Equine Fracture Repair

Equine Fracture Repair

Second Edition

Edited by

Alan J. Nixon, BVSc, MS, Diplomate ACVSProfessor of Orthopedic SurgeryDirector of Comparative Orthopaedics LaboratoryDepartment of Clinical SciencesCollege of Veterinary MedicineCornell UniversityIthaca, NY;Senior Orthopedic SurgeonCornell Ruffian Equine SpecialistsElmont, NY, USA

This edition first published 2020© 2020 John Wiley & Sons, Inc.

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The right of Alan J. Nixon to be identified as the author of this work has been asserted in accordance with law.

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Limit of Liability/Disclaimer of WarrantyThe contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.

Library of Congress Cataloging‐in‐Publication Data

Names: Nixon, Alan J., editor.Title: Equine fracture repair / edited by Alan J. Nixon.Description: 2nd edition. | Hoboken, NJ : Wiley-Blackwell, 2020. | Includes bibliographical references and index. | Identifiers: LCCN 2018054082 (print) | LCCN 2018055053 (ebook) | ISBN 9781119108740 (AdobePDF) |

ISBN 9781119108726 (ePub) | ISBN 9780813815862 (hardback)Subjects: LCSH: Horses–Fractures–Treatment. | Horses–Surgery. | MESH: Horses–surgery |

Fracture Fixation–veterinaryClassification: LCC SF959.F78 (ebook) | LCC SF959.F78 E68 2020 (print) | NLM SF 951 |

DDC 636.1/089705–dc23LC record available at https://lccn.loc.gov/2018054082

Cover image: WileyCover design: © Liu zishan/Shutterstock Photos by: Alan J. Nixon

Set in 10/12pt Warnock by SPi Global, Pondicherry, India

10 9 8 7 6 5 4 3 2 1

To Sally, for her passion for life, love, and encouragement throughout this project,and

My three children, Bridgette, Nicole, and Ryan, for their patience and understanding while I toiled and their unwavering love and support throughout these past few years.

vii

Contributors xiPreface to the Second Edition xivPreface to the First Edition xvAcknowledgments xvi

Part I Introduction 1

1 Bone Structure and the Response of Bone to Stress 3Mark D. Markel

2 Fracture Biomechanics 12Mark D. Markel

3 Fracture Healing 24Mark D. Markel

4 General Considerations for Fracture Repair 35Alan J. Nixon

5 Racetrack Fracture Management and Emergency Care 44Ian M. Wright

6 First Aid and Transportation of Equine Fracture Patients 83Larry R. Bramlage

7 Perioperative Considerations 91Alan J. Nixon

8 Surgical Equipment and Implants for Fracture Repair 107Joerg A. Auer

9 Principles of Fracture Fixation 127Alan J. Nixon, Joerg A. Auer , and Jeffrey P. Watkins

10 Application of the Locking Compression Plate (LCP) 156Dean W. Richardson

11 Bone Grafts and Bone Substitutes 163Mark D. Markel

Contents

Contentsviii

12 Biologic Agents to Enhance Fracture Healing 173Mark D. Markel and Howard Seeherman

13 Casting and Transfixation Casting Techniques 188Ashlee E. Watts and Lisa A. Fortier

Part II Specific Fractures 219

14 Fractures of the Distal Phalanx 221Alan J. Nixon, Norm G. Ducharme, and Alicia L. Bertone

15 Fractures of the Navicular Bone 242Michael C. Schramme and Roger K.W. Smith

16 Arthrodesis of the Distal Interphalangeal Joint 257Chad J. Zubrod and Robert K. Schneider

17 Fractures of the Middle Phalanx 264Jeffrey P. Watkins

18 Arthrodesis of the Proximal Interphalangeal Joint 277Jeffrey P. Watkins

19 Fractures of the Proximal Phalanx 295Dean W. Richardson

20 Fractures and Luxations of the Fetlock 320C. Wayne McIlwraith

21 Fractures of the Proximal Sesamoid Bones 341Ian M. Wright

22 Fractures of the Condyles of the Third Metacarpal and Metatarsal Bones 378Ian M. Wright and Alan J. Nixon

23 Arthrodesis of the Metacarpo/Metatarsophalangeal Joint 425Larry R. Bramlage

24 Fractures of the Third Metacarpal/Metatarsal Diaphysis and Metaphysis 436Robert K. Schneider and Sarah N. Sampson

25 Third Metacarpal Dorsal Stress Fractures 452Alan J. Nixon, Sue Stover, and David M. Nunamaker

26 Fractures of the Small Metacarpal and Metatarsal (Splint) Bones 465Alan J. Nixon and Lisa A. Fortier

27 Fractures of the Carpus 480C. Wayne McIlwraith

28 Arthrodesis of the Carpus 515Larry R. Bramlage and Alan J. Ruggles

Contents ix

29 Fractures of the Radius 527Joerg A. Auer

30 Fractures of the Ulna 545Alan J. Nixon

31 Fractures of the Humerus 567Alan J. Nixon and Jeffrey P. Watkins

32 Luxation of the Shoulder 588Ashlee E. Watts and Alan J. Nixon

33 Fractures of the Scapula 603Stephen B. Adams and Alan J. Nixon

34 Fractures and Luxations of the Hock 613Alan J. Nixon

35 Fractures of the Tibia 648Jeffrey P. Watkins and Sarah N. Sampson

36 Fractures of the Stifle 664Alan J. Nixon

37 Fractures of the Femur 688Alan J. Nixon, Larry R. Bramlage, and Steven R. Hance

38 Luxation and Subluxation of the Coxofemoral Joint 706Alan J. Nixon and Norm G. Ducharme

39 Fractures of the Pelvis 723Norm G. Ducharme and Alan J. Nixon

40 Fractures of the Vertebrae 734Alan J. Nixon

41 Fractures of the Head 770Anton E. Fuerst and Joerg A. Auer

42 Medical Aspects of Traumatic Brain Injury in Horses 800Stephen M. Reed

Part III Postoperative Aspects of Fracture Repair 805

43 Systems for Recovery from Anesthesia 807John B. Madison

44 Postanesthetic Myopathy 814Manuel Martin‐Flores and Robin D. Gleed

45 Implant Removal 823Alan J. Ruggles

Contentsx

46 Orthopedic Implant Failure 831David M. Nunamaker

47 Delayed Union, Nonunion, and Malunion 835Norm G. Ducharme and Alan J. Nixon

48 Osteomyelitis 851Laurie R. Goodrich

49 Stress‐induced Laminitis 874Scott Morrison

50 New Implant Systems 885Joerg A. Auer

Index 892

xi

Stephen B. Adams, DVM, MS, Diplomate ACVSProfessor of SurgeryDepartment of Veterinary Clinical SciencesSchool of Veterinary MedicinePurdue UniversityLynn Hall, West Lafayette, INUSAFractures of the Scapula

