Delee Drezs Orthopaedic Sports Medicine e Book 5th Edition Ebook PDF

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CONTRIBUTORS
Kathleen C. Abalos, MD Christian N. Anderson, MD Derek P. Axibal, MD

Department of Medicine Orthopaedic Surgeon Department of Orthopedics
Beth Israel Deaconess Medical Center Tennessee Orthopaedic Alliance/The University of Colorado School of Medicine
Boston, Massachusetts Lipscomb Clinic Aurora, Colorado
Nashville, Tennessee
Jeffrey S. Abrams, MD Bernard R. Bach Jr., MD
Clinical Professor Lindsay M. Andras, MD The Claude Lambert-Helen Thompson
School of Graduate Medicine Assistant Professor of Orthopaedic Surgery Professor of Orthopedic Surgery
Seton Hall University Children’s Orthopedic Center Rush University Medical Center
South Orange, New Jersey Children’s Hospital Los Angeles Chicago, Illinois
Clinical Associate Professor Los Angeles, California
Penn Medicine Princeton Medical Center Aaron L. Baggish, MD
Princeton, New Jersey James R. Andrews, MD Director, Cardiovascular Performance
Medical Director Program
Julie E. Adams, MD The Andrews Institute Massachusetts General Hospital
Professor of Orthopedic Surgery Gulf Breeze, Florida Boston, Massachusetts
Mayo Clinic Health System Medical Director
Austin, Minnesota and Rochester, Minnesota The American Sports Medicine Institute Wajeeh Bakhsh, MD
Birmingham, Alabama Surgical Resident, Department of
Bayan Aghdasi, MD Orthopaedics
Orthopaedic Surgery Michael Antonis, DO, RDMS, FACEP, University of Rochester Medical Center
University of Virginia CAQSM Rochester, New York
Charlottesville, Virginia Emergency Medicine & Sports Medicine
Georgetown University Christopher P. Bankhead, MD
Amiethab A. Aiyer, MD Washington, District of Columbia Resident, Orthopaedic Surgery
Assistant Professor, Chief Foot and Ankle University of New Mexico
Service Chad A. Asplund, MD, MPH Albuquerque, New Mexico
Department of Orthopaedics Director, Athletic Medicine
University of Miami, Miller School of Associate Professor, Health and Kinesiology Michael G. Baraga, MD
Medicine Georgia Southern University Assistant Professor of Orthopaedics
Miami, Florida Statesboro, Georgia UHealth Sports Medicine Institute
University of Miami, Miller School of
Nourbakhsh Ali, MD Rachid Assina, MD, RPH Medicine
Spine Surgeon Assistant Professor Miami, Florida
Wellstar Atlanta Medical Center Department of Neurological Surgery
Atlanta, Georgia Rutgers–New Jersey Medical School Jonathan Barlow, MD, MS
Newark, New Jersey Mayo Clinic
David W. Altchek, MD Rochester, Minnesota
Co-Chief Emeritus Ashley V. Austin, MD
Sports Medicine and Shoulder Service Resident Robert W. Battle, MD
Hospital for Special Surgery Family Medicine and Physical Medicine and Team Cardiologist
New York, New York Rehabilitation Associate Professor of Medicine and
University of Virginia Pediatrics
Raj M. Amin, MD Charlottesville, Virginia Department of Cardiology
Resident Physician University of Virginia Medical Center
Department of Orthopaedic Surgery Luke S. Austin, MD Charlottesville, Virginia
The Johns Hopkins Hospital Associate Professor of Orthopaedics
Baltimore, Maryland Rothman Institute Matthew Bessette, MD
Egg Harbor Township, New Jersey Sports Medicine Fellow
Kimberly K. Amrami, MD The Cleveland Clinic Foundation
Professor of Radiology John T. Awowale, MD Cleveland, Ohio
Chair, Division of Musculoskeletal Radiology Orthopedic Surgery
Mayo Clinic University of Wisconsin Hospitals and Thomas M. Best, MD, PhD
Rochester, Minnesota Clinics Professor of Orthopaedics
University of Wisconsin Research Director of Sports Performance
Madison, Wisconsin and Wellness Institute
University of Miami Sports Medicine Institute
Miami, Florida
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CONTRIBUTORS ix
Bruce Beynnon, PhD Stephen F. Brockmeier, MD Jon-Michael E. Caldwell, MD

McClure Professor of Musculoskeletal Associate Professor Resident, Department of Orthopedic
Research Department of Orthopaedic Surgery Surgery
Director of Research Fellowship Director, University of Virginia Columbia University Medical Center
Department of Orthopaedics and Sports Medicine Fellowship New York Presbyterian Hospital
Rehabilitation University of Virginia School of Medicine New York, New York
University of Vermont College of Medicine Charlottesville, Virginia
McClure Musculoskeletal Research Center Mary E. Caldwell, DO
Burlington, Vermont Jeffrey Brunelli, MD Assistant Professor of Physical Medicine and
Assistant Professor of Orthopaedic Surgery Rehabilitation and Sports Medicine
Kieran Bhattacharya, BS and Rehabilitation Medical College of Virginia
Research Assistant Chief, Sports Medicine and Shoulder Virginia Commonwealth University
Department of Orthopaedic Surgery Surgery Richmond, Virginia
University of Virginia University of Florida-Jacksonville College of
Charlottesville, Virginia Medicine Ryan P. Calfee, MD, MSc
Jacksonville, Florida Associate Professor of Orthopedics
Debdut Biswas, MD Washington University School of Medicine
Hinsdale Orthopaedics Jackie Buell, PhD, RD, CSSD, LD, ATC St. Louis, Missouri
Chicago, Illinois Assistant Professor, Clinical Health Sciences
and Medical Dietetics Christopher L. Camp, MD
Matthew H. Blake, MD The Ohio State University Assistant Professor of Orthopedics
Assistant Director, Sports Medicine Columbus, Ohio Mayo Clinic
Orthopaedic Sports Medicine Rochester, Minnesota
Avera McKennan Hospital and University Alissa J. Burge, MD
Health Center Assistant Professor of Radiology John T. Campbell, MD
Sioux Falls, South Dakota Weill Cornell Medicine Attending Orthopaedic Surgeon
New York, New York Institute for Foot and Ankle Reconstruction
Liljiana Bogunovic Mercy Medical Center
Assistant Professor Jessica L. Buschmann, MS, RD, CSSD, Baltimore, Maryland
Department of Orthopaedic Surgery LD
Washington University School of Medicine Clinical Dietician—Board Certified Kevin Caperton, MD
St. Louis, Missouri Specialist in Sports Dietetics Sports Department of Orthopedics and Sports
Medicine Medicine
Margaret Boushell, PhD Nationwide Children’s Hospital Georgetown Orthopedics
Department of Biomedical Engineering Columbus, Ohio Georgetown, Texas
Biomaterials and Interface Tissue
Engineering Laboratory Brian Busconi, MD Robert M. Carlisle, MD
Columbia University Medical Center Associate Professor of Orthopaedic Surgery Resident, Orthopaedic Surgery
New York Presbyterian Hospital Sports Medicine Greenville Health System
New York, New York University of Massachusetts Greenville, South Carolina
Worcester, Massachusetts
James P. Bradley, MD Rebecca A. Cerrato, MD
Clinical Professor Charles A. Bush-Joseph, MD Attending Orthopaedic Surgeon
Orthopaedic Surgery Professor of Orthopaedic Surgery Institute for Foot and Ankle Reconstruction
University of Pittsburgh Medical Center Division of Sports Medicine Baltimore, Maryland
Pittsburgh, Pennsylvania Rush University Medical Center
Chicago, Illinois Courtney Chaaban, PT, DPT, SCS
William Brady, MD, FAAEM, FACEP Doctoral Student
Professor of Medicine and Emergency Kadir Buyukdogan, MD Sports Medicine Research Laboratory
Medicine Department of Orthopaedic Surgery Department of Exercise and Sport Science
University of Virginia University of Virginia University of North Carolina at Chapel Hill
Charlottesville, Virginia Charlottesville, Virginia Chapel Hill, North Carolina
Jonathan T. Bravman, MD E. Lyle Cain Jr., MD Jorge Chahla, MD

Assistant Professor Founding Partner Regenerative Sports Medicine Fellow
Director of Sports Medicine Research Andrews Sports Medicine and Orthopaedic Center for Regenerative Sports Medicine
CU Sports Medicine Center Steadman Philippon Research Institute
Division of Sports Medicine and Shoulder Fellowship Director Vail, Colorado
Surgery American Sports Medicine Institute
University of Colorado Birmingham, Alabama
Denver, Colorado
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x CONTRIBUTORS
Peter N. Chalmers, MD Philip Chuang, PhD Shannon David, PhD, ATC

Assistant Professor Department of Biomedical Engineering Assistant Professor
University of Utah Department of Biomaterials and Interface Tissue Coordinator of Clinical Education
Orthopaedic Surgery Engineering Laboratory North Dakota State University
Salt Lake City, Utah Columbia University Medical Center Fargo, North Dakota
New York Presbyterian Hospital
Angela K. Chang, MD New York, New York Thomas M. DeBerardino, MD
Center for Outcomes-Based Orthopaedic Orthopaedic Surgeon
Research Nicholas J. Clark, MD The Orthopaedic Institute
Steadman Philippon Research Institute Orthopedic Surgeon Medical Director
Vail, Colorado Mayo Clinic Burkhart Research Institute for
Rochester, Minnesota Orthopaedics
Sonia Chaudhry, MD The San Antonio Orthopaedic Group
Assistant Professor of Orthopaedic Surgery John C. Clohisy, MD Co-Director, Combined Baylor College of
University of Connecticut School of Professor of Orthopaedic Surgery Medicine and The San Antonio
Medicine Washington University School of Medicine Orthopaedic Group, Texas Sports
Pediatric Orthopaedic, Hand, and St. Louis, Missouri Medicine Fellowship
Microvascular Surgery Professor of Orthopaedic Surgery
Connecticut Children’s Medical Center Christopher Coleman, MD Baylor College of Medicine
Hartford, Connecticut Department of Radiology San Antonio, Texas
University of Colorado
Austin W. Chen, MD Aurora, Colorado Richard E. Debski, PhD
Hip Preservation and Sports Medicine Professor
BoulderCentre for Orthopedics Francisco Contreras, MD Departments of Bioengineering and
Boulder, Colorado Department of Radiology Orthopaedic Surgery
Academic Faculty Jackson Memorial Hospital University of Pittsburgh
American Hip Institute University of Miami Hospital Pittsburgh, Pennsylvania
Chicago, Illinois Miami, Florida
Marc M. DeHart, MD
Edward C. Cheung, MD Joseph D. Cooper, MD Associate Professor of Orthopaedic Surgery
Resident Physician Resident, Orthopaedic Surgery Chief of Adult Reconstruction
Orthopaedic Surgery University of Southern California UT Health San Antonio
University of California, Los Angeles Los Angeles, California San Antonio, Texas
Medical Center
Los Angeles, California Chris A. Cornett, MD, MPT Arthur Jason De Luigi, DO, MHSA
Associate Professor of Orthopaedic Surgery Professor of Rehabilitation Medicine and
A. Bobby Chhabra, MD University of Nebraska Medical Center Sports Medicine
Lillian T. Pratt Distinguished Professor and Department of Orthopaedic Surgery and Georgetown University School of Medicine
Chair Rehabilitation Washington, District of Columbia
Orthopaedic Surgery Medical Director Physical/Occupational
University of Virginia Health System Therapy Elizabeth R. Dennis, MD, MS
Charlottesville, Virginia Co-Medical Director, Spine Program Resident, Department of Orthopedic
Nebraska Medicine Surgery
Woojin Cho, MD, PhD Omaha, Nebraska Columbia University Medical Center
Assistant Professor, Orthopaedic Surgery New York Presbyterian Hospital
Albert Einstein College of Medicine Paul S. Corotto, MD New York, New York
Chief of Spine Surgery Chief Fellow
Orthopaedic Surgery Department of Cardiology John J. Densmore, MD, PhD
Research Director University of Virginia Medical Center Associate Professor of Clinical Medicine
Multidisciplinary Spine Center Charlottesville, Virginia Division of Hematology/Oncology
Montefiore Medical Center University of Virginia
New York, New York Ryan P. Coughlin, MD, FRCSC Charlottesville, Virginia
Department of Orthopaedic Surgery
Joseph N. Chorley, MD Duke University Joshua S. Dines, MD
Associate Professor of Pediatrics Durham, North Carolina Sports Medicine and Shoulder Service
Baylor College of Medicine Hospital for Special Surgery
Houston, Texas Jared A. Crasto, MD New York, New York
Resident, Department of Orthopaedic
John Jared Christophel, MD, MPH Surgery Benjamin G. Domb, MD
Assistant Professor of Otolaryngology— University of Pittsburgh Medical Center Founder
Head and Neck Surgery Pittsburgh, Pennsylvania American Hip Institute
University of Virginia Chicago, Illinois
Charlottesville, Virginia
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CONTRIBUTORS xi
Jason Dragoo, MD Anthony Essilfie, MD J. Craig Garrison, PhD, PT, ATC, SCS
Associate Professor of Orthopaedic Surgery Resident Physician Director, Sports Medicine Research
Stanford University Orthopaedic Surgery Texas Health Sports Medicine
Stanford, California University of Southern California Texas Health
Los Angeles, California Fort Worth, Texas
Jeffrey R. Dugas, MD
Surgeon Jack Farr, MD R. Glenn Gaston, MD
Andrews Sports Medicine and Orthopaedic Professor of Orthopedics Hand and Upper Extremity Surgeon
Center Indiana University School of Medicine OrthoCarolina
American Sports Medicine Institute OrthoIndy Knee Preservation and Cartilage Chief of Hand Surgery
Birmingham, Alabama Restoration Center Division of Orthopedics
Indianapolis, Indiana Carolinas Medical Center
Guillaume D. Dumont, MD Charlotte, North Carolina
Assistant Professor of Orthopaedic Surgery Derek M. Fine, MD
University of South Carolina School of Associate Professor of Medicine William B. Geissler, MD
Medicine Fellowship Director Alan E. Freeland Chair of Hand Surgery
Columbia, South Carolina Division of Nephrology Professor and Chief
The Johns Hopkins University School of Division of Hand and Upper Extremity
Eric W. Edmonds, MD Medicine Surgery
Associate Professor of Clinical Orthopedic Baltimore, Maryland Chief, Arthroscopic Surgery and Sports
Surgery Medicine
University of California, San Diego Jake A. Fox, BS Department of Orthopaedic Surgery and
Director of Orthopedic Research and Sports Research Assistant Rehabilitation
Medicine Center for Outcomes-Based Orthopaedic University of Mississippi Health Care
Division of Orthopedic Surgery Research Jackson, Mississippi
Rady Children’s Hospital San Diego Steadman Philippon Research Institute
San Diego, California Vail, Colorado Brandee Gentile, MS, ATC
Athletic Trainer
Karen P. Egan, PhD Salvatore Frangiamore, MD, MS Department of Neurosurgery
Associate Sport Psychologist Summa Health Orthopaedic and Sports Rutgers–New Jersey Medical School
Department of Athletics Medicine Newark, New Jersey
University of Virginia Akron, Ohio
Charlottesville, Virginia J. Robert Giffin, MD, FRCSC, MBA
Rachel M. Frank, MD Professor of Orthopedic Surgery
Bassem T. Elhassan, MD Department of Orthopaedic Surgery Western University
Orthopedic Surgeon Rush University London, Ontario, Canada
Mayo Clinic Chicago, Illinois
Rochester, Minnesota Todd M. Gilbert, MD
Heather Freeman, PT, DHS Department of Orthopaedic Surgery and
Claire D. Eliasberg, MD Physical Therapist Rehabilitation
Resident, Orthopaedic Surgery Assistant Research Coordinator University of Nebraska Medical Center
Hospital for Special Surgery University of Indianapolis, Krannert School Omaha, Nebraska
New York, New York of Physical Therapy
Indianapolis, Indiana G. Keith Gill, MD
Fatih Ertem, MSc Department of Orthopaedics
Department of Biomechanics Jason Freeman, PhD University of New Mexico Health Sciences
Dokuz Eylul University Health Science Sport Psychologist Center
Institute Department of Athletics Albuquerque, New Mexico
Inciralti, Izmir, Turkey University of Virginia
Visiting Graduate Researcher Charlottesville, Virginia Thomas J. Gill, MD
Department of Orthopaedics and Professor of Orthopedic Surgery
Rehabilitation Nikhita Gadi, MD, MScBR Tufts Medical School
McClure Musculoskeletal Research Center Internal Medicine Resident, PGY-1 Chairman, Department of Orthopedic
Burlington, Vermont Hackensack University Medical Center Surgery
Hackensack, New Jersey St. Elizabeth’s Medical Center/Steward
Norman Espinosa Jr., MD Healthcare Network
Head of Foot and Ankle Surgery Seth C. Gamradt, MD Boston, Massachusetts
Institute for Foot and Ankle Reconstruction Associate Clinical Professor
FussInsitut Zurich Director of Orthopaedic Athletic Medicine Jacob D. Gire, MD
Zurich, Switzerland Orthopaedic Surgery Department of Orthopaedic Surgery
University of Southern California Stanford University
Los Angeles, California Palo Alto, California
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xii CONTRIBUTORS
Pau Golanó, MD Letha Y. Griffin, MD, PhD Hamid Hassanzadeh, MD

Professor of Human Anatomy Team Physician Assistant Professor
Laboratory of Arthroscopic and Surgical Georgia State University Department of Orthopaedic Surgery
Anatomy Atlanta, Georgia University of Virginia
Human Anatomy and Embryology Unit Staff Charlottesville, Virginia
Department of Pathology and Experimental Peachtree Orthopedics
Therapeutics Atlanta, Georgia Michael R. Hausman, MD
University of Barcelona–Spain Professor of Orthopaedic Surgery
Department of Orthopaedic Surgery Warren C. Hammert, MD Mount Sinai Medical Center
University of Pittsburgh School of Medicine Professor of Orthopaedic Surgery and New York, New York
Pittsburgh, Pennsylvania Plastic Surgery
Chief, Hand Surgery Stefan Hemmings, MBBS
Jorge E. Gómez, MD, MS Department of Orthopaedics and Post-Doctorate Fellow
Associate Professor of Adolescent Medicine Rehabilitation Division of Nephrology
and Sports Medicine University of Rochester Medical Center The Johns Hopkins University School of
Baylor College of Medicine Rochester, New York Medicine
Houston, Texas Baltimore, Maryland
Kyle E. Hammond, MD
Juan Gomez-Hoyos, MD Assistant Professor, Department of R. Frank Henn III, MD
Baylor University Medical Center at Dallas Orthopaedic Surgery Associate Professor of Orthopaedics
Hip Preservation Center Emory Sports Medicine Center University of Maryland School of Medicine
Dallas, Texas Atlanta, Georgia Baltimore, Maryland
Howard P. Goodkin, MD, PhD Joseph Hannon, PhD, PT, DPT, SCS, Daniel Herman, MD, PhD
The Shure Professor of Pediatric Neurology CSCS Assistant Professor
Director Research Physical Therapist Department of Orthopedics and Rehabilitation
Division of Pediatric Neurology Texas Health Sports Medicine Divisions of Physical Medicine and
Departments of Neurology and Pediatrics Texas Health Rehabilitation, Sports Medicine, and
University of Virginia Fort Worth, Texas Research
Charlottesville, Virginia University of Florida
Colin B. Harris, MD Gainesville, Florida
Gregory Grabowski, MD, FAOA Assistant Professor
Associate Professor Department of Orthopaedics Jay Hertel, PhD, ATC, FNATA
University of South Carolina School of Rutgers–New Jersey Medical School Joe H. Gieck Professor of Sports Medicine
Medicine Newark, New Jersey Departments of Kinesiology and
Department of Orthopedic Surgery Orthopaedic Surgery
Co-Medical Director Joshua D. Harris, MD University of Virginia
Palmetto Health USC Spine Center Orthopedic Surgeon Charlottesville, Virginia
Residency Program Director Associate Professor, Institute for Academic
Palmetto Health USC Orthopedic Center Medicine Daniel E. Hess, MD
Columbia, South Carolina Houston Methodist Orthopedics and Sports Department of Orthopaedic Surgery
Medicine University of Virginia
Tinker Gray, MA Houston, Texas Charlottesville, Virginia
The Shelbourne Knee Center at Community Assistant Professor of Clinical Orthopedic
East Hospital Surgery Carolyn M. Hettrich, MD
Indianapolis, Indiana Weill Cornell Medical College University of Iowa
New York, New York Iowa City, Iowa
James R. Gregory, MD
Assistant Professor of Pediatric Orthopedic Andrew Haskell, MD Benton E. Heyworth, MD
Surgery Chair, Department of Orthopedics Assistant Professor of Orthopedic Surgery
Department of Orthopedic Surgery Geographic Medical Director for Surgical Harvard Medical School
University of Oklahoma College of Services Attending Orthopedic Surgeon
Medicine Palo Alto Medical Foundation Department of Orthopedic Surgery
Oklahoma City, Oklahoma Palo Alto, California Division of Sports Medicine
Associate Clinical Professor Boston Children’s Hospital
Phillip Gribble, PhD Department of Orthopaedic Surgery Boston, Massachusetts
Professor of Rehabilitation Sciences University of California, San Francisco
University of Kentucky San Francisco, California
Lexington, Kentucky
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CONTRIBUTORS xiii
Ben Hickey, BM, MRCS, MSc, FRCS (Tr John V. Ingari, MD Robin N. Kamal, MD
& Orth), MD Division Chair, Hand Surgery Assistant Professor of Orthopaedic Surgery
Consultant Orthopaedic Foot and Ankle Department of Orthopaedic Surgery Chase Hand and Upper Limb Center
Surgeon The Johns Hopkins Hospital Stanford University
Wrexham Maelor Hospital Baltimore, Maryland Palo Alto, California
Wrexham, Wales, United Kingdom
Mary Lloyd Ireland, MD Thomas Kaminski, PhD, ATC, FNATA
Michael Higgins, PhD, ATC, PT, CSCS Professor Professor of Kinesiology and Applied
Professor, Kinesiology Department of Orthopaedics Physiology
University of Virginia University of Kentucky University of Delaware
Charlottesville, Virginia Lexington, Kentucky Newark, Delaware
Betina B. Hinckel, MD, PhD Todd A. Irwin, MD Abdurrahman Kandil, MD

