived
of nutrition, an important consideration for tendon
repair and rehabilitation.
TENDON HEALING
Biology of Tendon Healing
The extracellular matrix (ECM) is the principal compo­
nent of tendon tissue and is responsible for its material
properties.15-17 The major constituents of the ECM are
type I collagen; proteoglycans, principally decorin, but
also aggrecan in the gliding regions18-21; fibronectin; and
elastin. This matrix is synthesized by tendon cells, or
tenocytes. These cells are surrounded by the dense
matrix; thus, although they are metabolically active,
they do not participate much in the tendon healing
process. Instead, undifferentiated cells in the epitenon
do the heavy lifting for tendon healing, proliferating,
migrating into the gap between the tendon ends, and
finally uniting the cut tendon ends22,23 (Figure 2-2).
Unfortunately, this is a two-edged sword; if these same
cells migrate away from the tendon, toward the tendon
sheath, they form adhesions, which restrict tendon
OUTLINE
This chapter will review current knowledge on tendon
nutrition and healing. Tendon obtains nutrition from
both vascular sources and synovial fluid. The extracel­
lular matrix is the principal component of tendon
tissue, and is responsible for its material properties.
The major constituents are type I collagen; proteogly­
cans, principally decorin, but also aggrecan in the
gliding regions; fibronectin; and elastin. This matrix is
synthesized by tendon cells, or tenocytes. After tendon
injury, the extracellular matrix undergoes significant
changes, due to synthesis of new elements by the teno­
cytes, such as type III collagen, degradation of existing
elements by various matrix metalloproteases, and
remodeling of the resulting combination, under the
influence of cytokines as well as mechanical forces.
Physical factors, such as motion, loading and friction
affect the results of tendon repair. The concept of “safe
zone” was proposed to define the range of external
loading which does not disrupt the tendon repair
when the tendon is loaded during motion. Pharmaco­
logical manipulation of tendon healing, such as use
of 5-fluorouracil, may reduce adhesion formation
during tendon healing, and supplying stem cells or
cytokines may augment intrinsic healing capacity of
the injured tendon. Critical points are as follows.
Regarding nutrition, both synovial and vascular routes
are important; vascular route is affected by age and
injury, and the synovial route is affected by mobiliza­
tion. In healing, motion aids healing and reduces
adhesions. There is little evidence that loading, in the
absence of motion, is helpful, or that, once the tendon
is moving, more loading helps healing. We do know
that loading may lead to failure of the repair. The “safe
zone” involves enough loading to initiate motion but
not enough to risk the repair.
Traditionally, tendons have been thought of as being
inert, hypovascular structures.1,2 However, subsequent
research has shown that tendons are active metaboli­
cally, that tenocytes can replicate and heal experimental
injuries, and that adhesions, while common, are not
necessary for healing.3-6 This chapter will review current
knowledge on tendon nutrition and healing.

17
Chapter 2:  Tendon Nutrition and Healing
transforming growth factor (TGF)β as well as mechani­
cal forces. Manipulation of these processes, to augment
their action between the tendon ends while reducing
them at the tendon’s gliding surface, is the goal of much
research, as described later.
Healing of flexor tendons in zone 2 depends on the
ability of the injured tendon to recruit fibroblasts and
other cellular components to the site of injury.31 Nor­
mally these are circulating or locally derived undifferen­
tiated (i.e., stem) cells that are recruited to the injury
site by the expression of cytokines in the wound.24,27,32-34
Cytokine stimulation is also important in converting
these undifferentiated cells into the tendon phenotype,
characterized by the expression of markers such as
tenomodulin and scleraxis.35,36 Bone marrow–derived
stem cells (BMSCs) can also enter and participate in soft
tissue healing.37-39
EFFECT OF PHYSICAL FACTORS
Motion
Lacerated tendons that are immobilized, unless
extremely well nourished, will heal with adhesions.40-42
While these adhesions can remodel, especially in an
extrasynovial environment, in the region of the tendon
sheath such adhesions are invariably associated with
loss of motion. Thus, motion of flexor tendon repairs
in critical. Duran and Houser43 suggested observing
the repair intraoperatively and maintaining passive
motion sufficient to cause 4 mm of tendon gliding, and
separation of the profundus and superficialis repairs, if
both tendons are injured. Evans has discussed similar
concepts of limited active motion of repaired tendons.44
Loading
Clearly, some load must be applied to a flexor tendon
if it is to move. The loads applied to a tendon by passive
motion of a digit tend to be small, and tendons may
buckle instead of glide, especially if the tendon repair
has a high friction.45 A modification of the usual syner­
gistic passive motion protocol in which the metacarpo­
phalangeal joints are maintained in extension in both
the flexion and extension phases of motion seems to
provide better pull, on the order of 100 g, in both the
flexion and extension directions, and may be useful in
some cases.46,47 The use of higher loads, with active
motion protocols, is somewhat controversial.48-50 My
philosophy has been to tailor the loading to the stage
of healing, as emphasized by Groth,51 as further
described later.
Effect of Friction on the Results
of Tendon Repair
Animal studies over the past decade have shown
convincingly that high friction repairs with knots and/
or many loops on the surface, such as the modified
motion. Often this is indeed the case, as the relatively
ischemic tendon is surrounded by better vascularized
tissue, which sends out vascular buds under the stimula­
tion of vascular endothelial growth factor (VEGF).24-27
After tendon injury, the extracellular matrix under­
goes significant changes, due to synthesis of new ele­
ments by the tenocytes, such as type III collagen,28-30
degradation of existing elements by various matrix
metalloproteases, and remodeling of the resulting com­
bination, under the influence of cytokines such as
Figure 2-1  Tendon blood supply.
Figure 2-2  Epitenon cells migrating into the repair site 3
weeks after injury in a canine model of tendon injury
(hematoxylin-eosin, magnification ×100).

18
Section 1:  Basic Science
sufficient to overcome the forces of friction. It is for this
reason that low friction repairs are important—they
minimize the load needed to initiate movement. Fric­
tion, though, is not the only concern. The force needed
to overcome joint stiffness and to flex traumatized,
edematous tissues must also be considered, as well as
the weight of the distal digit itself; often these latter
forces will far outweigh the frictional ones in magni­
tude, especially in an injured digits. So the minimum
force needed to load the tendon will be a combination
of the frictional force and the force needed to move the
joints and soft tissues. The energy needed to flex the
digit is often called the “work of flexion”.69,77,78
One might imagine that the maximum load that
could be applied is the load that represents the breaking
strength of the tendon, but that would be incorrect: long
before the tendon breaks, it begins to gap, and gapping
also increases friction, setting up a vicious circle that can
lead to later rupture. So, really, the upper bound is not
breaking strength but the force needed to create a gap,
which is usually much less.50,62,79-87 The difference
between the two forces—the force to initiate unloaded
digital flexion and the gapping force—represents the
“safe zone” in which rehabilitation can occur88 (Figure
2-4). Early on, this safe zone will be bounded by strictly
mechanical parameters, related to the anatomy and bio­
mechanics of the repair. Over time, though, the effects
of tendon healing are added in; the general effect is
usually to gradually widen the safe zone, enabling the
rational use of a graded resistance program as outlined
by Groth.51 The details of such programs are reviewed
in Chapter 38.
