DOCSLIB.ORG

Epiphyseal Plate Repair Using Fat Interposition to Reverse Physeal

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Epiphyseal Plate Repair Using Fat Interposition to Reverse Physeal s.-ì E EPIPHYSEAL PLATE REPAIR USING FAT INTERPOSITION TO REVERSE PHYSEAL DEFOR}IITY An experimental study JI I j I I l l I Thesis submitted in March 1989 for the degree of Doctor of Medicine in the University of Adelaide by Bruce Kristian Foster, M.8., B.S. (Adel.), F.R.A.C.S. The work described was performed within the Department of Pathol ogy of the University of Adelaide I TABLE OF CONTENTS TITLE I TABLE OF CONTENTS II TABLE OF FIGURES IV TABLE OF TABLES VII SUMl'IARY X DECLARATION XII ACKNOl.lLEDGEMENTS XIII Chapter I GLOSSARY I Ghapter 2 AII'ls 2 Chapter 3 NOR]'IAL PHYSEAL FUNCTION 3 3.1 INTRODUCTION 3 3.2 MECHANICAL PHYSEAL INJURY 7 3.3 CLASSIFICATION OF FRACTURES l0 3.4 ANATOMY & PHYSIOLOGY 18 3.4. r Zone of Reserve Cel I s 3.4.2 Prol i ferati ng Cel I s 3.4.3 Hypertrophic Cells 3.4.4 Mi neral i zati on 3.4.5 Metaphysi s 3.4.6 Ci rcumferenti al Structures 3.4.7 Arti cul ar Cart'il age 3.5 BLOOD SUPPLY 30 3.6 BIO1'4ECHAN ICS 32 Chapter 4 DEVELOPMENT OF CLOSURE ]'IODEL 36 4.1 EXPERIMENTAL AIM 36 4.2 REVIEIil OF THE LITERATURE 44 4.3 MATERIALS & METHODS 4.3.1 Animal s 4.3.2 Operative Technique 4.3 .3 Radiol og'ical Techniques 4.3.4 Bone Deformity Index 4.3.5 C.T. Measurement 4.3.6 Spec'imen Measurements at Autopsy 4.4 RESULTS 58 4.5 D I SCUSS ION 7l 4.6 CONCLUS IONS 74 II Page No. Chapter 5 FAT INTERPOSITIONAL REVERSAL 75 5.1 EXPERIMENTAL AIM 75 5.2 REVIEI^, OF THE LITERATURE 75 5.3 MATERIALS & METHODS 84 5.3.1 Bone Brjdge Resection 5.3.2 Radiologìcaì Techniques 5.3.3 C.T. Measurements 5.4 HISTOLOGICAL QUANTI FICATION 93 5.5 RESULTS 0F l SQ. CM. DEFECTS 108 5.6 RESULTS OF 2 SQ. CM. DEFECTS t2t 5.7 RESULTS 0F 3 SQ. CM. DEFECTS 134 Chapter 6 DISCUSSION 145 Chapter 7 CONCLUSIONS & FUTURE DIRECTIONS 158 Chapter I APPENDICES t62 Chapter 9 BIBLIOGRAPHY 169 III TABLE OF FIGURES Paqe No 3.1 Growth arrest following trauma. 5&6 3.2 Poland's classification of physeal fracture. ll 3.3 Salter and Harris' classification of physeal l3 fracture. 3.4 Rang's classification of physeal fracture. 16 3.5 Ogden's classificatjon of physeal jniury. t7 3.6 Normal physeal anatomy. l9 3.7 Physeaì zonaì function. 20 3.8 Blood supp'ly to the epiphys'is. 31 3.9 Normal physeal radiology. 35 4.1 Summary of growth djsturbance caused by surgical 42 trauma to the ep'iphysea'l plate in immature dogs. 4.2 K-wi re marker pì acement. 47 4.3 Ep'iphyseal arrest by phys j odesi s, accordi ng 49 to Phemister. 4.4 Radioìogical bone deformity. 52 4.5 Measurement of bone lengthening ratio. 52 4.6 Computerized tomographic section of the tibial 54 physis. IV Page No. 4.7 Measurement of pin distances at autopsy. 56 4.8 Preparation of histologÌcal section. 57 4 .9 Macroscopi c vi ew of a prox'imal ti bi al fusi on . 59 4. 10 Radi ol ogi ca'l variati on of fusi on. 6l 4.ll Histologica'l evidence of fusion: bone response. 66 4.12 Histological evidence of fusion: physeal response. 67 4. 13 Histological evidence of non-fusion: physea'l 68 transpl antatj on. 4.14 Histological evidence of non-fusion I. 69 4.15 Histologica'l evjdence of non-fusion II. 70 5.1 0perati ve deta'i I s of physeal bridge resect'ion 85 and fat interposition. 5.2 Quantification of physeal area by computerized 94 tomography. 5.3 Hjstologicaì assessment of host tissue response 95 to implant - capsule formation. 5.4 Histological assessment of host tissue reaction 97 to implant - epiphyseal bone response. 5.5 Hjstolog'ical assessment of host tissue reaction l0l to'impìant - cortical bone remodel'ling. V 5.6 Hjstological assessment of fat autograft. 5.7 Histological assessment of bone brìdge reformation. 104 5.8 Hjstological assessment of host physeal response. 105 5.9 H j stol og'ica'l assessment of host physea'l 109 response - polarized light examination. 5. l0 Hi stol og'ical assessment of host physeal ll0 response - peripheral physis. 