Avascular Necrosis of Trochlea After Supracondylar Humerus Fractures in Children
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Investigating the Genetic and Genomic Basis of Osteochondrosis in Thoroughbred Horses from Australia and New Zealand
Investigating the genetic and genomic basis of osteochondrosis in Thoroughbred horses from Australia and New Zealand Kao Castle The University of Sydney A thesis submitted to the Faculty of Veterinary Science, The University of Sydney, in fulfilment of the requirements for the Degree of Doctor of Philosophy December 2012 i Declaration I declare that the work presented in this thesis is, to the best of my knowledge and belief, original, except as acknowledged in the text, and that the material has not been submitted, either in whole or in part, for a degree at this or any other university. (Kao Castle) 17 December 2012 ii Statement of Contributions The identities of the studs and horses that participated in the research described in this thesis are protected by confidentiality agreements. On this basis, the names of stud staff and veterinarians who provided data for this research are not listed as authors or named in the acknowledgements, although their input was invaluable. Chapter 2, Skeletal lesions and injuries in Australasian Thoroughbred weanling and yearling radiographs (draft manuscript). Castle K., Tammen I., Thomson P.C., Jeffcott L.B., Raadsma H.W. and Nicholas F.W. • Dr Tammen supervised components of this work, contributed to discussions, and provided feedback on the presentation of results. • Associate Professor Thomson provided advice on statistical techniques to compare results between the weanling and yearling populations, and provided feedback on the presentation of results. • Professors Jeffcott and Raadsma contributed to planning the data collection strategy, and provided feedback on the presentation of results. • Emeritus Professor Nicholas supervised components of this work, contributed to discussions and provided extensive feedback on the presentation of the results, and edited the manuscript. -
Upper Jaw Chronic Osteomyelitis. Report of Four Clinical Cases Osteomielitis Crónica Maxilar
www.medigraphic.org.mx Revista Odontológica Mexicana Facultad de Odontología Vol. 16, No. 2 April-June 2012 pp 105-111 CASE REPORT Upper jaw chronic osteomyelitis. Report of four clinical cases Osteomielitis crónica maxilar. Informe de 4 casos clínicos Alberto Wintergerst Fish,* Carlos Javier Iturralde Espinosa,§ Vladimir de la Riva Parra,II Santiago Reinoso QuezadaII ABSTRACT RESUMEN Osteomyelitis is an infl ammatory bone disease commonly related La osteomielitis es una enfermedad ósea infl amatoria, comúnmente to an infectious origin caused by germs, mainly pyogenic staphy- relacionada a un origen infeccioso por gérmenes piógenos funda- lococcus, and occasionally, streptococci, pneumococci and en- mentalmente estafi lococos y en algunas ocasiones por estreptoco- terobacteriae. Several treatments and classifi cations for osteomy- cos, neumococos y enterobacterias. Se han establecido diversas elitis have been established. These are based on clinical course, clasifi caciones y tratamientos para la osteomielitis, basadas en el pathologic-anatomical or radiologic features, etiology and patho- comportamiento clínico, características anatomo-patológicas, ra- genesis. Chronic osteomyelitis is a complication of non-treated or diográfi cas, etiología y patogenia. La osteomielitis crónica es una inadequately treated acute osteomyleitis. It can also be caused by a complicación de la osteomielitis aguda no tratada, manejada inade- low grade prolonged infl ammatory reaction. This study presents four cuadamente o como una reacción infl amatoria prolongada de bajo cases of maxillary osteomyelitis treated between 2007 and 2009. grado. Se presentan 4 casos de osteomielitis crónica en el maxilar Cases were treated with antimicrobial therapy. Preoperatively, pa- tratadas entre 2007 y 2009 mediante terapia antimicrobiana preo- tients were prescribed Clindamycin, 300 mg every eight hours, Ce- peratoriamente con clindamicina 300 mg, IV cada 8 h y ceftriaxona friaxone, 1 g IV every 12 hours. -
Osteomalacia and Osteoporosis D