Unfortunately, in some cases, early mobilization after
tendon repair is not possible by any method. Common
examples include situations with complex hand injury,
in which motion might jeopardize bone, skin, nerve
or vascular integrity; patients who are uncooperative
due to age or mental status; or situations where the
tendon repair is deemed to be too tenuous to tolerate
Becker/MGH or Tsuge repairs, result in abrasion of the
tendon sheath (Figure 2-3) and adhesion formation,
even when factors such as rehabilitation method are
optimized.52-54 Thus, the goal should be to use a high-
strength, low-friction repair construct, such as the modi­
fied Kessler, Tajima, or Pennington repairs, and a
low-friction suture material, of which there are many.
Most recently, I have been using 3-0 polyester suture and
a modified Pennington design.
Impact on Postoperative Management:
Concept of the “Safe Zone”
Until the mid 1960s, most flexor tendon repairs were
immobilized postoperatively for three weeks. This
policy was based on the research of Mason and Allen,55
who had shown that canine flexor tendon repairs
decreased in tensile strength for three weeks postopera­
tively. Subsequent clinical work by Verdan,56 Kleinert
et al,57 and Duran et al58 showed that human flexor
tendon repairs could be safely mobilized with a combi­
nation of active extension and passive flexion.
The use of early mobilization after tendon repair has
resulted in improved outcomes for flexor tendon inju­
ries.56,58-62 In animal models,45,53,63-67 earlier mobiliza­
tion results in better final tendon gliding and tensile
strength. More recently, the fine details of mobilization
have been studied, specifically the effect of timing68-70
and the effect of differential motion of the wrist and
finger joints on tendon loading and tendon gliding
during the healing period.49,53,71 Active motion protocols
have also been used, although, interestingly, the clinical
results are not reliably better than passive protocols.72-75
Moreover, the addition of loading to motion in animal
models has been shown to have little effect on the final
result in terms of strength and motion.49,67,76 Thus, the
available evidence suggests that motion, not load, is the
critical factor.
Of course, there must be some load on the tendon if
it is going to move; at the very least, the load must be
Figure 2-3  A, Abrasion of sheath 6 weeks after MGH repair in an in vivo canine model (scanning electron microscopy,
magnification, ×300). Compare with B, a similar image from a tendon repaired with a modified Kessler suture.
A
B

19
Chapter 2:  Tendon Nutrition and Healing
effects appear to be focal to the site of application and
titratable in terms of length of action.96-98 A 5-minute
exposure to 5-FU has been shown to significantly
decrease postoperative flexor tendon adhesions in
chicken and rabbit models.99,100 This beneficial effect is
thought to be due to the downregulation of TGFβ and
modulation of matrix metalloproteinase (MMP)-2 and
MMP-9 production.101,102 The effect on surface lubrica­
tion is unknown. No adverse effect was noted on tendon
healing in these studies. It is presumed therefore that
the topical 5-FU does not penetrate to affect the cells
below the tendon surface. Topical application of 5-FU
may well have a role in improving the outcomes in
selected cases of tenolysis.
AUGMENTATION OF INTRINSIC
TENDON HEALING
Stem Cells
BMSCs delivered on collagen sponges improve healing
in animal models of tendon repair,103,104 and stem cells
from other origins have been shown to be effective
in enhancing repair in several other tendon injury
models.105-108 Current research is focused on optimizing
the isolation and differentiation of stem cells into the
tendon phenotype. In the future, it is likely that cells
derived from the patient’s own bone marrow, fat, skin,
or muscle will be used as a “patch” to augment tendon
repair (Figure 2-5). My colleagues and I are pursuing
one such option in our laboratory now: a mixture of
collagen, growth factors, and stem cells from the patient’s
own tissues and lubricated with an engineered surface
containing hyaluronic acid and lubricin.109-112 Such a
graft could also be used to bridge flexor tendon defects,
and, finally, replace like with like.
Cytokines
Growth factors are the chemical signals that direct the
migration and proliferation of the tendon fibroblast
during the healing process. The role of growth factors
has been examined extensively in cutaneous wounds
and other soft tissue processes, yet we are only begin­
ning to known the specifics involved in flexor tendon
healing.17,113 The factors that appear to be involved
mobilization. In such cases, adhesions have been, up to
now, inevitable. It is possible, though, that the applica­
tion of a tissue engineered, biocompatible adhesion
barrier that is porous to nutrients might allow an immo­
bilized tendon to heal without adhesions. We are cur­
rently pursuing research to address this issue, using
carbodiimide derivatized hyaluronic acid and lubricin,
linked to collagen, as the proposed barrier, and hope to
have an update in time for the next edition of this book.
PHARMACOLOGICAL MANIPULATION
OF TENDON HEALING
Various pharmacological agents have been used in the
past in an attempt to modify adhesion formation. Ste­
roids, antihistamines, and beta-aminoproprionitrile
have not been shown to clinically decrease scar forma­
tion.89,90 Ibuprofen and indomethacin have been found
to have a small beneficial effect.91
The ideal pharmacological agent should have no
systemic side effects, should be limited to a single
application, and should be directed at growth factor
expression and ECM production. 5-Fluorouracil (5-FU)
may be such a drug. 5-FU is an antimetabolite that
is used not only as a cancer chemotherapeutic agent
but also to prevent adhesions in glaucoma filtration
surgery. The exposure of a surgical field to 5-FU pro­
duces a focal inhibition of scarring. Blumenkranz
et al92,93 has found that 5-FU is able to inhibit the pro­
liferation of fibroblasts in cell cultures and reduce retinal
scarring. Single exposures to 5-FU, for as short duration
as 5 minutes, can have antiproliferative effects on fibro­
blasts for several days. The suppression of fibroblast
proliferation has been observed for up to 36 hours
without signs of cell death.94,95 This time frame may be
adequate to inhibit tendon adhesions prior to begin­
ning postoperative motion protocols. Reversible pro­
longed inhibition of fibroblast function is attributed to
the drug’s inhibition of DNA and mRNA synthesis
through thymidylate syntheses. More important, these
Figure 2-4  The “safe zone” concept.
0.2
5
10
20
30
40N
Max strength
In Vitro
Max strength
1 wk. In Vitro
2 mm gap
Initial gap
Effect
of time
Friction
of the
repair
Initial “safe zone”
Initial strength of the repair
In Vitro
Repair
Figure 2-5  Conceptual model of stem cell patch to
augment tendon repair.