5.ll Rad'iolog'icaì evidence of fusion and reversal ll4 of deformity. 5.12 Bone bridge reformat'ion - peripheral . 120 5.13 Interst'iti aì physeal repair. t22 5. 14 Attempt at medial bone bridge reformation - 132 low power examination. 5. l5 Attempt at medial bone brjdge reformatjon - 133 high power examination. 5.16 Bone bridge reformation I. 742 5.17 Bone bridge reformation II. 143 6. I Physeal defect. t5l 6.2 Physeal repaÌr t52 6.3 Physeal growth. 155 VI LIST OF TABLES Page No. I Rel ative incidence of physeal 'iniuries 8 4A Provocation Series - Deform'ity index at 3 months 62 (i) bone lengthening ratio (i i ) pin angul ation 4B C.T. scan results 63 4C Direct measurements at 3 months autopsy of: 64 Bone p'in distance versus bone length difference 4D Radiology & histology correlatjon of fusion 7t 5A I sq. cm. defect - 3 month survival tt2 Deformity index at 3 months 5B I sq. cm. defect - 6 month survival ll3 Deformity index at 3 and 6 months 5C C.T. scan results for I sq.cm. defect 116 at 3 month and 6 month survival 5D H'istopathol ogy I sq. cm. reversal s - sheep tt7 autopsied at 3 months VII Page No. 5E Histopathology I sq. cm. reversals - sheep ll8 autopsied at 6 months 5F 2 sq. cm. defect - 3 month survival 124 Deformity index at 3 months 5G 2 sq. cm. defect - 6 month survival t25 Deformity index at 3 and 6 months 5H C.T. scan results for 2 sq. cm. defect t27 at 3 month and 6 month survival 5I Hi stopatho'logy 2 sq. cm. reversal s - sheep t28 autopsied at 3 months 5J Histopatho'logy 2 sq. cm. reversals - sheep t29 autopsied at 6 months 5K 3 sq. cm. defect - 3 month survival 135 Deformity 'index at 3 months 5L 3 sq. cm. defect - 6 month survival 137 Deformity index at 3 and 6 months VIII Page No. 5M C.T. scan results for 3 sq.cm. defect - 3 month 138 and 6 month survival 5N Histopathology 3 sq. cm. reversals - sheep 140 autopsied at 3 months 50 H'lstopathology 3 sq. cm. reversals - sheep 141 t 1 autopsied at 6 months I 1 ; I i ,trl '1 I I I l I I I I I IX SUMMARY A predi ctabl e method of reversal of physea'l (ep'iphyseaì pl ate) damage at the level of deformity is not current'ly avajlable. A reproduci bl e model of a periphera'l part'ia'l bone bridge to the proximal medjal tjbial physis v',as created jn lambs at the age of 6 weeks. Three months after the initial procedure, reversal of the bone bridge lesjon u,as achieved by excjsion of the bone bridge and autologous fat interposition from the ipsilateral knee fat pad. There v',ere 3 groups of animals with lesions to the phys'is. At reversal in the first group of animals, C.T. scans determined that the size of defects was 17.2 + 2.2% of the total physeal area. For the second group of anjmals, the size of the defect was 28.0 + 6.0%. For the thjrd group of animals, the lesion was 33.7 + 7.2%. Us'ing an unpaired Student's ú test, there u,as a statjst'ica'lly sign'ificant increase ìn sìze of lesion between groups (p < 0.0001). ldi th 'interposi t j on of fat radi ol og'ical cniteri a j ndi cated success j n the resumption of physeal growth jn 85.7% of cases in the first group, 54.5% in the second group, and 50.0% jn the third group. The survjval of the fat and its maintainjng of pos'ition I'rere critical factors to the success of the reversal procedures. For example, 'in the first series of experiments, success js 100% if two animals unable to satisfy both criteria are elimjnated from analys'is. Measurements of the areas of the physea'l defects us'ing C.T.'images between the initial (reversa'l) procedure and autopsy at three and six X months showed a decrease ìn size of the defects. These, hov'lever, failed to reach a statistically sign'ifjcant level of change in the size of the defects. This is presumptive evjdence of the ìnabiìity of physeal cartilage to repaìr. Histolog'ical assessment showed that there bras minimal evidence of physeal stimulation or resumption of a normal physis in the defects. A spur of cartilage cou'ld be seen to arjse centraì'ly from the phys'is and to point towards the metaphys'is. In this regÌon there was loss of normal physeaì chondrocyte organ'ization. Under polarized light mìcroscopy the phenotyp'icaì expression showed metapl asi a of the hyal 'ine cart'il age to f i brocart'il age. Chondrons of physeaì di sorgani zati on occurred. It is postulated that correction of deformity occurs by a non-union effect, which allows the rema'ining normal physis to functjon and groþ,, rather than by a process of interstitial physeal repa'ir.