Postgrad. med.J. (August 1968) 44, 621-625. Postgrad Med J: first published as 10.1136/pgmj.44.514.621 on 1 August 1968. Downloaded from Osteomalacia and osteoporosis D. B. MORGAN Department of Clinical Investigation, University ofLeeds OSTEOMALACIA and osteoporosis are still some- in osteomalacia is an increase in the alkaline times confused because both diseases lead to a phosphatase activity in the blood (SAP); there deficiency of calcium which can be detected on may also be a low serum phosphorus or a low radiographs of the skeleton. serum calcium. This lack of calcium is the only feature Our experience with the biopsy of bone is that common to the two diseases which are in all a large excess of uncalcified bone tissue (osteoid), other ways easily distinguishable. which is the classic histological feature of osteo- malacia, is only found in patients with the other Osteomalacia typical features of the disease, in particular the Osteomalacia will be discussed first, because it clinical ones (Morgan et al., 1967a). Whether or is a clearly defined disease which can be cured. not more subtle histological techniques will detect Osteomalacia is the result of an imbalance be- earlier stages of the disease remains to be seen. tween the supply of and the demand for vitamin Bone pains, muscle weakness, Looser's zones, D. The the following description of disease is raised SAP and low serum phosphate are the Protected by copyright. based on our experience of twenty-two patients most reliable aids to the diagnosis of osteomalacia, with osteomalacia after gastrectomy; there is no and approximately in that order. -
Osteochondrosis and Arthrosis in Pigs Ii
Acta vet. scand, 1974, 15, 26-42. From the Department of Pathology, Veterinary College of Norway, Oslo. OSTEOCHONDROSIS AND ARTHROSIS IN PIGS II. INCIDENCE IN BREEDING ANIMALS By Trygve Grendalen GR0NDALEN, TRYGVE: Osteochondrosis and arthrosis in pigs. 11. Incidence in breeding animals. Acta vet. scand. 1974, 15, 26-42. - Joint and bone lesions in breeding pigs are described on the background of an investdgatlon involving 174 sows and 155 boars from 7 months to 4% years old . Lesions, which consisted pre dominantly of arthrosis, degeneration of intervertebral discs, spon dylosis and epiphyseal separations, were demonstrated frequently in both sexes. Osteochondrosis, a condition previously demonstrated frequently in slaughter pigs, had either completely healed, undergone repair or developed into an arthrosis by the time the animal reached an age of about 1% years. Whereas a higher incidence of arthrosis of the intervertebral joints was found in boars than in sows, the reverse was true as regards degeneration of the intervertebral discs and anchylosing spondylosis. Possible reasons for this are discussed. Norwegian pigs show a higher incidence of lesions in the lumbar region of the vertebral column than has been described up to the present time in other countries. os teo c h 0 n d r 0 sis; art h r 0 sis; pig. A high incidence of osteochondrosis in joints and epiphyseal plates, and arthrosis, especially in the lumbar intervertebral joints, the distomedial hock joints, the elbow and stifle joint in pigs up to 120 kg live weight has been previously described (Grpndalen 1974). A review of the literature showed that osteo chondrosisand archrosis are widespread in pigs in various coun tries. -
Osteopetrosis J
Arch Dis Child: first published as 10.1136/adc.46.247.257 on 1 June 1971. Downloaded from Archives of Disease in Childhood, 1971, 46, 257. Osteopetrosis J. S. YU,* R. K. OATES, K. HELEN WALSH, and SUSAN J. STUCKEY From the Department of Child Health, University of Sydney, and Department of Dietetics, Royal Alexandra Hospital for Children, Camperdown, N.S.W., Australia Yu, J. S., Oates, R. K., Walsh, K. H., and Stuckey, S. J. (1971). Archives of Disease in Childhood, 46, 257. Osteopetrosis. The clinical histories of nine children with osteopetrosis are reported. Two of them had the malignant infantile variety of the disease: one died within 3 months of birth and the other has survived 20 months on a regimen of a low calcium intake, cellulose phosphate, and steroids. The beneficial effect of a low calcium intake, in early infancy, is supported by the clinical course in the infant with the malignant variety and in another child with the more benign form of the disease. No calcium balance studies were performed. This study suggests