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MILLER’S REVIEW OF
ORTHOPAEDICS
This page intentionally left blank

     
MILLER’S REVIEW OF

ORTHOPAEDICS
EIGHTH EDITION

MARK D. MILLER, MD
S. Ward Casscells Professor
Head, Division of Sports Division
Department of Orthopaedic Surgery
University of Virginia Health System
Charlottesville, Virginia
Team Physician
James Madison University
Harrisonburg, Virginia

STEPHEN R. THOMPSON, MD, MEd, FRCSC

Lead Physician
Northern Light Orthopaedics
Associate Professor
University of Maine
Northern Light Eastern Maine Medical Center
Bangor, Maine
Elsevier
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MILLER’S REVIEW OF ORTHOPAEDICS, EIGHTH EDITION ISBN: 978-0-323-60978-4

Copyright © 2020 by Elsevier, Inc. All rights reserved.

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Practitioners and researchers must always rely on their own experience and knowledge in evaluating
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contained in the material herein.

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an imprint of Elsevier Inc.

Library of Congress Control Number: 2019946571

Senior Content Strategist: Kristine Jones

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Printed in Canada

Last digit is the print number: 9 8 7 6 5 4 3 2 1

To the generation of orthopaedic surgeons that I have had the honor to teach. For
as long as I am able, I will continue to answer your questions, give my opinions,
and share my experiences. The collective and collegial commitment to lifelong
learning is both admirable and inspirational.
Mark D. Miller

For Linden, Harper, and Shannon.

Because, Linden, you deserve to be first this time!
Stephen R. Thompson
CONTRIBUTORS
Amiethab A. Aiyer, MD F. Winston Gwathmey, Jr., MD
Chief, Foot and Ankle Service Associate Professor
Assistant Professor Department of Orthopaedic Surgery
Department of Orthopaedic Surgery University of Virginia Health System
Miller School of Medicine Charlottesville, Virginia
University of Miami
Miami, Florida David J. Hak, MD, MBA, FACS
Hughston Orthopedic Trauma Group
Central Florida Regional Hospital
Gerasimos Bastas, MD, PhD
Sanford, Florida
Assistant Professor
Director, Limb Loss Rehabilitation Joe M. Hart, PhD, ATC
Department of Physical Medicine and Rehabilitation Associate Professor
Vanderbilt University Medical Center Department of Kinesiology
Nashville, Tennessee Director of Clinical Research
Department of Orthopaedic Surgery
James A. Browne, MD University of Virginia Health System
Associate Professor Charlottesville, Virginia
Department of Orthopaedic Surgery
University of Virginia Health System Ginger E. Holt, MD
Charlottesville, Virginia Professor
Department of Orthopaedic Surgery
James E. Christensen, MD Orthopaedic Oncologist
Orthopaedic Surgery Vanderbilt Medical Center
St. Mary’s Health System Nashville, Tennessee
Madison, Wisconsin Nitin Jain, MD, MSPH
Associate Professor
Marc M. DeHart, MD Director, PM&R Research
Associate Professor Co-Director, Orthopaedic Sports Medicine Research
Chief, Adult Reconstruction Department of Physical Medicine and Rehabilitation and
Department of Orthopaedic Surgery Orthopaedics
UT Health San Antonio Vanderbilt University Medical Center
San Antonio, Texas Nashville, Tennessee
Clinical Associate Professor
Department of Orthopaedics and Rehabilitation Anish R. Kadakia, MD
University of Texas Medical Branch Associate Professor of Orthopedic Surgery
Galveston, Texas Director, Foot and Ankle Program
Foot and Ankle Orthopedic Fellowship
Chan Gao, MD, PhD Feinberg School of Medicine
Resident Northwestern University
Physical Medicine and Rehabilitation, Department of Orthopedic Surgery
Vanderbilt University Medical Center Northwestern Memorial Hospital
Nashville, Tennessee Chicago, Illinois

Sanjeev Kakar, MD
George Keith Gill, MD
Professor
Department of Orthopaedic Surgery
Department of Orthopedic Surgery
University of Virginia Health System
College of Medicine
Charlottesville, Virginia
Mayo Clinic
Rochester, Minnesota
vi

Dustin Lybeck, MD
Orthopedic Surgeon
Musculoskeletal Oncology
Department of Orthopedic Surgery
San Antonio Military Medical Center
Fort Sam Houston, Texas
Cyril Mauffrey, MD, FACS, FRCS
Professor
Department of Orthopedic Surgery
Interim Director of Service
Department of Orthopedics
Denver Health Medical Center
Denver, Colorado
Edward J. McPherson, MD, FACS
Professor
Department of Orthopaedic Surgery
University of California, Los Angeles
Santa Monica, California
Mark D. Miller, MD
S. Ward Casscells Professor
Head, Division of Sports Division
Department of Orthopaedic Surgery
University of Virginia Health System
Charlottesville, Virginia
Team Physician
James Madison University
Harrisonburg, Virginia
Jessica Rivera, MD
Division Chief, Research
Department of Orthopedic Surgery
San Antonio Military Medical Center
Fort Sam Houston, Texas
Jeremy K. Rush, MD, FAAP
Pediatric Orthopaedic Surgeon
Sports Medicine Program Director
Department of Orthopaedics
Nemours Children’s Health System
Jacksonville, Florida
Contributors vii
Matthew R. Schmitz, MD
Chief, Pediatric Orthopaedics and Young Adult Hip
Preservation
Department of Orthopedic Surgery
San Antonio Military Medical Center
Fort Sam Houston, Texas
Francis H. Shen, MD
Warren G. Stamp Endowed Professor
Division Head, Spine Division
Director, Spine Center
Department of Orthopaedic Surgery
University of Virginia Health System
Charlottesville, Virginia
Adam Shimer, MD
Associate Professor
Director, Spine Fellowship
Medical Director, Orthopaedic Inpatient Unit
Department of Orthopaedic Surgery
University of Virginia Health System
Charlottesville, Virginia
Stephen R. Thompson, MD, MEd, FRCSC
Lead Physician
Northern Light Orthopaedics
Associate Professor
University of Maine
Northern Light Eastern Maine Medical Center
Bangor, Maine
Eric R. Wagner, MD
Assistant Professor
Department of Orthopaedic Surgery
Emory University
Atlanta, Georgia
Brian C. Werner, MD
Assistant Professor
Department of Orthopaedic Surgery
University of Virginia Health System
Charlottesville, Virginia
PREFACE
We are both humbled and honored to present the eighth
edition of Miller’s Review of Orthopaedics. Very few textbooks
make it to an eighth edition, and for those that do, there are
even fewer for which the senior editor is still contributing, or
even still on this Earth. For that, and for the help of my friend
and colleague, Steve Thompson, MD, I am very grateful.
So what is new for this edition of one of the most popu-
lar orthopaedic textbooks in history? The answer lies in the
very concept of this book—we tried to get even closer to the
bottom line. We completely reworked several chapters and
put the unwieldy basic science chapter on a crash diet in fur-
thering our efforts with each edition to find the most concise
approach to content. We added several new composite figures
that show multiple key testable concepts all in one image. We
renewed our “war on typos” and hopefully advanced the battle
lines at a very minimum. For those of you who have person-
ally emailed us or stopped us at meetings all across the world,
we are indebted to your contributions in this fight! We also
began the “battle of the purge” across all the chapters, seeking
to condense the material as much as is practical.
viii
Thank you for purchasing this textbook. We are well aware
of the millennial push to have everything digital and free.
Nonetheless, we still see value in having an actual book to put
on one’s professional shelf and to circle, highlight, and refer-
ence as experiences and pursuit of knowledge dictates. And,
for those who are going completely paperless, there is still an
electronic version that will allow you to access the book in an
interactive fashion.
As always, we remain indebted to our incredible team of
authors, who have devoted a tremendous amount of time and
effort in updating their respective chapters. We also want to
acknowledge the efforts of the editorial and professional staff
at Elsevier, including Laura Schmidt, Victoria Heim, and Kris-
tine Jones.
Finally, this book would not be possible without you, the
reader. Thank you for allowing us to help you prepare for
your career in musculoskeletal medicine, whatever path it
may travel!
Mark D. Miller
Stephen R. Thompson
CONTENTS

1 BASIC SCIENCES 1 3 PEDIATRIC ORTHOPAEDICS 218

Jeremy K. Rush, Dustin Lybeck, Jessica Rivera, and Matthew R. Schmitz and Jeremy K. Rush
Matthew R. Schmitz
SECTION 1 UPPER EXTREMITY
SECTION 1 ORTHOPAEDIC TISSUES 1 PROBLEMS 219
Bone 1 Brachial Plexus Palsy 219
Cartilage and Joint 34 Sprengel Deformity 219
Muscle 52 Fibrotic Deltoid Problems 220
Tendon 57 Congenital Pseudarthrosis of the Clavicle 220
Ligament 58 Poland Syndrome 220
Neural Tissue and Intervertebral Disc 59 Apert Syndrome 220

SECTION 2 ORTHOPAEDIC SECTION 2 LOWER EXTREMITY

BIOLOGY 61 PROBLEMS: GENERAL 221
Cellular and Molecular Biology and Immunology 61 Rotational Problems of the Lower Extremities 221
Infection and Microbiology 70 Leg Length Discrepancy 222

SECTION 3 PERIOPERATIVE AND SECTION 3 HIP AND FEMUR 223

ORTHOPAEDIC MEDICINE 79 Developmental Dysplasia of the Hip 223
Thromboprophylaxis 79 Congenital Coxa Vara 227
Perioperative Disease and Comorbidities 84 Legg-Calvé-Perthes Disease (Coxa Plana) 227
Slipped Capital Femoral Epiphysis 229
SECTION 4 OTHER BASIC Bladder Exstrophy 231
PRINCIPLES 89 Proximal Femoral Focal Deficiency 231
Lower Extremity Inflammation and Infection 231
Imaging and Special Studies 89
Biomaterials and Biomechanics 93 SECTION 4 KNEE AND LEG 234
TESTABLE CONCEPTS 107 Leg 234
Tibial Bowing 235
Osteochondritis Dissecans 237
2 ANATOMY 110 Osgood-Schlatter Disease 237
F. Winston Gwathmey, Jr. Discoid Meniscus 237
Congenital Dislocation of the Knee 237
SECTION 1 INTRODUCTION 110
Overview 110 SECTION 5 FOOT 238
Clubfoot (Congenital Talipes Equinovarus) 238
SECTION 2 UPPER EXTREMITY 111 Metatarsus Adductus and Skewfoot 239
Shoulder 111 Pes Cavus (Cavus Foot) 239
Arm 112 Congenital Vertical Talus (Congenital Convex Pes Valgus) 241
Forearm 116 Tarsal Coalitions 241
Wrist and Hand 116 Calcaneovalgus Foot 242
Juvenile Bunions 242
SECTION 3 LOWER EXTREMITY 149 Kohler Disease 243
Pelvis, Hip, and Thigh 149 Flexible Pes Planus 243
Knee and Leg 151 Idiopathic Toe Walking 243
Ankle and Foot 157 Accessory Navicular 243
Ball-and-Socket Ankle 243
SECTION 4 SPINE 196 Congenital Toe Disorders 243
Osteology 196
Arthrology 197 SECTION 6 PEDIATRIC SPINE 244
Surgical Approaches to the Spine 209 Adolescent Idiopathic Scoliosis 244
Early-Onset Scoliosis 247
TESTABLE CONCEPTS 216 Juvenile Idiopathic Scoliosis 247
ix
x Contents

Infantile Idiopathic Scoliosis 247 Beckwith-Wiedemann Syndrome 274

Congenital Spinal Deformities 248 Nail-Patella Syndrome (Hereditary Onychoosteodysplasia)
Neuromuscular Scoliosis 249 274
Neurofibromatosis 250
Kyphosis 251 SECTION 11 HEMATOPOIETIC AND
Cervical Spine Disorders 252 METABOLIC DISORDERS AND
Spondylolysis and Spondylolisthesis 253 ARTHRITIDES 274
Other Spinal Conditions 254 Gaucher Disease 274
Niemann-Pick Disease 274
SECTION 7 CEREBRAL PALSY 255 Sickle Cell Anemia 274
Introduction 255 Thalassemia 275
Classification 255 Hemophilia 275
Orthopaedic Assessment 257 Leukemia 275
Spasticity Treatment 257 Rickets 275
Gait Disorders 257 Osteogenesis Imperfecta 275
Spinal Disorders 257 Juvenile Idiopathic Arthritis 276
Hip Subluxation and Dislocation 258 Ankylosing Spondylitis 277
Knee Abnormalities 258
Foot and Ankle Abnormalities 258 TESTABLE CONCEPTS 277
Upper Extremity Management 259

SECTION 8 NEUROMUSCULAR 4 SPORTS MEDICINE 281

DISORDERS 260 James E. Christensen, Brian C. Werner,
Arthrogrypotic Syndromes 260 Stephen R. Thompson, and
Myelodysplasia (Spina Bifida) 261 Mark D. Miller
Myopathies (Muscular Dystrophies) 263
Polymyositis and Dermatomyositis 264 SECTION 1 KNEE 281
Hereditary Neuropathies 264 Anatomy 281
Myasthenia Gravis 265 Biomechanics 287
Anterior Horn Cell Disorders 265 Diagnostic Techniques 288
Acute Idiopathic Postinfectious Polyneuropathy (Guillain- Knee Arthroscopy 288
Barré Syndrome) 265 Meniscal Injuries 290
Overgrowth Syndromes 265 Ligament Injuries 297
Osteochondral Lesions 303
SECTION 9 BONE DYSPLASIAS Synovial Lesions 306
266 Patellofemoral Disorders 307
Introduction 266 Pediatric Knee Injuries 310
Achondroplasia 266
Pseudoachondroplasia 267 SECTION 2 PELVIS, HIP, AND
Multiple Epiphyseal Dysplasia 268 THIGH 311
Spondyloepiphyseal Dysplasia 269 Contusions 311
Chondrodysplasia Punctata 269 Muscle Injuries 311
Kniest Syndrome 270 Bursitis 312
Metaphyseal Chondrodysplasia 270 Nerve Entrapment Syndromes 312
Progressive Diaphyseal Dysplasia (Camurati-Engelmann Bone Disorders 312
Disease) 270 Intraarticular Disorders 312
Mucopolysaccharidosis 270 Femoroacetabular Impingement 313
Diastrophic Dysplasia 271 Other Hip Disorders 315
Cleidocranial Dysplasia (Dysostosis) 271 Hip Arthroscopy 315
Osteopetrosis 271
Infantile Cortical Hyperostosis (Caffey Disease) 272 SECTION 3 SHOULDER 316
Anatomy 316
SECTION 10 SYNDROMES WITH
Biomechanics 316
ORTHOPAEDIC MANIFESTATIONS Diagnostic Techniques 318
272 Shoulder Arthroscopy 320
Down Syndrome (Trisomy 21) 272 Shoulder Instability 321
Turner Syndrome 272 Subacromial Impingement Syndrome 328
Prader-Willi Syndrome 272 Rotator Cuff Disease 329
Marfan Syndrome 273 Subscapularis Tears 334
Homocystinuria 273 Rotator Cuff Tear Arthropathy 334
Ehlers-Danlos Syndrome 273 Subcoracoid Impingement 335
Fibrodysplasia Ossificans Progressiva 273 Internal Impingement 335
Rett Syndrome 274 SLAP Tears 336
 Contents xi