Department of Orthopaedic Surgery Director of Research Stanford University
Brigham and Women’s Hospital OrthoCarolina Foot and Ankle Institute Stanford, California
Harvard Medical School Associate Professor
Boston, Massachusetts Carolinas Medical Center Jonathan R. Kaplan, MD
Charlotte, North Carolina Attending Orthopaedic Surgeon
Gwendolyn Hoben, MD, PhD Orthopaedic Specialty Institute
Instructor Nona M. Jiang, MD Orange, California
Plastic and Reconstructive Surgery Department of Medicine
Medical College of Wisconsin University of Virginia Christopher A. Keen, MD
Milwaukee, Wisconsin Charlottesville, Virginia Citrus Orthopedic and Joint Institute
Lecanto, Florida
Christopher Hogrefe, MD, FACEP Darren L. Johnson, MD
Assistant Professor Director of Sports Medicine Mick P. Kelly, MD
Departments of Emergency Medicine, University of Kentucky Resident, Department of Orthopaedic
Medicine—Sports Medicine, and Lexington, Kentucky Surgery
Orthopaedic Surgery—Sports Medicine Rush University Medical Center
Northwestern Medicine Jared S. Johnson, MD Chicago, Illinois
Northwestern University Feinberg School of St. Luke’s Clinic–Sports Medicine: Boise
Medicine Boise, Idaho A. Jay Khanna, MD, MBA
Chicago, Illinois Professor and Vice Chair of Orthopaedic
Grant L. Jones, MD Surgery
Jason A. Horowitz, BA Associate Professor of Orthopaedic Surgery Department of Orthopaedic Surgery
Research Fellow The Ohio State University The Johns Hopkins University School of
Department of Orthopaedic Surgery Columbus, Ohio Medicine
University of Virginia Baltimore, Maryland
Charlottesville, Virginia Jean Jose, DO, MS
Associate Chief of Musculoskeletal Anthony Nicholas Khoury
Benjamin M. Howe, MD Radiology Baylor University Medical Center at Dallas
Associate Professor of Radiology Associate Professor of Clinical Radiology Hip Preservation Center
Mayo Clinic Division of Diagnostic Radiology University of Texas at Arlington
Rochester, Minnesota University of Miami Hospital Bioengineering Department
Miami, Florida Dallas, Texas
Korin Hudson, MD, FACEP, CAQSM
Associate Professor of Emergency Medicine Scott G. Kaar, MD Christopher Kim, MD
Team Physician, Department of Athletics Associate Professor of Orthopaedic Surgery Instructor of Orthopaedic Surgery
Georgetown University Saint Louis University Saint Louis University
Washington, District of Columbia St. Louis, Missouri St. Louis, Missouri
Catherine Hui, MD, FRCSC Anish R. Kadakia, MD Lucas R. King, MD, BS

Associate Clinical Professor Associate Professor of Orthopaedic Surgery Sports Orthopedic Surgeon
Division of Orthopaedic Surgery Northwestern Memorial Hospital Department of Orthopedic Surgery
University of Alberta Northwestern University Feinberg School of Parkview Medical Center
Edmonton, Alberta, Canada Medicine Pueblo, Colorado
Chicago, Illinois
R. Tyler Huish, DO
First Choice Physician Partners Samantha L. Kallenbach, BS
La Quinta, California Steadman Philippon Research Institute
The Steadman Clinic
Vail, Colorado
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xiv CONTRIBUTORS
Susan E. Kirk, MD Marshall A. Kuremsky, MD Peter Lawrence, MD

Associate Professor of Internal Medicine Orthopaedic Surgeon Wiley Barker Professor of Surgery
and Obstetrics and Gynecology Hand and Upper Extremity Surgeon Chief, Division of Vascular and
Division of Endocrinology and Metabolism, Sports Medicine and Arthroscopic Surgeon Endovascular Surgery
Maternal–Fetal Medicine EmergeOrtho University of California, Los Angeles
Associate Dean, Graduate Medical Raleigh, North Carolina Los Angeles, California
Education
University of Virginia Health System Shawn M. Kutnik, MD Adrian D.K. Le, MD
Charlottesville, Virginia Orthopedic Surgeon Department of Orthopedic Surgery
Archway Orthopedics and Hand Surgery Stanford University
Georg Klammer, MD St. Louis, Missouri Stanford, California
Consultant
Institute for Foot and Ankle Reconstruction Michael S. Laidlaw, MD Nicholas LeCursi, CO
FussInsitut Zurich Department of Orthopaedic Surgery Certified Orthotist
Zurich, Switzerland University of Virginia Vice President, Services
Charlottesville, Virginia Chief Technology Officer
Derrick M. Knapik, MD Becker Orthopedic
Orthopaedic Surgery Joseph D. Lamplot Troy, Michigan
University Hospitals Chief Resident
Cleveland Medical Center Department of Orthopaedic Surgery Sonya B. Levine, BA
Cleveland, Ohio Washington University School of Medicine Department of Orthopedic Surgery
St. Louis, Missouri Columbia University Medical Center
Lee M. Kneer, MD, CAQSM New York Presbyterian Hospital
Assistant Professor, Department of Drew Lansdown, MD New York, New York
Orthopaedic Surgery Section of Young Adult Hip Surgery
Assistant Professor, Department of Physical Division of Sports Medicine William N. Levine, MD, FAOA
Medicine and Rehabilitation Department of Orthopedic Surgery Frank E. Stinchfield Professor and
Emory Sports Medicine Center Rush Medical College Chairman of Orthopedic Surgery
Atlanta, Georgia Rush University Medical Center Columbia University Medical Center
Chicago, Illinois New York Presbyterian Hospital
Mininder S. Kocher, MD, MPH New York, New York
Professor of Orthopaedic Surgery Matthew D. LaPrade, BS
Harvard Medical School Steadman Philippon Research Institute Xudong Joshua Li, MD, PhD
Associate Director The Steadman Clinic Associate Professor of Orthopaedic Surgery
Division of Sports Medicine Vail, Colorado and Biomedical Engineering
Department of Orthopaedic Surgery University of Virginia
Boston Children’s Hospital Robert F. LaPrade, MD, PhD Charlottesville, Virginia
Boston, Massachusetts Chief Medical Research Officer
Steadman Philippon Research Institute Gregory T. Lichtman, DO
Gabrielle P. Konin, MD The Steadman Clinic Department of Orthopedic Surgery
Assistant Professor of Radiology Vail, Colorado Rowan University School of Osteopathic
Weill Cornell Medicine Medicine
New York, New York Christopher M. Larson, MD Stratford, New Jersey
Minnesota Orthopedic Sports Medicine
Matthew J. Kraeutler, MD Institute Christopher A. Looze, MD
Department of Orthopaedic Surgery Twin Cities Orthopedics Orthopaedic Surgeon
Seton Hall-Hackensack Meridian School of Edina, Minnesota MedStar Franklin Square
Medicine Baltimore, Maryland
South Orange, New Jersey Evan P. Larson, MD
University of Nebraska Medical Center Gary M. Lourie, MD
Alexander B. Kreines, DO Department of Orthopaedic Surgery and Hand Surgeon
Resident, Orthopaedic Surgery Rehabilitation The Hand and Upper Extremity Center of
Rowan University Omaha, Nebraska Georgia
Stratford, New Jersey Atlanta, Georgia
Samuel J. Laurencin, MD, PhD
Vignesh Prasad Krishnamoorthy, MD Department of Orthopaedic Surgery Helen H. Lu, PhD
Section of Young Adult Hip Surgery University of Connecticut School of Professor of Biomedical Engineering
Division of Sports Medicine Medicine Vice Chair, Department of Biomedical
Department of Orthopedic Surgery Farmington, Connecticut Engineering
Rush Medical College Columbia University Medical Center
Rush University Medical Center New York Presbyterian Hospital
Chicago, Illinois New York, New York
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CONTRIBUTORS xv
Timothy J. Luchetti, MD Scott D. Martin, MD Heather Menzer, MD

Resident, Orthopedic Surgery Director, MGH Joint Preservation Service Fellow, Orthopaedic Surgery
Rush University Medical Center Director, Harvard/MGH Sports Medicine University of Virginia
Chicago, Illinois Fellowship Program Charlottesville, Virginia
Associate Professor of Orthopaedic Surgery
Jessica A. Lundgren, MD Harvard Medical School Sean J. Meredith, MD
Lecturer Department of Orthopaedic Surgery Resident Physician
Department of Internal Medicine Massachusetts General Hospital Department of Orthopaedics
Division of Endocrinology and Metabolism Boston, Massachusetts University of Maryland School of Medicine
University of Virginia Health System Baltimore, Maryland
Charlottesville, Virginia Rebecca Martinie, MD
Assistant Professor of Pediatrics Dayne T. Mickelson, MD
Travis G. Maak, MD Baylor College of Medicine Department of Orthopaedic Surgery
Associate Professor of Orthopaedic Surgery Houston, Texas Duke University
University of Utah Durham, North Carolina
Salt Lake City, Utah Lyndon Mason, MB BCh, MRCS (Eng),
FRCS (Tr & Orth) Michael R. Mijares, MD
John M. MacKnight, MD Trauma and Orthopaedic Consultant Department of Orthopaedics
Professor of Internal Medicine and Aintree University Hospital Jackson Memorial Hospital
Orthopaedic Surgery Liverpool, England, United Kingdom Jackson Health System
Team Physician and Medical Director Miami, Florida
UVA Sports Medicine Augustus D. Mazzocca, MD
University of Virginia Health System Department of Orthopaedic Surgery Matthew D. Milewski, MD
Charlottesville, Virginia University of Connecticut School of Assistant Professor
Medicine Division of Sports Medicine
Nancy Major, MD Farmington, Connecticut Department of Orthopaedic Surgery
Department of Radiology Boston Children’s Hospital
University of Colorado School of Medicine David R. McAllister, MD Boston, Massachusetts
Aurora, Colorado Chief, Sports Medicine Service
Professor and Vice Chair Mark D. Miller, MD
Francesc Malagelada, MD Department of Orthopaedic Surgery S. Ward Casscells Professor of Orthopaedic
Foot and Ankle Unit David Geffen School of Medicine Surgery
Department of Trauma and Orthopaedic University of California, Los Angeles Head, Division of Sports Medicine
Surgery Los Angeles, California University of Virginia
Royal London Hospital Charlottesville, Virginia
Barts Health National Health Service Trust Meagan McCarthy, MD Adjunctive Clinical Professor and Team
London, England, United Kingdom Fellowship Trained Orthopaedic Sports Physician
Medicine Surgeon James Madison University
Michael A. Marchetti, MD Reno Orthopaedic Clinic Harrisonburg, Virginia
Assistant Attending, Dermatology Service Reno, Nevada
Department of Medicine Dilaawar J. Mistry, MD
Memorial Sloan Kettering Cancer Center Eric C. McCarty, MD Team Physician
New York, New York Chief, Sports Medicine and Shoulder Primary Care Sports Medicine
Surgery Western Orthopedics and Sports Medicine
Patrick G. Marinello, MD Associate Professor Grand Junction, Colorado
Hand and Upper Extremity Surgeon Department of Orthopaedics
Capital Region Orthopaedic Group University of Colorado School of Medicine Erik Mitchell, DO
Bone and Joint Center Director Sports Medicine, Head Team Valley Health Orthopaedics Front Royal
Albany, New York Physician Front Royal, Virginia
University of Colorado Department of
Hal David Martin, DO Athletics Andrew Molloy, MBChB, MRCS
Medical Director Associate Professor, Adjunct Consultant Orthopaedic Surgeon
Baylor University Medical Center at Dallas Department of Integrative Physiology Trauma and Orthopaedics
Hip Preservation Center University of Colorado University Hospital Aintree
Dallas, Texas Boulder, Colorado Honorary Clinical Senior Lecturer
Department of Musculoskeletal Biology
Sean McMillan, DO University of Liverpool
Chief of Orthopedics Consultant Orthopaedic Surgeon
Director of Orthopedic Sports Medicine Spire Liverpool
and Arthroscopy Liverpool, England, United Kingdom
Lourdes Medical Associates
Lourdes Medical Center at Burlington
Burlington, New Jersey
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xvi CONTRIBUTORS
Timothy S. Mologne, MD Carl W. Nissen, MD Evan Peck, MD

Sports Medicine Center Professor Section of Sports Health
Appleton, Wisconsin Department of Orthopaedics Department of Orthopaedic Surgery
University of Connecticut Cleveland Clinic Florida
Scott R. Montgomery, MD Elite Sports Medicine Weston, Florida
Franciscan Orthopedic Associates at St. Joseph Connecticut Children’s Medical Center Affiliate Assistant Professor of Clinical
Tacoma, Washington Farmington, Connecticut Biomedical Science
Charles E. Schmidt College of Medicine
Amy M. Moore, MD, FACS Blake R. Obrock, DO Florida Atlantic University
Associate Professor of Surgery Sports Medicine Fellow Boca Raton, Florida
Plastic and Reconstructive Surgery Department of Orthopaedics
Washington University School of Medicine University of New Mexico Liam Peebles, BA
St. Louis, Missouri Albuquerque, New Mexico Research Assistant
Center for Outcomes-Based Orthopaedic
Claude T. Moorman III, MD James Onate, PhD, ATC, FNATA Research
Professor of Orthopaedic Surgery Associate Professor Steadman Philippon Research Institute
Duke Center for Integrated Medicine School of Health and Rehabilitation Vail, Colorado
Durham, North Carolina Sciences
The Ohio State University Andrew T. Pennock, MD
Gina M. Mosich, MD Columbus, Ohio Associate Clinical Professor
Resident Physician Orthopedic Surgery
Orthopaedic Surgery Scott I. Otallah, MD University of California, San Diego
University of California, Los Angeles Carilion Children’s Pediatric Neurology San Diego, California
Los Angeles, California Roanoke, Virginia
Anthony Perera, MBChB, MRCS,
Michael R. Moynagh, MBBCh Brett D. Owens, MD MFSEM, PGDip Med Law, FRCS (Tr &
Assistant Professor of Radiology Professor of Orthopedics Orth)
Mayo Clinic Brown Alpert Medical School Consultant, Orthopaedic Foot and Ankle
Rochester, Minnesota Providence, Rhode Island Surgeon
University Hospital of Wales
Andrew C. Mundy, MD Gabrielle M. Paci, MD Cardiff, Wales, United Kingdom
Department of Orthopaedic Surgery Physician
The Ohio State University Orthopaedic Surgery Jose Perez, BS
Columbus, Ohio Stanford University Research Fellow
Palo Alto, California Department of Orthopedics
Colin P. Murphy, BA Sports Medicine
Research Assistant Richard D. Parker, MD Miami, Florida
Center for Outcomes-Based Orthopaedic Department of Orthopaedic Surgery
Research The Cleveland Clinic Foundation William A. Petri Jr., MD, PhD
Steadman Philippon Research Institute Cleveland, Ohio Chief, Division of Infectious Disease and
Vail, Colorado International Health
Jonathan P. Parsons, MD Wade Hampton Frost Professor of
Volker Musahl, MD Professor of Internal Medicine Epidemiology
Assistant Professor Department of Pulmonary, Critical Care, University of Virginia
Department of Orthopaedic Surgery and Sleep Medicine Charlottesville, Virginia
University of Pittsburgh Medical Center Wexner Medical Center
Pittsburgh, Pennsylvania The Ohio State University Frank A. Petrigliano, MD
Columbus, Ohio Assistant Professor of Orthopaedic Surgery
Jeffrey J. Nepple, MD David Geffen School of Medicine
Assistant Professor of Orthopaedic Surgery Neel K. Patel, MD University of California, Los Angeles
Director Department of Orthopaedic Surgery Los Angeles, California
Young Athlete Center University of Pittsburgh Medical Center
Washington University School of Medicine Pittsburgh, Pennsylvania Adam M. Pickett, MD
St. Louis, Missouri Faculty, West Point Sports Medicine
Thierry Pauyo, MD Fellowship
Shane J. Nho, MD, MS Fellow Department of Orthopaedic Surgery
Assistant Professor Department of Orthopaedic Surgery United States Military Academy
Head, Section of Young Adult Hip Surgery University of Pittsburgh Medical Center West Point, New York
Division of Sports Medicine Pittsburgh, Pennsylvania
Department of Orthopedic Surgery
Rush Medical College
Rush University Medical Center
Chicago, Illinois
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CONTRIBUTORS xvii
Matthew A. Posner, MD Eliott P. Robinson, MD Susan Saliba, PhD, ATC, MPT