that the active measures outlined may favourably influence the haematological and osteosclerotic course of the disease, pending further know- ledge of its aetiological basis, and more specific therapy. Osteopetrosis or marble bone disease is a rare positive calcium balance with a diet low in calcium metabolic bone disease characterized by dense and with steroids (Morrow et al., 1967). This bones (Albers-Schonberg, 1904; Karshner, 1926). approach to management has been recently criti- copyright. Two varieties have been clearly defined-an cized by Cohen (Children's Hospital Medical infantile progressive disease and a milder benign Center, Boston, 1965). -
Hematological Diseases and Osteoporosis
International Journal of Molecular Sciences Review Hematological Diseases and Osteoporosis , Agostino Gaudio * y , Anastasia Xourafa, Rosario Rapisarda, Luca Zanoli , Salvatore Santo Signorelli and Pietro Castellino Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy; [email protected] (A.X.); [email protected] (R.R.); [email protected] (L.Z.); [email protected] (S.S.S.); [email protected] (P.C.) * Correspondence: [email protected]; Tel.: +39-095-3781842; Fax: +39-095-378-2376 Current address: UO di Medicina Interna, Policlinico “G. Rodolico”, Via S. Sofia 78, 95123 Catania, Italy. y Received: 29 April 2020; Accepted: 14 May 2020; Published: 16 May 2020 Abstract: Secondary osteoporosis is a common clinical problem faced by bone specialists, with a higher frequency in men than in women. One of several causes of secondary osteoporosis is hematological disease. There are numerous hematological diseases that can have a deleterious impact on bone health. In the literature, there is an abundance of evidence of bone involvement in patients affected by multiple myeloma, systemic mastocytosis, thalassemia, and hemophilia; some skeletal disorders are also reported in sickle cell disease. Recently, monoclonal gammopathy of undetermined significance appears to increase fracture risk, predominantly in male subjects. The pathogenetic mechanisms responsible for these bone loss effects have not yet been completely clarified. Many soluble factors, in particular cytokines that regulate bone metabolism, appear to play an important role. An integrated approach to these hematological diseases, with the help of a bone specialist, could reduce the bone fracture rate and improve the quality of life of these patients. -
Osteochondrosis – Primary Epiphyseal (Articular/Subchondral) Lesion Can Heal Or Can Progress
60 120 180 1 distal humeral condyles 2 medial epicondyle 3 proximal radial epiphysis 4 anconeal process Lab Ret study N=1018 . Normal . Affected . Total 688 (67.6%) . Total 330 (32.4%) . Male 230 (62.2%) . Male 140 (37.8%) . Female 458 (70.7%) . Female 190 (29.3%) Affected dogs N=330 1affected site - 250 (75.7%) 2 affected sites - 68 (20.6%) 3 affected sites - 12 (3.6%) immature skeletal diseases denis novak technique for skeletal radiography tissue < 12 cm “non-grid” (“table-top”) technique “high detail” system radiation safety diagnosis X – rays examination Ultrasound CT bilateral lesions - clinical signs ? unilateral present > one type of lesion 2ry arthrosis Common Osteochondrosis – primary epiphyseal (articular/subchondral) lesion can heal or can progress Osteochondritis dissecans – free articular fragment will progress Arthrosis Osteochondrosis talus / tarsus Lumbosacral OCD Lumbosacral OCD Inflammatory diseases Panosteitis – non infectious Hypertrophic osteodystrophy (HOD) – perhaps infectious Osteomyelitis - infectious Panosteitis New medullary bone Polyostotic Multiple lesions in one bone Symmetrical or nonsymmetrical Sclerotic pattern B I L A T E R A L periosteal new bone forms with chronicity Cross sections of a tibia different locations Hypertrophic osteodystrophy (HOD) Dogs are systemically ill, febrile, anorectic, reluctant to walk most will recover Radiographic changes of HOD . Polyostotic . Metaphyseal . Symmetrical . Changes of lesion Early Mid Late lytic “plates” in acute case HOD - 4 m ret – lesions are present -
Spontaneous Healing of Osteitis Fibrosa Cystica in Primary Hyperparathyroidism