Proximal Biceps Tendon Pathology 338 Templating 364

Acromioclavicular and Sternoclavicular Injuries 339 Implant Fixation 364
Muscle Ruptures 340 Bone Ongrowth Fixation 367
Shoulder Stiffness 342 Hydroxyapatite 367
Nerve Disorders 343 Femoral Stem Loading 368
Other Shoulder Disorders 344 Femoral Stress Shielding 368
Femoral Stem Breakage 368
SECTION 4 MEDICAL ASPECTS
OF SPORTS MEDICINE 345 SECTION 6 REVISION THA 370
Preparticipation Physical Examination 345 Presentation 370
Cardiac Abnormalities in Athletes 345 Acetabular Side 370
Concussion 347 Femoral Side 372
Sickle Cell Disease 347
Metabolic Issues in Athletes 348 SECTION 7 ARTICULAR BEARINGS
Ergogenic Drugs 348 AND CORROSION IN THA 374
Female Athlete–Related Issues 348 Introduction 374
Infectious Disease in Athletes 351 Polyethylene 374
Miscellaneous Sports-Related Injuries and Issues 352 Polyethylene Wear and Osteolysis 376
Osteolysis Process 376
TESTABLE CONCEPTS 353 Osteolysis Around THA Prosthesis—Effective Joint Space 377
Particle Debris Formation—Linear Versus Volumetric
Wear 377
5 ADULT RECONSTRUCTION 356 Osteolysis—Radiographic Findings in THA 377
Edward J. McPherson, Brian C. Werner, George Keith Gill, Treatment of Polyethylene Wear 378
and James A. Browne Bearing Lubrication 379
Metal and Ceramic on PE 379
SECTION 1 EVALUATION OF Metal on Metal 379
THE ADULT PATIENT WITH HIP Hip Resurfacing 382
PAIN 357 Ceramic-on-Ceramic Bearing 382
Dual-Mobility Components 383
Physical Examination Tests for Hip Irritability 357 Trunnion Corrosion 383
Imaging 357
SECTION 8 PERIPROSTHETIC THA
SECTION 2 STRUCTURAL HIP
FRACTURE 384
DISORDERS IN THE ADULT 358
Time of Fracture 384
Natural History 358 Intraoperative Fracture 384
Spectrum of Presentation 358 Early Postoperative Fracture 384
Anatomy of Adult Hip Dysplasia 358 Late Fracture 384
Treatment of Dysplasia 358
Femoroacetabular Impingement 359 SECTION 9 THA—
Treatment of FAI 360 MISCELLANEOUS 385
SECTION 3 OSTEONECROSIS Nerve Injury 385
OF THE HIP 361 Anatomy 385
Specific Complications and Host Risk Factors 386
Occurrence 361 Venous Thrombosis 386
Etiology 361 Heterotopic Ossification 386
Clinical Presentation 361 Iliopsoas Impingement 386
Imaging 361 Implant Facts 386
Staging 361
Treatment 361 SECTION 10 THA—JOINT
Transient Osteoporosis of the Hip 362 STABILITY 387
SECTION 4 TREATMENT OF HIP Incidence of THA Dislocation 387
ARTHRITIS 362 Risk Factors for Dislocation 387
Assessment 387
Nonoperative 362 Treatment 392
Operative 363
SECTION 11 KNEE ARTHRITIS
SECTION 5 TOTAL HIP
ASSESSMENT 395
ARTHROPLASTY 364
Clinical Presentation 395
Indications 364 Imaging Studies 395
Surgical Approaches 364
xii Contents

SECTION 12 KNEE ARTHRITIS SECTION 19 SHOULDER

TREATMENT 396 HEMIARTHROPLASTY 430
Consensus Treatment 396 Indications 430
Requirements 430
SECTION 13 TOTAL KNEE Complications 431
ARTHROPLASTY 398 Conversion From Hemiarthroplasty to TSA 431
Indications 398 Hemiarthroplasty for Cuff Tear Arthropathy 431
Survival of TKA 398
Technical Goals 398 SECTION 20 TOTAL SHOULDER
Preoperative Planning 398 ARTHROPLASTY 431
Goals of Bone Cuts in TKA 399 Introduction 431
Coronal Plane Ligament Balancing 400 Requirements 431
Flexion Deformity (i.e., Flexion Contracture) 401 Component Positioning 431
Sagittal Plane Balancing 402 Rehabilitation 431
Perioperative Nerve Blocks 402 Complications 432
Postoperative Therapy 402
Complications 402 SECTION 21 REVERSE TOTAL
SHOULDER ARTHROPLASTY 432
SECTION 14 TKA DESIGN 409 Introduction 432
Design Categories 409 Requirements 432
Cruciate-Retaining Primary TKA Design 409 Component Positioning 432
Cruciate-Sacrificing Primary TKA Designs 410 Complications 432
Tibial Rotating Platform in Primary TKA 413
Modularity in Primary TKA 414 SECTION 22 INFECTION IN
All-Polyethylene Tibia (APT) 414 SHOULDER ARTHROPLASTY 433
Constraint in TKA 414 Introduction 433
Common Organisms 433
SECTION 15 REVISION TKA 417 History and Physical Examination 433
Preoperative Evaluation 417 Investigations 433
Surgical Approach 417 Microbiology 434
Implant System 417 Management 434
Modular Bearing Change for Premature
Excessive Wear 417 TESTABLE CONCEPTS 435
Technique of Revision TKA 417
Revision TKA—Patella 418

SECTION 16 PATELLAR TRACKING

6 DISORDERS OF THE FOOT AND
IN TKA 418 ANKLE 438
Introduction 418 Anish R. Kadakia and Amiethab A. Aiyer
Q Angle in TKA 418
TKA Techniques to Optimize Patellar Tracking 418 SECTION 1 BIOMECHANICS OF
Intraoperative Assessment of Maltracking 421 THE FOOT AND ANKLE 439
Postoperative Assessment of Maltracking 421 Anatomy 439
Patella Baja 421 Foot Positions Versus Foot Motions 442
Patellar Resurfacing Versus Nonresurfacing 421 Gait Cycle 442

SECTION 17 CATASTROPHIC SECTION 2 PHYSICAL

WEAR IN TKA 424 EXAMINATION OF THE FOOT
Premature Failure of TKA Implant 424 AND ANKLE 445
Factors Involved in Catastrophic Wear 424 Inspection 445
“Perfect Storm” Scenario for Catastrophic Wear 427 Gait Evaluation 445
Measures to Mitigate Catastrophic PE Wear 427 Vascular Examination 445
Neurologic Examination 446
SECTION 18 GLENOHUMERAL Motor Examination 446
ARTHRITIS 427 Palpation and Stability Assessment 447
Introduction 42 Range of Motion (ROM) 448
History and Physical Examination 428
Imaging 428 SECTION 3 RADIOGRAPHIC
Treatment 428 EVALUATION OF THE FOOT AND
ANKLE 449
 Contents xiii

SECTION 4 ADULT HALLUX SECTION 15 HEEL PAIN 492

VALGUS 450 Plantar Heel Pain 492
Achilles Disorders 492
SECTION 5 JUVENILE AND
ADOLESCENT HALLUX SECTION 16 ANKLE PAIN AND
VALGUS 456 SPORTS INJURIES 496
Ankle Sprains 496
SECTION 6 HALLUX VARUS 458 High Ankle Sprains 497
Ankle Impingement 497
SECTION 7 LESSER-TOE Osteochondral Lesions 497
DEFORMITIES 459 Chronic Exertional Compartment Syndrome 498
Technical Pearls for Ankle Arthroscopy 498
Anatomy and Function 459
Deformities 459 SECTION 17 THE DIABETIC
SECTION 8 HYPERKERATOTIC FOOT 499
PATHOLOGIES 464 Pathophysiology 499
Clinical Problems 499
Intractable Plantar Keratosis (IPK) 464
Bunionette Deformity (Tailor’s Bunion) 464 SECTION 18 TRAUMA 502
SECTION 9 SESAMOIDS 466 Phalangeal Fractures 502
Metatarsal Fractures 502
Anatomy 466
First MTP Joint Injuries 504
Deformities 466
Tarsometatarsal Fractures and Dislocations (Lisfranc Injury) 504
SECTION 10 ACCESSORY Midfoot Injuries (Excluding Lisfranc Injuries) 507
Talus Fractures 511
BONES 468
Calcaneus Fractures 516
Peritalar (Subtalar) Dislocations 518
SECTION 11 NEUROLOGIC Compartment Syndrome 519
DISORDERS 468 Ankle Fractures 521
Interdigital Neuritis (Morton Neuroma) 468 Pilon (Tibial Plafond) Fractures 526
Recurrent Neuroma 469
Tarsal Tunnel Syndrome 470 TESTABLE CONCEPTS 529
Plantar Nerve Problems 471
Anterior Tarsal Tunnel Syndrome 472
Superficial Peroneal Nerve Entrapment 472 7 HAND, UPPER EXTREMITY,
Sural or Saphenous Nerve Entrapment 472 AND MICROVASCULAR
Sequelae of Upper Motor Neuron Disorders 473
Charcot-Marie-Tooth (CMT) Disease 473 SURGERY 534
Peripheral Nerve Injury and Tendon Transfers 475 Eric R. Wagner and Sanjeev Kakar
Anatomy 534
SECTION 12 ARTHRITIC Distal Radius Fractures 537
DISEASE 476 Carpal Fractures and Instability 543
Crystalline Disease 476 Metacarpal and Phalangeal Injuries 550
Seronegative Spondyloarthropathy (SNSA) 476 Tendon Injuries and Overuse Syndromes 555
Rheumatoid Arthritis 477 Distal Radioulnar Joint, Triangular Fibrocartilage Complex,
Osteoarthritis 479 and Wrist Arthroscopy 560
Nail and Fingertip Injuries 562
SECTION 13 POSTURAL Soft Tissue Coverage and Microsurgery 566
DISORDERS 485 Vascular Disorders 569
Compression Neuropathy 572
Pes Planus (Flatfoot Deformity) 485
Nerve Injuries and Tendon Transfers 580
Pes Cavus Deformity 488
Arthritis 584
SECTION 14 TENDON Idiopathic Osteonecrosis of the Carpus 590
Dupuytren Disease 591
DISORDERS 490
Hand Tumors 593
Achilles Tendon 490 Hand Infections 597
Peroneal Tendons 490 Injection Injury 600
Posterior Tibial Tendon 491 Congenital Hand Differences 600
Anterior Tibial Tendon 491 Elbow 604
Flexor Hallucis Longus 491
TESTABLE CONCEPTS 611
xiv Contents

8 SPINE 618 10 REHABILITATION: GAIT,

Francis H. Shen and Adam Shimer AMPUTATIONS, PROSTHESES,
Introduction 618
Cervical Spine 621 ORTHOSES, AND NEUROLOGIC
Thoracic Spine 629 INJURY 706
Lumbar Spine 630 Chan Gao, Gerasimos Bastas, and Nitin Jain
Adult Deformity 640
Sacropelvis 642 SECTION 1 GAIT 706
Spinal Tumors 643 Walking 706
Spinal Infections and Inflammatory Arthritides 645 Gait Dynamics 707
Spinal Trauma 649 Determinants of Gait (Motion Patterns) 707
TESTABLE CONCEPTS 665 Muscle Action 709
Pathologic Gait 710

SECTION 2 AMPUTATIONS 711

9 ORTHOPAEDIC PATHOLOGY 669 Introduction 711
Ginger E. Holt Metabolic Cost of Amputee Gait 711
Load Transfer 711
SECTION 1 PRINCIPLES OF
Amputation Wound Healing 712
PRACTICE 669 Pediatric Amputation 712
Presentation 669 Amputation After Trauma 712
Imaging 669 Risk Factors 713
Biopsy (Bone and Soft Tissue) 672 Musculoskeletal Tumors 713
Molecular Biology (Bone and Soft Tissue) 673 Technical Considerations 714
Grading (Bone and Soft Tissue) 673 Complications 714
Staging (Bone and Soft Tissue) 673 Upper Limb Amputations 714
Treatment (Bone and Soft Tissue) 673 Lower Limb Amputations 716
SECTION 2 SOFT TISSUE SECTION 3 PROSTHESES 718
TUMORS 676 Upper Limb 718
Introduction 676 Lower Limb 718
Malignant Soft Tissue Tumors (Soft Tissue Sarcomas) 676
Soft Tissue Sarcoma Subtypes 677 SECTION 4 ORTHOSES 723
Benign Soft Tissue Tumors 679 Introduction 723
Tumors of Fibrous Tissue 679 Shoes 723
Tumors of Fatty Tissue 679 Foot Orthoses 723
Tumors of Neural Tissue 680 Ankle-Foot Orthoses 723
Vascular Tumors 680 Knee-Ankle-Foot Orthosis 723
Synovial Proliferative Disorders 680 Hip-Knee-Ankle-Foot Orthosis 723
Posttraumatic Conditions 680 Elbow Orthosis 728
Clinical Pearls for Soft Tissue Sarcoma 681 Wrist-Hand Orthosis 728
Fracture Braces 728
SECTION 3 BONE TUMORS 681 Pediatric Orthoses 728
Presentation 681 Spine Orthoses 728
Bone-Producing Lesions 681
Nonosteogenic Osteosarcoma/Malignant Fibrous SECTION 5 SURGERY FOR
­Hystiocytoma 685 STROKE AND CLOSED-HEAD
Chondrogenic Lesions 685 INJURY 728
Fibrous Lesions 688 Introduction 728
Notochordal Tissue Tumors 690 Lower Limb 729
Vascular Tumors 690 Upper Limb 729
Hematopoietic Tumors 690
Tumors of Unknown Origin 693 SECTION 6 POSTPOLIO
Tumorlike Conditions 695 SYNDROME 729
Metastatic Bone Disease 698
Cause 729
TESTABLE CONCEPTS 702 Treatment 729

TESTABLE CONCEPTS 730

 Contents xv

11 TRAUMA 731 12 PRINCIPLES OF PRACTICE 789

David J. Hak and Cyril Mauffrey Marc M. DeHart
Introduction 789
SECTION 1 CARE OF THE Medical Professionalism in the New Millennium: A Physician
MULTIPLY INJURED PATIENT 731 Charter (2002) 789
Principles of Trauma Care 731 Aspirational Documents 790
Care of Injuries to Specific Tissues 733 Standards of Professionalism 791
Biomechanics of Fracture Healing 737 Child, Elder, and Spousal Abuse 792
Biomechanics of Open Reduction and Internal Fixation Sexual Misconduct 793
(ORIF) 737 The Impaired Physician 793
Sports Medicine Issues 793
SECTION 2 UPPER EXTREMITY Research 793
738 Medical Liability 794
Shoulder Injuries 738
TESTABLE CONCEPTS 795
Humeral Injuries 741
Elbow Injuries 743
Forearm Fractures 744
Wrist Fractures 745 13 BIOSTATISTICS AND
Carpal Injuries 746 RESEARCH DESIGN 796
Hand Injuries 746 Joe M. Hart
Introduction 796
SECTION 3 LOWER EXTREMITY Selecting a Research Study Design 796
AND PELVIS 746 Evidence-Based Medicine 796
Pelvic and Acetabular Injuries 746 Clinical Research Designs 796
Femoral and Hip Injuries 754 Common Flaws in Research Designs 798
Knee Injuries 760 How Many Subjects Are Needed to Complete a Research
Tibial Injuries 763 Study? 799
What Outcomes Should Be Included in a Research Study? 799
SECTION 4 PEDIATRIC Describing Your Data With Simple Statistics 799
TRAUMA 766 Concepts in Epidemiologic Research Studies 800
Introduction 766 Testing Your Hypotheses With Statistics 802
Child Abuse 766 What Statistical Test to Use in Research Studies 803
Physeal Fractures 767 Validity and Reliability 804
Pediatric Polytrauma 768 Interpretation of Statistical Test Results 805
Shoulder and Arm Injuries 768
Elbow Injuries 769 TESTABLE CONCEPTS 806
Forearm Fractures 776
Pediatric Scaphoid Fracture 776
Lower Extremity Injuries 776