Joerg A. Auer, Dr Med Vet, Dr Med Vet HC, Diplomate ACVS, ECVSProfessor Emeritus, Veterinary SurgeryVetsuisse FacultyUniversity of ZurichZurich, SwitzerlandSurgical Equipment and Implants for Fracture Repair; Principles of Fracture Fixation; Fractures of the Radius; Fractures of the Head; New Implant Systems

Alicia L. Bertone, DVM, PhD, Diplomate ACVS, Diplomate ACVSMRTrueman Family Endowed Chair and Professor of SurgeryVice Provost for Graduate Studies and Dean of the Graduate SchoolDepartment of Veterinary Clinical Sciences The Ohio State UniversityColumbus, OHUSAFractures of the Distal Phalanx

Larry R. Bramlage, DVM, MS, Diplomate ACVSRood and Riddle Equine HospitalLexington, KY, USAFirst Aid and Transportation of Equine Fracture Patients; Arthrodesis of the Metacarpo/Metatarsophalangeal Joint; Arthrodesis of the Carpus; Fractures of the Femur

Norm G. Ducharme, DVM, MSc, Diplomate ACVSJames Law Professor of SurgeryDepartment of Clinical Sciences College of Veterinary Medicine

Cornell UniversityIthaca, NY;Chief Medical OfficerCornell Ruffian Equine SpecialistsElmont, NYUSAFractures of the Distal Phalanx; Luxation and Subluxation of the Coxofemoral Joint; Fractures of the Pelvis; Delayed Union, Nonunion, and Malunion

Lisa A. Fortier, DVM, PhD, DACVSJames Law Professor of SurgeryDepartment of Clinical Sciences College of Veterinary MedicineCornell UniversityIthaca, NYUSACasting and Transfixation Casting Techniques; Fractures of the Small Metacarpal and Metatarsal (Splint) Bones

Anton E. Fuerst, Dr Med Vet, Diplomate ECVSProfessor of Veterinary SurgeryDirector of Equine Surgery ClinicVetsuisse Faculty, University of ZurichZurich, SwitzerlandFractures of the Head

Robin D. Gleed, BVSc, MRCVS, DVA, DACVAProfessor of AnesthesiologyDepartment of Clinical Sciences College of Veterinary MedicineCornell UniversityIthaca, NYUSAPostanesthetic Myopathy

Laurie R. Goodrich, DVM, MS, PhDProfessor of SurgeryCollege of Veterinary MedicineColorado State UniversityFort Collins, CO, USAOsteomyelitis

Contributors

Contributorsxii

Steven R. Hance, LLC, DVMEquine Sales and Radiographic ConsultantOklahoma City, OKUSAFractures of the Femur

John B. Madison, VMD, Dip ACVSOcala Equine HospitalOcala, FLUSASystems for Recovery from Anesthesia

Mark D. Markel, DVM, PhDDean, Comparative Orthopaedic Research LaboratoryDepartment of Medical SciencesSchool of Veterinary MedicineUniversity of Wisconsin‐MadisonMadison, WIUSABone Structure and the Response of Bone to Stress; Fracture Biomechanics; Fracture Healing; Bone Grafts and Bone Substitutes; Biologic Agents to Enhance Fracture Healing

Manuel Martin‐Flores, MV, DACVADepartment of Clinical SciencesCollege of Veterinary MedicineCornell UniversityIthaca, NYUSAPostanesthetic Myopathy

C. Wayne McIlwraith, BVSc, PhD, Dr Med Vet (HC), DSc (HC), FRCVS, Diplomate ACVS, Diplomate ACVSMRUniversity Distinguished Professor of OrthopaedicsBarbara Cox Anthony Endowed University Chair in OrthopaedicsDepartment of Clinical SciencesCollege of Veterinary Medicine & Biomedical SciencesColorado State UniversityFort Collins, COUSAFractures and Luxations of the Fetlock; Fractures of the Carpus

Scott Morrison, DVMRood and Riddle Equine HospitalLexington, KY, USAStress‐induced Laminitis

Alan J. Nixon, BVSc, MS, Diplomate ACVSProfessor of Orthopedic SurgeryDirector of Comparative Orthopaedics LaboratoryDepartment of Clinical SciencesCollege of Veterinary MedicineCornell UniversityIthaca, NY;Senior Orthopedic SurgeonCornell Ruffian Equine SpecialistsElmont, NYUSAGeneral Considerations in Selecting Cases for Fracture Repair; Perioperative Considerations; Principles of Fracture Fixation; Fractures of the Distal Phalanx; Fractures of the Condyles of the Third Metacarpal and Metatarsal Bones; Third Metacarpal Dorsal Stress Fractures; Fractures of the Small Metacarpal and Metatarsal (Splint) Bones; Fractures of the Ulna; Fractures of the Humerus; Luxation of the Shoulder; Fractures of the Scapula; Fractures and Luxations of the Hock; Fractures of the Stifle; Fractures of the Femur; Luxation and Subluxation of the Coxofemoral Joint; Fractures of the Pelvis; Fractures of the Vertebrae; Delayed Union, Nonunion, and Malunion

David M. Nunamaker, VMD, PhD, Diplomate ACVSProfessor EmeritusDepartment of Clinical StudiesSchool of Veterinary MedicineUniversity of PennsylvaniaNew Bolton CenterKennett Square, PA, USAThird Metacarpal Dorsal Stress Fractures; Orthopedic Implant Failure

Stephen M. Reed, DVM, Dip ACVIMRood and Riddle Equine HospitalLexington, KY, USAMedical Aspects of Traumatic Brain Injury in Horses

Dean W. Richardson, DVM, Diplomate ACVSCharles W. Raker Professor of Equine SurgeryDepartment of Clinical Studies School of Veterinary MedicineUniversity of PennsylvaniaNew Bolton CenterKennett Square, PAUSAApplication of the Locking Compression Plate (LCP); Fractures of the Proximal Phalanx

Contributors xiii

Alan J. Ruggles, DVM, Diplomate ACVSRood and Riddle Equine HospitalLexington, KY, USAArthrodesis of the Carpus; Implant Removal

Sarah N. Sampson, DVM, PhD, Diplomate ACVS, Diplomate ACVSMRAssistant Professor of Equine Sports Medicine and ImagingDepartment of Large Animal Clinical SciencesCollege of Veterinary Medicine & Biomedical SciencesTexas A&M UniversityCollege Station, TXUSAFractures of the Third Metacarpal/Metatarsal Diaphysis and Metaphysis; Fractures of the Tibia

Robert K. Schneider, DVM, MS, Diplomate ACVSMcKinlay Peters Equine HospitalNewman Lake, WAUSAArthrodesis of the Distal Interphalangeal Joint; Fractures of the Third Metacarpal/Metatarsal Diaphysis and Metaphysis

Michael C. Schramme, Dr Med Vet, Cert EO, PhD, HDR, Diplomate ECVS, Diplomate ACVSProfesseur de Chirurgie EquineChef de CliniqueVetAgro SupClinéquine, Campus Veterinaire de LyonMarcy l’ÉtoileFranceFractures of the Navicular Bone