754 Gibbs, Millar, Smith Postgrad Med J: first published as 10.1136/pgmj.72.854.754 on 1 December 1996. Downloaded from Spontaneous healing of osteitis fibrosa cystica in primary hyperparathyroidism CJ Gibbs, JGB Millar, J Smith Summar biochemistry showed hypercalcaemia, hypo- A 24-year-old man with primary hyper- phosphataemia, elevated parathyroid hormone, parathyroidism and osteitis fibrosa cystica but normal alkaline phosphatase (table). developed acute hypocalcaemia. Sponta- Radiographs showed improvement in the neous healing of his bone disease was mandibular translucency and resolution of the confirmed radiographically and by correc- phalangeal tuft resorption and subperiosteal tion of the serum alkaline phosphatase. erosion (figures 1B, 2B). Thallium scan of the Hypercalcaemia associated with a raised neck showed no evidence of parathyroid serum parathyroid hormone recurred 90 activity and neck exploration failed to reveal weeks after the initial presentation. Dur- any parathyroid tissue. Venous sampling ing the fourth neck exploration a para- showed no step-up in parathyroid hormone thyroid adenoma was removed, resulting concentration in the neck or chest. Selective in resolution of his condition. Haemor- angiography suggested a parathyroid adenoma rhagic infarction of an adenoma was the behind the right clavicle but two further most likely cause of the acute hypocalcae- explorations revealed only one normal para- mic episode. thyroid gland. Computed tomography (CT) of the neck showed a low attenuation, non- Keywords: primary hyperparathyroidism, osteitis enhancing mass in the right lower pole of the fibrosa cystica, hypercalcaemia thyroid gland. Ultrasonography confirmed a hypo-echoic mass 1.5 x 0.5 cm in the right lobe of the thyroid. -
1019 2 Feb 11 Weisbrode FINAL.Pages
The Armed Forces Institute of Pathology Department of Veterinary Pathology Wednesday Slide Conference 2010-2011 Conference 19 2 February 2011 Conference Moderator: Steven E. Weisbrode, DVM, PhD, Diplomate ACVP CASE I: 2173 (AFIP 2790938). Signalment: 3.5-month-old, male intact, Chow-Rottweiler cross, canine (Canis familiaris). History: This 3.5-month-old male Chow-Rottweiler mixed breed dog was presented to a veterinary clinic with severe neck pain. No cervical vertebral lesions were seen radiographically. The dog responded to symptomatic treatment. A week later the dog again presented with neck pain and sternal recumbency. The nose was swollen, and the submandibular and popliteal lymph nodes were moderately enlarged. The body temperature was normal. A complete blood count (CBC) revealed a marked lymphocytosis (23,800 lymphocytes/uI). Over a 3-4 hour period there was a noticeable increase in the size of all peripheral lymph nodes. Treatment included systemic antibiotics and corticosteroids. The dog became ataxic and developed partial paralysis. The neurologic signs waxed and waned over a period of 7 days, and the lymphadenopathy persisted. The peripheral blood lymphocyte count 5 days after the first CBC was done revealed a lymphocyte count of 6,000 lymphocytes/uI. The clinical signs became progressively worse, and the dog was euthanized two weeks after the initial presentation. Laboratory Results: Immunohistochemical (IHC) staining of bone marrow and lymph node sections revealed that tumor cells were negative for CD3 and CD79α. Gross Pathology: Marked generalized lymph node enlargement was found. Cut surfaces of the nodes bulged out and had a white homogeneous appearance. The spleen was enlarged and meaty. -
Introduction to the Orthopedics
[ Color index : Important | Notes | Extra ] Editing file link Introduction to the Orthopedics Objectives: ★ To explain what Orthopedic is and what conditions will be discussed during this course ★ Explain what we mean by Red Flags ★ List the different causes of orthopedic disease. ★ Describe some of clinical examination tests ★ Introduce titles of Clinical Skills which will be taught during this course. Done by: Rana Albarrak & Lamya Alsaghan Edited By: Bedoor Julaidan Revised by: Dalal Alhuzaimi References: slides + Toronto notes + 433 team + 435 team group A Introduction Orthopedic specialty: ★ Branch of surgery concerned with conditions involving the musculoskeletal system. Orthopedic surgeons use both surgical and nonsurgical means to treat musculoskeletal trauma, spine diseases, sports injuries, degenerative diseases, infections, tumors, and congenital disorders. ★ It includes: bones, muscles, tendons, ligaments, joints, peripheral