TESTABLE CONCEPTS 783

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 CHAPTER
1
BASIC SCIENCES
Jeremy K. Rush, Dustin Lybeck, Jessica Rivera, and Matthew R. Schmitz
CONTENTS
SECTION 1 ORTHOPAEDIC TISSUES, 1
Bone, 1
Cartilage and Joint, 34
Muscle, 52
Tendon, 57
Ligament, 58
Neural Tissue and Intervertebral Disc, 59
SECTION 2 ORTHOPAEDIC BIOLOGY, 61
Cellular and Molecular Biology and Immunology, 61
Infection and Microbiology, 70
SECTION 1 ORTHOPAEDIC TISSUES
BONE
n Histologic features of bone
n Types (Fig. 1.1; Table 1.1)
• N ormal bone: lamellar or mature
• Immature and pathologic bone: woven, more random,
more osteocytes, increased turnover, weaker
• Lamellar bone is stress oriented; woven bone is not.
• Cortical (compact) bone
• Constitutes 80% of the skeleton
• Consists of tightly packed osteons or haversian
systems
• Connected by haversian (or Volkmann) canals
• Contains arterioles, venules, capillaries, nerves,
possibly lymphatic channels
• Interstitial lamellae: between osteons
• Fibrils connect lamellae but do not cross cement
lines.
• Cement lines define the outer border of an
osteon.
• Nutrition provided by intraosseous circulation
through canals and canaliculi (cell processes of
osteocytes)
• Characterized by slow turnover rate, higher Young’s
modulus of elasticity, more stiffness
• Cancellous bone (spongy or trabecular bone)
• Less dense, more remodeling according to lines of
stress (Wolff’s law)
• Characterized by high turnover rate, smaller Young’s
modulus, more elasticity
n Cellular biology (Fig. 1.2)
• Osteoblasts
• Appear as cuboid cells aligned in layers along
immature osteoid
• Are derived from undifferentiated mesenchymal stem
cells
SECTION 3 PERIOPERATIVE AND ORTHOPAEDIC
MEDICINE, 78
Thromboprophylaxis, 78
Perioperative Disease and Comorbidities, 84
SECTION 4 OTHER BASIC PRINCIPLES, 89
Imaging and Special Studies, 89
Biomaterials and Biomechanics, 93
TESTABLE CONCEPTS, 107
• T  hese stem cells line haversian canals, endosteum,
and periosteum.
• Become osteoblasts under conditions of low strain
and increased oxygen tension
• Transcription factor RUNX2 and bone
morphogenetic protein (BMP) direct
mesenchymal cells to the osteoblast lineage.
• Core-binding factor α-1 and β-catenin also
stimulate differentiation into osteoblast
• Become cartilage under conditions of intermediate
strain and low oxygen tension
• Become fibrous tissue under conditions of high
strain
• Have more endoplasmic reticulum, Golgi apparatus,
and mitochondria than do other cells (for synthesis
and secretion of matrix)
• Bone surfaces lined by more differentiated,
metabolically active cells
• Entrapped cells: less active cells in resting regions;
maintain the ionic milieu of bone
• Disruption of the active lining cell layer activates
entrapped cells.
• Receptor-effector interactions in osteoblasts are
summarized in Table 1.2.
• Osteoblasts produce the following:
• Alkaline phosphatase
• Osteocalcin (stimulated by 1,25dihydroxyvitamin
D [1,25(OH)2D3])
• Type I collagen
• Bone sialoprotein
• Receptor activator of nuclear factor (NF)-κβ ligand
(RANKL)
• Osteoprotegerin—binds RANKL to limit its activity
• Osteoblast activity stimulated by intermittent
(pulsatile) exposure to parathyroid hormone (PTH)
1
2 Basic Sciences

Cortical Immature

Cancellous Pathologic
(giant cell tumor)

Haversian
canal

Cement line Interstitial

lamellae

Canaliculi
Osteocyte

CORTICAL BONE DETAIL

FIG. 1.1 Types of bone. Cortical bone consists of tightly packed osteons. Cancellous bone consists of a meshwork of trabeculae. In immature
bone, unmineralized osteoid lines the immature trabeculae. Pathologic bone is characterized by atypical osteoblasts and architectural disor-
ganization. (Colorized from Brinker MR, Miller MD: Fundamentals of orthopaedics, Philadelphia, 1999, Saunders, p 2.)

Table 1.1   Types of Bone

MICROSCOPIC
APPEARANCE SUBTYPES CHARACTERISTICS EXAMPLES
Lamellar Cortical Structure is oriented along lines of stress Femoral shaft
Strong
Cancellous More elastic than cortical bone Distal femoral metaphysis
Woven Immature Not stress oriented Embryonic skeleton
Fracture callus
Pathologic Random organization Osteogenic sarcoma
Increased turnover Fibrous dysplasia
Weak
Flexible

Modified from Brinker MR, Miller MD: Fundamentals of orthopaedics, Philadelphia, 1999, Saunders, p 1.

• O steoblast activity inhibited by TNF-α • Osteocytes (see Fig. 1.1)

• Wnts are proteins that promote osteoblast survival
and proliferation.
• Deficient Wnt causes osteopenia; excessive Wnt
expression causes high bone mass.
• Wnts can be sequestered by other secreted
molecules such as sclerostin (Scl) and
Dickkopf-related protein 1 (Dkk-1).
• Inhibiting sclerostin or Dkk-1 will lead to
increased bone mass
• Maintain bone
• Constitute 90% of the cells in the mature skeleton
• Former osteoblasts surrounded by newly formed matrix
• High nucleus/cytoplasm ratio
• Long interconnecting cytoplasmic processes
projecting through the canaliculi
• Less active in matrix production than osteoblasts
• Important for control of extracellular calcium and
phosphorus concentration
 Basic Sciences 3

Stem cell
Myeloid
progenitor

Hematopoietic
progenitor

Pre-osteocytes
Monocyte
Myocyte

Cell-cell fusion
Adipocyte

Macrophage
Fibroblast

Chondroblast/
chondrocyte Multi-nuclear
osteoclast
Osteoblast/osteocyte

Osteocytes Chondroblasts
Perichondrium
Osteoblasts
Lacuna
Chondrocyte
Isogenic group

Extracellular
matrix

Myoblast Adipocyte

Stem cell

Haversian
canal

Multipotential Tri- or bipotential Osteoblast

daughter cell progenitor cells Chondroblast Fibroblast
FIG. 1.2 Cellular origins of bone and cartilage cells.

Table 1.2   Bone Cell Types, Receptor Types, and Effects

CELL TYPE RECEPTOR EFFECT
Osteoblast PTH Releases a secondary messenger (exact mechanism unknown) to stimulate osteoclastic activity
Activates adenylyl cyclase
1,25(OH)2 vitamin D3 Stimulates matrix and alkaline phosphatase synthesis and production of bone-specific proteins
(e.g., osteocalcin)
Glucocorticoids Inhibits DNA synthesis, collagen production, and osteoblast protein synthesis
Prostaglandins Activates adenylyl cyclase and stimulates bone resorption
Estrogen Has anabolic (bone production) and anticatabolic (prevents bone resorption) properties
Increases mRNA levels for alkaline phosphatase
Inhibits activation of adenylyl cyclase
Osteoclast Calcitonin Inhibits osteoclast function (inhibits bone resorption)
4 Basic Sciences

Liberated Proliferation
matrix-bound
Osteoprogenitor cells
growth factors

Inhibition of
osteoblast activity
Mechanical factors BMP
hormones Proliferation Sclerostin
Osteoclast cytokines and maturation
precursor

Surface Wnt Active osteoblasts LRP5/6

osteoblasts
β-catenin
Mediators of
osteoclastogenesis
Osteoclast

Osteocyte

Microdamage

FIG. 1.3 Paracrine crosstalk between osteoblasts and osteoclasts. (From Kumar V et al, editors: Bones, joints, and soft tissue tumors. In Robbins and Cotran
pathologic basis of disease, ed 9, Philadelphia, 2014, Saunders, Fig. 26-5.)

• D irectly stimulated by calcitonin, inhibited by PTH
• Sclerostin secreted by osteocytes helps negative
feedback on osteoblasts’ bone deposition (Fig. 1.3).
• Differentially regulated according to mechanical
loading, with decreased sclerostin in areas of
concentrated strain
• Downregulation is associated with increased bone
formation (via sclerostin antibody).
• Potential for use in fracture healing, bone loss,
osseous integration of implants, and genetic bone
diseases via upregulation of sclerostin
• Osteoclasts
• Multinucleated irregular giant cells
• Derived from hematopoietic cells in macrophage
lineage
• Monocyte progenitors form giant cells by fusion
• Function
• Bone resorption
• Bone formation and resorption are linked
• Stimulated primarily by RANKL binding to
RANK receptor on cell surface
• Osteoblasts (and tumor cells) express
RANKL (Fig. 1.4):
• Binds to receptors on osteoclasts
• Stimulates differentiation into mature
osteoclasts
• Inhibited by osteoprotegerin (OPG)
binding to RANKL
• Occurs both normally and in certain conditions,
including multiple myeloma and metastatic
bone disease
• Denosumab is a monoclonal antibody that
targets and inhibits RANKL binding to the
RANK receptor
• Resorption mechanism
• Osteoclasts possess a ruffled (brush) border and
surrounding clear zone
• B order consists of plasma membrane enfoldings
that increase surface area
• Bind to bone surfaces through cell
attachment (anchoring) proteins
• Integrin (αvβ3 or vitronectin receptor)
• Bone resorption occurs in depressions: Howship
lacunae.
• Effectively seal the space below the osteoclast
• Synthesize tartrate-resistant acid phosphate
• Produce hydrogen ions through carbonic
anhydrase
• Lower pH
• Increase solubility of hydroxyapatite crystals
• Organic matrix then removed by proteolytic
digestion through activity of the lysosomal
enzyme cathepsin K
• Signaling
• Have calcitonin receptors, which inhibit
osteoclastic resorption
• Interleukin-1 (IL-1): potent stimulator of
osteoclast differentiation and bone resorption
• Found in membranes surrounding loose total
joint implants
• In contrast, IL-10 suppresses osteoclasts.
n Matrix (Table 1.3)
• Organic components: 40% of dry weight of bone
• Collagen (90% of organic components)
• Primarily type I (mnemonic: bone contains the
word one)
• Type I collagen provides tensile strength of
bone
• Hole zones (gaps) exist within the collagen fibril
between the ends of molecules.
• Pores exist between the sides of parallel
molecules.
• Mineral deposition (calcification) occurs within the
hole zones and pores.
 Basic Sciences 5

• C ross-linking decreases collagen solubility and

Vit D
increases its tensile strength.
PTH
• Proteoglycans
• Matrix proteins (noncollagenous)
• Osteocalcin: most abundant noncollagenous
protein in bone
• Inhibited by PTH and stimulated by
1,25(OH)2D3
Osteoblast Osteoclast precursor • Can be measured in serum or urine as a marker
of bone turnover
− • Inorganic (mineral) components: 60% of dry
weight of bone
• Calcium hydroxyapatite [Ca10(PO4)6(OH)2]:
+ provides compressive strength
• Calcium phosphate (brushite)
n Tissues surrounding bone
Vit
• Periosteum
PTH • Connective tissue membrane that covers bone
• More highly developed in children
• Inner periosteum, or cambium, is loose and vascular
and contains cells capable of becoming osteoblasts.
• These cells enlarge the diameter of bone during
growth and form periosteal callus during fracture
Carbonic healing.
anhydrase
• Outer (fibrous) periosteum is less cellular and is
CA
Lysosome contiguous with joint capsules.
Hydrogen ions • Bone marrow—source of progenitor cells; controls
inner diameter of bone
• Red marrow
• Hematopoietic (40% water, 40% fat, 20% protein)
Integrins • Slowly changes to yellow marrow with age,
Lysosome
enzyme first in appendicular skeleton and later in axial
skeleton
• Yellow marrow
FIG. 1.4 Control and function of the osteoclast. Vit, vitamin. • Inactive (15% water, 80% fat, 5% protein)

Table 1.3   Components of Bone Matrix

TYPE OF MATRIX FUNCTION COMPOSITION TYPES NOTES
ORGANIC MATRIX
Collagen Provides tensile strength Primarily type I Constitutes 90% of organic matrix
collagen Structure: triple helix of one α2 and
two α1 chains, quarter-stag-
gered to produce a fibril
Proteoglycans Partly responsible for Glycosaminoglycan- Inhibits mineralization
compressive strength protein complexes
Matrix proteins Promote mineralization and Osteocalcin (bone Attracts osteoclasts; direct
(noncollagenous) bone formation γ-carboxyglutamic regulation of bone density; most
acid–containing abundant noncollagenous ma-
protein) trix protein (10%–20% of total)
Osteonectin (SPARC) Secreted by platelets and osteo-
blasts; postulated to have a role
in regulating calcium or organiz-
ing mineral in matrix
Osteopontin Cell-binding protein, similar to an
integrin
Growth factors and Aid in bone cell TGF-β Present in small amounts in bone
cytokines differentiation, IGF matrix
activation, growth, IL-1, IL-6
and turnover BMPs
INORGANIC MATRIX
Calcium hydroxyapa- Provides compressive Most of the inorganic matrix;
tite [Ca10(PO4)6(OH)2] strength primary mineralization in collagen
gaps (holes and pores), second-
ary mineralization on periphery
Osteocalcium Makes up the remaining inorganic
phosphate (brushite) matrix
6 Basic Sciences

n Bone vascular supply

• Bone receives 5%–10% of the cardiac output.
• Bones with a tenuous blood supply include the
A D
scaphoid, talus, femoral head, and odontoid.
• Hypoxia, hypercapnia, and sympathectomy increase flow.
• Long bones receive blood from three sources (systems)
• Nutrient artery system
• Branch from systemic arteries, enter the diaphyseal
cortex through the nutrient foramen, enter the
medullary canal, and branch into ascending and C
descending arteries (Figs. 1.5 and 1.6)
• Further branch into arterioles in the endosteal
cortex, which enables blood supply to at least the
inner two-thirds of the mature diaphyseal cortex
via the haversian system (see Fig. 1.6) FIG. 1.5 Intraoperative arteriogram (canine tibia) demonstrating
ascending (A) and descending (D) branches of the nutrient artery. C,
• BP in the nutrient artery system is high. Cannula. (From Brinker MR et al: Pharmacological regulation of the circulation of
• 60% of cortical bone vascularized by nutrient arteries bone, J Bone Joint Surg Am 72:964–975, 1990.)

Endosteal
vessels

Epiphysis

Metaphysis

Diaphysis

Periosteal vessels

Tendon

Muscular vessels

FIG. 1.6 Blood supply to bone. (From Standring S et al, editors: Functional anatomy of the musculoskeletal system. In Gray’s anatomy, ed 40, London, 2008, Elsevier,
Fig. 5-20.)