Howard Seeherman, PhD, VMDMusculoskeletal TherapiesWyeth Discovery ResearchWyeth PharmaceuticalsCambridge, MA, USABiologic Agents to Enhance Fracture Healing

Roger K.W. Smith, MA, VetMB, PhD, DEO, FHEA, ECVDI LA Assoc., Diplomate ECVS, FRCVSEuropean and RCVS Specialist in Equine Surgery (Orthopaedics)Professor of Equine OrthopaedicsDepartment of Clinical Sciences and ServicesThe Royal Veterinary CollegeLondon, UKFractures of the Navicular Bone

Sue Stover, DVM, PhD, Diplomate ACVSProfessor, Department of Anatomy, Physiology & Cell BiologyUniversity of CaliforniaDavis, CAUSAThird Metacarpal Dorsal Stress Fractures

Jeffrey P. Watkins, DVM, MS, Diplomate ACVSProfessor of SurgeryDepartment of Large Animal Clinical Sciences College of Veterinary Medicine & Biomedical SciencesTexas A&M UniversityCollege Station, TXUSAPrinciples of Fracture Fixation; Fractures of the Middle Phalanx; Arthrodesis of the Proximal Interphalangeal Joint; Fractures of the Humerus; Fractures of the Tibia

Ashlee E. Watts, DVM, Diplomate ACVSAssociate Professor of SurgeryDepartment of Large Animal Clinical Sciences College of Veterinary Medicine & Biomedical SciencesTexas A&M UniversityCollege Station, TXUSACasting and Transfixation Casting Techniques; Shoulder Luxation

Ian M. Wright, MA VetMB, DEO, Diplomate ECVS, FRCVSSenior SurgeonDirector of Clinical SciencesNewmarket Equine HospitalNewmarket, UKRacetrack Fracture Management and Emergency Care; Fractures of the Proximal Sesamoid Bones; Fractures of the Condyles of the Third Metacarpal and Metatarsal Bones

Chad J. Zubrod, DVM, MS, Diplomate ACVSOakridge Equine HospitalEdmond, OKUSAArthrodesis of the Distal Interphalangeal Joint

xiv

It has been many years since the first edition of this text was published, and it has long been out of print. During this period, changing focus at Elsevier has driven a change in publisher to Wiley. While I would like to thank Ray Kersey and Saunders/Elsevier for their previous interest in this text, it is a pleasure to see Ray now with Wiley, and to deal with the professional commissioning and production staff at Wiley Blackwell.

Much has happened in the field of equine fracture repair in this interval. The second edition is almost dou-ble the size of the first. Numerous new implant systems, concepts, approaches to the bones, and enhanced after-care and treatment of complications have improved the outcome following fracture repair in the horse. Many of the authors contributing to the first edition have kindly enhanced and updated their chapters with the wealth of experience gained over another 25 years. Asking senior surgeons to update chapters for a textbook was made easier by the profound interest and dedication of these individuals to seeing a new edition of Equine Fracture Repair become available. My profound gratitude is owed to these authors for updating previous chapters and providing unpublished case examples and statistics, and additionally to the new authors who have brought their own unique experiences to the second edition. The guiding principle for all chapters has been to request a contribution from those recognized as an outstanding authority in that area.

In this edition, we have retained the concept of introductory chapters in Part I, dealing with fracture concepts, surgical systems, emergency splinting, and enhancements to fracture healing. Part II then provides

comprehensive updated information on fractures of specific bones, including new chapters describing repair of fractures of the navicular bone, stifle, pelvis, and skull. Additionally, novel arthrodesis techniques, including for the distal interphalangeal, carpal, and shoulder joints, are added. The final part deals with the postoperative aspects of fracture repair, and provides extensive infor-mation on anesthesia and anesthetic recovery, implant failure and removal, and complications such as nonun-ion, osteomyelitis, and support limb laminitis. The final chapter introduces implant systems with real potential to make their way into equine fracture repair over the next few years.

The presentation of new techniques in fracture repair has been enhanced by the excellent artwork of Michael Simmons, who also contributed numerous drawings to the first edition. These illustrations provide a valuable teaching resource for both trainees and experienced surgeons. I am also pleased to acknowledge the exten-sive assistance of the surgery and imaging technicians in the preparation of the materials in many chapters of this book. In the period between the first and second editions, digital radiography has been introduced, which has meant that many of the examples are now represented by pre‐ and postoperative digital radio-graphs, and three‐dimensional imaging, of exquisite detail. Numerous examples of fractures and their variations are included to provide a comprehensive illustration of fracture types and repair choices. The patience of the Wiley team as we extensively updated and expanded this book into its second edition is much appreciated.

Preface to the Second Edition

xv

Equine orthopedic surgery has evolved enormously during the last 20 years. New procedures and implants, and in many instances a desire to treat serious orthopedic injuries, have advanced the state of equine orthopedics in many domains. Increasing application of the AO/ASIF implant systems and development or new implants spe-cific to the horse have improved the success rate associ-ated with equine fracture repair. Much new information has developed, and the purpose of this book is primarily to provide an informative and authoritative text on equine fractures and the current state of the art in fracture repair. The authors bring to this book considerable experience, and their individual efforts have been enormous. As a result, the book should provide valuable information to equine practitioners and specialists, as well as an in‐depth coverage of fracture repair for students and veterinarians in surgical training programs. The book provides exten-sive treatment, splinting, casting, surgical and follow‐up details on specific fractures, and, finally, on the complica-tions and future developments in fracture repair in the horse. In all sections on specific fractures, the book brings the personal experience of recognized leaders in the field. I am particularly indebted to these people, who took the time from already overburdened scheduled to provide

detailed coverage in these chapters. The results provide a current text dedicated specifically to equine orthopedics. Such considerable published information is now available that the general‐purpose textbook, covering all aspects of equine medicine and surgery, would be enormous. This book narrows the scope in an attempt to improve the quality and depth of information.

Many chapters are accompanied by medical illustra-tions and radiographs to assist in the preparation and surgical procedures. I am particularly grateful to Ms. Conery Calhoon and Mr. Tom McCracken for the extensive artwork provided in the specific procedures chapters. Their work enhances our understanding of these techniques and brings clarity to many complex procedures. Additionally, many photographs have been prepared by the staff in the Biomedical Communications Lab at Cornell, and their work is most appreciated. The revision and typing of manuscripts was expertly per-formed by Ms. Debbie Lent, whose assistance is greatly appreciated.

My editor at W.B. Saunders, Mr. Raymond Kersey, has always been encouraging, and the W.B. Saunders edito-rial and production staff deserve special mention for keeping the book on schedule.