Director, West Point Sports Medicine Orthopedic Surgeon Professor, Kinesiology
Fellowship OrthoGeorgia Orthopaedic Specialists University of Virginia
Department of Orthopaedic Surgery Macon, Georgia Charlottesville, Virginia
United States Military Academy
West Point, New York Scott A. Rodeo, MD Adil Samad, MD
Professor of Orthopaedic Surgery Florida Orthopaedic Institute
Tricia R. Prokop, PT, EdD, MS, CSCS Weill Cornell Medical College Tampa, Florida
Assistant Professor of Physical Therapy Co-Chief Emeritus, Sports Medicine and
Department of Rehabilitation Sciences Shoulder Service Anthony Sanchez, BS
University of Hartford Attending Orthopaedic Surgeon Medical Doctor Candidate
West Hartford, Connecticut Hospital for Special Surgery Oregon Health and Science University
New York, New York Portland, Oregon
Matthew T. Provencher, MD, CAPT, MC,
USNR Anthony A. Romeo, MD Laura W. Scordino, MD
Professor of Surgery and Orthopaedics Department of Orthopaedic Surgery Orthopaedic Surgeon
Uniformed Services University of the Health Rush University OrthoNY
Services Chicago, Illinois Albany, New York
Complex Shoulder, Knee, and Sports
Surgeon Kyle Rosen, MD Virgil P. Secasanu, MD
The Steadman Clinic Dartmouth College Clinical Instructor, Housestaff
Vail, Colorado Hanover, New Hampshire Department of Pulmonary, Critical Care,
and Sleep Medicine
Rabia Qureshi, MD William H. Rossy, MD Wexner Medical Center
Research Fellow Clinical Associate Professor The Ohio State University
Department of Orthopedic Surgery Penn Medicine Princeton Medical Center Columbus, Ohio
University of Virginia Princeton, New Jersey
Charlottesville, Virginia Terrance Sgroi, PT
Paul Rothenberg, MD Sports Medicine and Shoulder Service
Fred Reifsteck, MD Resident Physician Hospital for Special Surgery
Head Team Physician Department of Orthopaedics New York, New York
University Health Center University of Miami
University of Georgia Miami, Florida Jason T. Shearn, MD
Athens, Georgia Associate Professor
Todd A. Rubin, MD Department of Biomedical Engineering
David R. Richardson, MD Orthopaedic Surgeon University of Cincinnati
Associate Professor of Orthopaedic Surgery Hughston Clinic Orthopaedics Cincinnati, Ohio
University of Tennessee–Campbell Clinic Nashville, Tennessee
Memphis, Tennessee K. Donald Shelbourne, MD
Robert D. Russell, MD The Shelbourne Knee Center at Community
Dustin Richter, MD Orthopaedic Surgeon East Hospital
Assistant Professor, Sports Medicine OrthoTexas Indianapolis, Indiana
Sports Medicine Fellowship Assistant Frisco, Texas
Director Seth L. Sherman, MD
Director of Orthopaedics Sports Medicine David A. Rush, MD Department of Orthopaedic Surgery
Research Department of Orthopaedic Surgery and University of Missouri, Columbia
University of New Mexico Rehabilitation Columbia, Missouri
Albuquerque, New Mexico University of Mississippi Medical Center
Jackson, Mississippi Ashley Matthews Shilling, MD
Andrew J. Riff, MD Associate Professor of Anesthesiology
Assistant Professor of Clinical Orthopaedic Joseph J. Ruzbarsky, MD University of Virginia Medical Center
Surgery Resident, Orthopedic Surgery Charlottesville, Virginia
Indiana University Health Orthopedics and Department of Orthopaedics
Sports Medicine Hospital for Special Surgery Adam L. Shimer, MD
Indianapolis, Indiana New York, New York Assistant Professor of Orthopaedic Surgery
University of Virginia
Christopher J. Roach, MD Marc Safran, MD Charlottesville, Virginia
Chairman, Orthopaedic Surgery Professor of Orthopedic Surgery
San Antonio Military Medical Center Associate Director Anuj Singla, MD
San Antonio, Texas Department of Sports Medicine Instructor, Orthopaedics
Stanford University University of Virginia
Redwood City, California Charlottesville, Virginia
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xviii CONTRIBUTORS
David L. Skaggs, MD, MMM Eric Swanton, MBChB, FRACS (Orth) Jason Thompson, MD
Professor of Orthopaedic Surgery Orthopaedic Consultant Orthopedic Surgery Resident, UT Health
Keck School of Medicine of USC Department of Orthopaedics San Antonio
University of Southern California North Shore Hospital, Waitemata District Adult Reconstructive Surgery Fellow
Chief, Orthopaedic Surgery Health Board University of Western Ontario
Children’s Hospital Los Angeles Auckland, New Zealand London Health Sciences Centre
Los Angeles, California London, Ontario, Canada
Matthew A. Tao, MD
Mia Smucny, MD Assistant Professor Stephen R. Thompson, MD, MEd,
University of Washington Orthopaedic Surgery FRCSC
Seattle, Washington University of Nebraska Medical Center Associate Professor of Sports Medicine
Omaha, Nebraska Eastern Maine Medical Center
Niall A. Smyth, MD University of Maine
Resident, Orthopaedic Surgery Sandip P. Tarpada, BS Bangor, Maine
University of Miami, Miller School of Department of Orthopaedic Surgery
Medicine Montefiore Medical Center Fotios P. Tjoumakaris, MD
Miami, Florida Albert Einstein College of Medicine Associate Professor
New York, New York Department of Orthopedic Surgery
Frederick S. Song, MD Sidney Kimmel College of Medicine
Clinical Associate Professor Kenneth F. Taylor, MD Thomas Jefferson University
Penn Medicine Princeton Medical Center Department of Orthopaedics and Philadelphia, Pennsylvania
Princeton, New Jersey Rehabilitation
The Pennsylvania State University Drew Toftoy, MD
Kurt Spindler, MD Milton S. Hershey Medical Center Sports Medicine Fellow
Cleveland Clinic Foundation Hershey, Pennsylvania University of Colorado
Cleveland, Ohio Aurora, Colorado
Michael Terry, MD
Chad Starkey, PhD, AT, FNATA Professor John M. Tokish, MD, USAF MC
Professor Department of Orthopaedic Surgery Orthopedic Surgery Residency Program
Division of Athletic Training Northwestern Medicine Director
Ohio University Northwestern University Feinberg School of Tripler Army Medical Center
Athens, Ohio Medicine Honolulu, Hawaii
Chicago, Illinois
Siobhan M. Statuta, MD Gehron Treme, MD
Associate Professor of Family Medicine and Charles A. Thigpen, PhD, PT, ATC Associate Professor, Orthopaedics
Physical Medicine and Rehabilitation Senior Director of Practice Innovation and University of New Mexico
University of Virginia Analytics Albuquerque, New Mexico
Charlottesville, Virginia ATI Physical Therapy
Director, Program in Observational Clinical Rachel Triche, MD
Samuel R. H. Steiner, MD Research in Orthopedics Attending Orthopaedic Surgeon
Orthopedic Surgery Center for Effectiveness in Orthopedic Santa Monica Orthopaedic and Sports
Orthopaedic Associates of Wisconsin Research Medicine Group
Pewaukee, Wisconsin Arnold School of Public Health Santa Monica, California
University of South Carolina
John W. Stelzer, MD, MS Greenville, South Carolina David P. Trofa, MD
Research Fellow Resident, Department of Orthopaedic
Department of Orthopaedic Surgery Stavros Thomopoulos, PhD Surgery
Harvard Medical School Director, Carroll Laboratories for Columbia University Medical Center
Massachusetts General Hospital Orthopedic Surgery New York, New York
Boston, Massachusetts Vice Chair, Basic Research in Orthopedic
Surgery Gift Ukwuani, MD
Christopher L. Stockburger, MD Robert E. Carroll and Jane Chace Carroll Section of Young Adult Hip Surgery
Department of Orthopedic Surgery Professor of Biomechanics (in Division of Sports Medicine
Washington University School of Medicine Orthopedic Surgery and Biomedical Department of Orthopedic Surgery
St. Louis, Missouri Engineering) Rush Medical College
Columbia University Medical Center Rush University Medical Center
J. Andy Sullivan, MD New York Presbyterian Hospital Chicago, Illinois
Clinical Professor of Pediatric Orthopedic New York, New York
Surgery M. Farooq Usmani, MSc
Department of Orthopedic Surgery Department of Orthopaedic Surgery
University of Oklahoma College of The Johns Hopkins University School of
Medicine Medicine
Oklahoma City, Oklahoma Baltimore, Maryland
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CONTRIBUTORS xix
Ravi S. Vaswani, MD Benjamin R. Wilson, MD Yi-Meng Yen, MD, PhD

Resident, Department of Orthopaedic Resident Physician Assistant Professor, Harvard Medical School
Surgery Orthopaedic Surgery and Sports Medicine Boston Children’s Hospital
University of Pittsburgh Medical Center University of Kentucky Department of Orthopaedic Surgery
Pittsburgh, Pennsylvania Lexington, Kentucky Division of Sports Medicine
Boston, Massachusetts
Aaron J. Vaughan, MD Brian F. Wilson, MD
Family Physician Director of Orthopaedic Surgery Stormont Jane C. Yeoh, MD, FRCSC
Sports Medicine Director Vail Health Vancouver, British Columbia, Canada
Mountain Area Health Education Center Washburn University Orthopaedic Sports
Asheville, North Carolina Medicine M. Christopher Yonz, MD
Topeka, Kansas Summit Orthopaedics
Jordi Vega, MD Southeast Georgia Health System
Orthopaedic Surgeon Jennifer Moriatis Wolf, MD St. Marys, Georgia
Etzelclinic Professor
Pfäffikon, Schwyz, Switzerland Department of Orthopaedic Surgery and Tracy Zaslow, MD, FAAP, CAQSM
Rehabilitation Assistant Professor
Evan E. Vellios, MD University of Chicago Hospitals University of Southern California, Los
Resident Physician Chicago, Illinois Angeles
Department of Orthopedic Surgery Children’s Orthopaedic Center (COC) at
David Geffen School of Medicine Rick W. Wright, MD Children’s Hospital–Los
University of California, Los Angeles Jerome J. Gilden Distinguished Professor Angeles
Los Angeles, California Executive Vice Chairman Medical Director
Department of Orthopaedic Surgery COC Sports Medicine and Concussion
Armando F. Vidal, MD Washington University School of Medicine Program
Associate Professor St. Louis, Missouri Team Physician, LA Galaxy
Department of Orthopedics Los Angeles, California
University of Colorado School of Medicine Frank B. Wydra, MD
Aurora, Colorado Department of Orthopedics Andrew M. Zbojniewicz, MD
University of Colorado School of Medicine Department of Radiology
Michael J. Vives, MD Aurora, Colorado Michigan State University
Professor and Chief of Spine Surgery College of Human Medicine
Department of Orthopedics James Wylie, MD, MHS Advanced Radiology Services
Rutgers–New Jersey Medical School Director of Orthopedic Research Grand Rapids, Michigan
Newark, New Jersey Intermountain Healthcare Division of Pediatric Radiology
The Orthopedic Specialty Hospital Cincinnati Children’s Hospital Medical
James E. Voos, MD Murray, Utah Center
Associate Professor of Orthopaedic Surgery Cincinnati, Ohio
Division Chief, Sports Medicine Robert W. Wysocki, MD
Medical Director, Sports Medicine Institute Rush University Medical Center Connor G. Ziegler, MD
University Hospitals Chicago, Illinois New England Orthopedic Surgeons
Cleveland Medical Center Springfield, Massachusetts
Cleveland, Ohio Haoming Xu, MD
Dermatology Service Mary L. Zupanc, MD
Dean Wang, MD Department of Medicine Professor and Division Chief
Fellow in Sports Medicine and Shoulder Memorial Sloan Kettering Cancer Center Neurology and Pediatrics
Surgery New York, New York University of California, Irvine
Hospital for Special Surgery Children’s Hospital of Orange County
New York, New York Kent T. Yamaguchi, MD Orange, California
Resident Physician
Robert Westermann, MD Orthopaedic Surgery
University of Iowa University of California, Los Angeles
Iowa City, Iowa Los Angeles, California
Barbara B. Wilson, MD Jeffrey Yao, MD

Associate Professor of Dermatology Associate Professor of Orthopedic Surgery
University of Virginia Stanford University Medical Center
Charlottesville, Virginia Palo Alto, California
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V I D E O TA B L E O F C O N T E N T S
Chapter 1 Chapter 15
Video 1.1 Physiology and Pathophysiology of Musculoskeletal Video 15.1 Gastrointestinal Medicine in the Athlete—John M.
Tissues—Dean Wang, Claire D. Eliasberg, and Scott MacKnight
A. Rodeo
Chapter 16
Chapter 2 Video 16.1 Hematologic Medicine in the Athlete—John J.
Video 2.1 Basic Concepts in Biomechanics—Richard E. Debski, Densmore
Neel K. Patel, and Jason T. Shearn
Chapter 17
Chapter 4 Video 17.1 Infectious Diseases in the Athlete—Nona M. Jiang,
Video 4.1 Basic Science of Implants in Sports Medicine— Kathleen C. Abalos, and William A. Petri Jr.
Elizabeth R. Dennis, Jon-Michael Caldwell, Sonya
B. Levine, Philip Chuang, Margaret Boushell, Stavros Chapter 18
Thomopoulos, Helen H. Lu, and William N. Levine Video 18.1 The Athlete with Diabetes—Jessica A. Lundgren
and Susan E. Kirk
Chapter 5
Video 5.1 Orthobiologics: Clinical Application of Platelet- Chapter 19
Rich Plasma and Stem Cell Therapy—Adrian D.K. Video 19.1 Renal Medicine and Genitourinary Trauma in
Le and Jason Dragoo the Athlete—Stefan Hemmings and Derek M.
Fine
Chapter 7
Video 7.1 Imaging Overview—Francisco Contreras, Jose Perez, Chapter 22
and Jean Jose Video 22.1 Dermatologic Conditions—Haoming Xu, Barbara
B. Wilson, and Michael A. Marchetti
Chapter 8
Video 8.1 Basic Arthroscopic Principles—Michael R. Mijares Chapter 23
and Michael G. Baraga Video 23.1 Facial, Eye, Nasal, and Dental Injuries—John Jared
Christophel
Chapter 9
Video 9.1 Overview of Sport-Specific Injuries—Jared A. Crasto, Chapter 25
Ravi S. Vaswani, Thierry Pauyo, and Volker Musahl Video 25.1 Sports Nutrition—Jessica L. Buschmann and Jackie
Buell
Chapter 10
Video 10.1 Commonly Encountered Fractures in Sports Chapter 26
Medicine—Christopher Kim and Scott G. Kaar Video 26.1 Doping and Ergogenic Aids—Siobhan M. Statuta,
Aaron J. Vaughan, and Ashley V. Austin
Chapter 11
Video 11.1 Team Medical Coverage—Daniel Herman, Nikhita Chapter 27
Gadi, and Evan Peck Video 27.1 The Female Athlete—Letha Y. Griffin, Mary
Lloyd Ireland, Fred Reifsteck, Matthew H. Blake,
Chapter 12 and Benjamin R. Wilson
Video 12.1 Comprehensive Cardiovascular Care and Evaluation Video 27.2 The Female Athlete—Letha Y. Griffin, Mary
of the Elite Athlete—Paul S. Corotto, Robert W. Lloyd Ireland, Fred Reifsteck, Matthew H. Blake,
Battle, Dilaawar J. Mistry, and Aaron L. Baggish and Benjamin R. Wilson
Video 13.1 Exercise-Induced Bronchoconstriction—Virgil P. Video 28.1 The Para-Athlete—Daniel Herman, Mary E.
Secasanu and Jonathan P. Parsons Caldwell, and Arthur Jason De Luigi
Video 14.1 Deep Venous Thrombosis and Pulmonary Video 30.1 The Athletic Trainer—Chad Starkey and Shannon
Embolism—Marc M. DeHart and Jason Thompson David
xxiv
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VIDEO TABLE OF CONTENTS xxv
Video 31.1 Principles of Orthopaedic Rehabilitation—Courtney Video 55.1 Vascular Problems and Thoracic Outlet Syndrome—
Chaaban and Charles A. Thigpen Matthew A. Posner, Christopher J. Roach, Adam
M. Pickett, and Brett D. Owens
Chapter 32
Video 32.1 Modalities and Manual Techniques in Sports Medicine Chapter 56
Rehabilitation—Susan Saliba and Michael Higgins Video 56.1 Injury to the Acromioclavicular and Sternoclavicular
Joints—Connor G. Ziegler, Samuel J. Laurencin,
Chapter 38 Rachel M. Frank, Matthew T. Provencher, Anthony
Video 38.1 Glenohumeral Joint Imaging—Alissa J. Burge and A. Romeo, and Augustus D. Mazzocca
Gabrielle P. Konin
Chapter 57
Chapter 41 Video 57.1 Elbow Anatomy and Biomechanics—Marshall A.
Video 41.1 Posterior Shoulder Instability—James Bradley and Kuremsky, E. Lyle Cain Jr., Jeffrey R. Dugas, James
Fotios P. Tjoumakaris R. Andrews, and Lucas R. King
Video 42.1 Multidirectional Instability of the Shoulder—Robert Video 58.1 Elbow Diagnosis and Decision-Making—Nicholas
M. Carlisle and John M. Tokish J. Clark and Bassem Elhassan
Video 44.1 SLAP Tears—Sean Meredith and R. Frank Henn Video 59.1 Elbow Imaging—Benjamin M. Howe and Michael
III R. Moynagh
Video 45.1 The Thrower’s Shoulder—Matthew A. Tao, Video 61.1 Elbow Tendinopathies and Bursitis—Jennifer
Christopher L. Camp, Terrance Sgroi, Joshua S. Moriatis Wolf
Dines, and David W. Altchek
Chapter 62
Chapter 46 Video 62.1 Distal Biceps and Triceps Tendon Ruptures—
Video 46.1 Proximal Biceps Tendon Pathology—Samuel R.H. James Bradley, Fotios P. Tjoumakaris, Gregory T.
Steiner, John T. Awowale, and Stephen F. Brockmeier Lichtman, and Luke S. Austin
Video 47.1 Rotator Cuff and Impingement Lesions—Gina M. Video 63.1 Entrapment Neuropathies of the Arm, Elbow, and
Mosich, Kent T. Yamaguchi, and Frank A. Petrigliano Forearm—Wajeeh Bakhsh and Warren C. Hammert
Video 48.1 Subscapularis Injury—William H. Rossy, Frederick Video 64.1 Elbow Throwing Injuries—Marshall A. Kuremsky,
S. Song, and Jeffrey S. Abrams E. Lyle Cain Jr, Jeffrey R. Dugas, James R. Andrews,
and Christopher A. Looze
Chapter 49
Video 49.1 Revision Rotator Cuff Repair—Joseph D. Cooper, Chapter 65
Anthony Essilfie, and Seth C. Gamradt Video 65.1 Loss of Elbow Motion—Timothy J. Luchetti, Debdut
Biswas, and Robert W. Wysocki
Chapter 52
Video 52.1 Glenohumeral Arthritis in the Athlete—Jeffrey Chapter 66
Brunelli, Jonathan T. Bravman, Kevin Caperton, Video 66.1 Anatomy and Biomechanics of the Hand and
and Eric C. McCarty Wrist—Raj M. Amin and John V. Ingari
Video 53.1 Scapulothoracic Disorders—G. Keith Gill, Gehron Video 67.1 Hand and Wrist Diagnosis and Decision-Making—
Treme, and Dustin Richter Patrick G. Marinello, R. Glenn Gaston, Eliott P.
Robinson, and Gary M. Lourie
Chapter 54
Video 54.1 Nerve Entrapment—Daniel E. Hess, Kenneth F. Chapter 68
Taylor, and A. Bobby Chhabra Video 68.1 Imaging of the Wrist and Hand—Kimberly K. Amrami
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xxvi VIDEO TABLE OF CONTENTS
Video 69.1 Wrist Arthroscopy—William B. Geissler, David A. Video 87.1 Hip and Thigh Contusions and Strains—Blake R.
Rush, and Christopher A. Keen Obrock, Christopher P. Bankhead, and Dustin Richter
Video 71.1 Wrist Tendinopathies—Raj M. Amin and John V. Video 89.1 Knee Anatomy and Biomechanics of the Knee—
Ingari Matthew J. Kraeutler, Jorge Chahla, Francesc
Malagelada, Jordi Vega, Pau Golanó, Bruce
Chapter 72 Beynnon, Fatih Ertem, and Eric C. McCarty
Video 72.1 Disorders of the Distal Radioulnar Joint—Julie E.
Adams Chapter 90
Video 90.1 Knee Diagnosis and Decision-Making—Andrew
Chapter 73 J. Riff, Peter N. Chalmers, and Bernard R. Bach Jr.
Video 73.1 Tendon Injuries in the Hand—Robin N. Kamal
and Jacob D. Gire Chapter 92
Video 92.1 Basics of Knee Arthroscopy—Stephen R. Thompson
Chapter 74 and Mark D. Miller
Video 74.1 Digit Fractures and Dislocations—Christopher L.
Stockburger amd Ryan P. Calfee Chapter 94
Video 94.1 Meniscal Injuries—Joseph J. Ruzbarsky, Travis G.
Chapter 75 Maak, and Scott A. Rodeo
Video 75.1 Neuropathies of the Wrist and Hand—Gwendolyn
Hoben and Amy M. Moore Chapter 96
Video 96.1 Articular Cartilage Lesions—Michael S. Laidlaw,
Chapter 76 Kadir Buyukdogan, and Mark D. Miller
Video 76.1 Hip Anatomy and Biomechanics—Marc Safran and
Abdurrahman Kandil Chapter 98
Video 98.1 Anterior Cruciate Ligament Injuries—Edward C.
Chapter 77 Cheung, David R. McAllister, and Frank A. Petrigliano
Video 77.1 Hip Diagnosis and Decision-Making—Benjamin
G. Domb and Austin W. Chen Chapter 99
Video 99.1 Revision Anterior Cruciate Ligament Injuries—
Chapter 78 Joseph D. Lamplot, Liljiana Bogunovic, and Rick
Video 78.1 Hip Imaging—Brian Busconi, R. Tyler Huish, Erik W. Wright
Mitchell, and Sean McMillan
Chapter 100
Chapter 79 Video 100.1 Posterior Cruciate Ligament Injuries—Frank A.
Video 79.1 Hip Arthroscopy—Joshua D. Harris Petrigliano, Evan E. Vellios, Scott R. Montgomery,
Jared S. Johnson, and David R. McAllister
Chapter 80
Video 80.1 Femoroacetabular Impingement in Athletes—Shane Chapter 101
J. Nho, Vignesh Prasad Krishnamoorthy, Drew Video 101.1 Medial Collateral Ligament and Posterior Medial
Lansdown, Gift Ukwuani Corner Injuries—M. Christopher Yonz, Brian F.
Wilson, Matthew H. Blake, and Darren L. Johnson
Chapter 82
Video 82.1 Iliopsoas Pathology—Christian N. Anderson Chapter 102
Video 102.1 Lateral and Posterolateral Corner Injuries of the
Chapter 83 Knee—Ryan P. Coughlin, Dayne T. Mickelson, and
Video 83.1 Peritrochanteric Disorders—John W. Stelzer and Claude T. Moorman III
Scott D. Martin
Video 83.2 Peritrochanteric Disorders—John W. Stelzer and Chapter 103
Scott D. Martin Video 103.1 Multiligament Knee Injuries—Samantha L.
Video 83.3 Peritrochanteric Disorders—John W. Stelzer and Kallenbach, Matthew D. LaPrade, and Robert F.
Scott D. Martin LaPrade