• M etaphyseal-epiphyseal system
• Arises from the periarticular vascular plexus (e.g.,
geniculate arteries)
• Periosteal system
• Consists mostly of capillaries that supply the outer
third (at most) of the mature diaphyseal cortex
• BP in the periosteal system is low.
• Physiologic features
• Direction of flow
• Arterial flow in mature bone is centrifugal (inside
to outside), which is the net effect of the high-
pressure nutrient artery system and the low-
pressure periosteal system.
• When fracture disrupts the nutrient artery system,
the periosteal system pressure predominates and
blood flow is centripetal (outside to inside).
• Flow in immature developing bone is centripetal
because the highly vascularized periosteal system
is the predominant component.
• Venous flow in mature bone is centripetal.
• Cortical capillaries drain to venous sinusoids,
which drain to the emissary venous system.
• Regulation of bone blood flow
• Influenced by metabolic, humoral, and autonomic
inputs
• Arterial system: great potential for vasoconstriction
(from the resting state), less potential for vasodilation
• Vessels within bone: have several vasoactive
receptors (β-adrenergic, muscarinic, thromboxane/
prostaglandin)
• Bone blood flow is the major determinant of how
well a fracture heals.
• Initial response is a decrease in bone blood flow after
vascular disruption at the fracture site.
• Bone blood flow increases within hours to days (as
part of the regional acceleratory phenomenon), peaks
at approximately 2 weeks, and returns to normal in
3–5 months.
• Unreamed intramedullary nails preserve endosteal
blood supply.
• Reaming devascularizes the inner 50%–80% of the
cortex and delays revascularization of the endosteal
blood supply.
n Types of bone formation (Table 1.4)
Table 1.4   Types of Bone Formation
TYPE OF
OSSIFICATION MECHANISM
Enchondral Bone replaces a cartilage model
Intramembranous Aggregates of undifferentiated
mesenchymal cells
differentiate into osteoblasts,
which form bone
Appositional Osteoblasts lay down new bone
on existing bone
Basic Sciences 7
• Enchondral
• Examples:
• Embryonic formation of long bones
• Longitudinal growth (physis)
• Fracture callus
• Bone formed with demineralized bone matrix
• Undifferentiated cells secrete cartilaginous matrix
and differentiate into chondrocytes.
• Matrix mineralizes and is invaded by vascular buds
that bring osteoprogenitor cells.
• Osteoclasts resorb calcified cartilage; osteoblasts
form bone.
• Bone replaces the cartilage model; cartilage is not
converted to bone.
• Embryonic formation of long bones (Figs. 1.7 and 1.8)
• These bones are formed from the mesenchymal
anlage at 6 weeks’ gestation.
• Vascular buds invade the mesenchymal model,
bringing osteoprogenitor cells that differentiate
into osteoblasts and form the primary ossification
centers at 8 weeks.
• Differentiation stimulated in part by binding of
Wnt protein to the lipoprotein receptor–related
protein 5 (LRP5) or LRP6 receptor
• Marrow forms through resorption of the central
cartilage anlage by invasion of myeloid precursor
cells that are brought in by capillary buds.
• Secondary ossification centers develop at bone
ends, forming the epiphyseal centers (growth
plates) responsible for longitudinal growth.
• Arterial supply is rich during development, with
an epiphyseal artery (terminates in the proliferative
zone), metaphyseal arteries, nutrient arteries, and
perichondrial arteries (Fig. 1.9).
• Physis
• Two types of growth plates exist in immature long
bones: (1) horizontal (the physis) and (2) spherical
(growth of the epiphysis).
• The spherical plate is less organized than the
horizontal plate.
• Perichondrial artery—major source of nutrition of
growth plate
• Delineation of physeal cartilage zones is based on
growth (see Fig. 1.9) and function (Figs. 1.10
and 1.11).
EXAMPLES OF NORMAL EXAMPLES OF DISEASES WITH
MECHANISMS ABNORMAL OSSIFICATION
Embryonic formation of long bones Achondroplasia
Longitudinal growth (physis)
Fracture callus
Bone formed with the use of
demineralized bone matrix
Embryonic flat bone formation Cleidocranial dysostosis
Bone formation during distraction
osteogenesis
Blastema bone
Periosteal bone enlargement (width) Paget disease of bone
The bone formation phase of bone Infantile hyperostosis (Caffey
remodeling disease)
Melorheostosis
8 Basic Sciences

Epiphyseal ossification center (secondary)

Cartilage Bone
Diaphyseal ossification center (primary)

Calcified Arteries Diaphyseo-epiphyseal junction

cartilage

A1 B1 C1 D1

A B C D E F

Epiphyseal cartilage plate

Epiphysis

Diaphysis

Epiphysis

G H I J
FIG. 1.7 Enchondral ossification of long bones. Note that phases F through J often occur after birth. (From Moore KL: The developing human, Philadel-
phia, 1982, Saunders, p 346.)

• R eserve zone: cells store lipids, glycogen, and
proteoglycan aggregates; decreased oxygen tension
occurs in this zone.
• Lysosomal storage diseases (e.g., Gaucher
disease) can affect this zone.
• Proliferative zone: growth is longitudinal, with
stacking of chondrocytes (the top cell is the
dividing “mother” cell), cellular proliferation, and
matrix production; increases in oxygen tension
and proteoglycans inhibit calcification.
• Achondroplasia causes defects in this zone
(see Fig. 1.11).
• Growth hormone exerts its effect in the
proliferative zone.
• Hypertrophic zone:
• Divided into three zones: maturation,
degeneration, and provisional calcification
• N ormal matrix mineralization occurs in the
lower hypertrophic zone: chondrocytes increase
five times in size, accumulate calcium in their
mitochondria, die, and release calcium from
matrix vesicles.
• Chondrocyte maturation is regulated by systemic
hormones and local growth factors (PTH-related
peptide inhibits chondrocyte maturation; Indian
hedgehog protein is produced by chondrocytes
and regulates the expression of PTH-related
peptide).
• Osteoblasts migrate from sinusoidal vessels and
use cartilage as a scaffolding for bone formation.
• Low oxygen tension and decreased proteoglycan
aggregates aid in this process.
• This zone widens in rickets (see Fig. 1.11), with
little or no provisional calcification.
 Basic Sciences 9

Proliferating
Perichondrium hyaline cartilage

Hypertrophic calcifying Canals, containing

Periosteum cartilage capillaries, periosteal
mesenchymal cells,
Thin collar of cancellous
and osteoblasts
bone from periosteum
around diaphysis

At 8 weeks
At 9 weeks

Epiphyseal capillaries
Calcified
cartilage
Epiphyseal
(secondary)
ossification center
Cancellous endochondral
bone laid down on spicules Outer part of periosteal bone
of calcified cartilage transforming into compact bone

Primordial marrow cavities

Central marrow cavity

At 10 weeks At birth Articular cartilage

of head
Proliferating
Bone of
growth cartilage
proximal epiphysis
Hypertrophic
calcifying cartilage Proximal
Proximal
Epiphyseal metaphysis
epiphyseal
ossification growth
centers for plate Diaphysis; growth
head and in width occurs by
greater tubercle periosteal bone
Sites of formation
growth
in length Endochondral bone
of bone laid down
Epiphyseal
ossification on spicules
of degenerating Distal metaphysis
centers of Distal
lateral epicondyle and calcified cartilage
epiphyseal Bone of
medial epicondyle growth plate Hypertrophic
distal epiphysis
calcifying cartilage
Articular cartilage
Proliferating
Calcified cartilage growth cartilage
At 5 years At 10 years

FIG. 1.8 Development of a typical long bone: formation of the growth plate and secondary centers of ossification. (From Netter FH: CIBA collection of
medical illustrations, vol 8: Musculoskeletal system, part I: Anatomy, physiology and developmental disorders, Basel, Switzerland, 1987, CIBA, p 136.)
10 Basic Sciences

CLOSE-UP VIEW OF DEVELOPING EPIPHYSIS AND EPIPHYSEAL GROWTH PLATE

Articular cartilage

Epiphyseal growth plate

(poorly organized)

Secondary (epiphyseal)
ossification center

Epiphyseal artery
Reserve zone

Ossification groove Proliferative zone

of Ranvier
Maturation zone

Perichondrial fibrous Degeneration zone Hypertrophic

ring of La Croix zone
Zone of provisional
calcification
Perichondrial artery Primary spongiosa
Metaphysis
Last intact transverse Secondary spongiosa
cartilage septum

Metaphyseal artery

Periosteum
Diaphysis

Cartilage

Nutrient artery Calcified cartilage

Bone

FIG. 1.9 Structure and blood supply of a typical growth plate. (From Netter FH: CIBA collection of medical illustrations, vol 8: Musculoskeletal system, part I:
Anatomy, physiology and developmental disorders, Basel, Switzerland, 1987, CIBA, p 166.)
 Basic Sciences 11

FIG. 1.10 Zone structure, function, and physiologic features of the growth plate. (From Netter FH: CIBA collection of medical illustrations, vol 8: Musculo-
skeletal system, part I: Anatomy, physiology and developmental disorders, Basel, Switzerland, 1987, CIBA, p 164.)
12 Basic Sciences

Zones
Histology Functions Exemplary diseases Defect (if known)
Structures

Secondary bony
epiphysis
Epiphyseal
artery

Diastrophic dwarfism.................... Defective type II collagen

(also, defects in other zones) synthesis
Matrix production
Pseudoachondroplasia................. Defective processing and
Reserve zone (also, defects in other zones) transport of proteoglycans
Storage
Kneist syndrome........................... Defective processing of
(also, defects in other zones) proteoglycans

Gigantism...................................... Increased cell proliferation

Matrix production
Proliferative
zone Cellular proliferation
(longitudinal growth)
Achondroplasia.............................
Hypochondroplasia.......................
Malnutrition, irradiation...............
injury, glucocorticoid excess
(growth hormone increased)
Deficiency of cell proliferation
Less severe deficiency of cell
proliferation
Decreased cell proliferation
and/or matrix synthesis

Maturation
zone

Preparation
of matrix for Mucopolysaccharidosis................ Deficiencies of specific
calcification (Morquio syndrome, lysosomal acid hydrolases,
Hypertrophic zone

Hurler syndrome) with lysosomal storage of

mucopolysaccharides
Degenerative
zone

Zone of Rickets, osteomalacia.................... Insufficiency of Ca2+ and/or

provisional Calcification of matrix (also, defects in metaphysis) for normal calcification
calcification of matrix

Last intact Metaphyseal chondro-................. Extension of hypertrophic

transverse Vascular invasion and dysplasia (Jansen cells into metaphysis
septum resorption of transverse and Schmid types)
septa
Primary Acute hematogenous.................... Flourishing of bacteria due to
Bone formation osteomyelitis sluggish circulation, low PO2,
Metaphysis

spongiosa
reticuloendothelial deficiency

Osteopetrosis............................... Abnormality of osteoclasts

Secondary Remodeling (internal remodeling)
spongiosa Internal: removal of
Osteogenesis imperfecta............. Abnormality of osteoblasts
cartilage bars, replace-
and collagen synthesis
ment of fiber bone
Branches of with lamellar bone
Scurvy.......................................... Inadequate collagen formation
metaphyseal External: funnelization
and nutrient Metaphyseal dysplasia................. Abnormality of funnelization
arteries (Pyle disease) (external remodeling)

FIG. 1.11 Zone structure and pathologic defects of cellular metabolism. (From Netter FH: CIBA collection of medical illustrations, vol 8: Musculoskeletal
system, part I: Anatomy, physiology and developmental disorders, Basel, Switzerland, 1987, CIBA, p 165.)
 Basic Sciences 13

• M  ucopolysaccharide diseases (see Fig. 1.11) EPIPHYSIS

affect this zone, leading to chondrocyte
degeneration.
• Physeal fractures probably traverse several
zones, depending on the type of loading (Fig.
1.12).
• Slipped capital femoral epiphysis (SCFE) occurs
here.
• Except renal osteodystrophy (through
metaphyseal spongiosa)
• Metaphysis
• Adjacent to the physis and expands with skeletal
growth
• Osteoblasts from osteoprogenitor cells align
on cartilage bars produced by physeal
expansion.
• Primary spongiosa (calcified cartilage bars)
mineralizes to form woven bone and remodels to
form secondary spongiosa and a “cutback zone” at
the metaphysis.
• Groove of Ranvier: supplies chondrocytes to the
periphery for lateral growth (width)
• Perichondrial ring of La Croix: dense fibrous
tissue, primary membrane anchoring the periphery
of the physis
• Intramembranous ossification
• Occurs without a cartilage model
• Undifferentiated mesenchymal cells aggregate
into layers (or membranes), differentiate into
osteoblasts, and deposit an organic matrix that
mineralizes.
• Examples:
• Embryonic flat bone formation
• Bone formation during distraction osteogenesis
• Blastema bone (in young children with
amputations)
• Appositional ossification
• Osteoblasts align on the existing bone surface and
lay down new bone.
• Examples:
• Periosteal bone enlargement (width)
• Bone formation phase of bone remodeling
n Bone remodeling
• General
• Cortical bone and cancellous bone are continuously
remodeled throughout life by osteoclastic and
osteoblastic activity (Fig. 1.13).
• Wolff’s law: remodeling occurs in response to
mechanical stress.
• Increasing mechanical stress increases bone gain.
• Removing external mechanical stress increases
bone loss, which is reversible (to varying degrees)
on remobilization.
• Piezoelectric remodeling occurs in response to
electric charge.
• The compression side of bone is electronegative,
stimulating osteoblasts (formation).
• The tension side of bone is electropositive,
stimulating osteoclasts (resorption).
• Hueter-Volkmann law: remodeling occurs in small
packets of cells known as basic multicellular units (BMUs).
• Such remodeling is modulated by hormones and
cytokines.
PHYSIS
Germinal
Columnation
Tension
Shear
Hypertrophic
Ossification Compression
METAPHYSIS
FIG. 1.12 Histologic zone of failure varies with the type of loading
applied to a specimen. (From Moen CT, Pelker RR: Biomechanical and histo-
logical correlations in growth plate failure, J Pediatr Orthop 4:180–184, 1984.)
• C ompressive forces inhibit growth; tension
stimulates it.
• Suggests that mechanical factors influence
longitudinal growth, bone remodeling, and
fracture repair
• May play a role in scoliosis and Blount disease
• Cortical bone remodeling
• Osteoclastic tunneling (cutting cones; Fig. 1.14)
• The head of the cutting cone is made up
of osteoclasts followed by capillaries and
osteoblasts.
• Followed by layering of osteoblasts and successive
deposition of layers of lamellae
• Cancellous bone remodeling
• Osteoclastic resorption followed by deposition of
new bone by osteoblasts
n Bone injury and repair
n Fracture repair (Table 1.5)
• S tages of fracture repair
• Inflammation
• Fracture hematoma provides hematopoietic cells
capable of secreting growth factors.
• Subsequently, fibroblasts, mesenchymal cells,
and osteoprogenitor cells form granulation tissue
around the fracture ends.
• Osteoblasts (from surrounding osteogenic
precursor cells) and fibroblasts proliferate.
• Repair
• Primary callus response within 2 weeks
• For bone ends not in continuity, bridging (soft)
callus occurs.
• Soft callus is later replaced through enchondral
ossification by woven bone (hard callus).
• Medullary callus supplements the bridging
callus, forming more slowly and later.
• Fracture healing varies with treatment method
(Table 1.6).
14 Basic Sciences

• I n an unstable fracture, type II collagen is • I ncreases time to fracture healing

expressed early, followed by type I collagen. • Increases risk of nonunion (particularly in the tibia)
• Amount of callus is inversely proportional to • Decreases strength of fracture callus
extent of immobilization. • Increases risk of pseudarthrosis after lumbar
• Progenitor cell differentiation fusion by up to 500%
• High strain promotes development of fibrous • Nonsteroidal antiinflammatory drugs
tissue. • Have adverse effects on fracture healing and
• Low strain and high oxygen tension promote healing of lumbar spinal fusions
development of woven bone. • Cyclooxygenase-2 (COX-2) activity is
• Intermediate strain and low oxygen tension required for normal enchondral ossification
promote development of cartilage. during fracture healing.
• Remodeling • Quinolone antibiotics
• Remodeling begins in middle of repair phase and • Toxic to chondrocytes and inhibit fracture
continues long after clinical healing (up to 7 years). healing
• Allows bone to assume its normal configuration and • Ultrasound and fracture healing
shape according to stress exposure (Wolff’s law) • Low-intensity pulsed ultrasound (30 mW/cm2)
• Throughout, woven bone is replaced with lamellar accelerates fracture healing and increases the
bone. mechanical strength of callus
• Fracture healing is complete when the marrow • A cellular response to the mechanical energy of
space is repopulated. ultrasound has been postulated.
• Biochemistry of fracture healing (Table 1.7) • Effect of radiation on bone
• Growth factors of bone (Table 1.8) • High-dose irradiation causes long-term changes
• BMP-2: acute open tibial fractures within the haversian system and decreases
• BMP-3: no osteogenic activity cellularity.
• BMP-4: associated with fibrodysplasia • Diet and fracture healing
ossificans progressiva • Protein malnutrition results in negative effects on
• BMP-7: tibial nonunions fracture healing:
• BMPs activate intracellular signal molecules called • Decreased periosteal and external callus
SMADs to cause osteoblastic differentiation • Decreased callus strength and stiffness
• Endocrine effects on fracture healing (Table 1.9) • Increased fibrous tissue within callus
• Head injury • In experimental models, oral supplementation
• Can increase the osteogenic response to fracture with essential amino acids improves bone
• Nicotine (smoking) mineral density in fracture callus.