Preface to the First Edition

xvi

A specialized text such as this is considerably enhanced by case examples from numerous referring veterinarians and consulting surgeons, and I appreciate the permission to reproduce images throughout the text, and for case follow‐up in specific examples. I particularly appreciate the numerous cases provided by Drs. David Bogenrief, Ryland Edwards, David Murphy, Dean Richardson, Paddy Todhunter, and Ashlee Watts. I would also like to thank the Cornell University surgical operating room staff and imaging technicians, at both the Ithaca campus and the Cornell Ruffian Equine Specialists practice in New York City. Additionally, I would like to extend my sincere gratitude to the many surgical interns and resi-dents who provided diligent assistance in surgery and postoperative care, and to numerous surgical colleagues

in private practice and university clinics who offered valuable assistance and  sage advice with many cases. My thanks to the enormous task of typing and adminis-trative assistance provided by Amy Ingham, Lyn Park, Sue Branch, and Billy Chorley, and the extensive permis-sions work also undertaken by Billy Chorley. This text would not have been possible without the patience and expertise  of the Executive Commissioning editor at Wiley Blackwell, Erica Judisch. The Wiley team has been outstanding, including the expert editing of the manu-script by Sally Osborn, quality assessment by Purvi Patel, production and layout by Jerusha Govindakrishnan, and cover work and back matter developed under the super-vision of Susan Engelken. My thanks to such a skilled and professional team.

Acknowledgments

1

Part I

Introduction

Equine Fracture Repair, Second Edition. Edited by Alan J. Nixon. © 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.

3

IntroductIon

The skeleton serves many essential purposes in the body, including the protection of internal organs, the provision of rigid kinematic links to allow for locomotion, and the storage of calcium and phosphorous, acting as a dynamic mineral reserve bank.20,26,30 Bone, the principal compo-nent of the skeleton, is living connective tissue made rigid by the orderly deposition of minerals on an organic matrix.1 Bone has many unique structural characteristics which allow it to fulfill these functions. It is one of the hardest substances in the body, following only dentin and enamel of teeth. Its intricate structural organization, combined with its high metabolic activity, allows bone to respond rapidly to both physical and biochemical demands. Additionally, bone is highly vascular with an excellent capacity for self‐repair. The surfaces of bone are covered with osteoblasts and osteoclasts, which are responsible for constant bone turnover through simulta-neous bone formation and bone resorption.3 Osteocytes, the third major cellular component of bone, reside within bone tissue and communicate with adjacent osteocytes and osteoblasts through channels called canaliculi. All three cell types help bone respond quickly to mechanical and metabolic demands.

This chapter will describe the structure and function of bone and its response to stress, focusing on the cellu-lar and mechanical characteristics of bone structure.

Bone Structure

On the microscopic level, two types of bone are found in the mature skeleton. Hard, compact cortical bone occurs in the shafts of the long bones. Cancellous, or trabecular, bone is composed of a network of fine, interlacing parti-

tions, called trabeculae, enclosing the cavities within the bone that contain either hematopoietic or fatty marrow. Cancellous bone is found in most of the axial skeleton and in the ends of the long bones. Bones of the appen-dicular skeleton are generally long and cylindrical, with relatively narrow mid‐portions. The length of equine bones increases the moment arm of each muscle as it acts on the limb, enhancing a horse’s speed and power. The expanded ends of long bones diminish the stresses that act on the articular surfaces by distributing loads over a larger cross‐sectional area.

An immature long bone is divided into four distinct regions (Figure 1.1). The central region of bone is called the diaphysis, with the physis, epiphysis, and metaphysis at either end. The physis, present in one or both ends of the bone, separates the epiphysis and metaphysis, and is responsible for the majority of long bone growth in young animals through a process called endochondral ossifica-tion. As an animal matures, the physis ceases growth and closes, at which stage the entire expanded end of the bone is represented by the metaphysis, which is composed of trabecular (cancellous or spongy) bone surrounded by cortical and dense subchondral bone. The diaphysis is a hollow tube of cortical bone with a central cavity that con-tains the major arterial and venous blood supply to the bone and fatty marrow. Most of the hematopoiesis in the body occurs in the metaphyseal cancellous bone and in the bones of the axial skeleton, although the fatty marrow of the diaphysis does contain hematopoietic elements.

Bones of the appendicular skeleton are covered by periosteum, except in regions covered by articular cartilage or where ligaments, tendons, or joint capsules attach.1,3 The periosteum has two layers: an outer, fibrous layer permeated by blood vessels and nerves which act in a supportive capacity, and an inner, osteogenic layer which provides the osteoprogenitor cells necessary for fracture

1

Bone Structure and the response of Bone to StressMark D. Markel

Comparative Orthopaedic Research Laboratory, Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA

Part I Introduction4

healing and is responsible for appositional growth prior to skeletal maturity. During growth, the osteogenic layer of the periosteum is thick, highly vascular, and adhered to the bone. With maturity, the osteogenic layer thins and becomes only loosely adhered to the bone.

The microstructure of bone can be divided into three principal components which are intimately associated with one another to allow for rapid response to the mechanical and homeostatic requirements of the body. These components include the cells, the organic extracel-lular matrix, and the inorganic portion of bone.

cellular components

osteoblastsOsteoblasts, which develop from fibroblastic osteo-progenitor or mesenchymal cells, cover the majority of bone surfaces and are responsible for the formation of the organic matrix, called osteoid (Figure 1.2).3,17,27,39 Osteoblasts deposit osteoid on bone surfaces, enveloping themselves in osteoid seams.

Ultrastructurally, osteoblasts contain abundant endo-plasmic reticulum, ribosomes, Golgi apparatus, and mitochondria. These cellular components are responsi-ble for the osteoblasts’ high metabolic activity and productivity. Osteoblasts produce the majority of the organic components of bone, including collagen, proteo-glycans, and other noncollagenous proteins.

osteocytesApproximately 10% of the osteoblastic population become enclosed in matrix and are then referred to as osteocytes (Figure  1.3).17 Compared with osteoblasts, osteocytes have less endoplasmic reticulum and fewer cytoplasmic organelles. Osteocytes have numerous cytoplasmic pro-cesses that extend into the surrounding matrix and fill the canaliculi of bone (Figure  1.3). These processes contact the processes of other osteocytes and osteoblasts to form an intricate transport and communication system within the bone. This interconnection of deeply embedded oste-ocytes and surface‐lining osteoblasts regulates the flow of mineral ions from the extracellular space surrounding the osteoblasts to the osteocytes, from the osteocytes to the extracellular fluid surrounding them, and finally from this fluid to the mineral surrounding the osteocytes. This organizational structure allows the large surface area of the osteocyte population to regulate the exchange of mineral ion between the extracellular fluid and the bone by means of the canalicular system.

osteoclastsThe cell type responsible for the majority of bone resorption is the osteoclast.17 Osteoclasts are large, multinucleated cells on or near bone surfaces that reside within concavities called Howship’s lacunae, which are the active sites of bone resorption (Figure 1.4).

Epiphysis

Physis

Metaphysis

Diaphysis

Medullary cavity

Periosteum

Articular cartilage

Figure 1.1 Immature equine tibia showing the different regions of a long bone.

Figure 1.2 Light microscopic image of a 5 μm undecalcified section of bone showing osteoblasts (arrows) laying down osteoid on bone surface (Goldner Stain, magnification ×80).

