DOCSLIB.ORG

Palaeopathology

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

This page intentionally left blank Palaeopathology Paleopathology is designed to help bone specialists with diagnosis of diseases in skeletal assemblages. It suggests an innovative method of arriving at a diagnosis in the skeleton by applying ‘operational definitions’. The aim is to ensure that all those who study bones will use the same criteria for diagnosing disease, which will enable valid comparisons to be made between studies. This book is based on modern clinical knowledge and provides background information so that readers understand the natural history of bone diseases, which will enable them to draw reliable conclusions from their observations. Details of bone metabolism and the fundamentals of basic pathology are also provided, as well as a comprehensive and up- to-date bibliography. A short chapter on epidemiology provides information on how best to analyze and present the results of a study of human remains. Professor Tony Waldron teaches paleopathology at the Institute of Archaeology, University College London. The author of about 300 peer-reviewed papers in medical, scientific and archaeology journals, as well as books on occupational medicine and paleoepidemiology, Waldron is co-founder of the International Journal of Osteoarchaeology and served as co- editor for its first decade. He is a Fellow of the Royal College of Physicians of London, the Royal Society of Medicine, the Institute of Biology and the Royal Anthropological Institute. Cambridge Manuals in Archaeology General Editor Graeme Barker, University of Cambridge Advisory Editors Elizabeth Slater, University of Liverpool Peter Bogucki, Princeton University Cambridge Manuals in Archaeology is a series of reference handbooks designed for an inter- national audience of upper-level undergraduate and graduate students and professional archaeologists and archaeological scientists in universities, museums, research laboratories and field units. Each book includes a survey of current archaeological practice alongside essential reference material on contemporary techniques and methodology. Books in the Series Pottery in Archaeology, CLIVE ORTON, PAUL TYRES and ALAN VINCE Vertebrate Taphonomy, R LEE LYMAN Photography in Archaeology and Conservation, 2nd edition, PETER G DORRELL Alluvial Geoarchaeology, A G BROWN Shells, CHERYL CLAASEN Sampling in Archaeology, CLIVE ORTON Excavation, STEVE ROSKAMS Teeth, 2nd edition, SIMON HILLSON Lithics, 2nd edition, WILLIAM ANDREFFSKY JR Geographical Information System in Archaeology, JAMES CONOLLY and MARK LAKE Demography in Archaeology, ANDREW CHAMBERLAIN Analytical Chemistry in Archaeology, A M POLLARD, C M BATT, B STERN and S M M YOUNG Zooarchaeology, 2nd edition, ELIZABETH J REITZ and ELIZABETH S WING Quantitative Paleozoology, R LEE LYMAN Palaeopathology Tony Waldron Institute of Archaeology, University College London CAMBRIDGE UNIVERSITY PRESS Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo Cambridge University Press The Edinburgh Building, Cambridge CB2 8RU, UK Published in the United States of America by Cambridge University Press, New York www.cambridge.org Information on this title: www.cambridge.org/9780521861373 © Tony Waldron 2009 This publication is in copyright. Subject to statutory exception and to the provision of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published in print format 2008 ISBN-13 978-0-511-43711-3 eBook (EBL) ISBN-13 978-0-521-86137-3 hardback Cambridge University Press has no responsibility for the persistence or accuracy of urls for external or third-party internet websites referred to in this publication, and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. CONTENTS List of Figures page xiii Preface xv 1. Introduction and Diagnosis 1 Diagnosis in Palaeopathology 2 Other Comparisons 7 A Note on Health . 9 . and Mummies 10 2. Bone Metabolism and Pathology 12 Types of Bone 12 The Bone Matrix 14 Bone Cells and Cytokines 14 Bone Mass 17 Remodelling 17 Bone Pathology 19 Pathology, Pseudopathology and Normal Variation 21 3. Diseases of Joints, Part 1 24 Osteoarthritis 26 Precipitants of Osteoarthritis 28 The Natural History of Osteoarthritis 30 Diagnosis of Osteoarthritis 33 Osteoarthritis at Individual Sites 34 The Association Between Osteoarthritis and Other Conditions 39 Rotator Cuff Disease and Intervertebral Disc Disease 40 Schmorl’s Nodes 45 viii contents 4. Diseases of Joints, Part 2 46 Rheumatoid Arthritis 46 The Natural History of Rheumatoid Arthritis 49 Sero-Negative Arthropathies 53 Erosive Osteoarthritis 53 The Spondyloarthritides 56 Ankylosing Spondylitis 57 Reiter’s Syndrome (Reactive Spondyloarthropathy) 60 Psoriatic Arthropathy 62 Enteropathic Arthropathy 65 Undifferentiated