Load more

Recommended publications
  • Applications of Chondrocyte-Based Cartilage Engineering: an Overview
    Hindawi Publishing Corporation BioMed Research International Volume 2016, Article ID 1879837, 17 pages http://dx.doi.org/10.1155/2016/1879837 Review Article Applications of Chondrocyte-Based Cartilage Engineering: An Overview Abdul-Rehman Phull,1 Seong-Hui Eo,1 Qamar Abbas,1 Madiha Ahmed,2 and Song Ja Kim1 1 Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongjudaehakro 56, Gongju 32588, Republic of Korea 2Department of Pharmacy, Quaid-i-Azam University, Islamabad 45320, Pakistan Correspondence should be addressed to Song Ja Kim; [email protected] Received 14 May 2016; Revised 24 June 2016; Accepted 26 June 2016 Academic Editor: Magali Cucchiarini Copyright © 2016 Abdul-Rehman Phull et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Chondrocytes are the exclusive cells residing in cartilage and maintain the functionality of cartilage tissue. Series of biocomponents such as different growth factors, cytokines, and transcriptional factors regulate the mesenchymal stem cells (MSCs) differentiation to chondrocytes. The number of chondrocytes and dedifferentiation are the key limitations in subsequent clinical application of the chondrocytes. Different culture methods are being developed to overcome such issues. Using tissue engineering and cell based approaches, chondrocytes offer prominent therapeutic option specifically in orthopedics for cartilage repair and to treat ailments such as tracheal defects, facial reconstruction, and urinary incontinence. Matrix-assisted autologous chondrocyte transplantation/implantation is an improved version of traditional autologous chondrocyte transplantation (ACT) method. An increasing number of studies show the clinical significance of this technique for the chondral lesions treatment.
    [Show full text]
  • Studies on Brain and Spinal Cord Tumors
    Studies on Brain and Spinal Cord Tumors Chapter 1 Osteochondroma of the Spine Iraj Lotfinia Professor of Neurosurgery, Tabriz Universsity of medical science, Tabriz, Iran. Fax: 00984113340830; Email: [email protected] Abstract Osteochondroma (OC) is the most common benign tumor of the bones, and it remains the most common precursor for secondary chondrosarcoma, which often occurs in the long bones’ metaphyseal areas. Rarely, it is also found in the spine. This tumor comprises a cartilage capped bone projection and is observed in both solitary and multiple forms. In many cases, the lesion can be definitively diagnosed according to radiological characteristics, but the rarity of these lesions in the spine, gradual onset of symptoms, and the frequent lack of observation of lesions in plain radiography may delay the diagnosis or cause misdiagnosis. These lesions are be- nign and do not risk the patient’s life; however, they rarely may be found to be a malignant degeneration that transformed into chondrosarcoma. When the lesion has led to clinical symptoms or has faced the patient with cosmetic challenges, or when definitive diagnosis is unknown, treatment is required. The primary treatment is the surgical removal of the lesion. Timely diagnosis and complete resection of the le- sion using surgery lead to complete recovery and prevent recurrence. 1. Introduction According to the World Health Organization’s (WHO’s) definition in 2002, osteocar- tilaginous exostosis are benign bone neoplasms covered by a cartilaginous cap created at the outer surface of the bone by endochondral ossification [1]. Osteochondroma (OC) is the most common benign primary tumor of the bone.
    [Show full text]
  • The Epiphyseal Plate: Physiology, Anatomy, and Trauma*
    3 CE CREDITS CE Article The Epiphyseal Plate: Physiology, Anatomy, and Trauma* ❯❯ Dirsko J. F. von Pfeil, Abstract: This article reviews the development of long bones, the microanatomy and physiology Dr.med.vet, DVM, DACVS, of the growth plate, the closure times and contribution of different growth plates to overall growth, DECVS and the effect of, and prognosis for, traumatic injuries to the growth plate. Details on surgical Veterinary Specialists of Alaska Anchorage, Alaska treatment of growth plate fractures are beyond the scope of this article. ❯❯ Charles E. DeCamp, DVM, MS, DACVS athologic conditions affecting epi­ foramen. Growth factors and multipotent Michigan State University physeal (growth) plates in imma­ stem cells support the formation of neo­ ture animals may result in severe natal bone consisting of a central marrow P 2 orthopedic problems such as limb short­ cavity surrounded by a thin periosteum. ening, angular limb deformity, or joint The epiphysis is a secondary ossifica­ incongruity. Understanding growth plate tion center in the hyaline cartilage forming anatomy and physiology enables practic­ the joint surfaces at the proximal and distal At a Glance ing veterinarians to provide a prognosis ends of the bones. Secondary ossification Bone Formation and assess indications for surgery. Injured centers can appear in the fetus as early Page E1 animals should be closely observed dur­ as 28 days after conception1 (TABLE 1). Anatomy of the Growth ing the period of rapid growth. Growth of the epiphysis arises from two Plate areas: (1) the vascular reserve zone car­ Page E2 Bone Formation tilage, which is responsible for growth of Physiology of the Growth Bone is formed by transformation of con­ the epiphysis toward the joint, and (2) the Plate nective tissue (intramembranous ossifica­ epiphyseal plate, which is responsible for Page E4 tion) and replacement of a cartilaginous growth in bone length.3 The epiphyseal 1 Growth Plate Closure model (endochondral ossification).
    [Show full text]
  • Osteochondroma: Ignore Or Investigate?
    r e v b r a s o r t o p . 2 0 1 4;4 9(6):555–564 www.rbo.org.br Updating Article ଝ Osteochondroma: ignore or investigate? a b,c,∗ Antônio Marcelo Gonc¸alves de Souza , Rosalvo Zósimo Bispo Júnior a School of Medicine, Federal University of Pernambuco (UFPE), Recife, PE, Brazil b School of Medicine, Federal University of Paraíba (UFPB), João Pessoa, PB, Brazil c University Center of João Pessoa (UNIPÊ), João Pessoa, PB, Brazil a r a t i b s c t l e i n f o r a c t Article history: Osteochondromas are bone protuberances surrounded by a cartilage layer. They generally Received 23 August 2013 affect the extremities of the long bones in an immature skeleton and deform them. They usu- Accepted 31 October 2013 ally occur singly, but a multiple form of presentation may be found. They have a very charac- Available online 27 October 2014 teristic appearance and are easily diagnosed. However, an atypical site (in the axial skeleton) and/or malignant transformation of the lesion may sometimes make it difficult to iden- Keywords: tify osteochondromas immediately by means of radiographic examination. In these cases, Osteochondroma/etiology imaging examinations that are more refined are necessary. Although osteochondromas Osteochondroma/physiopathology do not directly affect these patients’ life expectancy, certain complications may occur, with Osteochondroma/diagnosis varying degrees of severity. Bone neoplasms © 2014 Sociedade Brasileira de Ortopedia e Traumatologia. Published by Elsevier Editora Ltda. All rights reserved. Osteocondroma: ignorar ou investigar? r e s u m o Palavras-chave: Osteocondromas são protuberâncias ósseas envolvidas por uma camada de cartilagem.
    [Show full text]
  • Inability of Low Oxygen Tension to Induce Chondrogenesis in Human Infrapatellar Fat Pad Mesenchymal Stem Cells
    fcell-09-703038 July 20, 2021 Time: 15:26 # 1 ORIGINAL RESEARCH published: 26 July 2021 doi: 10.3389/fcell.2021.703038 Inability of Low Oxygen Tension to Induce Chondrogenesis in Human Infrapatellar Fat Pad Mesenchymal Stem Cells Samia Rahman1, Alexander R. A. Szojka1, Yan Liang1, Melanie Kunze1, Victoria Goncalves1, Aillette Mulet-Sierra1, Nadr M. Jomha1 and Adetola B. Adesida1,2* 1 Laboratory of Stem Cell Biology and Orthopedic Tissue Engineering, Division of Orthopedic Surgery and Surgical Research, Department of Surgery, University of Alberta, Edmonton, AB, Canada, 2 Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of Alberta Hospital, Edmonton, AB, Canada Objective: Articular cartilage of the knee joint is avascular, exists under a low oxygen tension microenvironment, and does not self-heal when injured. Human infrapatellar fat pad-sourced mesenchymal stem cells (IFP-MSC) are an arthroscopically accessible source of mesenchymal stem cells (MSC) for the repair of articular cartilage defects. Human IFP-MSC exists physiologically under a low oxygen tension (i.e., 1–5%) Edited by: microenvironment. Human bone marrow mesenchymal stem cells (BM-MSC) exist Yi Zhang, physiologically within a similar range of oxygen tension. A low oxygen tension of Central South University, China 2% spontaneously induced chondrogenesis in micromass pellets of human BM-MSC. Reviewed by: Dimitrios Kouroupis, However, this is yet to be demonstrated in human IFP-MSC or other adipose tissue- University of Miami, United States sourced MSC. In this study, we explored the potential of low oxygen tension at 2% to Dhirendra Katti, Indian Institute of Technology Kanpur, drive the in vitro chondrogenesis of IFP-MSC.
    [Show full text]
  • Bone Cartilage Dense Fibrous CT (Tendons & Nonelastic Ligaments) Dense Elastic CT (Elastic Ligaments)
    Chapter 6 Content Review Questions 1-8 1. The skeletal system consists of what connective tissues? Bone Cartilage Dense fibrous CT (tendons & nonelastic ligaments) Dense elastic CT (elastic ligaments) List the functions of these tissues. Bone: supports the body, protects internal organs, provides levers on which muscles act, store minerals, and produce blood cells. Cartilage provides a model for bone formation and growth, provides a smooth cushion between adjacent bones, and provides firm, flexible support. Tendons attach muscles to bones and ligaments attach bone to bone. 2. Name the major types of fibers and molecules found in the extracellular matrix of the skeletal system. Collagen Proteoglycans Hydroxyapatite Water Minerals How do they contribute to the functions of tendons, ligaments, cartilage and bones? The collagen fibers of tendons and ligaments make these structures very tough, like ropes or cables. Collagen makes cartilage tough, whereas the water-filled proteoglycans make it smooth and resistant. As a result, cartilage is relatively rigid, but springs back to its original shape if it is bent or slightly compressed, and it is an excellent shock absorber. The extracellular matrix of bone contains collagen and minerals, including calcium and phosphate. Collagen is a tough, ropelike protein, which lends flexible strength to the bone. The mineral component gives the bone compression (weight-bearing) strength. Most of the mineral in the bone is in the form of hydroxyapatite. 3. Define the terms diaphysis, epiphysis, epiphyseal plate, medullary cavity, articular cartilage, periosteum, and endosteum. Diaphysis – the central shaft of a long bone. Epiphysis – the ends of a long bone. Epiphyseal plate – the site of growth in bone length, found between each epiphysis and diaphysis of a long bone and composed of cartilage.
    [Show full text]
  • The Histology of Epiphyseal Union in Mammals
    J. Anat. (1975), 120, 1, pp. 1-25 With 49 figures Printed in Great Britain The histology of epiphyseal union in mammals R. WHEELER HAINES* Visiting Professor, Department of Anatomy, Royal Free Hospital School of Medicine, London (Accepted 11 November 1974) INTRODUCTION Epiphyseal union may be defined as beginning with the completion of the first mineralized bridge between epiphyseal and diaphyseal bone and ending with the complete disappearance of the cartilaginous epiphyseal plate and its replacement by bone and marrow. The phases have been described by Sidhom & Derry (1931) and many others from radiographs, but histological material showing union in progress is rare, probably because of the rapidity with which union, once begun, comes to completion (Stephenson, 1924; Dawson, 1929). Dawson (1925, 1929) described the histology of 'lapsed union' in rats, where the larger epiphyses at the 'growing ends' of the long bones remain un-united through- out life. He and Becks et al. (1948) also discussed the early and complete type of union found at the distal end of the humerus in the rat. Here a single narrow per- foration pierced the cartilaginous plate near the olecranon fossa and later spread to destroy the whole plate. Lassila (1928) described a different type of union in the metatarsus of the calf, with multiple perforations of the plate. Apart from a few notes on human material (Haines & Mohiuddin, 1960, 1968), nothing else seems to have been published on the histology of union in mammals. In this paper more abundant material from dog and man is presented and will serve as a basis for discussion of the main features of the different types of union.
    [Show full text]
  • Skeletal System
    Skeletal system Anatomy Department Beni-Suef University Intended learning objectives (ILOs) By the end of this lecture the student will be able to: 1.Describe the functions of the skeletal system. 2.Classify the bones according to shape and location. 3.Describe the blood and nerve supply of bone. 4.Describe bone growth and remodeling. Functions of the bones: 1. Support. 2. Protection. 3. Assistance in movement. 4. Storage of minerals: e.g. calcium and phosphorus. 5. Blood cell production. 6. Triglyceride storage: Yellow bone marrow Classification of the bones: A. According to position in the body. B. According to shape. C. According to histological structure. D. According to the type of ossification. A. Classification according to the position in the body: I. Axial skeleton: skull, Mandible, Vertebral column and Bones of the thorax (ribs and sternum). II. Appendicular skeleton: bones of the upper and lower limbs and each limb is composed of limb girdle and free limb B. Classification according to the shape of the bones: I.Long bones II.Short long bones III.Short bones IV.Flat bones V.Irregular bones VI.Pneumatic bones VII. Sesamoid bones VIII. Sutural bones C. Classification according to the histological structure: I.Dense, compact bone II.Spongy, cancellous bone D. Classification of bones according to the type of ossification: I.Intramembranous ossification II.Endochondral ossification Structure of long bone •The hyaline articular cartilage •Epiphysis •The epiphyseal line •Diaphysis Growth of long bones: 1.Growth in length 2.2. Growth in width Functions of the periosteum: 1. a2achments of muscles and li aments.
    [Show full text]
  • Design and Characterization of Photopolymerizable Semi
    DESIGN AND CHARACTERIZATION OF PHOTOPOLYMERIZABLE SEMI- INTERPENETRATING NETWORKS FOR IN VITRO CHONDROGENESIS OF HUMAN MESENCHYMAL STEM CELLS by AMANDA NICOLE BUXTON Submitted in partial fulfillment of the requirements For the degree of Doctor of Philosophy Dissertation Adviser: Dr. Brian Johnstone Department of Biomedical Engineering CASE WESTERN RESERVE UNIVERSITY August, 2007 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of _____________Amanda N. Buxton______________________ candidate for the Doctor of Philosophy degree *. (signed)_____Roger Marchant______________ (chair of the committee) ________________Stuart Rowan____________________________ __________________Steve Eppell___________________________ __________________Brian Johnstone________________________ _______________Joseph Mansour___________________________ _______________Lloyd A. Culp_____________________________ (date) ___April 3, 2007____________________ *We also certify that written approval has been obtained for any proprietary material contained therein. TABLE OF CONTENTS List of Tables iii List of Figures iv Acknowledgements vii List of Abbreviations viii Glossary ix Abstract 1 Chapter One: Background & Significance 3 Structure & Function of Articular Cartilage 4 Formation of Cartilage 13 Articular Cartilage Pathology & Repair 17 Tissue Engineering Design Criteria 20 Cell Source 21 Scaffold Considerations 22 Addition of Bioactive Factors 25 Chapter Two: In Vitro Chondrogenesis in a Poly(ethylene glycol) Diacrylate
    [Show full text]
  • Hand Bone Age: a Digital Atlas of Skeletal Maturity
    V. Gilsanz/O. Ratib · Hand Bone Age Vicente Gilsanz · Osman Ratib Hand Bone Age A Digital Atlas of Skeletal Maturity With 88 Figures Vicente Gilsanz, M.D., Ph.D. Department of Radiology Childrens Hospital Los Angeles 4650 Sunset Blvd., MS#81 Los Angeles, CA 90027 Osman Ratib, M.D., Ph.D. Department of Radiology David Geffen School of Medicine at UCLA 100 Medical Plaza Los Angeles, CA 90095 This eBook does not include ancillary media that was packaged with the printed version of the book. ISBN 3-540-20951-4 Springer-Verlag Berlin Heidelberg New York Library of Congress Control Number: 2004114078 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag. Violations are liable to prosecution under the German Copyright Law. Springer-Verlag Berlin Heidelberg New York Springer is a part of Springer Science+Business Media http://www.springeronline.com A Springer-Verlag Berlin Heidelberg 2005 Printed in Germany The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from therelevantprotectivelawsandregulationsandthereforefreeforgeneraluse. Product liability: The publishers cannot guarantee the accuracy of any information about the application of operative techniques and medications contained in this book.