Lubricated surface
Patch containing cells,
growth factors and collagen

20
Section 1:  Basic Science
adhesions in a rabbit tendon model.122-125 TGFβ levels
can remain elevated for up to 8 weeks after tendon
injury.126,127
Neuropeptides may also play a role in tendon
healing.128-131 During the early phases of healing, tendons
exhibit nerve fiber ingrowth.128 This nerve ingrowth is
associated with the temporal release of substance P
(SP). SP promotes tendon regeneration through the
stimulation and proliferation of fibroblasts.132-135 Further
studies have found that tendon motion helps to modu­
late the release of SP.129 The injection of SP into the
peritendinous region of ruptured rat tendons improves
healing and increases tendon strength.136 Similarly,
growth and differentiation factor-5 (GDF-5), a member
of the TGF superfamily, have a potential to stimulate
BMSC proliferation and regulate BMSC differentiation
to tenocytes.137 Recent experiments have some beneficial
effect of GDF-5 on tendon healing as well.25,119,138
include TGFβ, platelet-derived growth factor (PDGF),
basic fibroblast growth factor (bFGF), insulin-like
growth factor (IGF), epidermal growth factor (EGF),
and VEGF.27,114,115 These same growth factors have also
been shown to optimize tissue-engineered constructs
used for tendon repair.27,104,114-117 Growth differentiation
factor-5 (GDF-5), a member of the TGFβ superfamily,
has also been shown to accelerate tendon healing in
multiple animal models.118-120
TGFβ stimulates the formation of the ECM. It signals
fibroblasts to produce collagen and fibronectin,
decreases protease production, and increases the forma­
tion of integrins, which promote cellular adhesions and
matrix assembly. In normal tissue, TGFβ becomes inac­
tivated once wound healing is complete; however, it
may remain active in tendon adhesion formation, con­
tinuing the cycle of matrix accumulation.121,122 Modula­
tion of TGFβ has been reported to reduce peritendinous
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24
CHAPTER
3 
TENDON FRICTION,
LUBRICATION, AND
BIOMECHANICS OF MOTION
Chunfeng Zhao, MD, Peter C. Amadio, MD, and
Kai Nan An, PhD
fingers, frictional force must be encountered. An et al1
developed a tendon/pulley gliding model to measure
the frictional force and calculate the frictional coeffi­
cient (Figure 3-1). If the impending motion of the cable
is from F1 to F2, then F2 is greater than F1 due to the
friction f, and f = F2 − F1. F2 is also related to F1 as F2
= F1eµø, where µ is the frictional coefficient. If a loga­
rithm is taken, LnF2/F1 = µø. If the values of F2, F1, and
ø are known and natural logarithms of F2/F1 are plotted
against angles in radians, the frictional coefficient can
be calculated as the slope of a line designed according
to the least-squares method.2
The assessment of frictional force at the tendon–
pulley interface with this method is an ideal model.
However, tendon gliding is far more complicated. In
classical theory, for friction without a lubricant, three
laws have been postulated3: (1) The frictional force is
directly proportional to the applied load; (2) frictional
force is independent of the apparent area of contact; and
(3) the kinetic frictional force is independent of the
sliding speed. However, these rules must be modified in
tendon, for several reasons. First, the tendon is a visco­
elastic tissue. Its properties are affected by the velocity
of tendon motion, and its surface deforms in response
to contact pressure. In addition, tendon is lubricated, at
least normally.
Moriya et al4 investigated three parameters that may
relate to tendon friction: temperature (4°C, 23°C, and
36°C), gliding velocity (2, 4, 6, 8, or 12 mm/sec), and
load (250, 500, 750, 1000, 1250, and 1500 g) applied
to the tendon using a flexor digitorum profundus
tendon and A2 pulley model. They found that the
tendon friction was proportional to load, but not,
within the ranges studied, to gliding velocity (Figure
3-2A and B). The temperature also affected the tendon
friction; the friction at 4°C was significantly higher than
that at body temperature, 36°C. This information is
useful to guide the experiments that relate to tendon
frictional testing. Some studies have also demonstrated
that tendon frictional force is dependent on joint posi­
tion or the direction of motion. Zhao et al5 found that
OUTLINE
Both physiological and pathological conditions
regarding tendon friction, lubrication, and motion are
discussed in this chapter. Tendon friction and lubrica­
tion mechanism vary according to tendon type. Intra­
synovial tendon, regularly located in high abrasion
areas, has less frictional force and greater durability
than the extrasynovial tendon. The lubrication mecha­
nism of the intrasynovial tendon is similar to that of
the articular cartilage. Proteoglycan, hyaluronic acid,
and phospholipid are the major lubricating compo­
nents. Extrasynovial tendon relies on the paratenon
sequential gliding phenomenon to reduce the direct
abrasion of the tendon with surrounding tissues.
However, this gliding unit is fragile. A hybrid of intra­
synovial and extrasynovial tendon occurs in the carpal
tunnel. Adequate tendon excursion is essential to
maintain normal muscle and joint function. An
increased tendon moment arm (such as bowstringing)
will affect both strength and excursion of the tendon.
A healthy tendon is essential to maintain the normal
functional performance of muscles and joints. Since the
tendons transmit both force and displacement from
muscle, the tensile strength of the tendon must be
strong enough to bear the range of anticipated loading,
and the tendon displacement must be long enough to
achieve full joint motion. Lose of either property would
not only jeopardize the tendon functional performance
but also affect muscle and joint function. Therefore, an
understanding of tendon friction, lubrication, and bio­
mechanics, in both physiological and pathological con­
ditions, is essential for clinicians who diagnose and treat
tendon disorders.
TENDON FRICTION
Tendon Friction in Physiological Conditions
When tendons glide against surrounding tissue, espe­
cially when passing through a series of pulleys in the

25
Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
the friction at the flexor tendon–transverse carpal liga­
ment interface was significantly higher in wrist flexion
compared to the neutral position. Heers et al6 studied
the frictional force of the long head of the biceps tendon
during shoulder motion and found that the frictional
force during abduction was significantly higher than
that of adduction.
Tendon Friction in Pathological Conditions
The normal tendon frictional force is small. The fric­
tional coefficient of flexor tendon in zone 2, where two
flexor tendons are enveloped by flexor sheath with syno­
vial fluid between, is comparable to that of cartilage.7-9
However, the frictional force after tendon injury and
repair dramatically increases, which impairs tendon
function. Sutures create roughness of the tendon surface
and increase friction. Sutures also increase the volume
of the tendon, and postinjury edema can increase fric­
tion as well. Afterward, the biological healing between
tendons and surrounding tissue forms adhesions, which
increase the frictional force and may in some cases
totally impede tendon gliding.
Strategies to reduce the fictional force after tendon
repair have been studied.7,10-12 Surface friction of a
repaired tendon can be reduced by burying knots
between tendon ends, or locating the knots away from
the anterior tendon surface, choosing low friction suture
materials, and using fewer suture loops and strands.13,14
Using a canine in vivo model, Zhao et al15 found that
Figure 3-1  Illustration of the tendon–pulley frictional measurement system, consisting of a mechanical actuator with a
linear potentiometer, two tensile load-transducers connecting distal (F1) and proximal (F2) to the A2 pulley, a mechanical
pulley (right), a Dacron cord, and a weight. FDP, Flexor digitorum profundus.