Video 85.1 Posterior Hip Pain—Hal David Martin, Anthony Video 108.1 Loss of Knee Motion—K. Donald Shelbourne,
Nicholas Khoury, and Juan Gomez-Hoyos Heather Freeman, and Tinker Gray
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VIDEO TABLE OF CONTENTS xxvii

Video 110.1 Foot and Ankle Biomechanics—Andrew Haskell Video 124.1 Imaging of the Spine—Adil Samad, M. Farooq
Usmani, and A. Jay Khanna
Chapter 115
Video 115.1 Ankle Arthroscopy—Niall A. Smyth, Jonathan R. Chapter 125
Kaplan, Amiethab A. Aiyer, John T. Campbell, Video 125.1 Emergency and Field-Side Management of the
Rachel Triche, and Rebecca A. Cerrato Spine-Injured Athlete—Korin Hudson, Michael
Antonis, and William Brady
Chapter 117
Video 117.1 Ligamentous Injuries of the Foot and Ankle—Paul Chapter 132
Rothenberg, Eric Swanton, Andrew Molloy, Video 132.1 Imaging Considerations in Skeletally Immature
Amiethab A. Aiyer, and Jonathan R. Kaplan Athletes—Andrew M. Zbojniewicz

Video 118.1 Tendon Injuries of the Foot and Ankle—Todd A. Video 133.1 Shoulder Injuries in the Young Athlete—Andrew
Irwin T. Pennock and Eric W. Edmonds

Video 119.1 Articular Cartilage Injuries and Defects—David Video 134.1 Elbow Injuries in Pediatric and Adolescent Athletes—
R. Richardson and Jane C. Yeoh James P. Bradley, Luke S. Austin, Alexander B.
Kreines, and Fotios P. Tjoumakaris
Chapter 121
Video 121.1 Forefoot Problems in Sport—Ben Hickey, Lyndon Chapter 137
Mason, and Anthony Perera Video 137.1 Knee Injuries in Skeletally Immature Athletes—
Matthew D. Milewski, James Wylie, Carl W. Nissen,
Chapter 122 and Tricia R. Prokop
Video 122.1 Head and Spine Anatomy and Biomechanics—Colin
B. Harris, Rachid Assina, Brandee Gentile, and Chapter 138
Michael J. Vives Video 138.1 Foot and Ankle Injuries in the Adolescent Athlete—J.
Andy Sullivan and James R. Gregory
Chapter 123
Video 123.1 Head and Spine Diagnosis and Decision-Making— Chapter 139
Rabia Qureshi, Jason A. Horowtiz, Kieran Video 139.1 Head Injuries in Skeletally Immature Athletes—
Bhattacharya, and Hamid Hassanzadeh Tracy Zaslow
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1
Physiology and Pathophysiology of
Musculoskeletal Tissues
Dean Wang, Claire D. Eliasberg, Scott A. Rodeo
TENDON AND LIGAMENT become taut throughout the range of motion.6 The alignment
of collagen fiber bundles within the ligament substance generally
Structure follows the lines of tension applied to the ligament. This is in
Tendons and ligaments are both dense, regularly arranged con- contrast to the alignment of collagen fiber bundles within the
nective tissues. The surface of the tendon is enveloped in a white, tendon, which is generally parallel to its longitudinal axis. In
glistening, synovial-like membrane, called the epitenon, which addition, thinner collagen fibrils extend the entire length of the
is continuous on its inner surface with the endotenon, a thin tendon. Light microscopic examination has shown that the col-
layer of connective tissue that binds collagen fibers and contains lagen bundles have a wave or crimp pattern. The crimp pattern
lymphatics, blood vessels, and nerves. In some tendons, the epi- of matrix organization may allow slight elongation of the liga-
tenon is surrounded by a loose areolar tissue called the paratenon, ment without incurring damage to the tissue.6 In some regions,
which functions as an elastic sheath through which the tendon the ligament cells align themselves in rows between collagen
can slide. In some tendons, the paratenon is replaced by a true fiber bundles, but in other regions, the cells lack apparent ori-
synovial sheath or bursa consisting of two layers lined by synovial entation relative to the alignment of the matrix collagen fibers.
cells, called the tenosynovium, within which the mesotendon Scattered blood vessels penetrate the ligament substance, forming
carries important blood vessels to the tendon.1 In the absence small-diameter, longitudinal vascular channels that lie parallel
of a synovial lining, the paratenon often is called a tenovagina. to the collagen bundles. Nerve fibers lie next to some vessels,
Together the epitenon and the paratenon compose the peritenon and, like tendon, nerve endings with the structure of mechano-
(Fig. 1.1). The blood supply to tendons has several sources, receptors have been found in some ligaments.4,7,8
including the perimysium, periosteal attachments, and surround- Tendon and ligament insertions vary in size, strength, angle
ing tissues. Blood supplied through the surrounding tissues of the ligament collagen fiber bundles relative to the bone, and
reaches the tendon through the paratenon, mesotenon, or vincula. proportion of ligament collagen fibers that penetrate directly
Vascular tendons are surrounded by a paratenon and receive into bone.4,5,9 Based on the angle between the collagen fibrils
vessels along their borders; these vessels then coalesce within and the bone and the proportion of the collagen fibers that
the tendon. The relatively avascular tendons are contained within penetrate directly into bone, investigators group tendon and
tendinous sheaths, and the mesotenons within these sheaths ligament insertions into two types: direct and indirect. Direction
function as vascularized conduits called vincula. The muscle- insertions typically occur at the apophysis or epiphysis of bone,
tendon and tendon-bone junctions, along with the mesotenon, often within or around a synovial joint, and consist of sharply
are the three types of vascular supply to the tendon inside the defined regions where the collagen fibers appear to pass directly
sheath. Other sources of nutrition2 include diffusional pathways into the cortex of the bone.9,10 Although the thin layer of super-
from the synovial fluid, which provide an important supply of ficial collagen fibers of direct insertions joins the fibrous layer
nutrients for the flexor tendons of the hand, for example. The of the periosteum, most of the tendon or ligament insertions
nervous supply to a tendon involves mechanoreceptors located consist of deeper fibers that directly penetrate the cortex, often
near the musculotendinous junction, which provide propriocep- at a right angle to the bone surface. The deeper collagen fibers
tive feedback to the central nervous system. pass through four zones with increasing stiffness: ligament sub-
Ligaments grossly appear as firm, white fibrous bands, sheets, stance, fibrocartilage, mineralized fibrocartilage, and bone.9,10
or thickened strips of joint capsule securely anchored to bone. This four-zone interface is known as the fibrocartilaginous enthe-
They consist of a proximal bone insertion, the substance of the sis.11 Dissipation of force is achieved effectively through this
ligament or the capsule, and a distal bone insertion. Because gradual transition from tendon to fibrocartilage to bone. A larger
most insertions are no more than 1 mm thick, they contribute area of fibrocartilage can be found on one side of the insertion,
only a small amount to the volume and the length of the liga- which is thought to be an adaptation to the compressive forces
ment. Bundles of collagen fibrils form the bulk of the ligament experienced by the tendon or ligament on that side.12 Conversely,
substance.3–5 Some ligaments consist of more than one band of indirect or oblique insertions, such as the tibial insertion of the
collagen fibril bundles. For example, the anterior cruciate liga- medial collateral ligament of the knee or the femoral insertion
ment (ACL) has a continuum of fiber lengths; different fibers of the lateral collateral ligament, typically occur at the metaphysis
2
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CHAPTER 1 Physiology and Pathophysiology of Musculoskeletal Tissues 2.e1
Abstract Keywords
Musculoskeletal structures contain tissue-specific cells, extracel- tendon
lular matrix, and fiber arrangements which impart their unique ligament
biologic and mechanical properties. Tendon, ligament, meniscus, meniscus
articular cartilage, and bone all have different structures that cartilage
determine their specific function. Furthermore, the healing articular
potential and response to injury of these tissues is highly variable bone
and dependent on a number of factors, including the presence physiology
of a surrounding vasculature and the ability of intrinsic cells to
replicate and remodel the injured matrix. In this chapter, we
review the structure, biology, healing response to injury, and
potential augmentative therapies of tendon, ligament, meniscus,
articular cartilage, and bone.
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CHAPTER 1 Physiology and Pathophysiology of Musculoskeletal Tissues 3
process. Tendons of the extremities possess small amounts of

this structural protein, whereas most ligaments have little elastin
(usually less than 5%), although a few, such as the nuchal liga-
Tendon ment and the ligamentum flavum, have high concentrations
(up to 75%). In most tendons, elastin is found primarily at
Peritendon the fascicle surface,19 comprising less than 1% of the tendon
by dry weight, and it is responsible for the crimp pattern of
Paratenon
Epitenon the tendon when viewed by a light microscope. Elastin forms
protein fibrils or sheets, but elastin fibrils lack the cross-banding
pattern of fibrillar collagen and differ in amino acid composition,
Endotenon
Fibroblast including two amino acids not found in collagen (desmosine and
Primary bundle isodesmosine). In addition, unlike collagen, elastin amino acid
chains form random coils when the molecules are unloaded.
Fibril This conformation of the amino acid chains makes it possible
Microfibril for elastin to undergo some deformation without rupturing or
Collagen fibril tearing and then, when the load is removed, to return to its
Tropocollagen original size and shape.
Fig. 1.1 Structural organization of tendon. Approximately 1% of the total dry weight of tendon and
ligament is composed of ground substance, which consists of
or diaphysis of bone without an intervening fibrocartilage zone. proteoglycans, glycosaminoglycans, structural glycoproteins,
They usually cover more bone surface area than do direct inser- plasma proteins, and a variety of small molecules. Most ligaments
tions, and their boundaries cannot be easily defined because the have a higher concentration of glycosaminoglycans than do
collagen fibers pass obliquely along the bone surface rather than tendons, due to the functional need for more rapid adaptation.18
directly into the cortex. Proteoglycans and glycosaminoglycans both have important roles
in organizing the extracellular matrix and control the water
Extracellular Matrix content of the tissue.4,20–23 Tendon and ligaments contain two
Tendons and ligaments consist of relatively few cells and an known classes of proteoglycans. Larger proteoglycans contain
abundant extracellular matrix primarily containing collagen, long negatively charged chains of chondroitin and keratan sulfate.
proteoglycans, and water. Tenocytes (tendon-specialized fibro- Smaller proteoglycans contain dermatan sulfate. Because of their
blasts) are the dominant cell of tendons, whereas fibroblasts are long chains of negative charges, the large articular cartilage-type
the dominant cells of ligaments. Tenocytes and fibroblasts form proteoglycans tend to expand to their maximal domain in solu-
and maintain the extracellular matrix. Within ligaments, fibro- tion until restrained by the collagen fibril network. As a result,
blasts vary in shape, activity, and density among regions of the they maintain water within the tissue and exert a swelling pres-
same tissue and with the age of the tissue.4,5,9,13 Both tenocytes sure, thereby contributing to the mechanical properties of the
and fibroblasts are spindle shaped, with fibroblasts being rounder, tissue and filling the regions between the collagen fibrils. The
and extend between the collagen fibrils.14 Endothelial cells of small leucine-rich proteoglycans usually lie directly on the surface
small vessels and nerve cell processes are also present.4,5,9,13 Studies of collagen fibrils and appear to affect formation, organization,
have shown that tendon and ligament contain a small population and stability of the extracellular matrix, including collagen fibril
of resident stem cells which function to maintain tissue homeo- formation and diameter. They may also control the activity of
stasis during growth and repair.15–17 growth factors by direct association.21,24
Type I collagen, which is the major component of the molecular Although noncollagenous proteins contribute only a small
framework, composes more than 90% of the collagen content percentage of the dry weight of dense fibrous tissues, they appear
of ligaments. Type III collagen constitutes approximately 10% to help organize and maintain the macromolecular framework
of the collagen, and small amounts of other collagen types also of the collagen matrix, aid in the adherence of cells to the frame-
may be present. Ligaments have a higher content of type III work, and possibly influence cell function. One noncollagenous
collagen than do tendons.18 All types of collagen have in common protein, fibronectin, has been identified in the extracellular matrix
a triple helical domain, which is combined differently with globu- of ligaments and may be associated with several matrix compo-
lar and nonhelical structural elements. The triple helix confor- nent molecules and with blood vessels. Other noncollagenous
mation of collagen is stabilized mainly by hydrogen bonds between proteins undoubtedly exist within the matrix, but their identity
glycine residues and between hydroxyl groups of hydroxyproline. and their functions have not yet been defined. Many of the non-
This helical conformation is reinforced by hydroxyproline-forming collagenous proteins also contain a few monosaccharides and
and proline-forming hydrogen bonds to the other two chains. oligosaccharides.4,5
The physical properties of collagen and its resistance to enzymatic
and chemical breakdown rely on covalent cross-links within and Injury
between the molecules. Acute strains and tears to tendons and ligaments disrupt the
Elastin is a protein that allows connective tissues to undergo matrix, damage blood vessels, and injure or kill cells. Damage
large changes in geometry while expending little energy in the to cells, matrices, and blood vessels and the resulting hemorrhage
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4 SECTION 1 Basic Principles
start a response that leads to a sequential process of inflamma- A review of patients with chronic tendinitis syndrome revealed
tion, repair, and remodeling.25,26 These events form a continuous similar findings of tendon degeneration.27,35 Nirschl35 described
sequence of cell, matrix, and vascular changes that begins with the pathology of chronic tendinitis as “angiofibroblastic hyper-
the release of inflammatory mediators and ends when remodel- plasia.” A characteristic pattern of fibroblasts and vascular, atypi-
ing ceases.25 As with any injury to biologic tissue, acute inflam- cal, granulation-like tissue can be seen microscopically.35,36 Cells
mation lasts 48 to 72 hours after the injury and then gradually characteristic of acute inflammation are virtually absent. These
resolves as repair progresses. Some of the events that occur during observations suggest that factors other than mechanical overuse
inflammation, including the release of cytokines or growth factors, play an important role in the pathogenesis of these tendon lesions.
may help to stimulate tissue repair.25 These mediators promote In several studies, a correlation between age and the incidence
vascular dilation and increase vascular permeability, leading to of chronic tendinopathy has been identified.37,38 In vitro studies
exudation of fluid from vessels in the injured region, which have shown decreased proliferative and metabolic responses of
causes tissue edema. Blood escaping from the damaged vessels aging tendon tissue.39 Other causative factors include the lack
forms a hematoma that temporarily fills the injured site. Fibrin of blood flow in certain areas (e.g., supraspinatus and Achilles
accumulates within the hematoma, and platelets bind to fibrillar tendon) that may predispose a tendon to rupture or may result
collagen, thereby achieving hemostasis and forming a clot con- in chronic tendinopathy.40 Biopsy specimens of young patients
sisting of fibrin, platelets, red cells, and cell and matrix debris. with symptoms of chronic tendinopathy have revealed a change
The clot provides a framework for vascular and fibroblast cell in the morphology of tenocytes adjacent to areas of collagen
invasion. As they participate in clot formation, platelets release degeneration.28
vasoactive mediators and various cytokines or growth factors
(e.g., transforming growth factor-β [TGF-β] and platelet-derived Repair
growth factor). Polymorphonuclear leukocytes appear in the Tendons and ligaments may possess both intrinsic and extrinsic
damaged tissue and the clot. Shortly thereafter, monocytes arrive capabilities for healing, and the contribution of each of these
and increase in number until they become the predominant cell two mechanisms probably depends on the location, extent, and
type. Enzymes released from the inflammatory cells help to digest mechanism of injury and the rehabilitation program used after the
necrotic tissue, and monocytes phagocytose small particles of injury. Several studies2,41–46 have suggested that the inflammatory
necrotic tissue and cell debris. Endothelial cells near the injury response is not essential to the healing process and that these
site begin to proliferate, creating new capillaries that grow toward tissues possess an intrinsic capacity for repair. Recent research
the region of tissue damage. Release of chemotactic factors and has isolated intrinsic stem cells within tendon and ligament,
cytokines from endothelial cells, monocytes, and other inflam- although their in vivo identities, niche, and role in healing remain
matory cells helps to stimulate migration and proliferation of controversial.17,47 Lindsay and Thomson43 were the first to show
the fibroblasts that begin the repair process.25 that an experimental tendon suture zone can be isolated from
Overuse tendon injury is one of the more common forms of the perisheath tissues and that healing progressed at the same
musculoskeletal injury and clinical causes of pain, although rate as when the perisheath tissues were intact. Later, in isolated
controversy exists in the literature about a universal classification segments of profundus tendon in rabbits, these researchers found
and the responsible pathologic entities. A classification of Achilles anabolic and catabolic enzymes, which showed that an active
tendon disorders27 provides a guide to the structural manifesta- metabolic process existed in the isolated tendon segments.44
tions of overuse injury as follows: (1) peritendinitis, or inflam- As in other areas in the body, tendon healing proceeds in
mation of the peritenon; (2) tendinosis with peritendinitis; (3) three phases: (1) an inflammatory stage, (2) a reparative or
tendinosis without peritendinitis; (4) partial rupture; and (5) collagen-producing stage, and (3) a remodeling phase.
total rupture. Other classifiers have added a sixth category, ten-
dinitis, in which the primary site of injury is the tendon, with Inflammatory Phase
an associated reactive peritendinitis.28 The classification is not Tendon and ligament healing begins with hematoma formation
universal because some tendons lack a paratenon and instead and an inflammatory reaction that includes an accumulation of
have synovial sheaths; furthermore, it is unclear if certain his- fibrin and inflammatory cells. A clot forms between the two
topathologic conditions are actually separate entities. For instance, ends and is invaded by cells resembling fibroblasts and migratory
human biopsy studies have been unable to show histologic evi- capillary buds. Within 2 to 3 days of the injury, fibroblasts within
dence of acute inflammation within the tendon substance.29 the wound begin to proliferate rapidly and synthesize new matrix.
Because of uncertainty regarding the histologic features of these They replace the clot and the necrotic tissue with a soft, loose
conditions, several authors have suggested use of the term ten- fibrous matrix containing high concentrations of water, glycos-
dinopathy rather than tendinitis.30,31 aminoglycans, and type III collagen. Inflammatory cells and
Studies have shown that in cases of chronic tendinosis, the fibroblasts fill this initial repair tissue. Within 3 to 4 days, vascular
pathologic lesion is typical of a degenerative process rather than buds from the surrounding tissue grow into the repair tissue
an inflammatory one and that this degeneration occurs in areas and then canalize to allow blood flow to the injured tissue and
of diminished blood flow. Several authors have documented the across small tissue defects. This vascular granulation tissue fills
existence of areas of marked degeneration without acute or the tissue defect and extends for a short distance into the sur-
chronic inflammatory cell accumulation in most of these cases.32–34 rounding tissue but has little tensile strength. The inflammatory
These changes are separate and distinct from the site of rupture. phase is evident until the 8th to 10th day after injury.
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by disrupting the repair tissue, leading to gap formation and