1 Bone Structure and the Response of Bone to Stress 5

Osteoclasts originate from blood monocytes, which circulate in the vascular system before arriving in bone. The size and number of nuclei in osteoclasts vary, but each nucleus usually is associated with a perinuclear Golgi apparatus, in which Golgi vesicles exist in various stages of development. Osteoclasts contain little endo-plasmic reticulum and few ribosomes, but they do have abundant mitochondria, Golgi apparatus, and Golgi vesicles. The contact area between osteoclasts and bone consists of two regions, the ruffled border and the sealing zone. The ruffled border is composed of finger‐like membranous folds that extend varying distances into the cytoplasm and are responsible for bone resorption. The sealing zone is characterized by a dense, homogenous cytoplasmic membrane that lies in close apposition to the bone and isolates the ruffled border, preventing leakage

and concentrating the lysosomal enzymes and hydrogen ions produced by the osteoclast at the site of resorption. Osteoclasts produce acid phosphatase and collagenase to first dissolve mineral and then remove the organic matrix to a depth of 1–2 μm. Hydroxyapatite crystals and collagen fibers can be observed in the extracellular space between the cytoplasmic folds of the ruffled border. After being degraded, these components are taken up via endocytosis, transported across the cell, and then extruded into the extracellular space.

organic Matrix

collagenThe organic matrix of bone acts as a supporting structure for the deposition and crystallization of inorganic salts. Organic matrix is 21% of the bone by weight, with the remainder of the bone made up of inorganic material (71%) and water (8%). Approximately 95% of the organic matrix is collagen, with type I collagen the predominant collagen in bone. Collagen is the most abundant protein in mam-mals, accounting for 20–50% of the dry weight of adult long bones, approximately 70% of the dry weight of skin, and approximately 90% of the dry weight of tendon.3,17,34

Collagen’s unique ultrastructure makes it exceedingly strong in tension. Collagen is composed of three tightly folded polypeptide chains, called alpha chains, each con-sisting of approximately 1000 amino acids. The basic unit of collagen is tropocollagen, composed of three pro-collagen polypeptide alpha chains, each coiled in a left‐handed helix, and the alpha chains are then further coiled around each other into a right‐handed triple helix (Figure 1.5). Tropocollagen molecules, which are approx-imately 1.4 nm in diameter and 300 nm long, polymerize

Figure 1.3 Brightfield (left) and grayscale composite of Z‐stacked confocal photomicrographs (right) of osteocytes surrounding an osteon Haversian canal (large arrow) in the third metacarpal bone in a racing Thoroughbred. A dense syncytial network of vital osteocytes and their canaliculi are demonstrated (small arrows) connecting adjacent lacunae before ultimately reaching the Haversian canal. Scale bar = 50 μm. Source: Courtesy Peter Muir, University of Wisconsin‐Madison.

Figure 1.4 Light microscopic image of a 5 μm undecalcified section of bone showing an osteoclast (arrow) residing within a Howship’s lacuna where bone is resorbed (Goldner Stain, magnification ×80).

Part I Introduction6

into larger collagen fibrils. Covalent cross‐links form between the tropocollagen molecules, adding to the fibrils’ high tensile strength. Individual fibrils are aligned in a quarter‐staggered array with fibril lengths of 640 Å. The fibrils are separated by 400 Å gaps called hole zones. The hole zones are thought to serve as the initial miner-alization site within collagen.

Individual alpha chains of type I collagen consist of repeating tripeptides, composed of the amino acid sequence glycine‐x‐y, where x and y can be proline, hydroxyproline, or hydroxylysine.4 Glycine accounts for one‐third of all the constituent amino acids in type I collagen, because it is the only amino acid small enough to fit in the center of the collagen triple helix. Type I collagen consists of two identi-cal alpha chains and one alpha chain of a different amino acid composition, [α1(I)]2α2(I).

Proteoglycans and GlycosaminoglycansThe remaining 5% of organic matrix is ground substance. The predominant constituents of ground substance are

proteoglycans and their constituent glycosaminoglycans. Proteoglycans are high molecular weight molecules, with acidic glycosaminoglycan side chains that provide flexi-bility and resilience to the connective tissue matrix.4

Proteoglycans are made up of a central protein core to which acidic glycosaminoglycan side chains are covalently attached. The individual glycosaminoglycans are large anionic molecules of repeating basic and acidic disaccharides. In bone, proteoglycans do not form the large aggregates that predominate in other tissues such as cartilage. Glycosaminoglycans also serve as the cementing substance between layers of mineralized collagen fibers in lamellar bone.

Inorganic componentThe mineral portion of bone consists primarily of cal-cium and phosphate, mainly in the form of small crystals that resemble synthetic hydroxyapatite crystals and have the composition Ca10(PO4)6(OH)2.

3,13 Bone mineral crystals are extremely small, ~25–75 Å in diameter and 200 Å in length, in contrast to geological apatite crystals which are much larger.29 Because of their small size, the microscopic crystals found in bone mineral are more soluble than geological apatites. They also contain more impurities than pure hydroxyapatite crystals. In addition to calcium and phosphorous, bone mineral contains car-bonate, magnesium, fluoride, and citrate in variable amounts. This structure of bone (hydroxyapatite in inti-mate apposition to the organic matrix) is responsible for its mechanical strength.

osteonAt the microstructural level, the fundamental unit of bone is the osteon or Haversian system (Figure 1.6). At the center of each osteon is a small channel, called a Haversian canal, that contains blood vessels, nerve fibers, and lymphatic‐type channels. Surrounding the central canal is a concentric series of layers, or lamellae, of mineralized bone (Figure 1.6). Along the boundaries of each lamella are small spaces known as lacunae, each of which contains individual osteo-cytes. Canaliculi radiate from these lacunae and connect with adjacent lamellae before ultimately reaching a Haversian canal (Figure 1.3). Cell processes extend from the osteocytes into the canaliculi, allowing nutrients from the blood vessels in the Haversian canal to reach the osteocyte.

At the periphery of each osteon is a cement line, a nar-row area of cement‐like ground substance composed primarily of glycosaminoglycans. The canaliculi of the osteon do not cross this cement line. Like the canaliculi, the collagen fibers in the bone matrix interconnect from one lamella to another within an osteon, but do not cross the cement line. This intertwining of collagen fibers within the osteon increases the bone’s resistance to mechanical stress and probably explains why the cement line is the weakest portion of the bone’s microstructure.

Alpha chain

Triple helix

Tropocollagen molecules

Collagen �bril

1.4 nm

300 nm

Figure 1.5 Molecular features of collagen structure from the alpha chain to the fibril. The flexible amino acid sequence in the alpha chain allows these chains to wind tightly into a right‐handed triple helix, forming the tropocollagen molecule. This tight triple helical arrangement contributes to the high tensile strength of the collagen fibril. The parallel alignment of the individual tropocollagen molecules, in which each molecule overlaps the other by about one‐quarter of its length, results in a repeating banded pattern of the collagen fibril. Source: Adapted from Nordin and Frankel 1989.30 Reproduced with permission of John Wiley and Sons.