F1
F2
α
β
A2
pulley
FDP
tendon
Load
Mechanical
actuator
and linear
potentiometer
0
5
10
15
20
35
40
45
50
55
60
65
65
60
55
50
45
40
35
30
25
10
5
0
70
70
75
75
80
80
85
85
90
a lower friction repair technique, the modified Kessler
repair, had fewer adhesions after 6 weeks compared to
a higher friction technique, the modified Becker repair.
However, these positive adhesion outcomes were com­
bined with higher rates of gap formation and rupture.
To balance the tensile strength and friction, several
studies have studied suture techniques with higher
tensile strength and lower friction. Momose et al16 used
a looped suture with a modified Kessler suture tech­
nique to repair flexor tendons and achieved high tensile
strength with relative low friction. Later, Tanaka et al17
demonstrated that the modified Pennington technique
possesses low friction and high strength.
Some alternative surgical techniques have been devel­
oped to minimize bulk after tendon repair. Resection of
one slip of the flexor digitorum superficialis (FDS)
tendon decreased the repaired flexor digitorum profun­
dus (FDP) tendon gliding resistance.18 Pulley plasty also
reduces friction.19 Trimming the pulley edge on an
oblique, rather than perpendicular to the long axis of
the bone, may also help the repaired tendon pass
through with less risk of triggering.20
The frictional force of a repaired tendon with a gap
has also been studied. The friction of repaired tendons
without gap mainly comes from surface roughness.
However, with gap formation, plowing friction, related
to surface shape, becomes dominant, which dramati­
cally increases the resistance. If a repaired tendon has a
3-mm or larger gap, the plowing frictional force may

26
Section 1:  Basic Science
increase sharply due to the trapping of the repaired
tendon edge on the pulley, eventually leading to repair
failure if the applied load exceeds the repair strength.21
The tendon frictional force may also increase in cir­
cumstances not related to tendon injury or repair. Joint
deformities that cause the tendon pulley gliding angle
Figure 3-3  Left, Intrasynovial tendon region,
the tendon surface is covered by epitenon,
which includes several layers of epitenon cells
seeding on the surface (top, hematoxylin-
eosin stain). Middle, Extrasynovial tendon that
is wrapped by loose connective tissue,
paratenon (top, hematoxylin-eosin stain).
Right, Hybrid region of the tendon that
wrapped by paratenon and synovial sheath
bursa (top, hematoxylin-eosin stain).
Surrounding
tissues
Tendon
Synovial
sheath
Epitenon
Paratenon
SSCT
Bursa
Intrasynovial
portion
Extrasynovial
portion
Hybrid
portion
Figure 3-2  The frictional force of tendon is proportional to
load applied to the tendon (A) but independent of the
gliding velocity (B).
250
0
0.2
0.4
0.6
0.8
Frictional force (N)
1
500
750
1000
FRICTION VS LOAD
1250
1500 (g)
2
A
B
0
0.1
0.2
Gliding velocity (mm/s)
0.3
0.4
Frictional force (N)
0.5
4
6
8
FRICTION VS VELOCITY
10
12
to increase, as in rheumatoid arthritis, also increase fric­
tional force.22 Trigger finger is another example where
increased bulk and decreased lubrication hamper
tendon gliding through the pulley. The integrity of the
flexor pulley system is also important to maintain
normal frictional force during finger motion. Resection
of the A3 pulley increases the gliding resistance between
tendon and A2 pulley.23 Increased carpal tunnel pres­
sure also increases tendon frictional force.24
Tendon Friction in Different Tendon
Surroundings
Tendons can be classified as intrasynovial and extrasy­
novial tendons based on their surrounding environ­
ment.25 Intrasynovial tendons are defined as tendons, or
parts of tendons, enclosed within a synovial sheath.
These tendons are lubricated by synovial fluid, and the
tendon surface is covered by a thin visceral synovial
membrane, the epitenon (Figure 3-3). The epitenon
cells are similar to synovial cells and secrete lubricants.
This unique structure effectively decreases friction,
reduces abrasion, and eliminates wear. Flexor tendons
in zone 2 area are typical intrasynovial tendons. Exten­
sor tendons in the dorsal wrist area, the long head of
the biceps brachii tendon, and the posterior tibial
tendon at the medial malleolus are other examples of
intrasynovial tendons. In contrast, the tendons located
within subcutaneous soft tissues are extrasynovial
tendons. These tendons are covered by loose connective
tissue, called paratenon (see Figure 3-3). In addition,
some tendons have a hybrid type. Ettema et al26 reported
that flexor tendons in zone 4 (within the carpal tunnel)
have a unique structure, in which the subsynovial con­
nective tissue (SSCT), a paratenon-like structure, covers
each flexor tendon. The SSCT and tendon are in turn
encased in a synovialized bursa. Therefore, the flexor
tendons in this region include both intrasynovial and
extrasynovial gliding mechanisms (see Figure 3-3).

27
Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
why tendons may form adhesions, increased friction is
certainly one of the major factors to consider, which
can be ameliorated if an intrasynovial graft is available.
Unfortunately, there are few intrasynovial tendons that
can be sacrificed for the purpose of tendon grafting. The
development of a tissue-engineered intrasynovial graft
is one object of our research.
TENDON LUBRICATION
Lubrication has been the focus of intense study in
articular cartilage, since cartilage degeneration is associ­
ated with mechanical abrasion and wear.32-34 Although
tendon does not bear as much compressive loading as
cartilage, the number of motion cycles experienced by
tendons is comparable to that of joints and was esti­
mated at over 1 million cycles per year.35,36 Therefore,
tendon lubrication is very important, especially for the
intrasynovial tendons in the hand, which experience
the most cyclic motion. Since the gliding structure of
the intrasynovial and extrasynovial tendon structure is
different, the lubrication mechanism is also totally
different.
Intrasynovial Tendon Lubrication Mechanism
As the intrasynovial tendon glides within a synovial fluid
environment, its lubrication mechanism is similar to
the cartilage in the articular joint, which associates two
lubricating phenomena (i.e., boundary lubrication and
fluid-film lubrication). Boundary lubrication mainly
relies on the tendon surface structure. The intrasynovial
tendon surface is covered by a highly resistant, tenacious
epitenon layer acting as a living boundary support load
and avoiding collagen wear. These cells also secrete
lubricants into the synovial fluid. In addition, some of
the secreted lubricants are bound to the intercellular
matrix, and thus remain adherent to the epitendinous
Although the gliding ability of the paratenon is not
as durable as the epitenon, it serves as a cushion and
sliding sleeve to protect the tendons from surrounding
tissues, such as muscle, bone, and neurovascular struc­
tures. It also serves as a network to protect the vessels
and nerves that provide the nutritional supply of
tendons.27
Due to the differences of anatomy and structure
between intrasynovial and extrasynovial tendons, the
frictional force of extrasynovial tendons is much higher
than that of intrasynovial tendons.28,29 Uchiyama et al
found that the frictional force of the palmaris longus
tendon increased with increasing loads. In contrast, the
frictional force of FDP tendon was nearly independent
of the load applied to the tendon (Figure 3-4). Several
studies have demonstrated that the frictional force of
extrasynovial tendons increases rapidly with cyclic
motion,29-31 while intrasynovial tendons maintain a
constant frictional force even after 1000 cycles of tendon
motion (Figure 3-5).