    [Show full text]
  • Bone and Bone Tissue Skeletal System = , , Bones Are Main Organs
    61 Chapter 6: Bone and Bone Tissue Skeletal system = , , Bones are main organs: - osseous tissue - dense regular and irregular CT, plus bone marrow Module 6.1: Introduction to Bones as Organs FunctionsFUNCTIONS of OF the THE Skeletal SKELETAL SYSTEM System • Functions: 1. Protection 2. Mineral storage and 3. Blood cell formation: involved in formation of blood cells (hematopoiesis or hemopoiesis) 4. Fat storage: in yellow bone marrow of 5. Movement: bones are sites for skeletal muscle attachment 6. Support: supports weight and provides BONE STRUCTURE CLASSIFICATION (based on shape) 1. Long bones - longer than they are wide; - include most bones in arms and legs 2. Short bones – roughly cube-shaped - include carpals and 62 3. Flat bones – thin and broad bones - ribs, pelvis, sternum and 4. Irregular bones – include and certain skull bones 5. Sesamoid bones – located within BONE STRUCTURE Structure of long bone: • Periosteum – membrane surrounds outer surface • Perforating fibers (Sharpey’s fibers) - anchors periosteum firmly to bone surface • Diaphysis – • Epiphysis - of long bone (proximal & distal) • Articular cartilage – hyaline cartilage • Marrow cavity – contains bone marrow (red or yellow) • Endosteum – thin membrane lining marrow cavity Compact bone - hard, dense outer region - allows bone to resist stresses (compression & twisting) • Spongy bone ( bone) - found inside cortical bone - honeycomb-like framework of bony struts; - resist forces from many directions • EpiphySeal lines – separates epiphyses from diaphysis - remnants of
    [Show full text]
  • Aandp1ch07lecture.Pdf
    Chapter 07 Lecture Outline See separate PowerPoint slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright © McGraw-Hill Education. Permission required for reproduction or display. 1 Introduction • In this chapter we will cover: – Bone tissue composition – How bone functions, develops, and grows – How bone metabolism is regulated and some of its disorders 7-2 Introduction • Bones and teeth are the most durable remains of a once-living body • Living skeleton is made of dynamic tissues, full of cells, permeated with nerves and blood vessels • Continually remodels itself and interacts with other organ systems of the body • Osteology is the study of bone 7-3 Tissues and Organs of the Skeletal System • Expected Learning Outcomes – Name the tissues and organs that compose the skeletal system. – State several functions of the skeletal system. – Distinguish between bones as a tissue and as an organ. – Describe the four types of bones classified by shape. – Describe the general features of a long bone and a flat bone. 7-4 Tissues and Organs of the Skeletal System • Skeletal system—composed of bones, cartilages, and ligaments – Cartilage—forerunner of most bones • Covers many joint surfaces of mature bone – Ligaments—hold bones together at joints – Tendons—attach muscle to bone 7-5 Functions of the Skeleton • Support—limb bones and vertebrae support body; jaw bones support teeth; some bones support viscera • Protection—of brain, spinal cord, heart, lungs, and more • Movement—limb movements, breathing, and other
    [Show full text]