Resting phase Activation

Osteoclasts

Lining cells

Osteocytes Osteocytes

Resorption Reversal Formation

Apoptotic osteoclasts
Osteoclasts
Osteoblasts

Preosteoblasts Osteoid

Osteocytes Osteocytes

FIG. 1.13 Bone remodeling. Osteoclasts dissolve the mineral from the bone matrix. Osteoblasts produce new bone (osteoid) that fills in the
resorption pit. Some osteoblasts are left within the bone matrix as osteocytes. (From Firestein GS et al, editors: Kelley’s textbook of rheumatology, ed 8,
Philadelphia, 2008, Saunders.)
 Basic Sciences 15

• E
 lectricity and fracture healing • S treaming potentials: occur when
• Definitions electrically charged fluid is forced over a cell
• Stress-generated potentials membrane that has a fixed charge
• Piezoelectric effect: tissue charges are • Transmembrane potentials: generated by
displaced secondary to mechanical forces. cellular metabolism

Developing
resorption
Time cavity
Cutting
cone
Osteoclast

Resorption
cavity
Reversal
zone

Fibroblast

Osteoblast
Closing Forming
cone osteon

Quiescent
osteoblast

Completed
osteon
Blood vessel

B C

FIG. 1.14 Cortical bone remodeling. (A) Longitudinal and cross sections of a time line illustrating formation of an osteon. Osteoclasts cut a
cylindrical channel through bone. Osteoblasts follow, laying down bone on the surface of the channel until matrix surrounds the central blood
vessel of the newly formed osteon (closing cone of a new osteon). (B) Photomicrograph of a cutting cone. (C) Higher-magnification photomi-
crograph; osteoclastic resorption can be more clearly appreciated. (A from Standring S et al, editors: Functional anatomy of the musculoskeletal system. In
Gray’s anatomy, ed 40, London, 2008, Elsevier, Fig. 5-19.)
16 Basic Sciences

Table 1.5   Biologic and Mechanical Factors Influencing • T

 ypes of electrical stimulation
Fracture Healing • Direct current: stimulates an inflammatory-
like response, resulting in decreased oxygen
Biologic factors Patient age
Comorbid medical conditions
concentrations and increase in tissue pH
Functional level (similar to effects of an implantable bone
Nutritional status stimulator).
Nerve function • Alternating current: “capacity-coupled
Vascular injury generators”; affects cyclic AMP (cAMP)
Hormones
Growth factors synthesis, collagen synthesis, and calcification
Health of the soft tissue envelope during repair stage
Sterility (in open fractures) • Pulsed electromagnetic fields (PEMFs): initiate
Cigarette smoke calcification of fibrocartilage (but not fibrous
Local pathologic conditions
Level of energy imparted
tissue)
Type of bone affected n Bone grafting (Table 1.10)
Extent of bone loss n Graft properties
Mechanical factors Soft tissue attachments to bone • O steoconductive matrix: acts as a scaffold or
Stability (extent of immobilization) framework for bone growth
Anatomic location
Level of energy imparted • Osteoinductive factors: growth factors (BMP) that
Extent of bone loss stimulate bone formation
• Osteogenic cells: primitive mesenchymal cells,
osteoblasts, and osteocytes
• Structural integrity
n Specific bone graft types
Table 1.6   Type of Fracture Healing Based on Type of
• Cortical bone graft
Stabilization • Slower incorporation: remodels existing haversian
TYPE OF STABILIZATION PREDOMINANT TYPE OF HEALING systems through resorption (weakens the graft)
Cast (closed treatment) Periosteal bridging callus and and then deposits new bone (restores
interfragmentary enchondral strength)
ossification • Resorption confined to osteon borders; interstitial
Compression plate Primary cortical healing (­cutting-
cone type or haversian
lamellae are preserved.
remodeling) • Used for structural defects
Intramedullary nail Early: periosteal bridging callus; • Insufficiency fracture eventually occurs in 25% of
enchondral ossification massive grafts.
Late: medullary callus and • Cancellous graft
intramembranous ossification
External fixator Dependent on extent of rigidity:
• Useful for grafting nonunion and cavitary defects
Less rigid: periosteal bridging • Revascularizes and incorporates quickly
callus; enchondral ossification • Osteoblasts lay down new bone on old
More rigid: primary cortical trabeculae, which are later remodeled (“creeping
healing; intramembranous substitution”).
ossification
Inadequate immobilization Hypertrophic nonunion (failed
with adequate blood enchondral ossification); type II
supply collagen predominates Table 1.7   Biochemical Steps of Fracture Healing
Inadequate immobilization Atrophic nonunion
STEP COLLAGEN TYPE
without adequate blood
supply Mesenchymal I, II, III, V
Inadequate reduction with Oligotrophic nonunion Chondroid II, IX
displacement at the Chondroid-osteoid I, II, X
fracture site Osteogenic I

Table 1.8   Growth Factors of Bone

GROWTH FACTOR ACTION NOTES
Bone morphogenetic Osteoinductive; stimulates bone formation Target cells of BMP are the undifferentiated perivascular
protein Induces metaplasia of mesenchymal cells into mesenchymal cells; signals through serine-threonine kinase
osteoblasts receptors
Intracellular molecules called SMADs serve as signaling
mediators for BMPs
Transforming growth Induces mesenchymal cells to produce type II Found in fracture hematomas; believed to regulate cartilage
factor–β collagen and proteoglycans and bone formation in fracture callus; signals through serine/
Induces osteoblasts to synthesize collagen threonine kinase receptors
Coating porous implants with TGF-β enhances bone ingrowth
IGF-2 Stimulates type I collagen, cellular proliferation, Signals through tyrosine kinase receptors
cartilage matrix synthesis, and bone formation
Platelet-derived Attracts inflammatory cells to the fracture site Released from platelets; signals through tyrosine kinase
growth factor (chemotactic) receptors
 Basic Sciences 17

• V ascularized bone graft • P rimary mechanism of rejection is cellular rather

• Although technically difficult to implant, allows
more rapid union and cell preservation; best for
irradiated tissues or large tissue defects (morbidity
may occur at donor site [e.g., fibula])
• Nonvascular bone grafts are more common
• Allograft bone
• Types
• Fresh: increased immunogenicity
• Fresh frozen: less immunogenic than fresh; BMP
preserved
• Freeze dried (lyophilized “croutons”): loses
structural integrity and depletes BMP, is least
immunogenic, is purely osteoconductive, has
lowest risk of viral transmission
• Bone matrix gelatin (a digested source of BMP):
demineralized bone matrix is osteoconductive and
osteoinductive.
• Osteoarticular (osteochondral) allograft
• Immunogenic (cartilage is vulnerable to
inflammatory mediators of immune response)
• Articular cartilage preserved with glycerol or
DMSO
• Cryogenically preserved grafts (leave few viable
chondrocytes)
• Tissue-matched (syngeneic) osteochondral grafts
(produce minimal immunogenic effects and
incorporate well)
• Antigenicity
• Allograft bone possesses a spectrum of potential
antigens, primarily from cell surface glycoproteins.
• Classes I and II cellular antigens in allograft are
recognized by T lymphocytes in the host.
Table 1.9   Endocrine Effects on Fracture Healing
HORMONE EFFECT MECHANISM
Cortisone − Decreased callus proliferation
Calcitonin +? Unknown
Thyroid hormone, PTH + Bone remodeling
Growth hormone + Increased callus volume
than humoral.
• Incorporation related to cellularity and MHC
incompatibility.
• Cellular components that contribute to antigenicity
are marrow origin, endothelium, and retinacular
activating cells.
• Marrow cells incite the greatest immunogenic
response.
• Extracellular matrix components that contribute to
antigenicity are as follows:
• Type I collagen (organic matrix): stimulates cell-
mediated and humoral responses
• Noncollagenous matrix (proteoglycans,
osteopontin, osteocalcin, other glycoproteins)
• Hydroxyapatite does not elicit immune response.
• Demineralized bone matrix
• Acidic extraction of bone matrix from allograft
• Osteoconductive without structural support
• Minimally osteoinductive despite preservation of
osteoinductive molecules
• Synthetic bone grafts: calcium, silicon, or aluminum
• Calcium phosphate–based grafts: capable of
osseoconduction and osseointegration
• Biodegrade very slowly
• Highest compressive strength of any graft material
• Many prepared as ceramics (heated apatite crystals
fused into crystals [sintered])
• Tricalcium phosphate
• Hydroxyapatite; purified bovine dermal fibrillar
collagen plus ceramic hydroxyapatite granules and
tricalcium phosphate granules
• Calcium sulfate: osteoconductive
• Rapidly resorbed
• Calcium carbonate (chemically unaltered
marine coral): resorbed and replaced by bone
(osteoconductive)
• Coralline hydroxyapatite: calcium carbonate skeleton
is converted to calcium phosphate through a
thermoexchange process.
• Silicate-based: incorporate silicon as silicate (silicon
dioxide); bioactive glasses and glass-ionomer cement

Table 1.10   Types of Bone Grafts and Bone Graft Properties

PROPERTIES

OSTEOGENIC
GRAFT OSTEOCONDUCTION OSTEOINDUCTION CELLS STRUCTURAL INTEGRITY OTHER PROPERTIES
Autograft
Cancellous Excellent Good Excellent Poor Rapid incorporation
Cortical Fair Fair Fair Excellent Slow incorporation
Allograft Fair Fair None Good Fresh has the highest
immunogenicity
Freeze dried is the least
immunogenic but has the
least structural integrity
(weakest)
Fresh frozen preserves BMP
Ceramics Fair None None Fair
Demineralized Good Fair None Poor
bone matrix
Bone marrow Poor Poor Good Poor

Modified from Brinker MR, Miller MD: Fundamentals of orthopaedics, Philadelphia, 1999, Saunders, p 7.
18 Basic Sciences
• A luminum oxide: alumina ceramic bonds to bone
in response to stress and strain between implant and
bone
n Five stages of graft healing (Urist) are listed in Table 1.11.
n Distraction osteogenesis
• Definition: distraction-stimulated formation of bone
• Clinical applications:
• Limb lengthening
• Deformity correction (via differential lengthening)
• Segmental bone loss (via bone transport)
• Biologic features:
• Under optimal stability, intramembranous
ossification occurs.
• Under instability, bone forms through enchondral
ossification.
• Under extreme instability, pseudarthrosis may
occur.
• Three histologic phases:
• Latency phase (5–7 days)
• Distraction phase (1 mm/day [≈1 inch/mo])
• Consolidation phase (typically twice as long as
distraction phase)
• Optimal conditions during distraction osteogenesis:
• Low-energy corticotomy/osteotomy
• Minimal soft tissue stripping at corticotomy site
(preserves blood supply)
• Stable external fixation and elimination of torsion,
shear, and bending moments
• Latency period (no lengthening) 5–7 days
• Distraction: 0.25 mm three or four times per day
(0.75–1.0 mm/day)
• Neutral fixation interval (no distraction) during
consolidation
• Normal physiologic use of the extremity, including
weight bearing
n Heterotopic ossification
• Ectopic bone forms in soft tissues.
• Most commonly in response to injury or surgical
dissection
• Myositis ossificans: heterotopic ossification in muscle
• Increased risk with traumatic brain injury
• Recurrence after resection is likely if neurologic
compromise is severe.
• Timing of surgery for heterotopic ossification after
traumatic brain injury is important:
• Time since injury (3–6 months)
• Evidence of bone maturation on radiographs
(sharp demarcation, trabecular pattern)
• Heterotopic ossification may be resected after total hip
arthroplasty (THA).
• Resection should be delayed for 6 months or longer
after THA.
• Adjuvant radiation therapy may prevent recurrence
of heterotopic ossification.
Table 1.11   Stages of Graft Healing
STAGE ACTIVITY
Inflammation Chemotaxis stimulated by necrotic
debris
Osteoblast differentiation From precursors
Osteoinduction Osteoblast and osteoclast function
Osteoconduction New bone forming over scaffold
Remodeling Process continues for years
• O ptimal therapy: single preoperative or postoperative
dose of 600–800 rad/cGy (6-8 Gy)
• Prevents proliferation and differentiation of primordial
mesenchymal cells into osteoprogenitor cells
• Preoperative radiation (600–800 rad/cGy) may be
given in a single fraction up to 24 hours prior to
surgery.
• Helps prevent heterotopic ossification after THA in
patients at high risk for this development
• Incidence of heterotopic ossification after THA
among patients with Paget disease is approximately
50%.
n Normal bone metabolism
n Calcium
• I mportant in muscle and nerve function, clotting, and
many other areas
• More than 99% of the body’s calcium is stored in bones.
• Plasma calcium is about equally free and bound
(usually to albumin).
• Approximately 400 mg of calcium is released from
bone daily.
• Absorbed in the duodenum by active transport
• Requires ATP and calcium-binding protein
• Regulated by 1,25(OH)2D3
• Absorbed in the jejunum by passive diffusion
• Kidney reabsorbs 98% of calcium (60% in proximal
tubule)
• Calcium may be excreted in stool.
• Primary homeostatic regulators of serum calcium
are PTH and 1,25(OH)2D3
• Dietary requirement for elemental calcium:
• Approximately 600 mg/day for children
• Approximately 1300 mg/day for adolescents and
young adults (ages 10–25 years)
• 750 mg/day for adults ages 25–50 years
• 1200–1500 for adults over age 50 years
• 1500 mg/day for pregnant women
• 2000 mg/day for lactating women
• 1500 mg/day for postmenopausal women and for the
patient with a healing fracture in a long bone
• Calcium balance is usually positive in the first three
decades of life and negative after the fourth decade.
n Phosphate
• A key component of bone mineral
• Approximately 85% of the body’s phosphate stores
are in bone.
• Plasma phosphate is mostly unbound.
• Also important in enzyme systems and molecular
interactions as a metabolite and buffer
• Dietary intake of phosphate is usually adequate.
• Daily requirement is 1000–1500 mg.
n Reabsorbed by the kidney (proximal tubule)
n Phosphate may be excreted in urine.
n Parathyroid hormone
• An 84–amino acid peptide
• Synthesized in and secreted from chief cells of the
(four) parathyroid glands
• N-terminal fragment 1-34 is the active portion.
• Teriparatide, the synthetic form of recombinant
human PTH, contains this active sequence.
• Used to treat some forms of osteoporosis
• Increased risk of osteosarcoma
• Effect of PTH mediated by the cAMP second-
messenger mechanism downstream in osteocytes
 Basic Sciences 19

Table 1.12   Regulation of Calcium and Phosphate Metabolism

PARAMETER PTH (PEPTIDE) 1,25(OH)2D (STEROID) CALCITONIN (PEPTIDE)
Origin Chief cells of parathyroid glands Proximal tubule of kidney Parafollicular cells of
thyroid gland
Factors stimulating Decreased serum Ca2+ Elevated PTH level Elevated serum Ca2+ level
production Decreased serum Ca2+ level
Decreased serum Pi
Factors inhibiting Elevated serum Ca2+ Decreased PTH Elevated serum Ca2+ Decreased serum Ca2+
­production Elevated 1,25(OH)2D Elevated serum Pi
Effect on end-organs
for hormone action:
Intestine No direct effect Strongly stimulates intestinal ?
Acts indirectly on bowel by stimulating absorption of Ca2+ and Pi
production of 1,25(OH)2D in kidney
Kidney Stimulates 25(OH)D 1α-hydroxylase in ? ?
mitochondria of proximal tubular cells to
convert 25(OH)D to 1,25(OH)2D
Increases fractional resorption of filtered Ca2+
Promotes urinary excretion of Pi
Bone Stimulates osteoclastic resorption of bone Strongly stimulates osteoclastic Inhibits osteoclastic
Stimulates recruitment of preosteoclasts resorption of bone resorption of bone
? Role in normal human
physiology
Net effect on Ca2+ and Increased serum Ca2+ level Increased serum Ca2+ level Decreased serum Ca2+
Pi concentrations in Decreased serum Pi level Increased serum Pi level level (transient)
extracellular fluid
and serum

Adapted from Netter FH: CIBA collection of medical illustrations, vol 8: Musculoskeletal system, part I: Anatomy, physiology and developmental
disorders, Basel, Switzerland, 1987, CIBA, p 179.

• P TH helps regulate plasma calcium. n Other hormones affecting bone metabolism

• Decreased calcium levels in extracellular fluid
stimulate β2 adrenoreceptors to release PTH,
which acts at the intestines, kidneys, and bones
(Table 1.12).
• PTH directly activates osteoblasts.
• PTH modulates renal phosphate filtration.
• PTH may accentuate bone loss in elderly persons.
• PTH-related protein and its receptor have been
implicated in metaphyseal dysplasia.
n Vitamin D
• Naturally occurring steroid
• Activated by ultraviolet radiation from sunlight or
utilized from dietary intake (Fig. 1.15)
• Hydroxylated to 25(OH)D3 in the liver and
hydroxylated a second time in the kidney to one of the
following:
• 1,25(OH)2D3, the active hormone
• 24,25(OH)2D3, the inactive form (Fig. 1.16)
• 1,25(OH)2D3 works at the intestines, kidneys, and
bones (see Table 1.12).
• Phenytoin (Dilantin) impairs metabolism of vitamin D.
n Calcitonin
• A 32–amino acid peptide hormone produced by clear
cells in the parafollicles of the thyroid gland
• Limited role in calcium regulation (see Table 1.12)
• Increased extracellular calcium levels cause secretion of
calcitonin.
• Controlled by a β2 receptor
• Inhibits osteoclastic bone resorption
• Osteoclasts have calcitonin receptors.
• Calcitonin decreases osteoclast number and activity.
• Decreases serum calcium level
• May also have a role in fracture healing and in
reducing vertebral compression fractures in high-
turnover osteoporosis
• Estrogen
• Prevents bone loss by inhibiting bone resorption
• Decrease in urinary pyridinoline cross-links
• Because bone formation and resorption are coupled,
estrogen therapy also decreases bone formation.
• Supplementation is helpful in postmenopausal
women only if started within 5–10 years after onset
of menopause.
• Risk of endometrial cancer is reduced when
estrogen therapy is combined with cyclic progestin
therapy.
• Certain regimens of hormone replacement therapy
may increase risks of heart disease and breast cancer.
• Other postmenopausal pharmacologic interventions
(alendronate, raloxifene) should be strongly considered.
• Corticosteroids
• Increase bone loss
• Decrease gut absorption of calcium by decreasing
binding proteins
• Decrease bone formation (cancellous more than
cortical) by inhibiting collagen synthesis and
osteoblast productivity
• Do not affect mineralization
• Alternate-day therapy may reduce the effects.
• Thyroid hormones
• Affect bone resorption more than bone formation
• Large (thyroid-suppressive) doses of thyroxine can
lead to osteoporosis.
• Regulates skeletal growth at the physis
• Stimulates chondrocyte growth, type X collagen
synthesis, and alkaline phosphatase activity
• Growth hormone
• Causes positive calcium balance by increasing gut
absorption of calcium more than it increases urinary
excretion
20 Basic Sciences

Solar 7-dehydrocholesterol Dietary sources of

UVB vitamins D2 and D3
radiation
Pre-D3
Heat
Vitamin D3
Skin
Via chylomicrons and
lymphatic system

Circulation Vit D DBP Vit D

DBP

Vitamin D

25-OHase Liver

Pi, Ca2+, FGF23 25(OH)-vitamin D

and other factors

+ –
24-OHase
1,25(OH)2-vitamin D 1-OHase 1,25(OH)2-vitamin D Calcitroic
acid
Kidney
Osteoblast
Urine
PTH –
RANKL
RANK
Preosteoclast PTH Intestine

Parathyroid
glands

Mature
osteoclast
Calcium and
Bone phosphorus
Ca2+ and HPO4 2– Ca2+ and HPO42–
release absorption

Bone Metabolic Neuromuscular

mineralization functions functions

FIG. 1.15 Vitamin D metabolism. DBP, vitamin D–binding protein; OHase, 1α-hydroxylase; Pi, inorganic phosphate. (From Kumar V et al, editors:
Robbins and Cotran pathologic basis of disease, Philadelphia, 2010, Saunders.)

• Insulin and somatomedins participate in this effect. ↓ Ca2+

• Growth factors ↓ Pi
• Transforming growth factor β (TGF-β), platelet- ↑ PTH
derived growth factor (PDGF), monokines, and 1,25(OH)2-vitamin D
(active metabolite)
lymphokines have roles in bone and cartilage repair. 25(OH)-vitamin D,
n Peak bone mass 1α-hydroxylase
• Believed to occur between 16 and 25 years of age 25(OH)-vitamin D
• Higher in men and in African Americans 25(OH)-vitamin D,
• After peak, bone loss occurs at a rate of 0.3%–0.5% per 24 hydroxylase
year 24,25(OH)2-vitamin D
(inactive metabolite)
• Rate of bone loss is 2%–3% per year in untreated ↑ Ca2+
women during the sixth through tenth years after ↑ Pi
menopause. ↓ PTH
• Affects trabecular more than cortical bone FIG. 1.16 Vitamin D metabolism in the renal tubular cell. (From Simon
• Increase in trabecular rods results in increased SR, editor: Orthopaedic basic science, Rosemont, IL, 1994, American Academy of
anisotropy. Orthopaedic Surgeons, p 165.)
 Basic Sciences 21

• C ortical bone becomes thinner and intracortical • I ncreased osteoclastic resorption and failure of
porosities increase. repair attempts (poor mineralization as a result of
• Cortical bone becomes more brittle, less strong, low phosphate level)
and less stiff. • Diagnosis:
• Long bones have greater inner and outer • Laboratory findings
diameters. • Increased serum calcium, PTH, and urinary
n Bone loss phosphate
• Occurs at the onset of menopause when both bone • Decreased serum phosphate
formation and resorption are accelerated • Bony changes
• A net negative change in calcium balance: • Osteopenia
menopause decreases intestinal absorption and • Osteitis fibrosa cystica (fibrous replacement of
increases urinary excretion of calcium. marrow)
• Both urinary hydroxyproline and pyridinoline cross- • Brown tumors: increased giant cells,
links are elevated when bone resorption occurs. extravasation of RBCs, hemosiderin staining,
• Serum alkaline phosphatase level is elevated when fibrous tissue hemosiderin
bone formation is increased. • Chondrocalcinosis
n Conditions of bone mineralization (Tables 1.13 through 1.17) • Radiographic findings
n Hypercalcemia • Deformed, osteopenic bones
• C an manifest in a number of ways • Fractures
• Polyuria, polydipsia, and nephrolithiasis • Shaggy trabeculae
• Excessive bony resorption with or without fibrotic • Radiolucent areas (phalanges, distal clavicle,
tissue replacement (osteitis fibrosa cystica) skull)
• CNS effects (confusion, stupor, weakness) • Destructive metaphyseal lesions
• GI effects (constipation) • Calcification of soft tissues
• Can also cause anorexia, nausea, vomiting, dehydration, • Histologic changes
and muscle weakness • Osteoblasts and osteoclasts active on both sides
• Primary hyperparathyroidism of the trabeculae (as in Paget disease)
• Overproduction of PTH usually a result of a parathyroid • Areas of destruction
adenoma (surgical parathyroidectomy is curative) • Wide osteoid seams
• Generally affects only one parathyroid gland • Other causes of hypercalcemia
• Reflected in a net increase in plasma calcium and • Familial syndromes
a decrease in plasma phosphate (as a result of • Pituitary adenomas associated with multiple
enhanced urinary excretion) endocrine neoplasia (MEN) types I and II

Table 1.13   Overview of Clinical and Radiographic Aspects of Metabolic Bone Diseases
DISEASE
Hypercalcemia
Hyperparathyroidism
Familial syndromes
Hypocalcemia
Hypoparathyroidism
PHP/Albright syndrome
Renal osteodystrophy
Rickets (osteomalacia)
Vitamin D–deficiency rickets
Vitamin D–dependent (types I
and II) rickets
Vitamin D–resistant (hypo-
phosphatemic) rickets
Hypophosphatasia
Osteopenia
Osteoporosis
Scurvy
Osteodensity
Paget disease of bone
Osteopetrosis
CAUSE
PTH overproduction: adenoma
PTH overproduction: MEN/renal
PTH underproduction: idiopathic
PTH receptor abnormality
Chronic renal failure: ↓ phosphate
excretion
↓ Vitamin D diet; malabsorption
See Table 1.16
↓ Renal tubular phosphate
resorption
↓ Alkaline phosphatase
↓ Estrogen: ↓ bone mass
Vitamin C deficiency: defective
collagen
Osteoclastic abnormality: ↑ bone
turnover
Osteoclastic abnormality: unclear
CLINICAL FINDINGS
Kidney stone, hyperreflexia
Endocrine and renal
­abnormalities
Neuromuscular irritability,
­cataracts
Short MC/MT, obesity
Renal abnormalities
Bone deformities, hypotonia
Total baldness
Bone deformities, hypotonia
Bone deformities, hypotonia
Kyphosis, fractures
Fatigue, bleeding, effusions
Deformities, pain, CHF, fractures
Hepatosplenomegaly, anemia
RADIOGRAPHIC FINDINGS
Osteopenia, osteitis fibrosa
cystica
Osteopenia
Calcified basal ganglia
Brachydactyly, exostosis
Rugger jersey spine
Rachitic rosary, wide growth
plates, fractures
Poor mineralization
Poor mineralization
Poor mineralization
Compression vertebral fractures,
hip fractures
Thin cortices, corner sign
Coarse trabeculae, picture-
frame vertebrae
Bone within bone

↓, Decreased; ↑, increased.
 Table 1.14   Laboratory Findings and Clinical Data Regarding Patients With Metabolic Bone Diseases Causing Hypercalcemia
CHANGES IN LEVEL OR CONCENTRATION

SERUM SERUM ALKALINE URINARY OTHER FINDINGS

DISORDER CALCIUM PHOSPHATASE PHOSPHATASE PTH 25(OH)D 1,25(OH)2D CALCIUM OR POSSIBLE FINDINGS TREATMENT COMMENTS
Primary ↑ None or ↓ None or ↑ ↑ None None or ↑ ↑ Active turnover Surgical excision of Most commonly caused by
hyperparathyroidism observed on bone parathyroid edema parathyroid adenoma
biopsy with Treatment of hyper- Because PTH stimulates
peritrabecular calcemia (see text) conversion of the inactive
fibrosis form to the active form
Brown tumors [1,25(OH)2D] in the kidney,
↑ production of PTH leads
to ↑ levels of 1,25(OH)2D
Malignancy with bony ↑ None or ↑ None or ↑ None None None or ↓ ↑ Destructive lesions in Treatment of cancer ↑ Calcium levels may lead to
­metastases or bone and hypercalcemia ↓ PTH production through
↓ (see text) feedback mechanism
↓ 1,25(OH)2D levels result
from ↓ PTH (responsible for
conversion of inactive to
active form of vitamin D in
the kidney)
Patients with multiple my-
eloma display abnormal
urinary and serum protein
electrophoresis
Hyperthyroidism ↑ None None None None None ↑ ↑ Free thyroxin index Treatment of ↑ Calcium levels caused by ↑
or ↓ Thyroid-stimulating ­hyperthyroidism bone turnover (hypermeta-
↓ hormone bolic state)
Tachycardia, tremors
Vitamin D i­ntoxication ↑ None or ↑ None or ↑ None ↑↑↑ None ↑ Normalization of History of excessive vitamin
or vitamin D intake D intake
↓ and levels Dietary vitamin D is convert-
ed to 25(OH)D in the liver;
very high concentrations
of 25(OH)D cross-react
with intestinal vitamin D
receptors to ↑ resorption
of calcium and cause
hypercalcemia

↓, Decreased; ↑, increased.
 Table 1.15   Laboratory Findings and Clinical Data Regarding Patients With Metabolic Bone Diseases Causing Hypocalcemia
CHANGES IN LEVEL OR CONCENTRATION

SERUM SERUM ALKALINE URINARY OTHER FINDINGS OR

DISORDER CALCIUM PHOSPHASTASE PHOSPHATASE PTH 25(OH)D 1,25(OH)2D CALCIUM POSSIBLE FINDINGS TREATMENT COMMENTS
Hypopara- ↓ ↑ None ↓ None ↓ ↓ Basal ganglia Calcium and ­vitamin D ↓ PTH production most
thyroidism calcification supplementation ­commonly follows surgical
Hypocalcemic ­ ablation of the thyroid (with
findings the parathyroid) gland
↓ PTH leads to ↓ serum ­calcium
and ↑ serum ­phosphate (as
result of ↓ urinary excretion
of phosphate)
Because PTH stimulates con-
version from the i­nactive to
the active form of vitamin D
(in the kidney), 1,25(OH)2D
is also ↓
Pseudohypopara- ↓ ↑ None None or ↑ None ↓ ↓ Hypocalcemic Calcium and ­vitamin D PTH has no effect on the
thyroidism f­indings supplementation target cells (in the kid-
ney, bone, and intestine)
because of a PTH receptor
abnormality
Leads to a ↓ in the active form
of vitamin D
Therefore, serum calcium
levels are ↓ as result of (1)
lack of effect of PTH on
bone and (2) ↓ levels of
1,25(OH)2D
Renal osteo- ↓ or none ↑↑↑ ↑ ↑↑↑ None ↓ — Findings of Correction of ↓ Renal phosphorus
dystrophy ­secondary underlying renal excretion leads to
(high-turnover hyperparathyroid- abnormality ­hyperphosphatemia
bone disease ism: rugger Maintenance of Phosphorus retention
resulting from jersey spine normal serum phos- leads to ↓ serum c ­ alcium
renal disease Osteitis fibrosa phorous and calcium and ↑↑↑ PTH (which
[secondary Amyloidosis Dietary phosphate can lead to secondary
hyperparathy- restriction ­hyperparathyroidism)
roidism]) Phosphate-binding ↑ BUN and creatinine levels
antacid (calcium Associated with long-term
carbonate) hemodialysis
Administration of the
active form of
vitamin D:
1,25(OH)2D (calcitriol)
Renal osteodys- ↑ or none None or ↑ ↑ None or None ↓ — Rugger jersey spine Treatment of the PTH levels may be sup-
trophy (low- mildly ↑ Osteitis fibrosa urinary obstruction or pressed because of (1)
turnover bone Amyloidosis kidney disease frequent episodes of
disease due to Osteomalacia may hypercalcemia and (2)
renal disease be observed direct inhibitory effect of
[aluminum aluminum on PTH
toxicity]) No secondary hyperparathy-
roidism is present
↑ BUN and creatinine levels
Associated with long-term
hemodialysis

↓, Decreased; ↑, increased.
 Table 1.16   Laboratory Findings and Clinical Data Regarding Patients With Rickets and Related Diseases

24
CHANGES IN LEVEL OR CONCENTRATION

SERUM SERUM ALKALINE URINARY OTHER FINDINGS OR

Basic Sciences
DISORDER CALCIUM PHOS PHOS PTH 25(OH)D 1,25(OH)2D CALCIUM POSSIBLE FINDINGS TREATMENT COMMENTS
Nutritional rick- ↓ or none ↓ ↑ ↑ ↓ ↓ ↓ Osteomalacia, Oral vitamin D With ↓ vitamin D intake, intestinal calcium
ets: vitamin D ­hypotonia ­(1000–6000 IU/day) and phosphate absorption is reduced,
­deficiency Muscle weakness, leading to hypocalcemia
tetany ↓ Serum calcium stimulates ↑ PTH
Bowing deformities ­(secondary hyperparathyroidism),
of the long bones leading to bone resorption and ↑
Rachitic rosary serum calcium (toward or to normal
levels)
Sources of vitamin D include sunlight,
fish-liver foods, and fortified milk
Nutritional rick- ↓ or none ↓ ↑ ↑ None ↑ or none ↓ Clinical findings Oral calcium (1000 mg/ Hypocalcemia leads to secondary
ets: calcium ­similar to those day) ­hyperparathyroidism
­deficiency for vitamin D ↑ PTH leads to enhanced renal
­deficiency ­conversion of 25(OH)D to 1,25(OH)2D
Nutritional rick- None ↓ ↑ None None ↑↑↑ None No changes of Oral supplementation Neither secondary hyperparathyroidism
ets: phosphate secondary hyper- of phosphate nor vitamin D deficiency is present
­deficiency parathyroidism are ↓ Serum phosphate leads to ↑ renal
observed ­production of 1,25(OH)2D
Hereditary vita- ↓ ↓ ↑ ↑ None or ↑ ↓↓↓ ↓ Osteomalacia Oral physiologic There is a defect in renal 25(OH)D
min D–depen- Clinical findings doses (1–2 μg/day) of ­1α-hydroxylase. This enzymatic defect
dent rickets similar to (but more 1,25(OH)2D inhibits conversion from the inactive
type I (pseu- severe than) those form [25(OH)D] to the active form
do–vitamin D of nutritional rick- [1,25(OH)2D] of vitamin D in the kidney
deficiency) ets due to vitamin
D deficiency
Hereditary ↓ ↓ ↑ ↑ None or ↑ ↑↑↑ ↓ Osteomalacia Long-term (3–6 mo) There is an intracellular receptor defect
vitamin D– Alopecia daily ­administration for 1,25(OH)2D
dependent Clinical findings of high-dose Patients with this disorder have the
rickets type similar to (but vitamin D analogue highest 1,25(OH)2D levels observed
II [hereditary more severe than) [1,25(OH)2D or (OH)D in humans; this ↑↑↑ level of 1,25(OH)2D
resistance to nutritional rickets 1α-hydroxylase] plus distinguishes hereditary vitamin D–­
1,25(OH)2D] caused by vitamin 3 g/day of elemental dependent rickets type II from type I,
D deficiency calcium in which the level of 1,25(OH)2D is ↓↓↓
Hypophospha- None ↓↓↓ ↑ None None None None or ↑ Osteomalacia First line treatment with There is an inborn error in phosphate
temic rickets No changes of burosumab (anti- transport (probably located in the
(also known ­secondary hyper- FGF23 monoclonal proximal nephron); this leads to failure
as vitamin parathyroidism antibody), second line of reabsorption of phosphate in the
D–resistant Classic triad: elemental phosphate kidney and “spilling” of phosphate
rickets and 1. Hypophos- (1–2g/day plus vita- (phosphate diabetes) in the urine
phosphate dia- phatemia min D 0.5–1 µg/day) Although the absolute levels of
betes; Albright 2. Lower limb Vitamin D administra- 1,25(OH)2D are normal, they are
syndrome is ­deformities tion is needed to inappropriately low with regard to the
an example 3. Stunted growth counterbalance degree of phosphaturia; production of
of a hypo- rate the hypocalcemic 1,25(OH)2D is normally stimulated by ↓
phosphatemic effect of phosphate serum phosphorous (see Table 1.12)
syndrome) administration, which This is the most commonly encountered
otherwise could lead form of rickets
to severe secondary
hyperparathyroidism
Hypophospha- ↑ ↑ ↓↓↓ None None None Osteomalacia There is no established There is an inborn error in the tissue-
tasia Early loss of teeth medical therapy nonspecific (kidney, bone, liver) isoen-
zyme of alkaline phosphatase
↑ Urinary phosphoethanolamine is diag-
nostic

↓, Decreased; ↑, increased; phos, phosphatase.

Table 1.17   Differential Diagnosis of Metabolic Bone Diseases Based on Blood Chemistry Findings
CALCIUM LEVEL PHOSPHORUS LEVEL

INCREASED DECREASED NORMAL INCREASED DECREASED NORMAL

Primary hyperparathyroidism
Hyperthyroidism
Vitamin D intoxication
Malignancy without bony
metastasis
Malignancy with bony me-
tastasis
Multiple myeloma
Lymphoma
Sarcoidosis
Milk-alkali syndrome
Severe generalized immobi-
lization
Multiple endocrine neoplasias
Addison disease
Steroid administration
Peptic ulcer disease
Hypophosphatasia
Pseudohypoparathyroidism
Renal osteodystrophy
Nutritional rickets: vitamin D
deficiency
Nutritional rickets: calcium
deficiency
Hereditary vitamin D–depen-
dent rickets (types I and II)
Hypoparathyroidism
Pseudohypoparathyroidism
Renal osteodystrophy (high-
turnover bone disease)
Nutritional rickets: vitamin D
deficiency
Nutritional rickets: calcium
deficiency
Hereditary vitamin D–depen-
dent rickets (types I and II)
Malignancy with bony me-
tastasis
Malignancy without bony
metastasis
Multiple myeloma
Lymphoma
Hyperthyroidism
Vitamin D intoxication
Sarcoidosis
Milk-alkali syndrome
Severe generalized immobi-
lization
Osteoporosis
Pseudohypoparathyroidism
Nutritional rickets: vitamin D
deficiency
Nutritional rickets: calcium
deficiency
Nutritional rickets: phos-
phate deficiency
Hypophosphatemic rickets
Osteoporosis
Malignancy with bony me-
tastasis
Multiple myeloma
Lymphoma
Vitamin D intoxication
Renal osteodystrophy (only
low-turnover bone disease)
Hypophosphatemic rickets
Hypophosphatasia
Sarcoidosis
Hyperthyroidism
Milk-alkali syndrome
Severe generalized immobi-
lization
Malignancy with bony me-
tastasis
Multiple myeloma
Lymphoma
Vitamin D intoxication
Hypoparathyroidism
Pseudohypoparathyroidism
Renal osteodystrophy
Hypophosphatasia
Sarcoidosis
Milk-alkali syndrome
Severe generalized immobi-
lization
Primary hyperparathyroidism
Nutritional rickets: calcium
deficiency
Nutritional rickets: phosphate
deficiency
Hereditary vitamin D–depen-
dent rickets type II
Sarcoidosis
Primary hyperparathyroidism
Malignancy without bony
metastasis
Nutritional rickets: vitamin D
deficiency
Nutritional rickets: calcium
deficiency
Nutritional rickets: phosphate
deficiency
Hereditary vitamin D–depen-
dent rickets (types I and II)
Hypophosphatemic rickets
Malignancy with bony me-
tastasis
Multiple myeloma
Lymphoma
Hypoparathyroidism
Pseudohypoparathyroidism
Renal osteodystrophy
Osteoporosis
Primary hyperparathyroidism
Malignancy with bony me-
tastasis
Multiple myeloma
Lymphoma
Hyperthyroidism
Vitamin D intoxication
Renal osteodystrophy (only
low-turnover bone disease)
Sarcoidosis
Milk-alkali syndrome
Severe generalized immobi-
lization
Nutritional rickets: calcium
deficiency
Hypophosphatemic rickets
Hypophosphatasia

Basic Sciences
25
26 Basic Sciences
• F amilial hypocalciuric hypercalcemia
• Poor renal clearance of calcium
• Malignancy (most common)
• Can be life threatening; commonly associated with
muscle weakness
• Initial treatment should include hydration with
normal saline (reverses dehydration).
• Can occur in the absence of extensive bone
metastasis
• Most commonly results from release of systemic
growth factors and cytokines that stimulate
osteoclastic bone resorption at bony sites not
involved in the tumor process (RANKL pathway)
• PTH-related protein secretion (lung carcinoma)
• Lytic bone metastases and lesions (e.g., multiple
myeloma)
• Hyperthyroidism
• Vitamin D intoxication
• Prolonged immobilization
• Addison disease
• Steroid administration
• Peptic ulcer disease (milk-alkali syndrome)
• Kidney disease
• Sarcoidosis
• Hypophosphatasia
• Treatment of hypercalcemia
• Hydration (saline diuresis)
• Loop diuretics
• Dialysis (for severe cases)
• Mobilization (prevents further bone resorption)
• Specific drugs (bisphosphonates, mithramycin,
calcitonin, and gallium nitrate)
n Hypocalcemia (Fig. 1.17)
• Findings
• Low plasma calcium
• Results from low levels of PTH or vitamin D3
• Neuromuscular irritability (tetany, seizures, Chvostek
sign), cataracts, fungal nail infections, ECG changes
(prolonged QT interval), and other signs and
symptoms
n Hypoparathyroidism
• Reduced PTH level causes decrease in plasma calcium
level and increase in plasma phosphate level
• Urinary excretion not enhanced because of the lack
of PTH
• Common findings:
• Fungal nail infections
• Hair loss
• Blotchy skin (pigment loss, vitiligo)
• Skull radiographs may show basal ganglia calcification.
• Iatrogenic hypoparathyroidism most commonly follows
thyroidectomy.
n Pseudohypoparathyroidism (PHP)
• A rare genetic disorder caused by lack of effect of PTH
on the target cells
• PTH is normal or high.
• PTH action is blocked by an abnormality at the
receptor, by the cAMP system, or by a lack of required
cofactors (e.g., Mg2+)
• Defect in GNAS gene from mother
• Albright hereditary osteodystrophy, a form of PHP
• Short first, fourth, and fifth metacarpals (MCs) and
metatarsals (MTs)
• Brachydactyly
Low serum Ca2+
↑ PTH
↑ 1,25(OH)2-vitamin D3
↑ Ca2+ ↑ Ca2+ ↑ Ca2+
↑ Pi ↑ Pi ↓ Pi
↑ Serum Ca2+
– Serum Pi
FIG. 1.17 Body’s reaction to hypocalcemia, with consequent resorp-
tion of bone. When calcium level falls, PTH is secreted, which re-
leases calcium and Pi from bone. PTH increases renal reabsorption
of calcium while inhibiting phosphate reabsorption. These actions in
combination restore calcium concentration. If hypocalcemia persists,
PTH stimulates renal production of 1,25(OH)2D3, which increases
intestinal calcium absorption. (From Goldman L, Ausiello D, editors: Cecil
medicine, ed 23, Philadelphia, 2008, Saunders Elsevier.)
• Exostoses
• Obesity
• Diminished intelligence
n Pseudo-pseudohypoparathyroidism (pseudo-PHP)
• Normocalcemic disorder that is phenotypically similar
to PHP
• However, response to PTH is normal.
• Renal osteodystrophy (Fig. 1.18)
• A spectrum of bone mineral metabolism disorders in
chronic renal disease.
• Due to impaired excretion, which compromises
mineral homeostasis
• Leads to abnormalities in bone mineral metabolism
• High-turnover renal bone disease
• Chronically elevated serum PTH level leads to
secondary hyperparathyroidism (hyperplasia of
parathyroid gland chief cells).
• Factors contributing to sustained PTH increase
and secondary hyperparathyroidism include:
• Diminished renal phosphorus excretion;
phosphorus retention promotes PTH
secretion by three mechanisms:
• Hyperphosphatemia lowers serum calcium,
stimulating PTH.
• Phosphorus impairs renal 1α-hydroxylase
activity, impairing production of
1,25(OH)2D3.
• Phosphorus retention may directly increase
the synthesis of PTH.
 Basic Sciences 27

• H ypocalcemia • I n amyloidosis, Congo red stain causes tissue

• I mpaired renal calcitriol [1,25(OH)2D3] material to turn pink.
• Alterations in the control of PTH gene • Laboratory findings:
transcription secretion • Abnormal glomerular filtration rate (GFR)
• Skeletal resistance to the actions of PTH • Increased alkaline phosphatase, blood urea
• Low-turnover renal bone disease (adynamic lesion of nitrogen (BUN), and creatinine levels
bone and osteomalacia) • Decreased venous bicarbonate level
• Secondary hyperparathyroidism is not • Treatment directed at relieving the urologic
characteristic with this condition. obstruction or kidney disease
• Serum PTH level is normal or mildly elevated. • Rickets (osteomalacia in adults; Box 1.1)
• Bone formation and turnover are reduced. • Failure of mineralization leading to changes in
• Excess deposition of aluminum into bone the physis in the zone of provisional calcification
(aluminum toxicity) negatively affects bone (increased width and disorientation) and bone
mineral metabolism. (cortical thinning, bowing)
• Impairs differentiation of precursor cells to
osteoblasts
• Impairs proliferation of osteoblasts Box 1.1   Causes of Rickets and Osteomalacia
• Impairs PTH release from the parathyroid gland NUTRITIONAL DEFICIENCY
• Disrupts the mineralization process Vitamin D deficiency
• Adynamic lesion: accounts for the majority of Dietary chelators (rare) of calcium
cases of low-turnover bone disease in patients Phytates
Oxalates (spinach)
with chronic renal failure PHOSPHORUS DEFICIENCY (UNUSUAL)
• Osteomalacia: defects in mineralization of newly Abuse of antacids (which contain aluminum), which leads to
formed bone severe dietary phosphate binding
• Radiographs may demonstrate a rugger jersey GASTROINTESTINAL ABSORPTION DEFECTS
spine (vertebral bodies appear to have increased Postgastrectomy (rare today)
Biliary disease (interference with absorption of fat-soluble
density in the upper and lower zones in a striated vitamin D)
appearance, like that in childhood osteopetrosis) Enteric absorption defects
and soft tissue calcification. Short bowel syndrome
• β2-Microglobulin may accumulate with long-term Rapid transit (gluten-sensitive enteropathy) syndromes
Inflammatory bowel disease
dialysis, leading to amyloidosis. Crohn disease
• Amyloidosis may be associated with carpal tunnel Celiac disease
syndrome, arthropathy, and pathologic fractures. RENAL TUBULAR DEFECTS (RENAL PHOSPHATE LEAK)
• X-linked dominant hypophosphatemic vitamin D–resistant
rickets or osteomalacia
• Classic Albright syndrome or Fanconi syndrome type I
• Fanconi syndrome type II
Osteitis • Phosphaturia and glycosuria
↓↓ [Ca2+]
fibrosa • Fanconi syndrome type III
• Phosphaturia, glycosuria, aminoaciduria
• Vitamin D–dependent rickets (or osteomalacia) type I—a
Decreased PTR ↑↑ PTH genetic or acquired deficiency of renal tubular 25(OH)D 1α-
tubular hyperplasia Osteomalacia hydroxylase enzyme that prevents conversion of 25(OH)D to
function the active polar metabolite 1,25(OH)2D
• Vitamin D–dependent rickets (or osteomalacia) type II—which
Decreased represents enteric end-organ insensitivity to 1,25(OH)D and is
1,25(OH)2-vitamin D3 probably caused by an abnormality in the 1,25(OH)2D nuclear
receptor)
• Renal tubular acidosis
Decreased • Acquired: associated with many systemic diseases
GFR • Genetic
Renal • Debré–De Toni–Fanconi syndrome
osteodystrophy • Lignac-Fanconi syndrome (cystinosis)
Phosphate • Lowe syndrome
Renal retention RENAL OSTEODYSTROPHY: MISCELLANEOUS CAUSES
failure
Soft tissue tumors secreting putative factors
Kion = [Ca2+][HPO42–] Fibrous dysplasia
Neurofibromatosis
Other soft tissue and vascular mesenchymal tumors
Hypocalcemia Decreased Anticonvulsant medication (induction of the hepatic P450
absorption of microsomal enzyme system by some anticonvulsants—e.g.,
calcium and phosphate phenytoin, phenobarbital, and primidone [Mysoline]—causes
increased degradation of vitamin D metabolites)
Heavy metal intoxication
Fecal loss of calcium Hypophosphatasia
and phosphate High-dose diphosphonates
Sodium fluoride
FIG. 1.18 Pathogenesis of bony changes in renal osteodystrophy.
PTR, proximal tubule reabsorption. (From McPherson RA, Pincus MR, Adapted from Simon SR, editor: Orthopaedic basic science, ed 2,
editors: Henry’s clinical diagnosis and management by laboratory methods, ed 21, Rosemont, IL, 1994, American Academy of Orthopaedic Surgeons,
Philadelphia, 2007, Saunders Elsevier.) p 169.
Another random document with
no related content on Scribd:
 (good)
Strawberry Isinglass Jelly 468
Fancy Jellies, and Jelly in 469
Belgrave mould
Queen Mab’s Pudding (an 470
elegant summer dish)
Nesselróde Cream 471
Crême à la Comtesse, or the 472
Countess’s Cream
An excellent Trifle 473
Swiss Cream, or Trifle (very 473
good)
Tipsy Cake, or Brandy Trifle 474
Chantilly Basket filled with 474
whipped Cream and fresh
Strawberries
Very good Lemon Cream, 475
made without Cream
Fruit Creams, and Italian 475
Creams
Very superior whipped 476
Syllabubs
Good common Blanc-mange, 476
or Blanc Manger (Author’s
receipt)
Richer Blanc-mange 477
Jaumange, or Jaune Manger; 477
sometimes called Dutch
Flummery
Extremely good Strawberry 477
Blanc-mange, or Bavarian
Cream
Quince Blanc-mange 478
(delicious)
Quince Blanc-mange, with 478
Almond Cream
Apricot Blanc-mange, or 479
Crême Parisienne
Currant Blanc-mange 479
Lemon Sponge, or Moulded 480
Lemon Cream
An Apple Hedgehog, or 480
Suédoise
Imperial Gooseberry-fool 480
Very good old-fashioned boiled 481
Custard
Rich boiled Custard 481
The Queen’s Custard 481
Currant Custard 482
Quince or Apple Custards 482
The Duke’s Custard 482
Chocolate Custards 483
Common baked Custard 483
A finer baked Custard 483
French Custards or Creams 484
German Puffs 484
A Meringue of Rhubarb, or 485
green Gooseberries
Creamed Spring Fruit, or 486
Rhubarb Trifle
Meringue of Pears, or other 486
fruit
An Apple Charlotte, or 486
 Charlotte de Pommes
Marmalade for the Charlotte 487
A Charlotte à la Parisienne 486
A Gertrude à la Créme 486
Pommes au Beurre (Buttered 488
Apples) (excellent)
Suédoise of Peaches 488
Aroce Doce, or Sweet Rice à la 489
Portugaise
Cocoa Nut Doce 490
Buttered Cherries (Cerises au 490
Beurre)
Sweet Macaroni 490
Bermuda Witches 491
Nesselróde Pudding 491
Stewed Figs (a very nice 492
Compote)
 CHAPTER XXIV.

PRESERVES.

Page

General Remarks on the use 493

and value of Preserved
Fruits
A few General Rules and 496
Directions for Preserving
To Extract the Juice of Plums 497
for Jelly
To weigh the Juice of Fruit 498
Rhubarb Jam 498
Green Gooseberry Jelly 498
Green Gooseberry Jam (firm 499
and of good colour)
To dry green Gooseberries 499
Green Gooseberries for Tarts 499
Red Gooseberry Jam 500
Very fine Gooseberry Jam 500
Jelly of ripe Gooseberries 500
(excellent)
Unmixed Gooseberry Jelly 501
Gooseberry Paste 501
To dry ripe Gooseberries with 501
Sugar
Jam of Kentish or Flemish 502
Cherries
To dry Cherries with Sugar (a 502
 quick and easy method)
Dried Cherries (superior 503
receipt)
Cherries dried without Sugar 503
To dry Morella Cherries 504
Common Cherry Cheese 504
Cherry Paste (French) 504
Strawberry Jam 504
Strawberry Jelly, a very 505
superior Preserve (new
receipt)
Another very fine Strawberry 505
Jelly
To preserve Strawberries or 506
Raspberries, for Creams or
Ices, without boiling
Raspberry Jam 506
Very rich Raspberry Jam, or 506
Marmalade
Good Red or White Raspberry 507
Jam
Raspberry Jelly for flavouring 507
Creams
Another Raspberry Jelly (very 508
good)
Red Currant Jelly 508
Superlative Red Currant Jelly 509
(Norman receipt)
French Currant Jelly 509
Delicious Red Currant Jam 509
Very fine White Currant Jelly 510
White Currant Jam, a beautiful 510
Preserve
Currant Paste 510
Fine Black Currant Jelly 511
Common Black Currant Jelly 511
Black Currant Jam and 511
Marmalade
Nursery Preserve 512
Another good common 512
Preserve
A good Mélange, or mixed 513
Preserve
Groseillée, (another good 513
Preserve)
Superior Pine-apple 513
Marmalade (a new receipt)
A fine Preserve of the green 514
Orange Plum (sometimes
called the Stonewood Plum)
Greengage Jam, or Marmalade 515
Preserve of the Magnum 515
Bonum, or Mogul Plum
To dry or preserve Mogul 515
Plums in syrup
Mussel Plum Cheese and Jelly 516
Apricot Marmalade 516
To dry Apricots (a quick and 517
easy method)
Dried Apricots (French receipt) 517
Peach Jam, or Marmalade 518
To preserve or to dry Peaches 518
 or Nectarines (an easy and
excellent receipt)
Damson Jam (very good) 519
Damson Jelly 519
Damson or Red Plum Solid 519
(good)
Excellent Damson Cheese 520
Red Grape Jelly 520
English Guava (a firm, clear, 520
bright Jelly)
Very fine Imperatrice Plum 521
Marmalade
To dry Imperatrice Plums (an 521
easy method)
To bottle Fruit for winter use 522
Apple Jelly 522
Exceedingly fine Apple Jelly 523
Quince Jelly 524
Quince Marmalade 523
Quince and Apple Marmalade 525
Quince Paste 525
Jelly of Siberian Crabs 526
To preserve Barberries in 526
bunches
Barberry Jam (First and best 506
receipt)
Barberry Jam (second receipt) 527
Superior Barberry Jelly, and 527
Marmalade
Orange Marmalade (a 527
Portuguese receipt)
Genuine Scotch Marmalade 528
Clear Orange Marmalade 529
(Author’s receipt)
Fine Jelly of Seville Oranges 530
(Author’s original receipt)
 CHAPTER XXV.

PICKLES.

Page

Observations on Pickles 531

To pickle Cherries 532
To pickle Gherkins 532
To pickle Gherkins (a French 533
receipt)
To pickle Peaches, and Peach 534
Mangoes
Sweet Pickle of Lemon 534
(Foreign receipt) (to serve
with roast meat)
To pickle Mushrooms 535
Mushrooms in brine, for winter 536
use (very good)
To pickle Walnuts 536
To pickle Beet-Root 537
Pickled Eschalots (Author’s 537
receipt)
Pickled Onions 537
To pickle Lemons and Limes 538
(excellent)
Lemon Mangoes (Author’s 538
original receipt)
To pickle Nasturtiums 539
To pickle red Cabbage 539
 CHAPTER XXVI.

CAKES.

Page

General Remarks on Cakes 540

To blanch and to pound 542
Almonds
To reduce Almonds to a Paste 542
(the quickest and easiest
way)
To colour Almonds or Sugar- 542
grains, or Sugar-candy, for
Cakes or Pastry
To prepare Butter for rich 543
Cakes
To whisk Eggs for light rich 543
Cakes
Sugar Glazings and Icings, for 543
fine Cakes and Pastry
Orange-Flower Macaroons 544
(delicious)
Almond Macaroons 544
Very fine Cocoa-nut 545
Macaroons
Imperials (not very rich) 545
Fine Almond Cake 545
Plain Pound or Currant Cake 546
(or rich Brawn Brack or
Borrow Brack)
Rice Cake 546
White Cake 546
A good Sponge Cake 547
A smaller Sponge Cake (very 547
good)
Fine Venetian Cake or Cakes 547
A good Madeira Cake 548
A Solimemne (a rich French 549
breakfast cake, or Sally
Lunn)
Banbury Cakes 549
Meringues 550
Italian Meringues 551
Thick, light Gingerbread 551
Acton Gingerbread 552
Cheap and very good Ginger 552
Oven-cake or Cakes
Good common Gingerbread 553
Richer Gingerbread 553
Cocoa-nut Gingerbread 553
(original receipts)
Delicious Cream Cake and 554
Sweet Rusks
A good light Luncheon-cake 554
and Brawn Brack
A very cheap Luncheon-biscuit, 555
or Nursery-cake
Isle of Wight Dough-nuts 556
Queen Cakes 556
Jumbles 556
A good Soda Cake 556
Good Scottish Short-bread 557
A Galette 557
Small Sugar Cakes of various 558
kinds
Fleed, or Flead Cakes 558
Light Buns of different kinds 559
Exeter Buns 559
Threadneedle-street Biscuits 560
Plain Dessert Biscuits and 560
Ginger Biscuits
Good Captain’s Biscuits 560
The Colonel’s Biscuits 561
Aunt Charlotte’s Biscuits 561
Excellent Soda Buns 561
 CHAPTER XXVII.

CONFECTIONARY.

Page

To clarify Sugar 562

To boil Sugar from Syrup to 563
Candy, or to Caramel
Caramel (the quickest way) 563
Barley-sugar 564
Nougat 564
Ginger-candy 565
Orange-flower Candy 565
Orange-flower Candy (another 566
receipt)
Cocoa-nut Candy 566
Everton Toffee 567
Chocolate Drops 567
Chocolate Almonds 568
Seville Orange Paste 568
 CHAPTER XXVIII.

DESSERT DISHES.

Page

Dessert Dishes 569

Pearled Fruit, or Fruit en 570
Chemise
Salad of mixed Summer Fruits 570
Peach Salad 570
Orange Salad 571
Tangerine Oranges 571
Peaches in Brandy (Rotterdam 571
receipt)
Brandied Morella Cherries 571
Baked Compôte of Apples (our 572
little lady’s receipt)
Dried Norfolk Biffins 572
Normandy Pippins 572
Stewed Pruneaux de Tours, or 573
Tours dried Plums
To bake Pears 573
Stewed Pears 573
Boiled Chestnuts 574
Roasted Chestnuts 574
Almond Shamrocks (very good 574
and very pretty)
Small Sugar Soufflés 575
Ices 575
 CHAPTER XXIX.

SYRUPS, LIQUEURS, ETC.

Page

Strawberry Vinegar, of 577

delicious flavour
Very fine Raspberry Vinegar 578
Fine Currant Syrup, or Sirop de 579
Groseilles
Cherry Brandy (Tappington 579
Everard receipt)
Oxford Punch 580
Oxford receipt for Bishop 580
Cambridge Milk Punch 581
To mull Wine (an excellent 581
French receipt)
A Birthday Syllabub 581
An admirable cool cup 582
The Regent’s, or George the 582
Fourth’s Punch
Mint Julep (an American 582
receipt)
Delicious Milk Lemonade 583
Excellent portable Lemonade 583
Excellent Barley Water (Poor 583
Xury’s receipt)
Raisin Wine, which, if long 583
kept, really resembles
foreign
Very good Elderberry Wine 584
Very Good Ginger Wine 584
Excellent Orange Wine 585
The Counsellor’s Cup 585
 CHAPTER XXX.

COFFEE, CHOCOLATE, ETC.

Page

Coffee 587
To roast Coffee 588
A few general directions for 589
making Coffee
Excellent Breakfast Coffee 590
To boil Coffee 591
Café Noir 592
Burnt Coffee, or Coffee à la 592
militaire (In France vulgarly
called Gloria)
To make Chocolate 592
A Spanish recipe for making 592
and serving Chocolate
To make Cocoa 593
 CHAPTER XXXI.

BREAD.

Page

Remarks on Home-made 594

Bread
To purify Yeast for Bread or 595
Cakes
The Oven 595
A few rules to be observed in 596
making Bread
Household Bread 596
Bordyke Bread (Author’s 597
receipt)
German Yeast (and Bread 598
made with German Yeast)
Professor Liebig’s Bavarian 599
Brown Bread (very nutritious
and wholesome)
English Brown Bread 599
Unfermented Bread 599
Potato Bread 600
Dinner or Breakfast Rolls 600
Geneva Rolls or Buns 601
Rusks 602
Excellent Dairy Bread, made 602
without Yeast (Author’s
receipt)
To keep Bread 603
To freshen stale Bread (and 603
Pastry, &c.) and preserve it
from mould
To know when Bread is 604
sufficiently baked
On the proper fermentation of 604
Dough
 CHAPTER XXXII.

FOREIGN AND JEWISH COOKERY.

Page

Foreign and Jewish Cookery 605

Remarks on Jewish Cookery 606
Jewish Smoked Beef 606
Chorissa (or Jewish Sausage) 607
with Rice
To fry Salmon and other Fish in 607
Oil (to serve cold)
Jewish Almond Pudding 608
The Lady’s or Invalid’s new 608
Baked Apple Pudding
(Author’s original receipt.
Appropriate to the Jewish
table)
A few general directions for the 609
Jewish table
Tomata and other Chatnies 609
(Mauritian receipt)
Indian Lobster Cutlets 610
An Indian Burdwan (Entrée) 611
The King of Oude’s Omlet 611
Kedgeree or Kidgeree, an 612
Indian breakfast-dish
A simple Syrian Pilaw 612
Simple Turkish or Arabian 613
Pilaw (From Mr. Lane, the