1 Bone Structure and the Response of Bone to Stress 7

A typical osteon is 200 μm in diameter, so no portion of an osteon is more than 100 μm from the centrally located blood supply. In the appendicular skeleton, the osteons run longitudinally, but they branch frequently and anasto-mose extensively with each other.

Interstitial lamellae span the regions between complete osteons and are continuous with the osteons. As in oste-ons, no point in the interstitial lamellae is farther than 100 μm from its blood supply. The interfaces between these lamellae contain numerous osteocytes lying within lacunae, which interconnect with each other through the canalicular system.

There are two distinct types of osteons present in lamellar bone, primary and secondary. Primary osteons form during appositional bone growth, when the bone is increasing in diameter.9,40 Osteoblasts on the surface of the bone deposit successive lamellae of new bone,

progressively diminishing the caliber of each vascular space. The resulting anastomosing, convoluted areas of bone, occupying what were previously vascular spaces, are called primary Haversian systems, or primary osteons.8,9,40 Primary osteons usually turn parallel to the long axis of the bone, may contain one to several vascular canals, and are always surrounded by woven bone.9,15

Secondary osteons form during the continuous pro-cess of remodeling that occurs throughout life.6,9,14,33,34 This process is initiated by the osteoclastic resorption of bone via a structure called a cutting cone, and results in anastomosing tubular cavities that are oriented longitu-dinally (Figure 1.7). Osteoblasts on the inner surface of the cutting cone then deposit successive layers of lamel-lae with an orderly fiber orientation. The caliber of each cavity is thereby gradually reduced until only a single small vascular canal remains. The newly formed cylinders

LacunaOsteocyte

Canaliculi

HaversiancanalInterstitial

lamellae

Circumferentiallamellae

Endosteum

Trabeculae

Haversiancanals

Lamellae

Haversian systems

Cement line

Periosteum (split)

Blood vessel

Branches ofperiostealblood vesselsVolkmann’s

canals

Figure 1.6 Microstructural arrangement of a long bone depicted without the marrow cavity. Secondary osteons are apparent as the structural units of cortical bone. In the center of the osteons are the Haversian canals, which form the main branches of the circulatory network. Each osteon is bounded by a cement line and consists of lamellae, formed by concentric rings of mineral matrix surrounding the Haversian canal. Along the boundaries of the lamellae are small cavities known as lacunae, each of which contains a single bone cell, or osteocyte. Radiating from the lacunae are tiny canals, or canaliculi, into which the cytoplasmic processes of the osteocytes extend. Source: Adapted from Nordin and Frankel 1989.30 Reproduced with permission of John Wiley and Sons.

Part I Introduction8

of bone are called secondary Haversian systems, or secondary osteons. Secondary osteons consist of con-centric sheets of lamellar bone. Unlike primary osteons, secondary osteons are always bounded by cement lines, which are formed where osteoclastic activity ceases and osteoblastic bone formation resumes (Figure 1.8).

Lamellar bone, which is composed of osteons, is not the only type of bone within the body.2,9,40 The other type, called woven bone, is the first bone to appear in embryonic development and in the repair of fractures. Woven bone is gradually replaced by lamellar bone and serves only as a temporary structure, except in special locations such as the dental alveolus and osseous laby-rinths. Woven bone is characterized by coarse fiber bundles, approximately 30 μm in diameter, running in a random or interlacing fashion. In contrast, lamellar bone consists of fine fiber bundles, 2–4 μm in diameter, that are arranged irregularly in parallel or concentric curving sheets.

On a macroscopic level, two types of bone are found in the mature skeleton: hard, compact cortical bone in the shafts of the long bones, and cancellous or trabecular bone which is composed of a network of fine, interlacing partitions, called trabeculae, enclosing the cavities within bone that contain either hematopoietic or fatty marrow. Cancellous bone is found in the majority of the axial skeleton and in the ends of the long bones.

reSPonSe oF Bone to StreSS

Normal daily activity imposes a complex pattern of forces on the skeletal system that cause small deforma-tions of the bone.9 The direction and magnitude of these deformations are dependent on the geometry of the bone, the direction and magnitude of the loads imposed on the bone, and the material properties of the bone tissue. The mechanical response of a bone to stress can be described by quantitatively assessing the relationships between various directional loads and their resultant deformations. These relationships reflect the structural behavior of the entire bone.

The imposition of forces on a bone also creates a complex pattern of internal forces and deformations throughout the bone structure. Local deformations within the bone are referred to as strains, and the local force intensities at these sites are the stresses, defined as a given force per unit area. The relationship between stress and strain at a particular point in the bone is governed by the material properties of the local bone tissue. If the whole bone is loaded with very high forces, the stresses and strains in one region may exceed the ultimate stresses or strains that the tissue can tolerate, and a fracture develops.

osteonal remodelingIn adult equine long bones, large areas of primary oste-onal bone are often present in the cortex. This primary bone is lamellar in nature (although not truly lamellar),

Figure 1.7 Light microscopic image of a 100 μm undecalcified section of a bone‐cutting cone with osteoclasts resorbing bone at the apex of the cone (arrows) (Goldner Stain, magnification ×80).

Figure 1.8 Backscatter electron microscopic image of a 100 μm undecalcified section of bone showing secondary osteons within cortical bone. Newly remodeled bone is darker, indicating less mineralization of the site (backscatter electron microscopy, magnification ×70).

1 Bone Structure and the Response of Bone to Stress 9

consisting of layers of woven bone which are separated by layers of primary osteons. Studies of the relationship between the structure and the mechanical properties of bone have emphasized the comparison between primary and secondary osteonal (Haversian) bone. Many investigators have suggested that primary oste-onal bone is stronger than secondary osteonal bone.8,9,12,16 Hert et al.22 showed that fully mineralized primary bone was as strong or stronger than secondary osteonal bone. Reilly and Burstein37 demonstrated that bovine primary osteonal bone was significantly stiffer than secondary bone. Their finding was supported by Carter and Spengler,9 who showed that primary bovine bone was more fatigue resistant and was stronger in tensile tests than secondary bone. Carter et  al.8 demonstrated that osteonal or Haversian remodeling of bovine primary osteonal bone reduces the tensile strength and fatigue resistance of bone by decreasing bone density and creating an inherently weaker structure.

Many investigators have demonstrated that equine bone remodels in response to the stresses that are placed on it. The nature of these stresses is important, especially given that not all mechanical stimuli result in the same effect. Bone adaptation is induced by dynamic strains rather than by static loading.25,41 In addition, the increase in cross‐sectional area of bone induced by an osteogenic response was found to be highly correlated to the rate of bone deformation. These results suggest that training requires a high loading rate to elicit a maximal osteo-genic response.