Reparative Phase ischemia, adverse changes in tendon matrix, and possible
As the repair progresses during the next several weeks, proliferat- rupture.4,25,54–56 However, controlled loading of tendon and liga-
ing fibroblasts continue to produce fibrous tissue containing a ment repair tissue can promote healing and enhance the mechani-
high proportion of type III collagen. Collagen synthesis reaches cal and biologic characteristics of tendon-to-bone healing.57 The
its maximal level after approximately 4 weeks, and at 3 months, optimal amount of tension necessary to promote an acceptable
collagen synthesis continues at a rate 3 to 4 times that of normal clinical response is currently not well understood and depends
tissue. Over time, water, glycosaminoglycan, and type III colla- on the type of tissue and healing environment, but it is clear
gen concentrations decline, the inflammatory cells disappear, and that remodeling of collagen scar tissue into mature tendon tissue
the concentration of type I collagen increases. Newly synthesized depends on the presence of tensile forces.58,59 The concept of
collagen fibrils increase in size and begin to form tightly packed immediate passive mobilization after flexor tendon repair in the
bundles, and the density of fibroblasts decreases. Matrix organiza- hand was introduced by Kleinert and coworkers,60 who showed
tion increases48–51 as the fibrils begin to align along the lines of stress, that, during limited active extension, reciprocal relaxation of
the number of blood vessels decreases, and small amounts of elastin the flexor tendons occurs, allowing passive extension of the
may appear within the site of injury. The tensile strength of the repaired tendon. This controlled passive motion was found to
repair tissue increases as the collagen concentration increases. be effective experimentally and clinically in decreasing the teth-
ering effect of adhesions and in improving the rates of tendon
Remodeling Phase repair, gliding function, and strength of the tendon.
Repair of many tendon and ligament injuries results in an exces-
sive volume of highly cellular tissue with limited mechanical Methods for Augmentation of Tendon and
properties and a poorly organized matrix. Remodeling reshapes Ligament Healing
and strengthens this tissue by removing, reorganizing, and replac- A large body of research has demonstrated the potential for
ing cells and matrix.25 In most tendon and ligament injuries, growth factors to improve tendon and ligament tissue healing
evidence of remodeling appears within several weeks of injury by stimulation of cell proliferation, chemotaxis, matrix synthesis,
as fibroblasts and macrophages decrease, fibroblast synthetic and cell differentiation (summarized in Table 1.1). In addition
activity decreases, and fibroblasts and collagen fibrils assume a to multifunctional cytokines such as TGF-β and platelet-derived
more organized appearance. As these changes occur in the repair growth factor, work has focused on recapitulating the cellular
tissue, collagen fibrils grow in diameter, the concentration of and molecular signals that are expressed during embryonic tendon
collagen and the ratio of type I to type III collagen increase, and development, such as scleraxis and TGF-β3.61 However, chal-
the water and proteoglycan concentrations decline. During the lenges in the delivery of these growth factors, specifically regarding
months after the injury occurs, the matrix continues to align, the optimal carrier vehicles and proper dosing regimen, to the
presumably in response to loads applied to the repair tissue. desired site still remain.
The most apparent signs of remodeling disappear within 4 to 6 Platelet-rich plasma (PRP), an autologous blood concentrate,
months of injury. However, removal, replacement, and reorga- can be used to locally deliver a high concentration “cocktail” of
nization of repair tissue continue to some extent for years.50,52,53 cytokines and has gained popularity as a treatment modality for
The mechanical strength of the healing tendon and ligament tendon and ligament injuries. Recent studies have reported poten-
increases as the collagen becomes stabilized by cross-links and tially promising results with the use of PRP to augment healing
the fibrils assemble into fibers. of rotator cuff repair62–64 and patellar tendinopathy.65 However,
the results of PRP for augmentation of tendon and ligament
Factors Affecting Healing healing have been variable, which can partially be attributed
Among the most important variables that affect healing of tendon to the lack of understanding of the optimal PRP formulation
and ligament are the type of tendon or ligament, the size of the for different tissues and pathologies, as well as the tremendous
tissue defect, and the amount of load applied to the repair tissue. variability in the methods of PRP production among commer-
For example, injuries to capsular and extra-articular ligaments cial systems.66,67 To complicate matters further, within a given
stimulate production of repair tissue that will fill most defects, but separation technique, there is a high degree of intersubject and
injuries to intra-articular ligaments, such as the ACL, often fail to intrasubject variability in the composition of PRP produced.68
produce a successful repair response. Treatments that achieve or Cell-based approaches appear promising for tendon and liga-
maintain apposition of torn tissue and that stabilize the injury ment tissue engineering and improvement of healing. Therapies
site decrease the volume of repair tissue necessary to heal the using mesenchymal stem cells (MSCs) derived from adipose and
injury, which can benefit the healing process. Such treatments bone marrow to augment tendon and ligament healing have
may also minimize scarring and help to provide near-normal garnered the most attention due to their multipotent potential
tissue length. For these reasons, avoidance of wide separation of and ability to exert a paracrine effect to modulate and control
ruptured tendon or ligament ends and selection of treatments inflammation, stimulate endogenous cell repair and prolifera-
that maintain some stability at the injured site during the initial tion, inhibit apoptosis, and improve blood flow.14,69 However,
stages of repair are generally desirable. like PRP augmentation therapy, continued research is needed
Early excessive loading in the immediate postoperative period to identify the optimal cell source and the ideal treatment pro-
may have a deleterious effect on tendon and ligament healing tocol needed to drive differentiation of these or neighboring
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TABLE 1.1 Growth Factors in Soft Tissue Repair

Biologic Factor Functions Reference
TGF-β Influx of mononuclear cells and fibroblasts Lee J et al: Iowa Orthop J 1998
Enhanced collagen deposition Spindler KP et al: J Orthop Res 2002
Spindler KP et al: J Orthop Res 2003
Kashiwagi K et al: Scand J Plast Reconstr Surg Hand Surg 2004
Kim HJ et al: Connect Tissue Res 2007
Kim HM et al: Connect Tissue Res 2011
Manning CN et al: J Orthop Res 2011
Kovacevic D et al: Am J Sports Med 2011
GDF 5/6/7 Influx of mononuclear cells and fibroblasts Wolfman NM et al: J Clin Invest 1997
Enhanced collagen deposition Aspenberg P et al: Acta Orthop Scand 1999
Rickert M et al: Growth Factors 2001
Forslund C et al: J Orthop Res 2003
Virchenko O et al: Scand J Med Sci Sports 2005
Fealy S et al: Am J Sports Med 2006
Dines JS et al: J Shoulder Elbow Surg 2007
Saiga K et al: Biochem Biophys Res Commun 2010
Date H et al: J Orthop Res 2010
IGF-1 Proliferation of fibroblasts Abrahamsson SO et al: J Orthop Res 1991
Enhanced collagen deposition Abrahamsson SO et al: J Orthop Res 1996
Kurtz CA et al: Am J Sports Med 1999
Dahlgren LA et al: J Orthop Res 2002
Dahlgren LA et al: J Orthop Res 2005
Provenzano PP et al: BMC Physiol 2007
PDGF-B Influx of mononuclear cells and fibroblasts Lee J et al: Iowa Orthop J 1998
Enhanced angiogenesis Hildebrand KA et al: Am J Sports Med 1998
Enhanced collagen deposition Nakamura N et al: Gene Ther 1998
Kobayashi M et al: J Shoulder Elbow Surg 2006
Uggen C et al: Arthroscopy 2010
Hee CK et al: Am J Sports Med 2011
bFGF Proliferation of fibroblasts Lee J et al: Iowa Orthop J 1998
Enhanced collagen deposition Cool SM et al: Knee Surg Sports Traumatol Arthrosc 2004
Saiga K et al: Biochem Biophys Res Commun 2010
Date H et al: J Orthop Res 2010
HGF Enhanced angiogenesis Ueshima K et al: J Orthop Sci 2011
Enhanced collagen deposition
PRP Enhanced angiogenesis Murray MM et al: J Orthop Res 2006
Enhanced collagen deposition Murray MM et al: J Orthop Res 2007
Joshi SM et al: Am J Sports Med 2009
VEGF Enhanced angiogenesis Boyer MI et al: J Orthop Res 2001
Enhanced collagen deposition Petersen W et al: Arch Orthop Trauma Surg 2003
BMP-12 Enhanced ossification Aspenberg P et al: Scand J Med Sci Sports 2000
Enhanced angiogenesis Lou J et al: J Orthop Res 2001
Enhanced collagen deposition Seeherman HJ et al: J Bone Joint Surg Am 2008
bFGF, Basic fibroblast growth factor; BMP-12, bone morphogenetic protein-12; GDF, growth/differentiation factor; HGF, human growth factor;
IGF-1, insulin-like growth factor-1; PDGF-β, platelet-derived growth factor-β; PRP, plasma-rich protein; TGF-β, transforming growth factor-β;
VEGF, vascular endothelial growth factor.
cells into mature tenocytes and fibroblasts. Recent studies have to augment Achilles tendon and rotator cuff tendon repair.
identified resident tissue-specific stem cells in the perivascular However, negative clinical results have been reported, includ-
regions of native tendon and ligament that detach from vessels ing inflammatory/immunologic response to the small intestine
in response to injury, migrate into the interstitial space, and submucosa material believed to be due to residual porcine DNA
deposit extracellular matrix,70,71 although their precise potential in the implant.72,73 Various other allografts and xenografts, such
for use in augmenting tendon and ligament healing remains to as collagen allograft matrices and porcine dermal xenografts, are
be elucidated. commercially available and differ from porcine small intestine
Research has also investigated scaffold materials to augment submucosa in both biologic and mechanical composition.74,75
tendon repair and ligament reconstruction. Porcine-derived Nanomaterials are promising for tendon and ligament tissue
small intestine submucosa has been used as a collagen scaffold engineering because the microstructure of the material mimics
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Superficial layer Deep layer of

of random collagen circumferential
fibers collagen fibers
A B
Fig. 1.2 (A) Diagram of collagen fiber architecture throughout the meniscus. Collagen fibers of the thin
superficial sheet are randomly distributed in the plane of the surface and are predominantly arranged in a
circumferential fashion deep in the substance of the tissue. (B) Macrophotograph of bovine medial meniscus
with the surface layer removed, showing the large circumferentially arranged collagen bundles of the deep
zone. ([A] Modified from Bullough PG, Munuera L, Murphy J, et al. The strength of the menisci of the knee
as it relates to their fine structure. J Bone Joint Surg Br. 1970;52:564–570. [B] From Proctor CS, Schmidt MB,
Whipple RR, et al. Material properties of the normal medial bovine meniscus. J Orthop Res. 1989;7:771–782.)
native extracellular matrix. Multiphasic scaffolds are being used Anterior

to create bone-ligament composites.76 In addition to various scaf- 30°
fold materials and cell types, it has become clear that mechani- 30°
cal stimulation of the neotissue is also critical to optimize the 60°
structure and composition of the tissue.77 The specific scaffold
can be modified in vitro by seeding marrow stromal cells on the 120°
scaffold and applying cyclic stretching to increase the alignment 90° 60°
of cells, as well as to improve the production and orientation of
collagen. When applied in vivo, such a tissue-engineered scaffold
could serve to accelerate the healing process, ultimately helping 120°
150°
to make a better neoligament or tendon. 90°
150°
MENISCUS Posterior
Structure Fig. 1.3 Radial collagen fiber bundles of the meniscus. Radial tie fibers
78 consisting of branching bundles of collagen fibrils extend from the periph-
Human menisci are semilunar in shape and consist of a sparse ery of the meniscus to the inner rim in every radial section throughout
distribution of cells surrounded by an abundant extracellular the meniscus. They are more abundant in the posterior sections and
matrix.79–81 The meniscus functions to optimize force transmis- gradually diminish in number as the sections progress toward the anterior
sion and provide stability to the knee. The medial meniscus is region of the meniscus. (Modified from Kelly MA, Fithian DC, Chern
the dominant secondary stabilizer in an ACL-deficient knee KY, et al. Structure and function of meniscus: basic and clinical implica-
tions. In: Mow VC, Ratcliffe A, Woo SL, eds. Biomechanics of Diarthrodial
during the Lachman maneuver,82 whereas the lateral meniscus Joints. Vol 1. New York: Springer-Verlag; 1990.)
is the dominant secondary stabilizer in an ACL-deficient knee
during the pivot shift maneuver.83 Within the meniscus lies an
anisotropic, inhomogeneous, and highly ordered arrangement Radial sections of meniscus (Fig. 1.3) show radially oriented
of collagen fibrils. The meniscal surface is composed of a ran- bundles of collagen fibrils, or “radial tie fibers,” among the cir-
domly woven mesh of fine collagen type II fibrils that lie parallel cumferential collagen fibril bundles, weaving from the periphery
to the surface. Below this surface layer, large, circumferentially of the meniscus to the inner region.85,86 These tie fibers help to
arranged collagen fiber bundles (mostly type I) spread through increase the stiffness and the strength of the tissue in a radial
the body of the tissue (Fig. 1.2).84,85 These circumferential col- direction, thereby resisting longitudinal splitting of the collagen
lagen bundles give menisci great tensile stiffness and strength framework. In cross section, these radial tie fibers appear to be
parallel to their orientation.85 The collagen bundles insert into more abundant in the posterior sections than in the anterior
the anterior and the posterior meniscal attachment sites on the sections of the meniscus.87
tibial plateau, providing for rigid and strong attachment sites. Unlike articular cartilage, the peripheral 25% to 30% of the
Fig. 1.2A illustrates these large fiber bundles and the thin super- lateral meniscus and the peripheral 30% of the medial menis-
ficial surface layer. Fig. 1.2B is a photograph of a bovine medial cus78,88–90 have a blood supply, and the peripheral regions of the
meniscus with the surface layer removed, showing the large col- meniscus, especially the meniscal horns,91,92 have a nerve supply
lagen bundles of the deep zone. as well. Branches from the geniculate arteries form a capillary
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plexus along the peripheral borders of the menisci, with the of large aggregating proteoglycans suggests that they probably
medial inferior geniculate artery supplying the peripheral medial contribute less to the properties of meniscus than to the proper-
meniscus and the lateral inferior geniculate artery supplying the ties of articular cartilage.94,95 As with the quantitatively minor
peripheral lateral meniscus.88,89 Small radial branches project collagens, the smaller nonaggregating meniscal proteoglycans
from these circumferential parameniscal vessels into the meniscal may help to organize and stabilize the matrix, but currently their
substance.90 The central aspects of the meniscus do not have a exact function remains unknown.
direct arterial supply and instead receive nutrients primarily Noncollagenous proteins also form part of the macromolecular
through synovial fluid diffusion. framework of the meniscus and may contribute as much as 10%
of the dry weight of the tissue in some regions.80 Two specific
Extracellular Matrix noncollagenous proteins, link protein and fibronectin, have been
The mechanical functions of the menisci depend on a highly identified in the meniscus.80 Link protein is required for the
organized extracellular matrix consisting of fluid and a macro- formation of the stable proteoglycan aggregates that are capable
molecular framework formed of collagen (types I, II, III, V, and of forming strong networks.105,106 Fibronectin serves as an attach-
VI), proteoglycans, elastin, and noncollagenous proteins, along ment protein for cells in the extracellular matrix.107 Other non-
with the cells that maintain this matrix. collagenous proteins such as thrombospondin108 may serve as
Based on morphologic characteristics, two major types of adhesive proteins in the tissue, thus contributing to the structure
meniscal cells exist.80,93 Near the surface, the cells have flattened and the mechanical strength of the matrix; however, the exact
ellipsoid or fusiform shapes and are considered more fibroblastic; details of their composition and function in the meniscus remain
in the deep zone, the cells are spherical or polygonal and con- largely unknown.
sidered more chondrocytic. The superficial and the deep meniscal Finally, elastin contributes less than 1% of the dry weight of
cells appear to have different metabolic functions and perhaps the meniscus.80 The contribution of elastin to the mechanical
different responses to loading.94 Like most other mesenchymal properties of meniscal tissue is not well understood because the
cells, these cells lack cell-to-cell contacts. Because most of the sparsely distributed elastic fibers are unlikely to play a significant
cells lie at a distance from blood vessels, they rely on diffusion role in the organization of the matrix or in determining the
through the matrix for transport of nutrients and metabolites. mechanical properties of the tissue.
The membranes of meniscal cells attach to matrix macromol-
ecules through adhesion proteins (e.g., fibronectin, thrombos- Injury
pondin, and type VI collagen).80 The matrix, particularly the Traumatic meniscal tears occur most frequently in young, active
pericellular region, protects the cells from damage due to physi- people. Tension, compression, or shear forces that exceed the
ologic loading of the tissue. Deformation of the macromolecular strength of the meniscal matrix in any direction can lead to
framework of the matrix causes fluid flow through the matrix94,95 tissue failure. Acute traumatic injuries of normal meniscal sub-
and influences meniscal cell function. Because meniscal tissue stance usually produce longitudinal or transverse tears, although
is more fibrous than is hyaline cartilage, some authors have pro- the morphology of these tears can be highly variable, including
posed that meniscal cells be called fibrochondrocytes.80,96 oblique, radial horizontal, bucket-handle, and complex tears.
Water comprises 65% to 75% of the total weight of the menis- The configuration of tears due to overloading of normal menis-
cus.94,95,97 Some portion of this water may reside within the cal tissue depends strongly on the direction of the load and the
intrafibrillar space of the collagen fibers.98,99 Most of the water rate of stretch.94 Unlike acute traumatic tears through apparently
is retained within the tissue in the solvent domains of the pro- normal meniscal tissue, degenerative meniscal tears occur as a
teoglycans due to both their strong hydrophilic tendencies and result of age-related changes in the tissue. These degenerative
the Donnan osmotic pressure exerted by the counter ions associ- tears are most common in persons older than 40 years. Often,
ated with the negative charge groups on the proteoglycans.94,100,101 these persons do not recall a specific injury, or they recall only
Because the pore size of the tissue is extremely small (<60 nm), a minor load applied to the knee. Degenerative tears often have
very large hydraulic pressures are required to overcome the impact complex shapes or may appear as horizontal clefts or flaps, as
of frictional resistance when forcing fluid flow through the tissue. though they were produced by shear failure. Multiple degenera-
These interactions between water and the macromolecular frame- tive tears often occur within the same meniscus. These features
work of the matrix significantly influence the viscoelastic prop- of degenerative meniscal tears suggest that they result more from
erties of the tissue. age-related changes in the collagen-proteoglycan solid matrix
Some meniscal regions have a proteoglycan concentration of than from specific acute trauma.
up to 3% of their dry weight.80,81,95,102 Like proteoglycans from The response of meniscal tissue to tears depends on whether
other dense fibrous tissues, meniscal proteoglycans can be divided the tear occurs through a vascular or an avascular portion of the
into two general types. The large, aggregating proteoglycans meniscus.89 The peripheral, vascular regions respond to injury as
expand to fill large volumes of matrix and contribute to tissue other vascularized, dense fibrous tissues do. The tissue damage
hydration and the mechanical properties of the tissue. The smaller, initiates a sequence of cellular and vascular events including
nonaggregating proteoglycans usually have a close relationship inflammation, repair, and remodeling109 that can result in healing
with fibrillar collagen.80,103,104 The large aggregating meniscal and restoration of tissue structure and function. Although tears
proteoglycans have the same structure as the large aggregating through the vascular regions of the meniscus can typically
proteoglycans from articular cartilage.81,104 The concentration heal, tears through the avascular regions do not typically heal
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spontaneously, resulting in tissue deficiency.78,89 Therefore strate- connective tissue growth factor have been evaluated in rabbit
gies for meniscal repair in the avascular zone are continuously models,118,119 and vascular endothelial growth factor has been
being explored.110 tested in a sheep meniscus tear model.120,121 Although these cyto-
kines appear to have a positive effect on basic meniscal fibro-
Meniscal Repair chondrocyte biology, the challenge at this time is to identify the
Factors Affecting Healing optimal carrier vehicles and dosage to translate these preclinical
Repair in vascular regions of the meniscus. Partial meniscal data to clinical trials. Although some studies have suggested that
resection through the peripheral vascularized region or complete PRP, as a source of cytokines, may confer some benefit in menis-
meniscal resection initiates production of repair tissue that can cus healing,122,123 other studies have demonstrated no differences
extend from the remaining peripheral tissue into the joint.111–116 in outcomes or reoperation rates.124 In addition, in an animal
Although the repair cells usually fail to replicate normal meniscal model of meniscus injury, PRP treatment increased hypertrophic
tissue, many authors have referred to this phenomenon as menis- fibrous tissue rather than meniscal cartilage.125 Thus further
cal regeneration.114,116 Some repaired menisci grossly resemble investigation is necessary to better elucidate the role of growth
normal menisci, but the functional capabilities and mechanical factors and PRP in meniscal healing.
properties of this “regenerated” meniscal tissue have not been Cell-based approaches have also been evaluated for augmen-
comprehensively studied. Surgeons have reported meniscal regen- tation of biologic healing mechanisms. Various sources of both
eration in many clinical situations. Investigators have also exam- autogenous126 and allogeneic cells127 have been evaluated using
ined the tissue produced by meniscal regeneration in animals. different carrier materials. Both differentiated cells, such as chon-
Meniscal regeneration can occur repeatedly in the same knee115 drocytes, and undifferentiated cells, such as MSCs,128,129 have
and occasionally occurs after total knee replacement.114 In rabbits, been tested in animal models. Few human studies investigating
meniscal regeneration occurs more frequently on the medial the role of MSCs for meniscal repair have been performed.130–133
side of the knee than on the lateral side, and development of Although the authors suggest that MSCs may be effective in
degenerative changes in articular cartilage after a meniscectomy repairing meniscal tears, these studies are limited, and more
is inversely correlated with the extent of meniscal regeneration.111–113 rigorous, placebo-controlled trials are necessary.134
Synovectomy appears to prevent meniscal regeneration, which Scaffolds. The use of scaffold materials to replace a portion
suggests that synovial cells contribute to the formation of menis- of the damaged meniscus or to replace the entire structure is
cal repair tissue. The mechanisms and conditions that promote an appealing option and has the theoretical benefit of provid-
this type of repair, its functional importance, and the factors ing mechanical stability to the injured site while allowing for
related to the predictability and frequency of meniscal regenera- cell attachment and proliferation.135,136A collagen-based scaffold
tion remain unknown. (Collagen Meniscus Implant, Menaflex, ReGen Biologics, Glen
Repair in avascular portions of the meniscus. The response Rock, NJ) and a resorbable porous polyurethane-based scaffold
of meniscal tissue to tears in the avascular portion resembles (Actifit, Orteq Sport Medicine, London, United Kingdom) have
the response of articular cartilage to lacerations in many respects. demonstrated satisfactory clinical outcome in up to 80% of cases
Experimental studies show that a penetrating injury to the avas- at up to 10 years and 2 years of follow-up, respectively.137,138 Both
cular region of the meniscus causes no apparent repair or inflam- of these devices are designed for partial meniscus replacement.
matory reaction. Meniscal cells in the injured region, like Although it remains unclear whether the use of such scaffolds
chondrocytes in the region of an injury limited to the articular can affect the long-term sequelae of meniscectomy, early results
cartilage, may proliferate and synthesize new matrix, but they are promising and may represent a new horizon in the treat-
appear to be incapable of migrating to the site of the defect or ment of these complex injuries. Further optimization of these
producing enough new matrix to fill it. The ineffective response materials may occur by incorporating undifferentiated cells into
of meniscal cells in the avascular region of the meniscus has led the scaffold.
investigators to develop novel methods to stimulate repair. Some
promising approaches include creation of a vascular access channel
to the injury site and stimulation of cell migration to the avas-
ARTICULAR CARTILAGE
cular region using implantation of a fibrin clot, an artificial Synovial joints allow the rapid controlled movements necessary
matrix, or growth factors.117 Synovial abrasion has also been to support joint motion and to participate in sports. Normal
shown to stimulate proliferation of the synovial fringe into the function of these complex diarthrodial structures depends on
meniscus and allows blood vessels to enter the avascular regions. the structural integrity and macromolecular composition of
Although early results appear promising, the quality of the repair articular cartilage. Sports-related traumatic disruptions of car-
tissue, its biomechanical properties, and the long-term results tilage structure and alterations in the macromolecular composi-
of these methods have not been evaluated. tion or organization change the biomechanical properties of the
tissue, compromise joint function, and can lead to progressive
Augmentation of Meniscus Healing pain and disability.
Given the well-established poor intrinsic healing potential of The specialized composition and organization of hyaline
the meniscus, particularly in avascular regions, intense interest articular cartilage impart its unique biomechanical properties
exists regarding methods to augment healing using cytokines, that permit normal synovial joint function. In the joint, cartilage
exogenous cells, and scaffolds. Fibroblast growth factor-2 and distributes the loads of articulation, thereby minimizing peak
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stresses acting on the subchondral bone. The tensile strength of the distance from the cell.109 Morphologic changes in articular car-
tissue provides its structural integrity under such loads. Alterations tilage cells and matrix from the articular surface to the subchon-
in the mechanical properties of cartilage due to injury, disease, dral bone make it possible to identify four zones or layers of
or increasing age have not been well defined, but the available articular cartilage.
information shows that these properties change with age and
loss of structural integrity. Cartilage from skeletally immature Zones of Articular Cartilage
joints (open growth plates) is much stiffer than cartilage from Superficial zone. The thinnest zone, the superficial tangential
skeletally mature joints (closed growth plates).139 Older cartilage zone, has two layers. A sheet of fine fibrils without cells covers
and fibrillated cartilage have much lower tensile stiffness and the joint surface (see Fig. 1.4). On phase-contrast microscopy,
strength.109 Participation in sports often subjects the articular it appears as a narrow bright line, the “lamina splendens.” In the
cartilage to intense repetitive, compressive high-energy impact next layer of the superficial zone, flattened ellipsoid chondrocytes
forces that can cause tissue injury. These abnormally large forces are arranged so that their major axes are parallel to the articular
generate high shear stresses at the cartilage-subchondral bone surface (see Fig. 1.4). They synthesize a matrix that has a high
junction, causing matrix disruption and death of the articular collagen concentration and a low proteoglycan concentration
chondrocytes that may lead to early osteoarthritis.140,141 Because relative to the other cartilage zones. Water content is the highest
cartilage is aneural, patients with pure chondral injuries can in this zone, averaging 80%.143 In addition, a specific protein,
remain asymptomatic. called lubricin (or PRG4) is also only produced in this zone.
Lubricin plays an important role in joint lubrication and in
Structure and Composition of Articular Cartilage allowing frictionless articulation.145–147
Like the dense fibrous tissues and meniscus, articular cartilage Transitional zone. The transitional (middle) zone has several
consists of cells, matrix water, and a matrix macromolecular times the volume of the superficial zone (see Fig. 1.4). The cells
framework.142 Unlike the most dense fibrous tissues, cartilage of this zone assume a spheroidal shape and synthesize a matrix
lacks nerves, blood vessels, and a lymphatic system. The com- with collagen fibrils of a larger diameter and a higher concentra-
position, organization, and mechanical properties of the matrix tion of proteoglycans than is found in the superficial zone. In
of articular cartilage and the cell morphology and function vary this zone, the proteoglycan concentration is higher than in the
according to the depth from the articular surface (Fig. 1.4).143,144 superficial zone, but the water and the collagen concentrations
Matrix composition, organization, and function also vary with are lower.148
Articular surface
STZ (10%–20%)
Middle zone (40%–60%)
Deep zone (30%)
Calcified zone
A B
Subchondral bone
Fig. 1.4 Normal articular cartilage structure. Histologic (A) and schematic (B) views of a section of normal
articular cartilage. The tissue consists of four zones: the superficial tangential zone (STZ), the middle zone,
the deep zone, and the calcified zone. Notice the differences in cell alignment among zones. The cells of
the superficial zone have an ellipsoidal shape and lie with their long axes parallel to the articular surface. The
cells of the other zones have a more spheroidal shape. In the deep zone, they tend to align themselves in
columns perpendicular to the joint surface. (Schematic from Nordin M, Frankel VH. Basic Biomechanics of
the Musculoskeletal System. 2nd ed. Philadelphia: Lea & Febiger; 1989.)
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Deep zone. The chondrocytes in the deep zone resemble those

of the middle zone, but they tend to align in columns perpen- Cell-Matrix Interactions
dicular to the joint surface (see Fig. 1.4). This zone contains the Maintenance of cartilage depends on continual complex interac-
collagen fibrils with the largest diameter, the highest concentrations between chondrocytes and the matrix they synthesize.
tion of proteoglycans, and the lowest concentration of water. Normal degradation of matrix macromolecules, especially pro-
The collagen fibers of this zone pass through the tidemark (a teoglycans, requires that the chondrocytes continually synthesize
thin basophilic line seen on light microscopic sections that marks new molecules.143,144 If the cells did not replace the lost proteo-
the boundary between calcified and uncalcified cartilage)141 into glycans, the tissue would deteriorate. Mechanical loading also
the calcified zone.149 affects cartilage homeostasis.156,157
Calcified cartilage zone. A zone of calcified cartilage lies Chondrocytes respond to changes in patterns of matrix defor-
between the deep zone of uncalcified cartilage and the subchon- mation due to persistent changes in joint use. Both mechanical
dral bone. The calcified layer plays an integral role in securing and physicochemical events during matrix deformation likely
the cartilage to bone by anchoring the collagen fibrils of the play significant roles. A chondrocyte embedded in the charged
deep zone to the subchondral bone. In this zone, the cell popula- extracellular matrix may exist in either an undeformed state or
tion is scarce and chondrocytes are hypertrophic. Type X collagen a deformed state. Deformation during compression alters the
is present in the calcified cartilage. charge density around the cells and induces a streaming potential
throughout the tissue. These physicochemical effects vary accord-
Chondrocytes ing to proteoglycan concentration relative to depth from the
The chondrocyte is the predominant cell in cartilage. Chondro- surface in the different zones of the charged collagen-proteoglycan
cytes contribute only 5% or less to the total volume of cartilage. extracellular matrix143,144 and are important in modulating chon-
Like other mesenchymal cells, chondrocytes surround themselves drocyte proteoglycan biosynthesis.152,158–161 In addition to these
with their extracellular matrix and rarely form cell-to-cell contacts. events, biochemical agents such as growth factors,162 cytokines,
In normal cartilage, they are isolated. Because the tissue lacks and enzymes are also potent stimulators of chondrocytes. Alto-
blood vessels, the cells depend on diffusion through the matrix gether, studies addressing these important questions offer great
for their nutrition and rely primarily on anaerobic metabolism. challenges for the future.
After completion of skeletal growth, chondrocytes rarely divide,
but throughout life they synthesize and maintain the extracel- Relevance for Articular Cartilage Repair
lular matrix that gives cartilage its essential material properties. The typical tissue response of vascularized connective tissues to
Synthesis and turnover of proteoglycans are relatively fast, whereas injury follows a cascade of inflammation, repair, and scar remod-
collagen synthesis and turnover are very slow.150,151 The limited eling, which is facilitated by cells and other mediators brought
potential for chondrocyte replication contributes to the limited in from the surrounding vasculature. However, because hyaline
inherent capacity of cartilage to regenerate or heal after injury. cartilage is avascular, this vital response cannot be generated,
and the intrinsic reparative ability of cartilage is very low.163–165
Extracellular Matrix In healthy cartilage, a homeostasis of extracellular matrix metabo-
Water contributes up to 80% of the wet weight of articular car- lism balances the degradation of macromolecules with their
tilage. The interaction of water with the matrix macromolecules, replacement through newly synthesized products. Insult to the
particularly the large aggregating proteoglycans, significantly influ- cartilage can lead to imbalance of this equilibrium and a shift
ences the material properties of the articular cartilage.109,143,152,153 toward degradation, leading to progression of the chondral defect
This tissue fluid contains gases, small proteins, metabolites, and a and potentially, osteoarthritis. Factors associated with this physi-
high concentration of cations that balance the negatively charged ologic imbalance and repair response include joint loading, depth
proteoglycans.152,154 The interaction between proteoglycans and of the defect, size of the defect, and patient age.
tissue fluid significantly influences the compressive stiffness and
resilience of articular cartilage.139,152 Joint Loading
Collagens contribute approximately 60% of the dry weight Acute or repetitive direct blunt trauma or abnormal loading can
of cartilage, proteoglycans contribute 25% to 35%, and the non- cause a spectrum of cartilage injuries ranging from those isolated
collagenous proteins and glycoproteins contribute 15% to 20%. to microscopic matrix damage to those that lead to visible fis-
Collagens are distributed relatively uniformly throughout the sures causing matrix disruption and chondrocyte death. Abnormal
depth of the cartilage except in the collagen-rich region near loading can be caused by mechanical malalignment or concomi-
the surface. The collagen fibrillar meshwork and cross-linking tant ligament injury that leads to excessive focal stresses on the
give cartilage its form and tensile strength.139,155 Proteoglycans cartilage. Loss of proteoglycans typically occurs before other
and noncollagenous proteins bind to the collagenous meshwork signs of tissue injury166,167 and may be due to either increased
or become mechanically entrapped within it, and water fills this degradation or altered synthesis of the molecules, including the
molecular framework. Proteoglycans give cartilage its stiffness collagen fibrils, thus increasing the vulnerability of the tissue to
in compression and its resilience. Some noncollagenous proteins damage from further impact loading.166–168 Disruption of the
organize and stabilize the matrix macromolecular framework, surface collagen matrix leads to increased hydration, fissuring
whereas others bind chondrocytes to the macromolecules of the in the cartilage, and thickening of subchondral bone. A study
matrix. of the response of human articular cartilage to blunt trauma
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showed that impact loads exceeding 25 N/m2 (25 megapascal restorative potential, has demonstrated promising early results
[MPa]) caused chondrocyte death and cartilage fissures.149 for treatment of cartilage defects of the knee.179,180 Future devel-
opments include improved scaffolds,178,181 augmentation with
Depth of the Defect therapeutic factors such as proteins or genes,182 and the use of
Articular cartilage defects are generally classified as chondral or MSCs.182,183 Furthermore, small molecules and activation of
osteochondral, depending on the depth. Chondral defects can endogenous repair (homing of intrinsic progenitors/MSCs) are
be further classified into partial thickness or full thickness (i.e., potential forthcoming therapeutic avenues.184,185
down to subchondral bone). The repair response depends on
whether the injury extends down to the subchondral vascular BONE
bone marrow. For partial-thickness chondral injuries, the local
response depends entirely on chondrocytes near the injury site, Types of Bone
which proliferate and increase the synthesis of matrix macro- Normal bone is lamellar and can be classified as cortical or can-
molecules.109,169 However, the newly synthesized matrix and the cellous. Immature bone and pathologic bone are woven and, in
proliferating chondrocytes are unable to fill the tissue defect, contrast to lamellar bone, have more random orientation with
and soon after injury, the increased proliferative and synthetic more osteocytes, increased turnover, and inferior integrity. Lamel-
activity ceases. Because chondrocytes cannot repair these matrix lar bone is stress oriented, whereas woven bone is not stress
injuries, the fissures either remain unchanged or progress. Injuries oriented.
that extend down into the subchondral bone marrow lead to Cortical bone (compact bone) (Fig. 1.5) makes up 80% of
migration of osteoprogenitor cells into the defect region and the skeleton and is composed of tightly packed osteons or haver-
synthesis of a new fibrocartilaginous tissue. However, this repair sian systems which are connected by haversian (or Volkmann)
tissue is biomechanically and structurally inferior to hyaline canals. These canals contain arterioles, venules, capillaries, nerves,
cartilage and thus prone to breakdown with time and loading.170,171 and possibly lymphatic channels. Interstitial lamellae lie between
the osteons. Fibrils frequently connect lamellae but do not cross
Size of the Defect cement lines. Cement lines define the outer border of an osteon
Smaller defects are less likely to affect the stress distribution on and represent the area where bone resorption has stopped and
the subchondral bone and progress in size, whereas larger defects new bone formation has begun. Nutrition occurs through the
are more likely to progress due to increased rim stresses and an intraosseous circulation, which involves networks of canals and
inadequate repair response. A study in horses revealed that defects
less than 3 mm in diameter may lead to complete repair after 9
months, whereas those larger in size (up to 21 mm in diameter)
failed to heal.172
Age
Immature
Articular cartilage undergoes significant structural, matrix com- Cortical
position, and mechanical changes with age.104,139,173,174 As with
most type of cells in the body, mitotic and synthetic activities
of chondrocytes decline with age.175 These changes are responsible
for higher incidence of chondral lesions and development of Cancellous
Pathologic
osteoarthritis in older patients. As a result, any reparative response (giant cell
tumor)
or ability to maintain extracellular matrix homeostasis decreases
with older age. Animal studies in rabbits have demonstrated a
better reparative response for chondral defects in younger animals Cement line
compared with older ones.176,177 Interstitial lamellae
Canaliculi
Clinical Relevance and Further Developments
Small, symptomatic chondral defects may be treated by marrow- Osteocyte
stimulating techniques such as microfracture. However, the Haversian canal
resultant fibrocartilage repair tissue after microfracture is his-
tologically different and biomechanically inferior to native hyaline
cartilage.178 For larger lesions, a myriad of options is available, Cortical bone detail
including osteochondral autografts or allografts, autologous
chondrocyte implantation (ACI), or matrix-induced autologous
chondrocyte implantation (MACI). Osteochondral grafts are Fig. 1.5 Types of bone. Cortical bone consists of tightly packed osteons.
Cancellous bone consists of a meshwork of trabeculae. In immature
able to treat defects that extend into the subchondral bone,
bone, unmineralized osteoid lines the immature trabeculae. In pathologic
whereas ACI and MACI require well-preserved bone stock at bone, atypical osteoblasts and architectural disorganization are seen.
the base of the chondral defect. The use of particulated juvenile (From Brinker MR, Miller MD. Fundamentals of Orthopaedics. Philadel-
cartilage allograft, which may have increased proliferative and phia: WB Saunders; 1999.)
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DANCE ON STILTS AT THE GIRLS’ UNYAGO, NIUCHI
Newala, too, suffers from the distance of its water-supply—at least

the Newala of to-day does; there was once another Newala in a lovely
valley at the foot of the plateau. I visited it and found scarcely a trace
of houses, only a Christian cemetery, with the graves of several
missionaries and their converts, remaining as a monument of its
former glories. But the surroundings are wonderfully beautiful. A
thick grove of splendid mango-trees closes in the weather-worn
crosses and headstones; behind them, combining the useful and the
agreeable, is a whole plantation of lemon-trees covered with ripe
fruit; not the small African kind, but a much larger and also juicier
imported variety, which drops into the hands of the passing traveller,
without calling for any exertion on his part. Old Newala is now under
the jurisdiction of the native pastor, Daudi, at Chingulungulu, who,
as I am on very friendly terms with him, allows me, as a matter of
course, the use of this lemon-grove during my stay at Newala.
FEET MUTILATED BY THE RAVAGES OF THE “JIGGER”
(Sarcopsylla penetrans)
The water-supply of New Newala is in the bottom of the valley,

some 1,600 feet lower down. The way is not only long and fatiguing,
but the water, when we get it, is thoroughly bad. We are suffering not
only from this, but from the fact that the arrangements at Newala are
nothing short of luxurious. We have a separate kitchen—a hut built
against the boma palisade on the right of the baraza, the interior of
which is not visible from our usual position. Our two cooks were not
long in finding this out, and they consequently do—or rather neglect
to do—what they please. In any case they do not seem to be very
particular about the boiling of our drinking-water—at least I can
attribute to no other cause certain attacks of a dysenteric nature,
from which both Knudsen and I have suffered for some time. If a
man like Omari has to be left unwatched for a moment, he is capable
of anything. Besides this complaint, we are inconvenienced by the
state of our nails, which have become as hard as glass, and crack on
the slightest provocation, and I have the additional infliction of
pimples all over me. As if all this were not enough, we have also, for
the last week been waging war against the jigger, who has found his
Eldorado in the hot sand of the Makonde plateau. Our men are seen
all day long—whenever their chronic colds and the dysentery likewise
raging among them permit—occupied in removing this scourge of
Africa from their feet and trying to prevent the disastrous
consequences of its presence. It is quite common to see natives of
this place with one or two toes missing; many have lost all their toes,
or even the whole front part of the foot, so that a well-formed leg
ends in a shapeless stump. These ravages are caused by the female of
Sarcopsylla penetrans, which bores its way under the skin and there
develops an egg-sac the size of a pea. In all books on the subject, it is
stated that one’s attention is called to the presence of this parasite by
an intolerable itching. This agrees very well with my experience, so
far as the softer parts of the sole, the spaces between and under the
toes, and the side of the foot are concerned, but if the creature
penetrates through the harder parts of the heel or ball of the foot, it
may escape even the most careful search till it has reached maturity.
Then there is no time to be lost, if the horrible ulceration, of which
we see cases by the dozen every day, is to be prevented. It is much
easier, by the way, to discover the insect on the white skin of a
European than on that of a native, on which the dark speck scarcely
shows. The four or five jiggers which, in spite of the fact that I
constantly wore high laced boots, chose my feet to settle in, were
taken out for me by the all-accomplished Knudsen, after which I
thought it advisable to wash out the cavities with corrosive
sublimate. The natives have a different sort of disinfectant—they fill
the hole with scraped roots. In a tiny Makua village on the slope of
the plateau south of Newala, we saw an old woman who had filled all
the spaces under her toe-nails with powdered roots by way of
prophylactic treatment. What will be the result, if any, who can say?
The rest of the many trifling ills which trouble our existence are
really more comic than serious. In the absence of anything else to
smoke, Knudsen and I at last opened a box of cigars procured from
the Indian store-keeper at Lindi, and tried them, with the most
distressing results. Whether they contain opium or some other
narcotic, neither of us can say, but after the tenth puff we were both
“off,” three-quarters stupefied and unspeakably wretched. Slowly we
recovered—and what happened next? Half-an-hour later we were
once more smoking these poisonous concoctions—so insatiable is the
craving for tobacco in the tropics.
Even my present attacks of fever scarcely deserve to be taken
seriously. I have had no less than three here at Newala, all of which
have run their course in an incredibly short time. In the early
afternoon, I am busy with my old natives, asking questions and
making notes. The strong midday coffee has stimulated my spirits to
an extraordinary degree, the brain is active and vigorous, and work
progresses rapidly, while a pleasant warmth pervades the whole
body. Suddenly this gives place to a violent chill, forcing me to put on
my overcoat, though it is only half-past three and the afternoon sun
is at its hottest. Now the brain no longer works with such acuteness
and logical precision; more especially does it fail me in trying to
establish the syntax of the difficult Makua language on which I have
ventured, as if I had not enough to do without it. Under the
circumstances it seems advisable to take my temperature, and I do
so, to save trouble, without leaving my seat, and while going on with
my work. On examination, I find it to be 101·48°. My tutors are
abruptly dismissed and my bed set up in the baraza; a few minutes
later I am in it and treating myself internally with hot water and
lemon-juice.
Three hours later, the thermometer marks nearly 104°, and I make
them carry me back into the tent, bed and all, as I am now perspiring
heavily, and exposure to the cold wind just beginning to blow might
mean a fatal chill. I lie still for a little while, and then find, to my
great relief, that the temperature is not rising, but rather falling. This
is about 7.30 p.m. At 8 p.m. I find, to my unbounded astonishment,
that it has fallen below 98·6°, and I feel perfectly well. I read for an
hour or two, and could very well enjoy a smoke, if I had the
wherewithal—Indian cigars being out of the question.
Having no medical training, I am at a loss to account for this state
of things. It is impossible that these transitory attacks of high fever
should be malarial; it seems more probable that they are due to a
kind of sunstroke. On consulting my note-book, I become more and
more inclined to think this is the case, for these attacks regularly
follow extreme fatigue and long exposure to strong sunshine. They at
least have the advantage of being only short interruptions to my
work, as on the following morning I am always quite fresh and fit.
My treasure of a cook is suffering from an enormous hydrocele which
makes it difficult for him to get up, and Moritz is obliged to keep in
the dark on account of his inflamed eyes. Knudsen’s cook, a raw boy
from somewhere in the bush, knows still less of cooking than Omari;
consequently Nils Knudsen himself has been promoted to the vacant
post. Finding that we had come to the end of our supplies, he began
by sending to Chingulungulu for the four sucking-pigs which we had
bought from Matola and temporarily left in his charge; and when
they came up, neatly packed in a large crate, he callously slaughtered
the biggest of them. The first joint we were thoughtless enough to
entrust for roasting to Knudsen’s mshenzi cook, and it was
consequently uneatable; but we made the rest of the animal into a
jelly which we ate with great relish after weeks of underfeeding,
consuming incredible helpings of it at both midday and evening
meals. The only drawback is a certain want of variety in the tinned
vegetables. Dr. Jäger, to whom the Geographical Commission
entrusted the provisioning of the expeditions—mine as well as his
own—because he had more time on his hands than the rest of us,
seems to have laid in a huge stock of Teltow turnips,[46] an article of
food which is all very well for occasional use, but which quickly palls
when set before one every day; and we seem to have no other tins
left. There is no help for it—we must put up with the turnips; but I
am certain that, once I am home again, I shall not touch them for ten
years to come.
Amid all these minor evils, which, after all, go to make up the
genuine flavour of Africa, there is at least one cheering touch:
Knudsen has, with the dexterity of a skilled mechanic, repaired my 9
× 12 cm. camera, at least so far that I can use it with a little care.
How, in the absence of finger-nails, he was able to accomplish such a
ticklish piece of work, having no tool but a clumsy screw-driver for
taking to pieces and putting together again the complicated
mechanism of the instantaneous shutter, is still a mystery to me; but
he did it successfully. The loss of his finger-nails shows him in a light
contrasting curiously enough with the intelligence evinced by the
above operation; though, after all, it is scarcely surprising after his
ten years’ residence in the bush. One day, at Lindi, he had occasion
to wash a dog, which must have been in need of very thorough
cleansing, for the bottle handed to our friend for the purpose had an
extremely strong smell. Having performed his task in the most
conscientious manner, he perceived with some surprise that the dog
did not appear much the better for it, and was further surprised by
finding his own nails ulcerating away in the course of the next few
days. “How was I to know that carbolic acid has to be diluted?” he
mutters indignantly, from time to time, with a troubled gaze at his
mutilated finger-tips.
Since we came to Newala we have been making excursions in all
directions through the surrounding country, in accordance with old
habit, and also because the akida Sefu did not get together the tribal
elders from whom I wanted information so speedily as he had
promised. There is, however, no harm done, as, even if seen only
from the outside, the country and people are interesting enough.
The Makonde plateau is like a large rectangular table rounded off
at the corners. Measured from the Indian Ocean to Newala, it is
about seventy-five miles long, and between the Rovuma and the
Lukuledi it averages fifty miles in breadth, so that its superficial area
is about two-thirds of that of the kingdom of Saxony. The surface,
however, is not level, but uniformly inclined from its south-western
edge to the ocean. From the upper edge, on which Newala lies, the
eye ranges for many miles east and north-east, without encountering
any obstacle, over the Makonde bush. It is a green sea, from which
here and there thick clouds of smoke rise, to show that it, too, is
inhabited by men who carry on their tillage like so many other
primitive peoples, by cutting down and burning the bush, and
manuring with the ashes. Even in the radiant light of a tropical day
such a fire is a grand sight.
Much less effective is the impression produced just now by the
great western plain as seen from the edge of the plateau. As often as
time permits, I stroll along this edge, sometimes in one direction,
sometimes in another, in the hope of finding the air clear enough to
let me enjoy the view; but I have always been disappointed.
Wherever one looks, clouds of smoke rise from the burning bush,
and the air is full of smoke and vapour. It is a pity, for under more
favourable circumstances the panorama of the whole country up to
the distant Majeje hills must be truly magnificent. It is of little use
taking photographs now, and an outline sketch gives a very poor idea
of the scenery. In one of these excursions I went out of my way to
make a personal attempt on the Makonde bush. The present edge of
the plateau is the result of a far-reaching process of destruction
through erosion and denudation. The Makonde strata are
everywhere cut into by ravines, which, though short, are hundreds of
yards in depth. In consequence of the loose stratification of these
beds, not only are the walls of these ravines nearly vertical, but their
upper end is closed by an equally steep escarpment, so that the
western edge of the Makonde plateau is hemmed in by a series of
deep, basin-like valleys. In order to get from one side of such a ravine
to the other, I cut my way through the bush with a dozen of my men.
It was a very open part, with more grass than scrub, but even so the
short stretch of less than two hundred yards was very hard work; at
the end of it the men’s calicoes were in rags and they themselves
bleeding from hundreds of scratches, while even our strong khaki
suits had not escaped scatheless.
NATIVE PATH THROUGH THE MAKONDE BUSH, NEAR

MAHUTA
I see increasing reason to believe that the view formed some time
back as to the origin of the Makonde bush is the correct one. I have
no doubt that it is not a natural product, but the result of human
occupation. Those parts of the high country where man—as a very
slight amount of practice enables the eye to perceive at once—has not
yet penetrated with axe and hoe, are still occupied by a splendid
timber forest quite able to sustain a comparison with our mixed
forests in Germany. But wherever man has once built his hut or tilled
his field, this horrible bush springs up. Every phase of this process
may be seen in the course of a couple of hours’ walk along the main
road. From the bush to right or left, one hears the sound of the axe—
not from one spot only, but from several directions at once. A few
steps further on, we can see what is taking place. The brush has been
cut down and piled up in heaps to the height of a yard or more,
between which the trunks of the large trees stand up like the last
pillars of a magnificent ruined building. These, too, present a
melancholy spectacle: the destructive Makonde have ringed them—
cut a broad strip of bark all round to ensure their dying off—and also
piled up pyramids of brush round them. Father and son, mother and
son-in-law, are chopping away perseveringly in the background—too
busy, almost, to look round at the white stranger, who usually excites
so much interest. If you pass by the same place a week later, the piles
of brushwood have disappeared and a thick layer of ashes has taken
the place of the green forest. The large trees stretch their
smouldering trunks and branches in dumb accusation to heaven—if
they have not already fallen and been more or less reduced to ashes,
perhaps only showing as a white stripe on the dark ground.
This work of destruction is carried out by the Makonde alike on the
virgin forest and on the bush which has sprung up on sites already
cultivated and deserted. In the second case they are saved the trouble
of burning the large trees, these being entirely absent in the
secondary bush.
After burning this piece of forest ground and loosening it with the
hoe, the native sows his corn and plants his vegetables. All over the
country, he goes in for bed-culture, which requires, and, in fact,
receives, the most careful attention. Weeds are nowhere tolerated in
the south of German East Africa. The crops may fail on the plains,
where droughts are frequent, but never on the plateau with its
abundant rains and heavy dews. Its fortunate inhabitants even have
the satisfaction of seeing the proud Wayao and Wamakua working
for them as labourers, driven by hunger to serve where they were
accustomed to rule.
But the light, sandy soil is soon exhausted, and would yield no
harvest the second year if cultivated twice running. This fact has
been familiar to the native for ages; consequently he provides in
time, and, while his crop is growing, prepares the next plot with axe
and firebrand. Next year he plants this with his various crops and
lets the first piece lie fallow. For a short time it remains waste and
desolate; then nature steps in to repair the destruction wrought by
man; a thousand new growths spring out of the exhausted soil, and
even the old stumps put forth fresh shoots. Next year the new growth
is up to one’s knees, and in a few years more it is that terrible,
impenetrable bush, which maintains its position till the black
occupier of the land has made the round of all the available sites and
come back to his starting point.
The Makonde are, body and soul, so to speak, one with this bush.
According to my Yao informants, indeed, their name means nothing
else but “bush people.” Their own tradition says that they have been
settled up here for a very long time, but to my surprise they laid great
stress on an original immigration. Their old homes were in the
south-east, near Mikindani and the mouth of the Rovuma, whence
their peaceful forefathers were driven by the continual raids of the
Sakalavas from Madagascar and the warlike Shirazis[47] of the coast,
to take refuge on the almost inaccessible plateau. I have studied
African ethnology for twenty years, but the fact that changes of
population in this apparently quiet and peaceable corner of the earth
could have been occasioned by outside enterprises taking place on
the high seas, was completely new to me. It is, no doubt, however,
correct.
The charming tribal legend of the Makonde—besides informing us
of other interesting matters—explains why they have to live in the
thickest of the bush and a long way from the edge of the plateau,
instead of making their permanent homes beside the purling brooks
and springs of the low country.
“The place where the tribe originated is Mahuta, on the southern
side of the plateau towards the Rovuma, where of old time there was
nothing but thick bush. Out of this bush came a man who never
washed himself or shaved his head, and who ate and drank but little.
He went out and made a human figure from the wood of a tree
growing in the open country, which he took home to his abode in the
bush and there set it upright. In the night this image came to life and
was a woman. The man and woman went down together to the
Rovuma to wash themselves. Here the woman gave birth to a still-
born child. They left that place and passed over the high land into the
valley of the Mbemkuru, where the woman had another child, which
was also born dead. Then they returned to the high bush country of
Mahuta, where the third child was born, which lived and grew up. In
course of time, the couple had many more children, and called
themselves Wamatanda. These were the ancestral stock of the
Makonde, also called Wamakonde,[48] i.e., aborigines. Their
forefather, the man from the bush, gave his children the command to
bury their dead upright, in memory of the mother of their race who
was cut out of wood and awoke to life when standing upright. He also
warned them against settling in the valleys and near large streams,
for sickness and death dwelt there. They were to make it a rule to
have their huts at least an hour’s walk from the nearest watering-
place; then their children would thrive and escape illness.”
The explanation of the name Makonde given by my informants is
somewhat different from that contained in the above legend, which I
extract from a little book (small, but packed with information), by
Pater Adams, entitled Lindi und sein Hinterland. Otherwise, my
results agree exactly with the statements of the legend. Washing?
Hapana—there is no such thing. Why should they do so? As it is, the
supply of water scarcely suffices for cooking and drinking; other
people do not wash, so why should the Makonde distinguish himself
by such needless eccentricity? As for shaving the head, the short,
woolly crop scarcely needs it,[49] so the second ancestral precept is
likewise easy enough to follow. Beyond this, however, there is
nothing ridiculous in the ancestor’s advice. I have obtained from
various local artists a fairly large number of figures carved in wood,
ranging from fifteen to twenty-three inches in height, and
representing women belonging to the great group of the Mavia,
Makonde, and Matambwe tribes. The carving is remarkably well
done and renders the female type with great accuracy, especially the
keloid ornamentation, to be described later on. As to the object and
meaning of their works the sculptors either could or (more probably)
would tell me nothing, and I was forced to content myself with the
scanty information vouchsafed by one man, who said that the figures
were merely intended to represent the nembo—the artificial
deformations of pelele, ear-discs, and keloids. The legend recorded
by Pater Adams places these figures in a new light. They must surely
be more than mere dolls; and we may even venture to assume that
they are—though the majority of present-day Makonde are probably
unaware of the fact—representations of the tribal ancestress.
The references in the legend to the descent from Mahuta to the
Rovuma, and to a journey across the highlands into the Mbekuru
valley, undoubtedly indicate the previous history of the tribe, the
travels of the ancestral pair typifying the migrations of their
descendants. The descent to the neighbouring Rovuma valley, with
its extraordinary fertility and great abundance of game, is intelligible
at a glance—but the crossing of the Lukuledi depression, the ascent
to the Rondo Plateau and the descent to the Mbemkuru, also lie
within the bounds of probability, for all these districts have exactly
the same character as the extreme south. Now, however, comes a
point of especial interest for our bacteriological age. The primitive
Makonde did not enjoy their lives in the marshy river-valleys.
Disease raged among them, and many died. It was only after they
had returned to their original home near Mahuta, that the health
conditions of these people improved. We are very apt to think of the
African as a stupid person whose ignorance of nature is only equalled
by his fear of it, and who looks on all mishaps as caused by evil
spirits and malignant natural powers. It is much more correct to
assume in this case that the people very early learnt to distinguish
districts infested with malaria from those where it is absent.
This knowledge is crystallized in the
ancestral warning against settling in the
valleys and near the great waters, the
dwelling-places of disease and death. At the
same time, for security against the hostile
Mavia south of the Rovuma, it was enacted
that every settlement must be not less than a
certain distance from the southern edge of the
plateau. Such in fact is their mode of life at the
present day. It is not such a bad one, and
certainly they are both safer and more
comfortable than the Makua, the recent
intruders from the south, who have made USUAL METHOD OF
good their footing on the western edge of the CLOSING HUT-DOOR
plateau, extending over a fairly wide belt of
country. Neither Makua nor Makonde show in their dwellings
anything of the size and comeliness of the Yao houses in the plain,
especially at Masasi, Chingulungulu and Zuza’s. Jumbe Chauro, a
Makonde hamlet not far from Newala, on the road to Mahuta, is the
most important settlement of the tribe I have yet seen, and has fairly
spacious huts. But how slovenly is their construction compared with
the palatial residences of the elephant-hunters living in the plain.
The roofs are still more untidy than in the general run of huts during
the dry season, the walls show here and there the scanty beginnings
or the lamentable remains of the mud plastering, and the interior is a
veritable dog-kennel; dirt, dust and disorder everywhere. A few huts
only show any attempt at division into rooms, and this consists
merely of very roughly-made bamboo partitions. In one point alone
have I noticed any indication of progress—in the method of fastening
the door. Houses all over the south are secured in a simple but
ingenious manner. The door consists of a set of stout pieces of wood
or bamboo, tied with bark-string to two cross-pieces, and moving in
two grooves round one of the door-posts, so as to open inwards. If
the owner wishes to leave home, he takes two logs as thick as a man’s
upper arm and about a yard long. One of these is placed obliquely
against the middle of the door from the inside, so as to form an angle
of from 60° to 75° with the ground. He then places the second piece
horizontally across the first, pressing it downward with all his might.
It is kept in place by two strong posts planted in the ground a few
inches inside the door. This fastening is absolutely safe, but of course
cannot be applied to both doors at once, otherwise how could the
owner leave or enter his house? I have not yet succeeded in finding
out how the back door is fastened.
MAKONDE LOCK AND KEY AT JUMBE CHAURO

This is the general way of closing a house. The Makonde at Jumbe
Chauro, however, have a much more complicated, solid and original
one. Here, too, the door is as already described, except that there is
only one post on the inside, standing by itself about six inches from
one side of the doorway. Opposite this post is a hole in the wall just
large enough to admit a man’s arm. The door is closed inside by a
large wooden bolt passing through a hole in this post and pressing
with its free end against the door. The other end has three holes into
which fit three pegs running in vertical grooves inside the post. The
door is opened with a wooden key about a foot long, somewhat
curved and sloped off at the butt; the other end has three pegs
corresponding to the holes, in the bolt, so that, when it is thrust
through the hole in the wall and inserted into the rectangular
opening in the post, the pegs can be lifted and the bolt drawn out.[50]
MODE OF INSERTING THE KEY
With no small pride first one householder and then a second

showed me on the spot the action of this greatest invention of the
Makonde Highlands. To both with an admiring exclamation of
“Vizuri sana!” (“Very fine!”). I expressed the wish to take back these
marvels with me to Ulaya, to show the Wazungu what clever fellows
the Makonde are. Scarcely five minutes after my return to camp at
Newala, the two men came up sweating under the weight of two
heavy logs which they laid down at my feet, handing over at the same
time the keys of the fallen fortress. Arguing, logically enough, that if
the key was wanted, the lock would be wanted with it, they had taken
their axes and chopped down the posts—as it never occurred to them
to dig them out of the ground and so bring them intact. Thus I have
two badly damaged specimens, and the owners, instead of praise,
come in for a blowing-up.
The Makua huts in the environs of Newala are especially
miserable; their more than slovenly construction reminds one of the
temporary erections of the Makua at Hatia’s, though the people here
have not been concerned in a war. It must therefore be due to
congenital idleness, or else to the absence of a powerful chief. Even
the baraza at Mlipa’s, a short hour’s walk south-east of Newala,
shares in this general neglect. While public buildings in this country
are usually looked after more or less carefully, this is in evident
danger of being blown over by the first strong easterly gale. The only
attractive object in this whole district is the grave of the late chief
Mlipa. I visited it in the morning, while the sun was still trying with
partial success to break through the rolling mists, and the circular
grove of tall euphorbias, which, with a broken pot, is all that marks
the old king’s resting-place, impressed one with a touch of pathos.
Even my very materially-minded carriers seemed to feel something
of the sort, for instead of their usual ribald songs, they chanted
solemnly, as we marched on through the dense green of the Makonde
bush:—
“We shall arrive with the great master; we stand in a row and have
no fear about getting our food and our money from the Serkali (the
Government). We are not afraid; we are going along with the great
master, the lion; we are going down to the coast and back.”
With regard to the characteristic features of the various tribes here
on the western edge of the plateau, I can arrive at no other
conclusion than the one already come to in the plain, viz., that it is
impossible for anyone but a trained anthropologist to assign any
given individual at once to his proper tribe. In fact, I think that even
an anthropological specialist, after the most careful examination,
might find it a difficult task to decide. The whole congeries of peoples
collected in the region bounded on the west by the great Central
African rift, Tanganyika and Nyasa, and on the east by the Indian
Ocean, are closely related to each other—some of their languages are
only distinguished from one another as dialects of the same speech,
and no doubt all the tribes present the same shape of skull and
structure of skeleton. Thus, surely, there can be no very striking
differences in outward appearance.
Even did such exist, I should have no time
to concern myself with them, for day after day,
I have to see or hear, as the case may be—in
any case to grasp and record—an
extraordinary number of ethnographic
phenomena. I am almost disposed to think it
fortunate that some departments of inquiry, at
least, are barred by external circumstances.
Chief among these is the subject of iron-
working. We are apt to think of Africa as a
country where iron ore is everywhere, so to
speak, to be picked up by the roadside, and
where it would be quite surprising if the
inhabitants had not learnt to smelt the
material ready to their hand. In fact, the
knowledge of this art ranges all over the
continent, from the Kabyles in the north to the
Kafirs in the south. Here between the Rovuma
and the Lukuledi the conditions are not so
favourable. According to the statements of the
Makonde, neither ironstone nor any other
form of iron ore is known to them. They have
not therefore advanced to the art of smelting
the metal, but have hitherto bought all their
THE ANCESTRESS OF
THE MAKONDE
iron implements from neighbouring tribes.
Even in the plain the inhabitants are not much
better off. Only one man now living is said to
understand the art of smelting iron. This old fundi lives close to
Huwe, that isolated, steep-sided block of granite which rises out of
the green solitude between Masasi and Chingulungulu, and whose
jagged and splintered top meets the traveller’s eye everywhere. While
still at Masasi I wished to see this man at work, but was told that,
frightened by the rising, he had retired across the Rovuma, though
he would soon return. All subsequent inquiries as to whether the
fundi had come back met with the genuine African answer, “Bado”
(“Not yet”).
BRAZIER
Some consolation was afforded me by a brassfounder, whom I

came across in the bush near Akundonde’s. This man is the favourite
of women, and therefore no doubt of the gods; he welds the glittering
brass rods purchased at the coast into those massive, heavy rings
which, on the wrists and ankles of the local fair ones, continually give
me fresh food for admiration. Like every decent master-craftsman he
had all his tools with him, consisting of a pair of bellows, three
crucibles and a hammer—nothing more, apparently. He was quite
willing to show his skill, and in a twinkling had fixed his bellows on
the ground. They are simply two goat-skins, taken off whole, the four
legs being closed by knots, while the upper opening, intended to
admit the air, is kept stretched by two pieces of wood. At the lower
end of the skin a smaller opening is left into which a wooden tube is
stuck. The fundi has quickly borrowed a heap of wood-embers from
the nearest hut; he then fixes the free ends of the two tubes into an
earthen pipe, and clamps them to the ground by means of a bent
piece of wood. Now he fills one of his small clay crucibles, the dross
on which shows that they have been long in use, with the yellow
material, places it in the midst of the embers, which, at present are
only faintly glimmering, and begins his work. In quick alternation
the smith’s two hands move up and down with the open ends of the
bellows; as he raises his hand he holds the slit wide open, so as to let
the air enter the skin bag unhindered. In pressing it down he closes
the bag, and the air puffs through the bamboo tube and clay pipe into
the fire, which quickly burns up. The smith, however, does not keep
on with this work, but beckons to another man, who relieves him at
the bellows, while he takes some more tools out of a large skin pouch
carried on his back. I look on in wonder as, with a smooth round
stick about the thickness of a finger, he bores a few vertical holes into
the clean sand of the soil. This should not be difficult, yet the man
seems to be taking great pains over it. Then he fastens down to the
ground, with a couple of wooden clamps, a neat little trough made by
splitting a joint of bamboo in half, so that the ends are closed by the
two knots. At last the yellow metal has attained the right consistency,
and the fundi lifts the crucible from the fire by means of two sticks
split at the end to serve as tongs. A short swift turn to the left—a
tilting of the crucible—and the molten brass, hissing and giving forth
clouds of smoke, flows first into the bamboo mould and then into the
holes in the ground.
The technique of this backwoods craftsman may not be very far
advanced, but it cannot be denied that he knows how to obtain an
adequate result by the simplest means. The ladies of highest rank in
this country—that is to say, those who can afford it, wear two kinds
of these massive brass rings, one cylindrical, the other semicircular
in section. The latter are cast in the most ingenious way in the
bamboo mould, the former in the circular hole in the sand. It is quite
a simple matter for the fundi to fit these bars to the limbs of his fair
customers; with a few light strokes of his hammer he bends the
pliable brass round arm or ankle without further inconvenience to
the wearer.
SHAPING THE POT
SMOOTHING WITH MAIZE-COB
CUTTING THE EDGE

FINISHING THE BOTTOM
LAST SMOOTHING BEFORE

BURNING
FIRING THE BRUSH-PILE

LIGHTING THE FARTHER SIDE OF
THE PILE
TURNING THE RED-HOT VESSEL
NYASA WOMAN MAKING POTS AT MASASI

Pottery is an art which must always and everywhere excite the
interest of the student, just because it is so intimately connected with
the development of human culture, and because its relics are one of
the principal factors in the reconstruction of our own condition in
prehistoric times. I shall always remember with pleasure the two or
three afternoons at Masasi when Salim Matola’s mother, a slightly-
built, graceful, pleasant-looking woman, explained to me with
touching patience, by means of concrete illustrations, the ceramic art
of her people. The only implements for this primitive process were a
lump of clay in her left hand, and in the right a calabash containing
the following valuables: the fragment of a maize-cob stripped of all
its grains, a smooth, oval pebble, about the size of a pigeon’s egg, a
few chips of gourd-shell, a bamboo splinter about the length of one’s
hand, a small shell, and a bunch of some herb resembling spinach.
Nothing more. The woman scraped with the
shell a round, shallow hole in the soft, fine
sand of the soil, and, when an active young
girl had filled the calabash with water for her,
she began to knead the clay. As if by magic it
gradually assumed the shape of a rough but
already well-shaped vessel, which only wanted
a little touching up with the instruments
before mentioned. I looked out with the
MAKUA WOMAN closest attention for any indication of the use
MAKING A POT. of the potter’s wheel, in however rudimentary
SHOWS THE a form, but no—hapana (there is none). The
BEGINNINGS OF THE embryo pot stood firmly in its little
POTTER’S WHEEL
depression, and the woman walked round it in
a stooping posture, whether she was removing
small stones or similar foreign bodies with the maize-cob, smoothing
the inner or outer surface with the splinter of bamboo, or later, after
letting it dry for a day, pricking in the ornamentation with a pointed
bit of gourd-shell, or working out the bottom, or cutting the edge
with a sharp bamboo knife, or giving the last touches to the finished
vessel. This occupation of the women is infinitely toilsome, but it is
without doubt an accurate reproduction of the process in use among
our ancestors of the Neolithic and Bronze ages.
There is no doubt that the invention of pottery, an item in human
progress whose importance cannot be over-estimated, is due to
women. Rough, coarse and unfeeling, the men of the horde range
over the countryside. When the united cunning of the hunters has
succeeded in killing the game; not one of them thinks of carrying
home the spoil. A bright fire, kindled by a vigorous wielding of the
drill, is crackling beside them; the animal has been cleaned and cut
up secundum artem, and, after a slight singeing, will soon disappear
under their sharp teeth; no one all this time giving a single thought
to wife or child.
To what shifts, on the other hand, the primitive wife, and still more
the primitive mother, was put! Not even prehistoric stomachs could
endure an unvarying diet of raw food. Something or other suggested
the beneficial effect of hot water on the majority of approved but
indigestible dishes. Perhaps a neighbour had tried holding the hard
roots or tubers over the fire in a calabash filled with water—or maybe
an ostrich-egg-shell, or a hastily improvised vessel of bark. They
became much softer and more palatable than they had previously
been; but, unfortunately, the vessel could not stand the fire and got
charred on the outside. That can be remedied, thought our
ancestress, and plastered a layer of wet clay round a similar vessel.
This is an improvement; the cooking utensil remains uninjured, but
the heat of the fire has shrunk it, so that it is loose in its shell. The
next step is to detach it, so, with a firm grip and a jerk, shell and
kernel are separated, and pottery is invented. Perhaps, however, the
discovery which led to an intelligent use of the burnt-clay shell, was
made in a slightly different way. Ostrich-eggs and calabashes are not
to be found in every part of the world, but everywhere mankind has
arrived at the art of making baskets out of pliant materials, such as
bark, bast, strips of palm-leaf, supple twigs, etc. Our inventor has no
water-tight vessel provided by nature. “Never mind, let us line the
basket with clay.” This answers the purpose, but alas! the basket gets
burnt over the blazing fire, the woman watches the process of
cooking with increasing uneasiness, fearing a leak, but no leak
appears. The food, done to a turn, is eaten with peculiar relish; and
the cooking-vessel is examined, half in curiosity, half in satisfaction
at the result. The plastic clay is now hard as stone, and at the same
time looks exceedingly well, for the neat plaiting of the burnt basket
is traced all over it in a pretty pattern. Thus, simultaneously with
pottery, its ornamentation was invented.
Primitive woman has another claim to respect. It was the man,
roving abroad, who invented the art of producing fire at will, but the
woman, unable to imitate him in this, has been a Vestal from the
earliest times. Nothing gives so much trouble as the keeping alight of
the smouldering brand, and, above all, when all the men are absent
from the camp. Heavy rain-clouds gather, already the first large
drops are falling, the first gusts of the storm rage over the plain. The
little flame, a greater anxiety to the woman than her own children,
flickers unsteadily in the blast. What is to be done? A sudden thought
occurs to her, and in an instant she has constructed a primitive hut
out of strips of bark, to protect the flame against rain and wind.
This, or something very like it, was the way in which the principle
of the house was discovered; and even the most hardened misogynist
cannot fairly refuse a woman the credit of it. The protection of the
hearth-fire from the weather is the germ from which the human
dwelling was evolved. Men had little, if any share, in this forward
step, and that only at a late stage. Even at the present day, the
plastering of the housewall with clay and the manufacture of pottery
are exclusively the women’s business. These are two very significant
survivals. Our European kitchen-garden, too, is originally a woman’s
invention, and the hoe, the primitive instrument of agriculture, is,
characteristically enough, still used in this department. But the
noblest achievement which we owe to the other sex is unquestionably
the art of cookery. Roasting alone—the oldest process—is one for
which men took the hint (a very obvious one) from nature. It must
have been suggested by the scorched carcase of some animal
overtaken by the destructive forest-fires. But boiling—the process of
improving organic substances by the help of water heated to boiling-
point—is a much later discovery. It is so recent that it has not even
yet penetrated to all parts of the world. The Polynesians understand
how to steam food, that is, to cook it, neatly wrapped in leaves, in a
hole in the earth between hot stones, the air being excluded, and
(sometimes) a few drops of water sprinkled on the stones; but they
do not understand boiling.
To come back from this digression, we find that the slender Nyasa
woman has, after once more carefully examining the finished pot,
put it aside in the shade to dry. On the following day she sends me
word by her son, Salim Matola, who is always on hand, that she is
going to do the burning, and, on coming out of my house, I find her
already hard at work. She has spread on the ground a layer of very
dry sticks, about as thick as one’s thumb, has laid the pot (now of a
yellowish-grey colour) on them, and is piling brushwood round it.
My faithful Pesa mbili, the mnyampara, who has been standing by,
most obligingly, with a lighted stick, now hands it to her. Both of
them, blowing steadily, light the pile on the lee side, and, when the
flame begins to catch, on the weather side also. Soon the whole is in a
blaze, but the dry fuel is quickly consumed and the fire dies down, so
that we see the red-hot vessel rising from the ashes. The woman
turns it continually with a long stick, sometimes one way and
sometimes another, so that it may be evenly heated all over. In
twenty minutes she rolls it out of the ash-heap, takes up the bundle
of spinach, which has been lying for two days in a jar of water, and
sprinkles the red-hot clay with it. The places where the drops fall are
marked by black spots on the uniform reddish-brown surface. With a
sigh of relief, and with visible satisfaction, the woman rises to an
erect position; she is standing just in a line between me and the fire,
from which a cloud of smoke is just rising: I press the ball of my
camera, the shutter clicks—the apotheosis is achieved! Like a
priestess, representative of her inventive sex, the graceful woman
stands: at her feet the hearth-fire she has given us beside her the
invention she has devised for us, in the background the home she has
built for us.
At Newala, also, I have had the manufacture of pottery carried on
in my presence. Technically the process is better than that already
described, for here we find the beginnings of the potter’s wheel,
which does not seem to exist in the plains; at least I have seen
nothing of the sort. The artist, a frightfully stupid Makua woman, did
not make a depression in the ground to receive the pot she was about
to shape, but used instead a large potsherd. Otherwise, she went to
work in much the same way as Salim’s mother, except that she saved
herself the trouble of walking round and round her work by squatting
at her ease and letting the pot and potsherd rotate round her; this is
surely the first step towards a machine. But it does not follow that
the pot was improved by the process. It is true that it was beautifully
rounded and presented a very creditable appearance when finished,
but the numerous large and small vessels which I have seen, and, in
part, collected, in the “less advanced” districts, are no less so. We
moderns imagine that instruments of precision are necessary to
produce excellent results. Go to the prehistoric collections of our
museums and look at the pots, urns and bowls of our ancestors in the
dim ages of the past, and you will at once perceive your error.
MAKING LONGITUDINAL CUT IN
BARK
DRAWING THE BARK OFF THE LOG
REMOVING THE OUTER BARK

BEATING THE BARK
WORKING THE BARK-CLOTH AFTER BEATING, TO MAKE IT

SOFT
MANUFACTURE OF BARK-CLOTH AT NEWALA

To-day, nearly the whole population of German East Africa is
clothed in imported calico. This was not always the case; even now in
some parts of the north dressed skins are still the prevailing wear,
and in the north-western districts—east and north of Lake
Tanganyika—lies a zone where bark-cloth has not yet been
superseded. Probably not many generations have passed since such
bark fabrics and kilts of skins were the only clothing even in the
south. Even to-day, large quantities of this bright-red or drab
material are still to be found; but if we wish to see it, we must look in
the granaries and on the drying stages inside the native huts, where
it serves less ambitious uses as wrappings for those seeds and fruits
which require to be packed with special care. The salt produced at
Masasi, too, is packed for transport to a distance in large sheets of
bark-cloth. Wherever I found it in any degree possible, I studied the
process of making this cloth. The native requisitioned for the
purpose arrived, carrying a log between two and three yards long and
as thick as his thigh, and nothing else except a curiously-shaped
mallet and the usual long, sharp and pointed knife which all men and
boys wear in a belt at their backs without a sheath—horribile dictu!
[51]
Silently he squats down before me, and with two rapid cuts has
drawn a couple of circles round the log some two yards apart, and
slits the bark lengthwise between them with the point of his knife.
With evident care, he then scrapes off the outer rind all round the
log, so that in a quarter of an hour the inner red layer of the bark
shows up brightly-coloured between the two untouched ends. With
some trouble and much caution, he now loosens the bark at one end,
and opens the cylinder. He then stands up, takes hold of the free
edge with both hands, and turning it inside out, slowly but steadily
pulls it off in one piece. Now comes the troublesome work of
scraping all superfluous particles of outer bark from the outside of
the long, narrow piece of material, while the inner side is carefully
scrutinised for defective spots. At last it is ready for beating. Having
signalled to a friend, who immediately places a bowl of water beside
him, the artificer damps his sheet of bark all over, seizes his mallet,
lays one end of the stuff on the smoothest spot of the log, and
hammers away slowly but continuously. “Very simple!” I think to
myself. “Why, I could do that, too!”—but I am forced to change my
opinions a little later on; for the beating is quite an art, if the fabric is
not to be beaten to pieces. To prevent the breaking of the fibres, the
stuff is several times folded across, so as to interpose several
thicknesses between the mallet and the block. At last the required
state is reached, and the fundi seizes the sheet, still folded, by both
ends, and wrings it out, or calls an assistant to take one end while he
holds the other. The cloth produced in this way is not nearly so fine
and uniform in texture as the famous Uganda bark-cloth, but it is
quite soft, and, above all, cheap.
Now, too, I examine the mallet. My craftsman has been using the
simpler but better form of this implement, a conical block of some
hard wood, its base—the striking surface—being scored across and
across with more or less deeply-cut grooves, and the handle stuck
into a hole in the middle. The other and earlier form of mallet is
shaped in the same way, but the head is fastened by an ingenious
network of bark strips into the split bamboo serving as a handle. The
observation so often made, that ancient customs persist longest in
connection with religious ceremonies and in the life of children, here
finds confirmation. As we shall soon see, bark-cloth is still worn
during the unyago,[52] having been prepared with special solemn
ceremonies; and many a mother, if she has no other garment handy,
will still put her little one into a kilt of bark-cloth, which, after all,
looks better, besides being more in keeping with its African
surroundings, than the ridiculous bit of print from Ulaya.
MAKUA WOMEN

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DeLee & Drez’s Orthopaedic Sports

Medicine E Book 5th Edition, (Ebook

Kathleen C. Abalos, MD Christian N. Anderson, MD Derek P. Axibal, MD

Bruce Beynnon, PhD Stephen F. Brockmeier, MD Jon-Michael E. Caldwell, MD

Jonathan T. Bravman, MD E. Lyle Cain Jr., MD Jorge Chahla, MD

Peter N. Chalmers, MD Philip Chuang, PhD Shannon David, PhD, ATC

Pau Golanó, MD Letha Y. Griffin, MD, PhD Hamid Hassanzadeh, MD

Betina B. Hinckel, MD, PhD Todd A. Irwin, MD Abdurrahman Kandil, MD

Catherine Hui, MD, FRCSC Anish R. Kadakia, MD Lucas R. King, MD, BS

Susan E. Kirk, MD Marshall A. Kuremsky, MD Peter Lawrence, MD

Timothy J. Luchetti, MD Scott D. Martin, MD Heather Menzer, MD

Timothy S. Mologne, MD Carl W. Nissen, MD Evan Peck, MD

Matthew A. Posner, MD Eliott P. Robinson, MD Susan Saliba, PhD, ATC, MPT

Ravi S. Vaswani, MD Benjamin R. Wilson, MD Yi-Meng Yen, MD, PhD

Barbara B. Wilson, MD Jeffrey Yao, MD

Chapter 85 Chapter 108

Chapter 110 Chapter 124

Chapter 118 Chapter 133

Chapter 119 Chapter 134

process. Tendons of the extremities possess small amounts of

by disrupting the repair tissue, leading to gap formation and

TABLE 1.1 Growth Factors in Soft Tissue Repair

Superficial layer Deep layer of

native extracellular matrix. Multiphasic scaffolds are being used Anterior

Middle zone (40%–60%)

Deep zone (30%)

Deep zone. The chondrocytes in the deep zone resemble those

Newala, too, suffers from the distance of its water-supply—at least

The water-supply of New Newala is in the bottom of the valley,

NATIVE PATH THROUGH THE MAKONDE BUSH, NEAR

MAKONDE LOCK AND KEY AT JUMBE CHAURO

MODE OF INSERTING THE KEY

With no small pride first one householder and then a second

Some consolation was afforded me by a brassfounder, whom I

SMOOTHING WITH MAIZE-COB

CUTTING THE EDGE

LAST SMOOTHING BEFORE

FIRING THE BRUSH-PILE

TURNING THE RED-HOT VESSEL

NYASA WOMAN MAKING POTS AT MASASI

DRAWING THE BARK OFF THE LOG

REMOVING THE OUTER BARK

WORKING THE BARK-CLOTH AFTER BEATING, TO MAKE IT

MANUFACTURE OF BARK-CLOTH AT NEWALA

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