nerves (peripheral neuropathy of hand and foot), , vertebral column, spinal cord and its nerves. NOT only bones. ★ Subspecialties: General, pediatric, sport and reconstructive (commonly ACL “anterior cruciate ligament” injury), trauma, arthroplasty, spinal surgery, foot and ankle surgery, oncology, hand surgery (usually it is a mixed speciality depending on the center. Orthopedics = up to the wrist joint. Orthopedics OR plastic surgery = from carpal bones and beyond, upper limb (new) elbow & shoulder. will be discussed in details in a separate lectures Red Flags: ★ Red Flags = warning symptoms or signs = necessity for urgent or different action/intervention. ★ Should always be looked for and remembered. you have to rule out red flags with all emergency cases! Fever is NOT a red flag! Do not confuse medicine with ortho. Post-op day 1 fever is considered normal! ★ There are 5 main red flags: 1. -
Osteochondrosis
Osteochondrosis (Abnormal Bone Formation in Growing Dogs) Basics OVERVIEW • Long bones (such as the humerus, radius and ulna in the foreleg and the femur and tibia in the rear leg) have three sections: the end of the bone, known as the “epiphysis”; the shaft or long portion of the bone, known as the “diaphysis”; and the area that connects the end and the shaft of the bone, known as the “metaphysis” • The metaphysis is the area where bone growth occurs in puppies; the long bones in the body grow in length at specific areas known as “growth plates”; these areas usually continue to produce bone until the bones are fully developed, at which time, no further growth is needed; the growth plates then “close” and become part of the hard bone • Bone is formed by the replacement of calcified cartilage at the growth plates; the bone-forming cells (known as “osteoblasts”) form bone on the cartilage structure; this process is known as “endochondral ossification” • “Osteochondrosis” is a disorder of bone formation in the growth plates (areas where bone grows in length in the young pet) of the bone; it is a disease process in growing cartilage, primarily characterized by a disturbance of the change from cartilage to bone (known as “endochondral ossification”) during bone development that leads to excessive retention of cartilage GENETICS • Multiple genes are involved (known as “polygenetic transmission”)—expression determined by an interaction of genetic and environmental factors • Heritability index—depends on breed, 0.25-0.45 SIGNALMENT/DESCRIPTION -
Bone Homeostasis and Pathology
Bone Homeostasis and Pathology Instructor: Roman Eliseev Outline: § Bone anatomy and composi<on § Bone remodeling § Factors regulang bone homeostasis § Disorders of bone homeostasis: -Bone loss -Abnormal bone acquisi<on § Methods and Mouse Models Adult Skeleton Axial Skeleton Appendicular Skeleton 206 bones Image from www.pngall.com Adult Bone Architecture Cor<cal bone Marrow cavity Diaphysis Metaphysis Epiphysis Trabecular bone Bone Histology Subchondral bone Trabecular bone Marrow fat Bone marrow Cor<cal bone Bone Composion Bone is a mineralized organic matrix composed of: • Type I collagen and non-collagenous proteins (osteoid) • Hydroxyapate crystals (Ca5(PO4)3(OH)) Osteoblasts Bone Bone-forming cells are osteoblasts (OB) that produce collagen I and deposit HA Bone is Formed by Osteoblasts OBs originate from Bone Marrow Stromal (a.k.a. Mesenchymal Stem) Cells (BMSC) and terminally differen<ate into osteocytes (OT). Wagner et al., PPAR Res., 2010 Bone is Resorbed by Osteoclasts Image from SciencePhotoLibrary Osteoclasts (OC) are bone resorbing mul<nucleated cells that originate from hematopoie<c cells (monocyte/macrophage) Homeostasis = equilibrium (Greek: ὁμοίως + στάσις) Bone Formaon vs Resorp<on = Dynamic Equilibrium (~10% of adult human skeleton is replaced annually) Bone Bone rosorp<on formaon Intact Bone BMSC – bone marrow stromal Blood vessel (a.k.a. mesenchymal stem) cell BMSC OB – osteoblast OT – osteocyte Apoptosis OB (~70%) Lining cells BONE OT TGFb, IGF1, OCN Collagen I Remodeling: Ini<al Phase BMSC – bone marrow stromal (a.k.a. mesenchymal stem) cell Blood vessel HSC OB – osteoblast BMSC OT – osteocyte HSC – hematopoie<c stem cell RANKL, OCP – osteoclast precursor ? m-CSF OCP OB Lining cells BONE OT Remodeling: Resorp<on Pit BMSC – bone marrow stromal (a.k.a.