The rate at which musculoskeletal tissues adapt varies with tissue, age, and exercise regime.41 Age is a potent factor in determining the extent of adaptation. The immature skeleton is much more responsive than the adult skeleton, although this varies among species. Animals that show limited morphologic change with aging, such as rodents, likely exhibit less reduction in the responsiveness of the skeleton with age, compared to the more typical aging phenotypes such as the human and the horse. In bone, adaptation can be initiated through brief cyclic‐loading periods given on a number of days per week. This type of exercise, if prolonged or intro-duced too rapidly, may also lead to fatigue damage and

microcrack development within the bone, with the potential to cause catastrophic fracture of the bone.5,18

Several research studies have reported the impact of evaluated training regimens on bone modeling and frac-ture. Short bursts of high‐speed gallop during training reduced the risk of fracture during subsequent racing.32 Nunamaker and colleagues5 proposed exercise regimens for young Thoroughbreds in training, based on experi-mental data where short‐distance, high‐speed gallops rather than longer, slower gallops led to improved bone strength and minimized fatigue fracture and the risk of catastrophic failure.

Track surface can also significantly affect the adaptive response of bone. Young et al.,44 in a study evaluating the effects of training regimens and track surfaces on bone remodeling, found that the cancellous bone component of the equine proximal sesamoid bone of horses trained on dirt tracks had significantly lower porosity than that of untrained horses, enabling the bone to withstand the higher loads of racing.7,11,28,44 Track surface had a greater effect on the cancellous morphology of the proximal ses-amoid bone than a variety of training regimens.33,44

Young and coworkers45 also demonstrated that equine carpal bone remodels in response to the stresses placed on it. This phenomenon, in which bone gains or loses cancellous or cortical bone or both in response to the level of stress sustained, is summarized as Wolff ’s law, which states that bone is laid down where it is needed and resorbed where it is not needed.10,12,24,31,36,38,43 Both theoretical and experimental evidence supports the pre-vailing hypothesis that trabeculae within bone align with the maximum and minimum principal stresses placed on the bone.7,19,23,36,42,44 Structural anisotropy is expected to be greatest in regions of primary tension or compression, in contrast to porosity and trabecular width, which cor-relate best with shear stress.21 The osteogenic response of bone to remodeling stimuli has been shown to be most dependent on strain magnitude and strain rate.24,38,44 Significant decreases in porosity have been demon-strated after controlled, impulsive loading of joints in rabbits and after exercising of sheep on concrete.35,36 The nature of the remodeling stimulus in these studies is believed to be associated with the high loading rate and the peak magnitude of the applied loads.36

reFerenceS

1 Arnoczky, S.P. and Wilson, J.W. (1990). The connective tissues. In: Canine Orthopedics (ed. W.G. Whittick), 21–41. Philadelphia: Lea & Febiger.

2 Ascenzi, A., Bonucci, E., and Bocciarelli, D.S. (1965). An electron microscope study of osteon calcification. J. Ultrastruct. Res. 12: 287–303.

3 Boskey, A.L. (1981). Current concepts of the physiology and biochemistry of calcification. Clin. Orthop. 167: 225–257.

4 Boskey, A.L. (1985). Connective tissues of the musculoskeletal system. In: Textbook of Small Animal Surgery (ed. D.H. Slatter), 1926–1939. Philadelphia: WB Saunders.

Part I Introduction10

5 Boston, R.C. and Nunamaker, D.M. (2000). Gait and speed as exercise components of risk factors associated with onset of fatigue injury of the third metacarpal bone in 2‐year‐old Thoroughbred racehorses. Am. J. Vet. Res. 61: 602–608.

6 Boyde, A. and Hobdell, M.H. (1969). Scanning electron microscopy of primary membrane bone. Z. Zellforsch. 99: 98–108.

7 Carter, D.R. and Hayes, W.C. (1977). The compressive behavior of bone as a two‐phase porous structure. J. Bone Joint Surg. Am. 59: 954–962.

8 Carter, D.R., Hayes, W.C., and Schurman, D.J. (1976). Fatigue life of compact bone II. Effects of microstructure and density. J. Biomech. 9: 211–218.

9 Carter, D.R. and Spengler, D.M. (1978). Mechanical properties and composition of cortical bone. Clin. Orthop. 135: 192–217.

10 Chamay, A. and Tschantz, P. (1972). Mechanical influences in bone remodeling. Experimental research on Wolff ’s law. J. Biomech. 5: 173–180.

11 Cowin, S.C. (1983). The mechanical and stress adaptive properties of bone. Ann. Biomed. Eng. 11: 263–295.

12 Dempster, W.T. and Coleman, R.F. (1960). Tensile strength of bone along and across the grain. J. Appl. Physiol. 16: 355.

13 Eanes, E.D. and Posner, A.S. (1970). Structure and chemistry of bone mineral. In: Biological Calcification (ed. H. Schraer), 1–26. Amsterdam: North Holland.

14 Enlow, D.H. (1962). The functional significance of the secondary osteon. Anat. Rec. 142: 230.

15 Enlow, D.H. (1966). An evaluation of the use of bone histology in forensic medicine and anthropology. In: Studies on the Anatomy and Function of Bone and Joints (ed. F.G. Evans), 93–113. New York: Springer‐Verlag.

16 Evans, F.J. and Bang, S. (1967). Differences and relations between the physical properties and the microscopic structure of human femoral, tibial, and fibular cortical bone. Am. J. Anat. 120: 79.

17 Fetter, A.W. (1985). Structure and function of bone. In: Textbook of Small Animal Orthopaedics (ed. C.D. Newton and D.M. Nunamaker), 9–12. Philadelphia: JB Lippincott.

18 Firth, E.C., Goodship, A.E., Delahunt, J. et al. (1999). Osteoinductive response in the dorsal aspect of the carpus of young Thoroughbreds in training occurs within months. Equine Vet. J. Suppl. 30: 552–554.

19 Fyhrie, D.P. and Carter, D.R. (1986). A unifying principle relating stress to trabecular bone morphology. J. Orthop. Res. 4: 304–317.

20 Hayes, W.C. and Carter, D.R. (1979). Biomechanics of bone. In: Skeletal Research: An Experimental Approach (ed. D.J. Simmons and A.S. Kunin), 263–300. New York: Academic Press.

21 Hayes, W.C. and Snyder, B. (1981). Toward a quantitative formulation of Wolff ’s law in trabecular bone. In: Mechanical Properties of Bone. AMD, vol. 45 (ed. S.C. Cowin), 43–68. New York: American Society of Mechanical Engineers.

22 Hert, J., Kucera, P., Vavra, M., and Volenik, V. (1965). Comparison of the mechanical properties of both primary and Haversian bone tissue. Acta Anat. 61: 412–423.

23 Lanyon, L.E. (1974). Experimental support for the trajectory theory of bone structure. J. Bone Joint Surg. Br. 56: 160–166.

24 Lanyon, L.E. (1982). Mechanical function and bone remodeling. In: Bone in Clinical Orthopedics (ed. G. Sumner‐Smith), 273–304. Philadelphia: WB Saunders Co.

25 Lanyon, L.E. and Rubin, C.T. (1984). Static vs dynamic loads as an influence on bone remodeling. J. Biomech. 17 (12): 897–905.