Tendon surface morphology has been studied with
the use of electron microscopy. These studies show that
the intrasynovial tendon surface has a smooth surface,
with no collagen fibrils exposed on the surface. After
cyclic motion, this smooth surface is maintained. In
contrast, the paratenon on the extrasynovial tendon
surface wears off with cyclic motion, exposing increas­
ing amounts of collagen fibrils with increasing number
of motion cycles (Figure 3-6). One could argue that
extrasynovial tendon rarely glides against a pulley, but
this is only true normally. When an extrasynovial tendon
is used as a graft to reconstruct an intrasynovial tendon,
which is a common clinical situation, then the tendon
does glide against a pulley. While there are many reasons
Figure 3-4  The slope of friction versus load for the
extrasynovial tendon (palmaris longus [PL]) was higher than
that for the intrasynovial tendon (FDP). (Data from Uchiyama
S, Amadio PC, Coert JH, et al: Gliding resistance of
extrasynovial and intrasynovial tendons through the A2
pulley, J Bone Joint Surg Am 79:219–224, 1997.)
FDP
PL
Friction force (N)
0
0
4
8
Load (N)
12
16
1.0
2.0
Figure 3-5  The friction of the extrasynovial tendons rises
up rapidly with cyclic motion. The intrasynovial tendon
remains at the same level of frictional force even after 1000
cycles of tendon motion.
Friction (N)
0
0
200
400
600
800
1000
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
Number of cycles
PL tendon
FDP tendon

28
Section 1:  Basic Science
moves, the paratenon layer closest to the tendon starts
to move. This stretches the collagen fibers crosslinking
between the paratenon layers, leading to the next layer’s
subsequent motion. This sequential small motion
among paratenon layers effectively reduces the total
tendon excursion related to the surrounding tissue
surface. The extracellular matrix of the epitenon layer
has similar components and structure as the superficial
zone of the cartilage, including collagen, hyaluronic
acid, proteoglycans, and phospholipids. The structural
collagen in tendon is type I collagen. Hyaluronic acid
(HA) is an important component on the tendon surface.
Proteoglycans bind to HA in the presence of HA binding
protein (Figure 3-7),37,38 forming large highly negatively
harged aggregates. These aggregates imbibe water to
form a highly viscous layer to decrease friction and wear
during tendon motion. The major lubricating proteogly­
can on the tendon surface is lubricin.39,40 Phospholipids,
existing on the cell surface and extracellular matrix, are
also important for lubrication.41,42 These three compo­
nents (i.e., HA, lubricin, and phospholipid) are present
in the synovial fluid as well.
The removal of any of these three lubricating sub­
stances results in increased friction.43 Conversely, exog­
enously applied lubricants on the tendon surface
decrease the frictional force, especially in combination,
and
when
chemically
bound
to
the
tendon
surface.29-31,44
Extrasynovial Tendon Lubrication
In contrast to intrasynovial tendon, the extrasynovial
tendon has no synovial fluid environment. The lubrica­
tion mechanism relies on the paratenon sliding unit.27
The paratenon gliding mechanism of extrasynovial
tendon has been well studied recently, using flexor
tendon in zone 4 as a model.26,45,46 When the tendon
Figure 3-6  The morphological appearances under scanning electron microscopy (SEM) of the intrasynovial tendon
(A, normal tendon before testing; B, after 1000 cycle motion in low magnification; and C, after 1000 cycle motion in high
magnification) display a smooth surface compared to the extrasynovial tendon (D, normal tendon before testing; E, after
1000 cycle motion in low magnification; and F, after 1000 cycle motion in high magnification paratenon on the extrasynovial
tendon surface wears off with collagen exposed under tendon cyclic motion against pulley).
Before testing
A
B
C
D
E
F
After 1000-cycle
After 1000-cycle
FDP tendon
PL tendon
Figure 3-7  Intrasynovial tendon surface structure.
Core protein
Chondroitin
sulfate
Keratan
sulfate
HA
HA–binding
domain
Proteoglycan
Hyaluronic
acid (HA)
Epitenon cell
Collagen
Phospholipids

29
Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
collagen molecules form a microfibril, and groups of
microfibrils assemble a subfibril, which then combine
to form larger fibrils. Fibrils are packed in parallel
bundles with proteoglycans and water to form the fas­
cicles. The numbers of fascicles, which are wrapped by
the endotenon, compose a tendon bundle.48,49 Some
tendons have only one tendon bundle; others have
several. For example, the canine flexor digitorum pro­
fundus tendon in zone 2 has two bundles.50
The tendon stress-strain curve includes three phases:
a toe region, a linear region, and a failure region (Figure
3-9). The toe region is the initial loading phase, in
which a small axial load can reach a large elongation.
and decreases abrasion during tendon motion (Figure
3-8).47 Any pathological changes of the paratenon, such
as fibrosis, could alter this sequential motion pattern,
which in turn may lead to clinical problems. Indeed, a
disruption of this mechanism has been suggested as a
cause of carpal tunnel syndrome.26
BIOMECHANICS OF TENDON MOTION
Flexor tendons cross over multiple joints, including the
wrist, metacarpophalangeal (MCP) joint, proximal
interphalangeal (PIP) joint, and distal interphalangeal
(DIP) joint. Therefore, a large excursion is needed to
achieve full joint motion. Flexor tendons also bear large
tensile loads during forceful hand motion and experi­
ence a huge number of repetitive motion cycles during
routine activities. It is essential therefore to understand
the mechanical properties and motion characteristics of
the flexor tendons.
Mechanical Properties of Tendon
Mechanical properties of tendon are determined by its
basic structure, molecular organization, cellular arrange­
ment, and extracellular crosslinking. The tendon con­
sists of 60% to 80% water in its wet weight. The major
extracellular matrix is type I collagen, which is estimated
to comprise about 80% of the tendon’s dry weight.
Proteoglycans and elastin make up 1% to 5% and 2%
of the dry weight, respectively.48 Collagen’s hierarchical
structure has been well described. The collagen mole­
cule itself is a triple helix of polypeptide chains linked
by covalent and hydrogen bonds. Five crosslinked
Figure 3-8  Extrasynovial tendon gliding mechanism. When a tendon moves from A to B, the paratenon layer that closes to
the tendon moves first and then transmit to the next layer by the connecting collagen fibers shown by the scanning electron
microscopy (SEM) left (relaxed) and right (stretched). This sequential motion of the multi–paratenon-layer motion decreases
the relative motion between tendon and surrounding tissue.
Outer paratenon
displacement
Tendon displacement
Paratenon
Tendon
A
B
Figure 3-9  Tendon mechanical properties can be typically
presented by its stress-strain curve, which includes three
phases: a toe region, a linear region, and a failure region.
Sress (N/ma)
Toe region
Linear region
Failure region
Strain

30
Section 1:  Basic Science
Biomechanics of Tendon Motion
The flexor tendon excursion depends on the range of
joint motion and applied tension.58-60 In the pathologi­
cal condition, there are other factors, such as tendon
adhesions, joint contracture, bone shortening, or pulley
resections, that also affect excursion.61-63 Wehbe et al58
measured tendon excursion radiographically in 36
hands in which the flexor tendons were tagged with
buried wire sutures. The flexor digitorum profundus
tendon excursion averaged 32 mm and the flexor digi­
torum superficialis tendon averaged 24 mm with the
wrist in the neutral position. With wrist range of motion
added, the amplitude of the profundus tendon excur­
sion increased to 50 mm and the superficialis tendon to
49 mm.58
The correlation between tendon excursion and joint
motion has been well studied.64,65 For single joint
motion, the ratio of the joint motion and tendon excur­
sion is determined by the joint moment arm. Since the
moment arm is different for different joints, the relation
of tendon excursion and joint motion is different at
different joints. The larger the moment arm, the greater
the tendon excursion must be to produce a given angle
of joint rotation. For example, at the DIP joint, every 10
degrees of motion requires 1.2 mm of FDP tendon
excursion, while at the MCP joint every 10 degrees of
motion requires 2.2 mm of FDP tendon excursion.59
The tendon excursion also can be mathematically
calculated based on the joint moment arm.61,64,65 The
moment arm is defined as the perpendicular distance
between the joint center rotation and the central longi­
tudinal axis of the tendon (Figure 3-11). To best under­
stand the relationship between tendon excursion, joint
angular motion, and moment arm, the geometric
concept of the radian has been introduced (Figure
3-12).64 The basic concept is that the joint is like a
wheel, and the tendon is like a rope going around the
outer edge of the wheel. As the rope is pulled, the wheel
turns. For one complete rotation of the wheel (360
degrees) the rope must move the full circumference of
the wheel, which is 2πr. The moment arm, or distance
from the center of rotation to the closest point on the
tendon, is also the radius of the circle, or r, which means
that when the joint moves roughly 57.29 degrees
(360/2π), the tendon will have moved a distance equal
to r. This angular rotation, 57.29 degrees, is called a
radian.
The moment arms of the hand joints have been
reported with 12.5 mm at the wrist, 10 mm at the MCP
joint, 7.5 mm at the PIP joint, and 5 mm at the DIP
joint.64,66 Based on the angular motion of the finger
joints (MCP, 85 degrees; PIP, 110 degrees; DIP, 65
degrees), the excursion was calculated as 14.8 mm in
the MCP joint, 14.4 mm in the PIP joint, and 5.7 mm
in the DIP joint (see Figure 3-12). These results indeed
were similar to excursion that was experimentally
This behavior is attributed to the collagen at the molecu­
lar level unfolding from an initial relaxed state. The
linear region demonstrates the fundamental tendon
mechanical properties, in which the tendon elongation
is constant under a given load. The slope of the stress
to strain represents Young’s modulus of elasticity. In
the failure region the collagen crosslinks gradually
break until complete disruption occurs. Since the
tendon is a viscoelastic tissue, the mechanical behavior
of tendon can be also characterized by creep and stress
relaxation. Creep is a time-dependent elongation of the
tendon under a constant load (Figure 3-10A). Stress
relaxation represents the concomitant decrease in load
as the tendon is subjected to a constant elongation
(Figure 3-10B).
In the normal tendon, Young’s modulus ranges from
1200 to 1800 Mpa, the ultimate strength ranges from
50 to 150 MPa, and the ultimate strain to failure ranges
from 9% to 35%.48 However, the true strain is probably
less. The strains noted in publication are measured from
the places where the tendon is gripped. More detailed
studies of strain within the tendon suggest that there is
always some slippage at the grips, and the intratendi­
nous true strain to failure is less.
Tendons are rarely subjected to within 30% of the
tendon ultimate force and stress values, even for the
most vigorous activity.51,52 This high safety factor may
explain why tendon rupture is usually at the muscle–
tendon conjunction or tendon–bone insertion, rather
than within the tendon substance,53,54 unless the tendon
is damaged by disease or trauma.55-57
Figure 3-10  A, Creep is the time-dependent elongation of
the tendon under a constant load. B, Stress relaxation
presents the concomitant decrease in load as the tendon is
subjected to a constant elongation.
Elongation
Load
Elongation
Load
Time (load control)
A
Creep
Constant load
Elongation
Load
Time (displacement control)
B
Constant elongation
Stress
relaxation
Elongation
Load

31
Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
arm, leading to a need for more tendon excursion to
produce a given arc of motion.
The flexor tendon–pulley system elegantly balances
the force generation and tendon movement.66 Tendon
excursion has an upper limit, so moment arms need to
be small to affect the most motion. However, tendons
transmit force, so moment arms should be big to apply
more force. The volar plate–based annular pulleys, A1,
A3, and A5, provide this flexibility, because the moment
arms begin short with the finger extended and then
gradually increase as the finger flexes, and the volar plate
bows away from the joint center of rotation. Using this
concept, many postoperative rehabilitation protocols
have been developed.71,73-76
The tendon motion or excursion can also be affected
by the tendon friction within the flexor sheath. This
effect may not be obvious since the normal frictional
force is very small. We have already discussed some
pathological conditions that cause the friction to
measured using human fingers.58,59 This mathematical
calculation model provides a useful tool for the valida­
tion of in vivo measurement of tendon excursion.67-69
Tendon excursion is also dependent on the force
applied to the tendon. The excursion with active motion
is longer than the excursion with passive motion due to
the difference of the force applied to the tendon.60,70,71
Although joint passive motion can induce a pushing
force from distally towards proximally which is able to
create tendon motion, this passive tendon excursion is
limited by tendon buckling, if the resistance to passive
motion exceeds the passive force applied to the
tendon.71,72 In contrast, active motion not only elimi­
nates this tendon buckling effect but also elongates the
tendon viscoelastically, to create more tendon excursion
even without joint motion. In addition, the active force
on the tendon boosts the bowstring effect, especially
when the joint is in flexion position (Figure 3-13). This
bowstring effect will increase the tendon–joint moment
Figure 3-11  The moment arm is the
perpendicular distance between the joint
center rotation and the central
longitudinal axis of the tendon.
Moment
arm
Figure 3-12  The FDP tendon excursion can be calculated by the joint moment arm and its range of motion based on the
principle that the excursion is equal to moment arm when joints move 57.29 degrees (1 radian).
5 mm
DIP
140° ~ 30 mm
110° ~ 14.4 mm
85° ~ 14.8 mm
65° ~ 5.7 mm
1 Radian = 57.29°
7.5 mm
PIP
10 mm
MP
12.5 mm
Wrist

32
Section 1:  Basic Science
599% for high-friction repair technique, which then
make up 24% and 31% of total work of flexion, res­
pectively.81 External resistance can also dramatically
increases after trauma and surgical procedures due to
soft tissue edema, joint swelling, and pain-induced
antagonist muscle contraction. As the total resistance
increases, more tendon force is needed to move the
finger during active motion. Therefore, the tendon repair
strength has to be strong enough to bear the loading
without gapping or rupture of the tendon during active
motion. With passive motion, however, since the exter­
nal resistance is overcome by the passive manipulation,
motion of the tendon only needs to overcome the inter­
nal resistance between the tendon surface and surround­
ing tissues. However, the force applied to the tendon
with passive motion is also small. Therefore, the fric­
tional force of the repaired tendon becomes an impor­
tant issue if a passive rehabilitation is chosen. A low
frictional repair technique should be considered if a
passive rehabilitation is used clinically.
In summary, tendon friction, lubrication, and the
biomechanics of tendon motion are the fundamental if
a hand surgeon is to understand hand function and
pathological alterations. Normally, the tendon in zone
2 is almost frictionless, because of its unique structure
and effective lubricating surface. However, any patho­
logical disorders that disrupt tendon lubrication could
jeopardize the tendon motion. A better understanding
of the evolution of resistance to finger motion, tendon
strength after repair, and postoperative rehabilitation
will guide future improvement in treatment of these
complex injuries.
increase, potentially hindering tendon motion, such as
trigger finger or tendon repair.7,17,74,77-80
Mechanical resistance to tendon gliding is composed
of external sources of resistance and internal sources of
resistance. The external sources of resistance consists of
joint stiffness, surrounding soft tissue resistance, mass
of the digit, and resistance of antagonist muscles. The
internal resistance includes surface friction between
tendon and sheath, the bulk friction due to the fit of
the tendon within the flexor sheath, and biological
adhesions. The energy expended by internal resistance
in only a small portion (10%) of total work of flexion.
However, the internal resistance after tendon repair
increases 274% for low-friction repair techniques and
Figure 3-13  Moment arm of the PIP joint increases with
the joint flexion due to bowstring effect when a tension (10
Newton) is applied to the FDP tendon.
Moment arm
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technique on adhesion formation after flexor tendon repair
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Crit Care 51:917–921, 2001.
16. Momose T, Amadio PC, Zhao C, et al: Suture techniques with
high breaking strength and low gliding resistance: Experi­
ments in the dog flexor digitorum profundus tendon, Acta
Orthop Scand 72:635–641, 2001.
17. Tanaka T, Amadio PC, Zhao CF, et al: Gliding characteristics
and gap formation for locking and grasping tendon repairs:
A biomechanical study in a human cadaver model, J Hand
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18. Zhao C, Amadio PC, Zobitz ME, et al: Resection of the flexor
digitorum superficialis reduces gliding resistance after zone II
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27:316–321, 2002.
19. Paillard PJ, Amadio PC, Zhao C, et al: Pulley plasty versus
resection of one slip of the flexor digitorum superficialis after
repair of both flexor tendons in zone II: A biomechanical
study, J Bone Joint Surg (Am) 84:2039–2045, 2002.
20. Kutsumi K, Amadio PC, Zhao C, et al: Gliding resistance of
the flexor pollicis longus tendon after repair: Does partial
excision of the oblique pulley affect gliding resistance? Plast
Reconstr Surg 118:1423–1428, 2006.
21. Zhao CF, Amadio PC, Tanaka T, et al: Effect of gap size on
gliding resistance after flexor tendon repair, J Bone Joint Surg
(Am) 86:2482–2488, 2004.
22. Taguchi M, Zhao CF, Zobitz ME, et al: Effect of finger ulnar
deviation on gliding resistance of the flexor digitorum pro­
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Surg (Am) 31:113–117, 2006.
23. Zhao CF, Amadio PC, Berglund L, et al: The A3 pulley, J Hand
Surg (Am) 25:270–276, 2000.
24. Zhao C, Ettema AM, Berglund LJ, et al: Gliding resistance of
flexor tendon associated with carpal tunnel pressure: A bio­
mechanical cadaver study, J Orthop Res 29:58–61, 2011.
25. Lundborg G: Experimental flexor tendon healing without
adhesion formation—A new concept of tendon nutrition and
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8:235–238, 1976.
26. Ettema AM, Zhao C, Amadio PC, et al: Gliding characteristics
of flexor tendon and tenosynovium in carpal tunnel syn­
drome: A pilot study, Clin Anat 20:292–299, 2007.
27. Guimberteau JC, Delage JP, McGrouther DA, et al: The micro­
vacuolar system: how connective tissue sliding works, J Hand
Surg (Eur) 35:614–622, 2010.
28. Uchiyama S, Amadio PC, Coert JH, et al: Gliding resistance
of extrasynovial and intrasynovial tendons through the A2
pulley, J Bone Joint Surg (Am) 79:219–224, 1997.
29. Taguchi M, Zhao CF, Sun YL, et al: The effect of surface treat­
ment using hyaluronic acid and lubricin on the gliding resis­
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(Am) 34:1276–1281, 2009.
30. Momose T, Amadio PC, Sun YL, et al: Surface modification
of extrasynovial tendon by chemically modified hyaluronic
acid coating, J Biomed Mater Res 59:219–224, 2002.
31. Sun YL, Yang C, Amadio PC, et al: Reducing friction by chemi­
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32. Linn FC,Radin EL: Lubrication of animal joints. 3. The effect
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69. Manal K, Cowder JD, Buchanan TS: A hybrid method for
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71. Zhao C, Amadio PC, Momose T, et al: Effect of synergistic
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35
CHAPTER
4 
BIOMECHANICS OF CORE AND
PERIPHERAL TENDON REPAIRS
Jin Bo Tang, MD, and Ren Guo Xie, MD
The end-to-end repair commonly consists of two
parts: (1) core sutures that provide essential strength and
(2) peripheral sutures (also called epitendinous sutures)
that serve to “tidy up” the tendon approximation.
Strength of the repairs relates to the tendons’ resistance
to gapping at the repair site and to complete failure
during tendon movement, which consequently relates
closely to adhesions and ruptures of the tendons. The
essential goal of a surgical repair is to provide the tendon
with strength sufficient to withstand early active tendon
motion postsurgery but offering minimal resistance to
tendon gliding. A surgical repair should also be simple
(or at least uncomplicated) for most surgeons to learn
and to practice. Therefore, understanding the biome­
chanics of tendon repairs is imperative not only to
design and planning of an optimal repair technique but
also to its appropriate application to clinical cases and
to guide postoperative rehabilitation. Surgeons or thera­
pists should also be aware of the mechanical properties
of surgical repairs when establishing postoperative
therapies.
ESSENTIAL MECHANICAL REQUIREMENTS
OF A SURGICAL REPAIR
Forces generated during normal hand action range from
1 to 35 N, except tip pinch, according to in vivo mea­
surements.1 Schuind et al1 measured tendon forces up
to 6 N during passive mobilization of the wrist, up to 9
N during passive mobilization of the fingers, and up to
35 N during active unrestricted finger motion. There­
fore, a surgically repaired tendon should be able to
withstand at least 40 N, with power sufficient to resist
gap formation. The repair should be able to withstand
cyclic loads under both linear and curvilinear load con­
ditions. In vitro laboratory tests have shown that a con­
ventional two-strand core repair plus running peripheral
sutures yields a maximal strength of 20 to 30 N2; this is
lower than forces generated during normal hand actions
and explains why some such repairs are disrupted during
postoperative motion exercise. Studies have shown that
forces necessary to cause failure of four-strand repairs
are around or beyond 40 N3-5; six-strand repairs fail with
loads over 50 to 60 N.6,7
OUTLINE
Surgical sutures with core and epitendinous stitches
are the mainstay of tendon repair. Adequate mechani­
cal strength is essential for a repair to resist gapping
and failure. A repair using conventional two-strand
core sutures is weak; repairs using four- or six-strand
core sutures are stronger. To ensure surgical repair
strength, a sufficient number of strands (four or more)
passing through the repair site, an optimal core suture
purchase (0.7 to 1.2 cm), appropriate suture calibers
(4-0 or 3-0), and optimal size (2 mm) of locking or
grasping anchors are essential. Maintaining a certain
baseline tension on the core suture during surgery
greatly benefits gap resistance. It should be realized
that repair strength decreases considerably as the
finger flexes, and traumatized tendon ends tend to
soften during the first 2 weeks postsurgery, thus reduc­
ing the holding power of the suture. The innately weak
and slow biological healing creates a “no gain” lag
period in tendon strength during the first 3 to 4 weeks
after surgery. We should ensure that the strength of
surgical repairs is greater than the forces generated
during unresisted active finger flexion (1 to 35 N for
a normal adult) plus a certain safety margin.
The gap resistance, ultimate strength, and stiffness of
repaired tendons are the primary parameters that define
the mechanical properties of a surgical repair. To evalu­
ate a surgical repair, the tendon is usually tested under
a single cycle load-to-failure or under cyclic loading;
both generate load-displacement curves. The cycle
numbers at which gapping occurs and the repair com­
pletely fails indicate performance of the repair.
Surgical repairs of the tendon are divided into end-
to-end repairs (for acutely lacerated tendons), repairs of
tendon–bone junctions, and tendon repairs by other
methods (such as interweave repairs for tendon grafting
or transfer). This chapter will be devoted to end-to-end
repairs for primary tendon surgery. These repairs have
received the most attention, and their success is most
dependent on repair mechanics. Strong surgical repair
is the mechanical basis of early tendon mobilization
and a prerequisite for biological healing.

36
Section 1:  Basic Science
mechanical properties of the repairs. Human and porcine
tendons are the most common materials used in in vitro
tests of repair strength,2-5 though tendons from sheep,
rabbits, monkeys, and cows are also reported.7,8 Canine,
rabbit, and chicken are used in in vivo investigations.9-12
CURRENT TENDON REPAIR TECHNIQUES
Techniques currently available are, first, repair with core
and peripheral sutures. Core suture repairs are further
divided according to the number of strands passing
through the repair site: two-strand (conventional) and
multistrand (including four-strand, six-strand, and
eight-strand) repairs.2-8,13,14 Alternatively, suture repairs
can be categorized by type of tendon–suture junctions:
grasping, locking, and mixed grasping-locking repairs.
A repair is often referred to using the type of tendon–
suture junctions and the number of strands (e.g., a
locking four-strand repair). Peripheral sutures include
interrupted, simple running, locking running, cross-
stitch (Silfverskiöld),15 locking cross-stitch (Dona),16
interlocking horizontal mattress (IHM),16 and horizon­
tal mattress (Halsted) sutures.17 Second, repair can be
Clinically, patients are encouraged to start moving
the tendons in the first few days after surgery. Edema of
traumatized tissues (tendons, subcutaneous tissue,
sheath, and pulleys), bulkiness of the tendons, and the
normal healing responses of tissues increase the resis­
tance of the tendons. In the first 1 to 2 weeks, the tendon
ends tend to soften, which decreases their power to hold
the sutures. Therefore, a certain safety margin should be
maintained by increasing the baseline surgical repair
strength. Taking these points into consideration, one
expects a baseline ultimate strength of 40 to 50 N and
the capacity to resist gapping of 20 to 30 N for a surgi­
cally repaired tendon.
HISTORICAL REVIEWS
The main body of information regarding the biome­
chanics of tendon repair was accrued over the past few
decades; the principal contributing research groups are
summarized in Box 4-1. The investigatory topics
included (1) development of new repair methods; (2)
comparisons of existing repairs; (3) factors affecting
strength; and (4) new means to test or to record the
Amadio-Mayo Group: In vitro model: human, canine tendons; in vitro model: canine tendons
Gliding friction of the tendon against sheath and pulley (Uchiyama et al), gapping and resistance of grasping and locking
repairs (Tanaka et al), partial tendon repairs (Zobitz et al), effects of different repairs, knot sizes and locations (Momose
et al), and relation of gap sizes and gliding resistance (Zhao et al).
Gelberman–St Louis Group: In vitro and in vivo models: canine tendons
Significance of gap formation on adhesion and repair failure (Gelberman et al), effects of forces of rehabilitation on the
healing strength (Boyer et al), zone 1 flexor tendon repair including tendon–bone junction (Silva, Dinopoulos, et al), and
development of eight-strand repair (Winster et al).
Manske–St Louis Group: In vitro model: human, canine tendons; in vivo model: canine, chicken tendons
Development of tendon splint repair (Aoki et al), knot locations (Pruitt et al), cyclic loading (Pruitt et al), differences between
grasping and locking loops (Hotokezaka and Manske), effects of area of locking loops, suture sizes, and development of
the modified Pennington locks (Hatanaka and Manske), and tendon strength during early mobilization (Kubuta, et al).
Mass-Chicago Group: In vitro model and in vivo models: human tendons
In situ tendon repair strength in curvilinear test model using cadaveric hands (Komanduri et al), comparison of repair
strength of different techniques (Angeles et al), repair strength during cyclic load (Choueka et al), and partial tendon
repairs (Manning et al)
Tang-Nantong Group: In vitro model: human, porcine tendons; in vivo model: chicken tendons
Development of four- and six-strand repairs (Wang et al), effects of sizes and configurations of locks (Xie et al), core suture
purchase (Cao et al) and oblique or partial tendon cuts (Tan et al), effects of tension direction and tendon curvature
(Tang et al), strength of the healing tendon (Wu et al), and effects of a major pulley on strength (Cao and Tang).
Trumble-Seattle Group: In vitro model: human tendons
In situ test of repair strength in cadaveric hands and cyclic loading (Thurman et al), zone 1 tendon repairs (McCallister
et al), and repair with Fiberwire (Miller et al and Hwang et al).
Wolfe–Yale–New York Group: In vitro model: human tendons
Development of the cruciate repair (McLarney et al), cyclic loading test of locked repairs and gap formation (Barrie et al),
effect of peripheral suture purchase (Merrell et al), and comparisons of four-strand repairs with Teno Fix (Wolfe et al)
Box 4-1 
Groups Contributing to Major Information of Tendon Repair Biomechanics
(Listed in Alphabetic Order of the Leading Investigators)