Spondyloarthritides 66 Juvenile Arthritis 66 Gout 67 Bunions 70 5. Bone forming and DISH 72 Bone Forming and Bone Formers 72 Diffuse Idiopathic Skeletal Hyperostosis (DISH) 73 Ossification in the Posterior Longitudinal Ligament 77 Hyperostosis Frontalis Interna 78 Heterotopic Ossification 79 Osteopetrosis 82 6. Infectious Diseases 83 Osteomyelitis 84 Special Forms of Osteomyelitis 87 Tuberculosis 90 Leprosy 97 Venereal Syphilis 102 The Origins of Syphilis 104 Changes in the Skeleton 105 Poliomyelitis 109 Smallpox 110 Fungal Infections of Bone 111 Parasitic Disease 111 Non-Specific Infections 113 7. Metabolic Diseases 118 Osteoporosis 118 Paget’s Disease of Bone (PDB) 122 contents ix Rickets and Osteomalacia 127 Osteomalacia 130 Scurvy 130 Other Metabolic Diseases 133 Thyroid Disease 134 Hyperparathyroidism 134 Diabetes 136 Anaemia 136 8. Trauma 138 Fractures and Dislocations 138 Fractures 141 Treatment of Fractures 142 Complications of Fractures 143 Healing of fractures 146 The Epidemiology of Fractures 148 Comments of the Aetiology of Some Fractures 151 Osteochondritis Dissecans (OCD) 153 Dislocations and Subluxations 155 Dislocation of the Shoulder 155 Wounding 156 Gunshot Wounds 157 Amputation 158 Trephination 161 The Autopsy 162 Legalised Trauma 165 Beheading 165 Hanging 165 9. Tumours 168 Epidemiology of Bone Tumours 168 The Diagnosis of Tumours in Human Remains 170 Benign Tumours 170 Tumours Arising from Bone 171 Tumours Arising from Cartilage 174 Malignant Tumours 177 Primary Malignant Bone Tumours 178 The Periosteal Response to Malignant Bone Tumours 178 Ewing’s Sarcoma 181 Metastatic Bone Tumours 184 Diagnosing Secondary Tumours 189 x contents 10. Disorders of Growth and Development 191 Normal Growth 191 Abnormal Growth and Development 195 Dwarfism 195 Pituitary Dwarfism 196 Turner’s Syndrome 197 Achondroplasia 197 Other Forms of Dwarfism 206 Gigantism 207 Disorders of Skull Growth 208 Cleft Palate 209 Developmental Disorders of the Hips 210 Fibrous Dysplasia 213 Kyphosis and Scoliosis 215 Klippel-Feil Syndrome 218 Other Spinal Anomalies 218 11. Soft Tissue Diseases 221 Cardio-Vascular Lesions 224 Neurological Lesions 227 Stones and Cysts 233 12. Dental Disease 236 Caries 236 Ante-Mortem Tooth Loss 238 Periodontal Disease 239 Dental Calculus 240 Periapical Cavities 241 Developmental Defects of Enamel 243 Ectopic Teeth and Morphological Variation 245 Dental Tumours 246 Dental Cysts 247 13. An Introduction to Epidemiology 249 Disease Frequency 249 Incidence 250 Prevalence 252 Outcome Variables 255 Missing Data 256 Overall Prevalence 257 contents xi Denominator-Free Methods 258 Ranking 258 Proportional Morbidity or Mortality Ratio 259 Analytical Epidemiology 261 Case-Control Studies in Palaeopathology 263 Planning a Study 264 ANoteaboutTeeth 265 Select Bibliography 267 Index 269 LIST OF FIGURES 2.1. Diagram to show different phases of bone remodelling. page 18 2.2. Diagram of remodelling unit. 19 3.1. Diagram of normal synovial joint. 26 3.2. Model of aetiology of osteoarthritis. 29 3.3. Secondary osteoarthritis of the hip. 30 3.4. Osteoarthritis of the patello-femoral compartment of the knee. 32 3.5. Osteoarthritis of the hip. 32 3.6. Cervical vertebrae (C3–C5) with disc disease. 44 4.1. Diagram to show relationship of the different joint diseases. 47 4.2. Model of aetiology of rheumatoid arthritis. 50 4.3. Rheumatoid arthritis of the elbow. 52 4.4. Radiograph of erosive osteoarthritis. 55 4.5. Ankylosing spondylitis. 57 4.6. Model to show aetiology of reactive arthritis. 62 4.7.Radiographofankle. 69 4.8. Simplified diagram to show the differentiation between the various forms of erosive arthropathy. 70 5.1. Thoracic spine of Giso. 74 5.2. Two large plaques of heterotopic bone. 80 6.1. Posterior view of left femur with osteomyelitis. 86 6.2. Thoracic spine with tuberculosis. 93 6.3. Frontal bone of skull affected with syphilis. 106 6.4. Left and right tibia and femur from a presumptive case of polio. 110 7.1. Model of aetiology of Paget’s disease of bone. 125 8.1. Healedfractureoftherightankle. 144 8.2. Fourth lumbar vertebra with spondylolysis. 152 xiv list of figures 8.3. Skull from Anglo-Saxon male showing healed wound. 156 8.4. Distal end of amputated femur from an eighteenth-century context. 160 8.5. Skeleton from late eighteenth or early nineteenth century. 164 9.1. Frontal bone showing the presence of a small button osteoma. 173 9.2. Skull of elderly female from eighteenth century context showing the presence of several holes. 186 10.1. Diagram to show four hypothetical cohorts of children. 194 10.2. Scheme for differentiating between the more common forms of dwarfism. 206 10.3. Diagram of a cross-section of the spine in scoliosis.
Recommended publications
  • Abstracts from the 9Th Biennial Scientific Meeting of The

    Abstracts from the 9Th Biennial Scientific Meeting of The

    International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):15 DOI 10.1186/s13633-017-0054-x MEETING ABSTRACTS Open Access Abstracts from the 9th Biennial Scientific Meeting of the Asia Pacific Paediatric Endocrine Society (APPES) and the 50th Annual Meeting of the Japanese Society for Pediatric Endocrinology (JSPE) Tokyo, Japan. 17-20 November 2016 Published: 28 Dec 2017 PS1 Heritable forms of primary bone fragility in children typically lead to Fat fate and disease - from science to global policy a clinical diagnosis of either osteogenesis imperfecta (OI) or juvenile Peter Gluckman osteoporosis (JO). OI is usually caused by dominant mutations affect- Office of Chief Science Advsor to the Prime Minister ing one of the two genes that code for two collagen type I, but a re- International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):PS1 cessive form of OI is present in 5-10% of individuals with a clinical diagnosis of OI. Most of the involved genes code for proteins that Attempts to deal with the obesity epidemic based solely on adult be- play a role in the processing of collagen type I protein (BMP1, havioural change have been rather disappointing. Indeed the evidence CREB3L1, CRTAP, LEPRE1, P4HB, PPIB, FKBP10, PLOD2, SERPINF1, that biological, developmental and contextual factors are operating SERPINH1, SEC24D, SPARC, from the earliest stages in development and indeed across generations TMEM38B), or interfere with osteoblast function (SP7, WNT1). Specific is compelling. The marked individual differences in the sensitivity to the phenotypes are caused by mutations in SERPINF1 (recessive OI type obesogenic environment need to be understood at both the individual VI), P4HB (Cole-Carpenter syndrome) and SEC24D (‘Cole-Carpenter and population level.
  • Program Nr: 1 from the 2004 ASHG Annual Meeting Mutations in A

    Program Nr: 1 from the 2004 ASHG Annual Meeting Mutations in A

    Program Nr: 1 from the 2004 ASHG Annual Meeting Mutations in a novel member of the chromodomain gene family cause CHARGE syndrome. L.E.L.M. Vissers1, C.M.A. van Ravenswaaij1, R. Admiraal2, J.A. Hurst3, B.B.A. de Vries1, I.M. Janssen1, W.A. van der Vliet1, E.H.L.P.G. Huys1, P.J. de Jong4, B.C.J. Hamel1, E.F.P.M. Schoenmakers1, H.G. Brunner1, A. Geurts van Kessel1, J.A. Veltman1. 1) Dept Human Genetics, UMC Nijmegen, Nijmegen, Netherlands; 2) Dept Otorhinolaryngology, UMC Nijmegen, Nijmegen, Netherlands; 3) Dept Clinical Genetics, The Churchill Hospital, Oxford, United Kingdom; 4) Children's Hospital Oakland Research Institute, BACPAC Resources, Oakland, CA. CHARGE association denotes the non-random occurrence of ocular coloboma, heart defects, choanal atresia, retarded growth and development, genital hypoplasia, ear anomalies and deafness (OMIM #214800). Almost all patients with CHARGE association are sporadic and its cause was unknown. We and others hypothesized that CHARGE association is due to a genomic microdeletion or to a mutation in a gene affecting early embryonic development. In this study array- based comparative genomic hybridization (array CGH) was used to screen patients with CHARGE association for submicroscopic DNA copy number alterations. De novo overlapping microdeletions in 8q12 were identified in two patients on a genome-wide 1 Mb resolution BAC array. A 2.3 Mb region of deletion overlap was defined using a tiling resolution chromosome 8 microarray. Sequence analysis of genes residing within this critical region revealed mutations in the CHD7 gene in 10 of the 17 CHARGE patients without microdeletions, including 7 heterozygous stop-codon mutations.
  • Bioarchaeology (Anthropological Archaeology) - Mario ŠLAUS

    Bioarchaeology (Anthropological Archaeology) - Mario ŠLAUS

    PHYSICAL (BIOLOGICAL) ANTHROPOLOGY - Bioarchaeology (Anthropological Archaeology) - Mario ŠLAUS BIOARCHAEOLOGY (ANTHROPOLOGICAL ARCHAEOLOGY) Mario ŠLAUS Department of Archaeology, Croatian Academy of Sciences and Arts, Zagreb, Croatia. Keywords: Bioarchaeology, archaeological, forensic, antemortem, post-mortem, perimortem, traumas, Cribra orbitalia, Harris lines, Tuberculosis, Leprosy, Treponematosis, Trauma analysis, Accidental trauma, Intentional trauma, Osteological, Degenerative disease, Habitual activities, Osteoarthritis, Schmorl’s nodes, Tooth wear Contents 1. Introduction 1.1. Definition of Bioarchaeology 1.2. History of Bioarchaeology 2. Analysis of Skeletal Remains 2.1. Excavation and Recovery 2.2. Human / Non-Human Remains 2.3. Archaeological / Forensic Remains 2.4. Differentiating between Antemortem/Postmortem/Perimortem Traumas 2.5. Determination of Sex 2.6. Determination of Age at Death 2.6.1. Age Determination in Subadults 2.6.2. Age Determination in Adults. 3. Skeletal and dental markers of stress 3.1. Linear Enamel Hypoplasia 3.2. Cribra Orbitalia 3.3. Harris Lines 4. Analyses of dental remains 4.1. Caries 4.2. Alveolar Bone Disease and Antemortem Tooth Loss 5. Infectious disease 5.1. Non–specific Infectious Diseases 5.2. Specific Infectious Disease 5.2.1. Tuberculosis 5.2.2. Leprosy 5.2.3. TreponematosisUNESCO – EOLSS 6. Trauma analysis 6.1. Accidental SAMPLETrauma CHAPTERS 6.2. Intentional Trauma 7. Osteological and dental evidence of degenerative disease and habitual activities 7.1. Osteoarthritis 7.2. Schmorl’s Nodes 7.3. Tooth Wear Caused by Habitual Activities 8. Conclusion Glossary Bibliography Biographical Sketch ©Encyclopedia of Life Support Systems (EOLSS) PHYSICAL (BIOLOGICAL) ANTHROPOLOGY - Bioarchaeology (Anthropological Archaeology) - Mario ŠLAUS 1. Introduction 1.1. Definition of Bioarchaeology Bioarchaeology is the study of human biological remains within their cultural (archaeological) context.
  • Absolute Risk, 252 Acetabular Dysplasia, 38, 211, 213 Acetabular Protrusion, 38 Achondroplasia, 195, 197, 199–200, 205 Genetic

    Absolute Risk, 252 Acetabular Dysplasia, 38, 211, 213 Acetabular Protrusion, 38 Achondroplasia, 195, 197, 199–200, 205 Genetic

    Cambridge University Press 978-0-521-86137-3 - Palaeopathology Tony Waldron Index More information Index absolute risk, 252 angular kyphosis acetabular dysplasia, 38, 211, 213 in Scheuermann’s disease, 45 acetabular protrusion, 38 in tuberculosis, 93–4 achondroplasia, 195, 197, 199–200, 205 ankylosing spondylitis, 57–60, 65 genetic defect in, 199 ankylosis in, 58 skeletal changes in, 200 bamboo spine in, 59 acoustic neuroma, 229–31 erosions in, 59 acromegaly, 78, 207–8 first description, 57 and DISH, 208 HLA B27 58 and, skeletal changes in, 208 operational definition of, 59 acromelia, 198 prevalence of, 58 aDNA sacroiliitis and, 59 in leprosy, 101 skip lesions in, 59 in syphilis, 108 ankylosis, 51 in tuberculosis, 92, 95–6 following fracture, 146 Albers-Schonberg˝ disease, see in ankylosing spondylitis, 58 osteopetrosis in brucellosis, 96 Alstrom syndrome, 78 in DISH, 73 alveolar margin, see periodontal disease in erosive osteoarthritis, 55 amputation, 158–61 in rheumatoid arthritis, 51 indications for, 160–1 in septic arthritis, 89 ancient DNA, see aDNA in tuberculosis, 93–4 anaemia, 136–7 annulus fibrosus, 42–3, 45 cribra obitalia and, 136–7 ante-mortem tooth loss, 238–9 aneurysms, 224–7 and periodontal disease, 238–9 aortic, 224–5 and scurvy, 132 and syphilis, 224 causes of, 238 of vertebral artery, 225–6 anterior longitudinal ligament popliteal, 226 in ankylosing spondylitis, 59 aneurysmal bone cyst, 177 in DISH, 73 angiosarcoma, 182 anti-CCP antibodies, 49, 53 © Cambridge University Press www.cambridge.org Cambridge University Press
  • Fall Quarter 2018 Class Schedule

    Fall Quarter 2018 Class Schedule

    FALL QUARTER 2018 CLASS SCHEDULE COURSE NUMBER COURSE TITLE SPECIAL TOPIC (IF APPLICABLE) INSTRUCTOR Core Course Archaeology M201A Graduate Core Seminar Monica Smith Archaeology C220 Archaeology of Death John Papadopoulos Anthropology 219 Selected Topics in Anthropological/Archaeological Theory Issues in Indigenous Archaeology Stephen Acabado Ancient Near East 260 Seminar: Ancient Near Eastern Archaeology Elizabeth Carter Ancient Near East 261 Practical Field Archaeology Archaeological Fieldwork (Ethiopia) Willeke Wendrich Graduate Art and Architecture of Ancient Egypt, Predynastic Period to Ancient Near East C267A Kara Cooney Seminars New Kingdom Art History C216A Middle Byzantine Art & Architecture Sharon Gerstel Art History C248A Art and Material Culture, Neolithic to 210 B.C. Art & Material Culture of Early China Lothar von Falkenhausen Art History C249A Selected Topics in Chinese Art Lothar von Falkenhausen Classics 245 Computing and Classics Chris Johanson Classics 250 Topics in Greek and Roman Culture and Literature Women's History Amy Richlin Archaeology M205A Selected Laboratory Topics in Archaeology Experimental Archaeology Tom Wake Conservation M210L Cultural Materials Science Laboratory: Technical Study Ioanna Kakoulli Conservation 231 Conservation Laboratory: Stone and Adobe Christian Fischer Conservation 238 Conservation Laboratory: Organic Materials II Ellen Pearlstein Lab Courses Conservation Laboratory: Rock Art, Wall Paintings, and Conservation M250 Ioanna Kakoulli Mosaics Structure, Properties, and Deterioration of
  • Metabolic Bone Disease 5

    Metabolic Bone Disease 5

    g Metabolic Bone Disease 5 Introduction, 272 History and examination, 275 Osteoporosis, 283 STRUCTURE AND FUNCTION, 272 Investigation, 276 Paget’s disease of bone, 288 Structure of bone, 272 Management, 279 Hyperparathyroidism, 290 Function of bone, 272 DISEASES AND THEIR MANAGEMENT, 280 Hypercalcaemia of malignancy, 293 APPROACH TO THE PATIENT, 275 Rickets and osteomalacia, 280 Hypocalcaemia, 295 Introduction Calcium- and phosphate-containing crystals: set in a structure• similar to hydroxyapatite and deposited in holes Metabolic bone diseases are a heterogeneous group of between adjacent collagen fibrils, which provide rigidity. disorders characterized by abnormalities in calcium At least 11 non-collagenous matrix proteins (e.g. osteo- metabolism and/or bone cell physiology. They lead to an calcin,• osteonectin): these form the ground substance altered serum calcium concentration and/or skeletal fail- and include glycoproteins and proteoglycans. Their exact ure. The most common type of metabolic bone disease in function is not yet defined, but they are thought to be developed countries is osteoporosis. Because osteoporosis involved in calcification. is essentially a disease of the elderly, the prevalence of this condition is increasing as the average age of people Cellular constituents in developed countries rises. Osteoporotic fractures may lead to loss of independence in the elderly and is imposing Mesenchymal-derived osteoblast lineage: consist of an ever-increasing social and economic burden on society. osteoblasts,• osteocytes and bone-lining cells. Osteoblasts Other pathological processes that affect the skeleton, some synthesize organic matrix in the production of new bone. of which are also relatively common, are summarized in Osteoclasts: derived from haemopoietic precursors, Table 3.20 (see Chapter 4).
  • The Global History of Paleopathology

    The Global History of Paleopathology

    OUP UNCORRECTED PROOF – FIRST-PROOF, 01/31/12, NEWGEN TH E GLOBA L H ISTORY OF PALEOPATHOLOGY 000_JaneBuikstra_FM.indd0_JaneBuikstra_FM.indd i 11/31/2012/31/2012 44:03:58:03:58 PPMM OUP UNCORRECTED PROOF – FIRST-PROOF, 01/31/12, NEWGEN 000_JaneBuikstra_FM.indd0_JaneBuikstra_FM.indd iiii 11/31/2012/31/2012 44:03:59:03:59 PPMM OUP UNCORRECTED PROOF – FIRST-PROOF, 01/31/12, NEWGEN TH E GLOBA L H ISTORY OF PALEOPATHOLOGY Pioneers and Prospects EDITED BY JANE E. BUIKSTRA AND CHARLOTTE A. ROBERTS 3 000_JaneBuikstra_FM.indd0_JaneBuikstra_FM.indd iiiiii 11/31/2012/31/2012 44:03:59:03:59 PPMM OUP UNCORRECTED PROOF – FIRST-PROOF, 01/31/12, NEWGEN 1 Oxford University Press Oxford University Press, Inc., publishes works that further Oxford University’s objective of excellence in research, scholarship, and education. Oxford New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With o! ces in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland " ailand Turkey Ukraine Vietnam Copyright © #$%# by Oxford University Press, Inc. Published by Oxford University Press, Inc. %&' Madison Avenue, New York, New York %$$%( www.oup.com Oxford is a registered trademark of Oxford University Press All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Oxford University Press. CIP to come ISBN-%): ISBN $–%&- % ) * + & ' ( , # Printed in the United States of America on acid-free paper 000_JaneBuikstra_FM.indd0_JaneBuikstra_FM.indd iivv 11/31/2012/31/2012 44:03:59:03:59 PPMM OUP UNCORRECTED PROOF – FIRST-PROOF, 01/31/12, NEWGEN To J.
  • A Case of Osteitis Fibrosa Cystica (Osteomalacia?) with Evidence of Hyperactivity of the Para-Thyroid Bodies

    A Case of Osteitis Fibrosa Cystica (Osteomalacia?) with Evidence of Hyperactivity of the Para-Thyroid Bodies

    A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA-THYROID BODIES. METABOLIC STUDY II Walter Bauer, … , Fuller Albright, Joseph C. Aub J Clin Invest. 1930;8(2):229-248. https://doi.org/10.1172/JCI100262. Research Article Find the latest version: https://jci.me/100262/pdf A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA- THYROID BODIES. METABOLIC STUDY IIF By WALTER BAUER,2 FULLER ALBRIGHT3 AND JOSEPH C. AUB (From the Medical Clinic of the Massachutsetts General Hospital, Boston) (Received for publication February 5, 1929) INTRODUCTION In a previous paper (1) we have pointed out certain characteristic responses in the calcium and phosphorus metabolisms resulting from parathormone4 administration to essentially normal individuals. In the present paper, similar studies will be reported on a patient who presented a condition suggestive of idiopathic hyperparathyroidism. CASE HISTORY The patient, Mr. C. M., sea captain, aged 30, was transferred from the Bellevue Hospital Service to the Special Study Ward of the Massachusetts General Hospital through the courtesy of Dr. Eugene F. DuBois, for further investigation of his calcium metabolism and for consideration of parathyroidectomy. His complete case history has been reported by Hannon, Shorr, McClellan and DuBois (2). It describes a man invalided for over three years with symptoms resulting from a generalized skeletal decalcification. (See x-rays, figs. 1 to 4.) 1 This is No. VII of the series entitled "Studies of Calcium and Phosphorus Metabolism" from the Medical Clinic of the Massachusetts General Hospital. 2 Resident Physician, Massachusetts General Hospital. ' Research Fellow, Massachusetts General Hospital and Harvard Medical School.
  • Paleopathological Analysis of a Sub-Adult Allosaurus Fragilis (MOR

    Paleopathological Analysis of a Sub-Adult Allosaurus Fragilis (MOR

    Paleopathological analysis of a sub-adult Allosaurus fragilis (MOR 693) from the Upper Jurassic Morrison Formation with multiple injuries and infections by Rebecca Rochelle Laws A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in Earth Sciences Montana State University © Copyright by Rebecca Rochelle Laws (1996) Abstract: A sub-adult Allosaurus fragilis (Museum of the Rockies specimen number 693 or MOR 693; "Big Al") with nineteen abnormal skeletal elements was discovered in 1991 in the Upper Jurassic Morrison Formation in Big Horn County, Wyoming at what became known as the "Big Al" site. This site is 300 meters northeast of the Howe Quarry, excavated in 1934 by Barnum Brown. The opisthotonic position of the allosaur indicated that rigor mortis occurred before burial. Although the skeleton was found within a fluvially-deposited sandstone, the presence of mud chips in the sandstone matrix and virtual completeness of the skeleton showed that the skeleton was not transported very far, if at all. The specific goals of this study are to: 1) provide a complete description and analysis of the abnormal bones of the sub-adult, male, A. fragilis, 2) develop a better understanding of how the bones of this allosaur reacted to infection and trauma, and 3) contribute to the pathological bone database so that future comparative studies are possible, and the hypothesis that certain abnormalities characterize taxa may be evaluated. The morphology of each of the 19 abnormal bones is described and each disfigurement is classified as to its cause: 5 trauma-induced; 2 infection-induced; 1 trauma- and infection-induced; 4 trauma-induced or aberrant, specific origin unknown; 4 aberrant; and 3 aberrant, specific origin unknown.
  • WHO Manual of Diagnostic Imaging Radiographic Anatomy and Interpretation of the Musculoskeletal System

    WHO Manual of Diagnostic Imaging Radiographic Anatomy and Interpretation of the Musculoskeletal System

    The WHO manual of diagnostic imaging Radiographic Anatomy and Interpretation of the Musculoskeletal System Editors Harald Ostensen M.D. Holger Pettersson M.D. Authors A. Mark Davies M.D. Holger Pettersson M.D. In collaboration with F. Arredondo M.D., M.R. El Meligi M.D., R. Guenther M.D., G.K. Ikundu M.D., L. Leong M.D., P. Palmer M.D., P. Scally M.D. Published by the World Health Organization in collaboration with the International Society of Radiology WHO Library Cataloguing-in-Publication Data Davies, A. Mark Radiography of the musculoskeletal system / authors : A. Mark Davies, Holger Pettersson; in collaboration with F. Arredondo . [et al.] WHO manuals of diagnostic imaging / editors : Harald Ostensen, Holger Pettersson; vol. 2 Published by the World Health Organization in collaboration with the International Society of Radiology 1.Musculoskeletal system – radiography 2.Musculoskeletal diseases – radiography 3.Musculoskeletal abnormalities – radiography 4.Manuals I.Pettersson, Holger II.Arredondo, F. III.Series editor: Ostensen, Harald ISBN 92 4 154555 0 (NLM Classification: WE 141) The World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full. Applications and enquiries should be addressed to the Office of Publications, World Health Organization, CH-1211 Geneva 27, Switzerland, which will be glad to provide the latest information on any changes made to the text, plans for new editions, and reprints and translations already available. © World Health Organization 2002 Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved.
  • Effect of the Combination of Ipriflavone and 1

    Effect of the Combination of Ipriflavone and 1

    PEDIATRIC DENTAL JOURNAL 14(1): 5–15, 2004 5 Effect of the combination of ipriflavone and 1␣-OH-D3 on debilitant bone in growing rats —Ultrastructural study of endochondral ossification— Kazushige Ueda, Ikuko Nishida, Bin Xia, Iwan Tofani, Jianguo Wang, Yasuhiro Nishikawa and Mitsutaka Kimura Department of Pediatric Dentistry, Kyushu Dental College 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu City, Fukuoka 803-8580, JAPAN Abstract Five-week-old male Wistar rats were used to study the effect of Key words dietary therapy with ipriflavone combined with 1␣-OH-D3. Ultrastructural alter- 1␣-OH-D3, ations in the metaphysis of debilitated tibia were observed in the growing rats. Growing rats, I. Light microscopy findings Ipriflavone, In the low-calcium diet • standard diet with supplementary ipriflavone and Metaphysis tibia 1␣-OH-D3 group, calcification of the chondral matrix and ossification were active, and the tibia grew normally as in the control group. II. Scanning electron microscopy findings In the low-calcium diet • standard diet with supplementary ipriflavone and 1␣-OH-D3 group, dense calcospherites, distinct chondral lacunae, regularly running collagen fibers, and distinct border lines were noted. III. Transmission electron microscopy findings In the low-calcium diet • standard diet with supplementary ipriflavone and 1␣-OH-D3 group we found that the osteoblasts were active, the ruffled border of osteoclast was decrease, indicated this osteoclast is inactive. In conclusion, insufficient calcium intake during the developmental period resulted in debilitated(3etaphysis tibia, whereas dietary therapy using combined ipriflavone and 1␣-OH-D3 promoted recovery. Introduction patients become refractory after several days of administration, which is known as the calcitonin Recently dietary therapies, physiologic active sub- escape phenomenon, therefore, it is not considered stances, exercise, and/or bone resorption inhibitors a suitable therapy for osteoporosis3).
  • The Geoarchaeology of Mound Key, an Anthropogenic Island in Southwest Florida, USA

    The Geoarchaeology of Mound Key, an Anthropogenic Island in Southwest Florida, USA

    RESEARCH ARTICLE From Shell Midden to Midden-Mound: The Geoarchaeology of Mound Key, an Anthropogenic Island in Southwest Florida, USA Victor D. Thompson1☯*, William H. Marquardt2☯, Alexander Cherkinsky3‡, Amanda D. Roberts Thompson4‡, Karen J. Walker2‡, Lee A. Newsom5‡, Michael Savarese6‡ 1 Center for Archaeological Sciences and Department of Anthropology, University of Georgia, Athens, Georgia, United States of America, 2 Florida Museum of Natural History, University of Florida, Gainesville, a11111 Florida, United States of America, 3 Center for Applied Isotope Studies, University of Georgia, Athens, Georgia, United States of America, 4 Laboratory of Archaeology, University of Georgia, Athens, Georgia, United States of America, 5 Department of Anthropology, Pennsylvania State University, State College, Pennsylvania, United States of America, 6 Department of Marine and Ecological Science, Florida Gulf Coast University, Ft. Myers, Florida, United States of America ☯ These authors contributed equally to this work. ‡ These authors also contributed equally to this work. * [email protected] OPEN ACCESS Citation: Thompson VD, Marquardt WH, Cherkinsky A, Roberts Thompson AD, Walker KJ, Newsom LA, et al. (2016) From Shell Midden to Midden-Mound: Abstract The Geoarchaeology of Mound Key, an Mound Key was once the capital of the Calusa Kingdom, a large Pre-Hispanic polity that Anthropogenic Island in Southwest Florida, USA. PLoS ONE 11(4): e0154611. doi:10.1371/journal. controlled much of southern Florida. Mound Key, like other archaeological sites along the pone.0154611 southwest Gulf Coast, is a large expanse of shell and other anthropogenic sediments. The Editor: Karen Hardy, ICREA at the Universitat challenges that these sites pose are largely due to the size and areal extent of the deposits, Autònoma de Barcelona, SPAIN some of which begin up to a meter below and exceed nine meters above modern sea levels.