26 Markel, M.D. (2006). Bone biology and fracture healing. In: Equine Surgery, 3e (ed. J.A. Auer and J.A. Stick), 991–1000. St. Louis: Saunders Elsevier.

27 Marks, S.C. (1983). The origin of osteoclasts: evidence, clinical implications and investigative challenges of an extra‐skeletal source. J. Oral Pathol. 12: 226–256.

28 Martin, R.B. (1982). Porosity and specific surface of bone. CRC Crit. Rev. Biomed. Eng. 10: 179–222.

29 Menczel, L.J., Posner, A.S., and Harper, R.A. (1965). Age changes in the crystallinity of rat bone apatite. Isr. J. Med. Sci. 1: 251–252.

30 Nordin, M. and Frankel, V.H. (1989). Biomechanics of bone. In: Basic Biomechanics of the Musculoskeletal System, 2e (ed. M. Nordin and V.H. Frankel), 3–29. Philadelphia: Lea & Febiger.

31 Nunamaker, D.M., Butterweck, D.M., and Provost, M.T. (1989). Some geometric properties of the third metacarpal bone: a comparison between the Thoroughbred and Standardbred racehorse. J. Biomech. 22: 129–134.

32 Parkin, T.D., Clegg, P.D., French, N.P. et al. (2005). Risk factors for fatal lateral condylar fracture of the third metacarpus/metatarsus in UK racing. Equine Vet. J. 37: 192–199.

33 Pratt, G.W. (1982). The response of highly stressed bone in the race horse. In: Proceedings of the American Association of Equine Practitioners, vol. 27, 31–37. Lexington, KY: AAEP.

34 Pritchard, J.J. (1972). General morphology of bone. In: The Biochemistry and Physiology of Bone, vol. 1 (ed. G.H. Bourne), 1–20. New York: Academic Press.

35 Radin, E.L., Martin, R.B., Barr, D.B. et al. (1984). Effects of mechanical loading on the tissues of the rabbit knee. J. Orthop. Res. 2: 221–234.

1 Bone Structure and the Response of Bone to Stress 11

36 Radin, E.L., Orr, R.B., Kelman, J.L. et al. (1982). Effect of prolonged walking on concrete on the knees of sheep. J. Biomech. 15: 487–492.

37 Reilly, D.T. and Burstein, A.H. (1974). The mechanical properties of cortical bone. J. Bone Joint Surg. Am. 56: 1001–1022.

38 Rubin, C.T. and Lanyon, L.E. (1987). Osteoregulatory nature of mechanical stimuli: function as a determinant for adaptive remodeling in bone. J. Orthop. Res. 5: 300–310.

39 Simmons, D.J., Kent, G.N., Jilka, R.L. et al. (1982). Formation of bone by isolated, cultured osteoblasts in millipore diffusion chambers. Calcif. Tissue Int. 34: 291–294.

40 Smith, J.W. (1960). Collagen fibre patterns in mammalian bone. J. Anat. 94: 329–344.

41 Smith, R.K.W. and Goodship, A.E. (2008). The effect of early training and the adaption and conditioning of skeletal tissues. Vet. Clin. North Am. Equine Pract. 24: 37–51.

42 Townsend, P.R., Miegel, R.E., Rose, R.M. et al. (1976). Structure and function of the human patella: the role of cancellous bone. J. Biomed. Mater. Res. Symp. 7: 605–611.

43 Woo, S.L.‐Y., Kuei, S.C., Amiel, D. et al. (1981). The effect of prolonged physical training on the properties of long bone: a study of Wolff ’s law. J. Bone Joint Surg. Am. 63: 780–787.

44 Young, D.R., Nunamaker, D.M., and Markel, M.D. (1991). Quantitative evaluation of the remodeling response of the proximal sesamoid bones to training‐related stimuli in Thoroughbreds. Am. J. Vet. Res. 52: 1350–1356.

45 Young, D.R., Richardson, D.W., Markel, M.D. et al. (1991). Mechanical and morphometric analysis of the third carpal bone of Thoroughbreds. Am. J. Vet. Res. 52: 402–409.

Equine Fracture Repair, Second Edition. Edited by Alan J. Nixon. © 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.

12

IntroductIon

Fracture repair in horses remains an arduous process, fraught with difficulties. During the repair of adult long‐bone fractures, equine surgeons routinely work at the mechanical limits of fracture fixation devices, and in regions of the bone that are often poorly covered by soft tissues, leading to a wide range of complications. Precarious stability accompanied by a relatively poor fracture healing response in these regions increases the risk of fixation failure or contralateral limb laminitis before fracture union occurs. In contrast, such fractures are not an issue in human orthopedic repairs, in which patients can be instructed to bear partial weight or to remain non‐weight bearing after surgery, and in small animal orthopedic repairs, in which implants are used that are routinely far stronger than that required for a successful outcome. It is imperative, therefore, that equine surgeons understand the biomechanics of bone and fracture repair, in order to enhance the likelihood of success. In this chapter, we will define (i) the basic biomechanical terminology needed to understand frac­ture mechanics; (ii) the forces causing various fracture configurations; (iii) the biomechanical principles of fracture repair; and (iv) the directional loads acting on equine long bones during normal activities.

BasIc BIomechanIcal termInology

load‐deformation curveThe most important mechanical properties of bone are its strength and stiffness. These mechanical characteris­tics can be assessed best by examining the behavior of the structure when it is subjected to externally applied forces,

called loads.19 Loading a structure such as bone causes deformation, or a change in dimension such as decreased or increased length. When a load of known direction is imposed on the structure, the deformation of that struc­ture can be measured and plotted as a load‐deformation curve. Essential information regarding the structure’s mechanical properties can be gathered from this curve.

A typical load‐deformation curve for bone is illustrated in Figure 2.1.19 The initial linear portion of the curve, called the elastic region, is a measure of the elasticity of a struc­ture. If the object is loaded only through the elastic region of the curve, it will return to its original shape when the load is removed. As loading continues, however, the substance of the structure begins to yield. Yield is defined as the point beyond which the structure will no longer return to its orig­inal shape when the load is removed. As the load exceeds the yield point, the structure exhibits plastic behavior, reflected in the second, flatter portion of the curve, the plas­tic region. In this region, the structure deforms to a much greater extent for a given load (the structure is less stiff) than in the elastic region of the curve. If the load is progres­sively increased, the structure will fail at some point. This load is the ultimate failure point on the curve.4,16,19

Three parameters for determining the strength of a structure are reflected in the load‐deformation curve: (i) the load that the structure can sustain before failing; (ii) the deformation that it can sustain before failing; and (iii) the energy that it can store before failing, known as toughness.4,16,19 The strength of the structure in terms of load and deformation, or ultimate strength, is indicated on the curve by the ultimate failure point. The toughness of the structure in terms of energy storage is equal to the area under the curve. Toughness can be divided into elastic energy (the area under the curve up to the yield point) and plastic energy (the area under the curve from the yield point to the ultimate failure point).

2

Fracture BiomechanicsMark D. Markel

Comparative Orthopaedic Research Laboratory, Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA