Injuries and Normal Variants of the Pediatric Knee
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Soft Tissue Calcification and Ossification
Soft Tissue Calcification and Ossification Soft-tissue Calcification Metastatic Calcification =deposit of calcium salts in previously normal tissue (1) as a result of elevation of Ca x P product above 60-70 (2) with normal Ca x P product after renal transplant Location:lung (alveolar septa, bronchial wall, vessel wall), kidney, gastric mucosa, heart, peripheral vessels Cause: (a)Skeletal deossification 1.1° HPT 2.Ectopic HPT production (lung / kidney tumor) 3.Renal osteodystrophy + 2° HPT 4.Hypoparathyroidism (b)Massive bone destruction 1.Widespread bone metastases 2.Plasma cell myeloma 3.Leukemia Dystrophic Calcification (c)Increased intestinal absorption =in presence of normal serum Ca + P levels secondary to local electrolyte / enzyme alterations in areas of tissue injury 1.Hypervitaminosis D Cause: 2.Milk-alkali syndrome (a)Metabolic disorder without hypercalcemia 3.Excess ingestion / IV administration of calcium salts 1.Renal osteodystrophy with 2° HPT 4.Prolonged immobilization 2.Hypoparathyroidism 5.Sarcoidosis 3.Pseudohypoparathyroidism (d)Idiopathic hypercalcemia 4.Pseudopseudohypoparathyroidism 5.Gout 6.Pseudogout = chondrocalcinosis 7.Ochronosis = alkaptonuria 8.Diabetes mellitus (b) Connective tissue disorder 1.Scleroderma 2.Dermatomyositis 3.Systemic lupus erythematosus (c)Trauma 1.Neuropathic calcifications 2.Frostbite 3.Myositis ossificans progressiva 4.Calcific tendinitis / bursitis (d)Infestation 1.Cysticercosis Generalized Calcinosis 2.Dracunculosis (guinea worm) (a)Collagen vascular disorders 3.Loiasis 1.Scleroderma -
Development of the Endochondral Skeleton
Downloaded from http://cshperspectives.cshlp.org/ on September 24, 2021 - Published by Cold Spring Harbor Laboratory Press Development of the Endochondral Skeleton Fanxin Long1,2 and David M. Ornitz2 1Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110 2Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110 Correspondence: fl[email protected] SUMMARY Much of the mammalian skeleton is composed of bones that originate from cartilage templates through endochondral ossification. Elucidating the mechanisms that control endochondral bone development is critical for understanding human skeletal diseases, injury response, and aging. Mouse genetic studies in the past 15 years have provided unprecedented insights about molecules regulating chondrocyte formation, chondrocyte maturation, and osteoblast differ- entiation, all key processes of endochondral bone development. These include the roles of the secreted proteins IHH, PTHrP, BMPs, WNTs, and FGFs, their receptors, and transcription factors such as SOX9, RUNX2, and OSX, in regulating chondrocyte and osteoblast biology. This review aims to integrate the known functions of extracellular signals and transcription factors that regulate development of the endochondral skeleton. Outline 1 Introduction 5 Osteoblastogenesis 2 Mesenchymal condensation 6 Closing remarks 3 Chondrocyte differentiation References 4 Growth plate development Editors: Patrick P.L. Tam, W. James Nelson, and Janet Rossant Additional Perspectives on Mammalian Development available at www.cshperspectives.org Copyright # 2013 Cold Spring Harbor Laboratory Press; all rights reserved; doi: 10.1101/cshperspect.a008334 Cite this article as Cold Spring Harb Perspect Biol 2013;5:a008334 1 Downloaded from http://cshperspectives.cshlp.org/ on September 24, 2021 - Published by Cold Spring Harbor Laboratory Press F. -
Bone Grafting in Brodie's Absc Rafting in Brodie's Abscess
Case Report Bone Grafting in Brodie’s Abscess Athar Ahemad Department of Orthopaedics, Indian Institute of Medical Sciences and Research, Warudi, Tq. Badnapur, Jalna, Maharashtra, INDIA. Email: [email protected] Abstract Brodie’s abscess is a localized infection of the bone manifesting on radiographs as an osteolytic lesion limited by sclerotic bone. It was first described by Sir Benjamin Brodie 1in the year 1832 as a localized abscess in the tibia seen in an amputation stump. It is most commonly seen in proximal tibia follo wed by femur and then in humerus. Various treatments have been described in the literature ranging from antibiotics alone to debridement alone to curettage and filling of defect by bone graft or cement 2,3,4. Here, we report 2 cases of Brodie’s abscess tre ated successfully by surgical debridement and bone grafting. Address for Correspondence Dr. Athar Ahemad, Department of Orthopaedics, Indian Institute of Medical Sciences and Research, Warudi, Tq. Badnapur, Jalna, Maharashtra, INDIA. Email: [email protected] Received Date: 13/09/2014 Accepted Date: 17 /0 9/2014 hydrogen peroxide. The cavity was debrided till there was Access this article online bleeding bone all around. Since the bone defect was large (5x3x3cm), fresh cancellous autograft from ipsilateral Quick Response Code: Website: iliac crest was used to fill the defect. Muscle flap st itched www.medpulse.in over the window as a local flap. A long knee brace was given to prevent pathological fracture. DOI: 18 September 2014 INTRODUCTION Case 1 A 24 year old male manual laborer presented to us with complaints of throbbing pain in the upper part of leg on Photo 1: Cavity of the abscess being debrided with a curette which and off since last 4 years especially at night. -
Diagnosis and Treatment of Intramedullary Osteosclerosis
Abe et al. BMC Musculoskeletal Disorders (2020) 21:762 https://doi.org/10.1186/s12891-020-03758-5 CASE REPORT Open Access Diagnosis and treatment of intramedullary osteosclerosis: a report of three cases and literature review Kensaku Abe, Norio Yamamoto, Katsuhiro Hayashi, Akihiko Takeuchi* , Shinji Miwa, Kentaro Igarashi, Takashi Higuchi, Yuta Taniguchi, Hirotaka Yonezawa, Yoshihiro Araki, Sei Morinaga, Yohei Asano and Hiroyuki Tsuchiya Abstract Background: Intramedullary osteosclerosis (IMOS) is a rare condition without specific radiological findings except for the osteosclerotic lesion and is not associated with family history and infection, trauma, or systemic illness. Although the diagnosis of IMOS is confirmed after excluding other osteosclerotic lesions, IMOS is not well known because of its rarity and no specific feature. Therefore, these situations might result in delayed diagnosis. Hence, this case report aimed to investigate three cases of IMOS and discuss imaging findings and clinical outcomes. Case presentation: All three cases were examined between 2015 and 2019. The location of osteosclerotic lesions were femoral diaphyses in the 60-year-old man (Case 1) and 41-year-old woman (Case 2) and tibial diaphysis in the 44-year-old woman (Case 3). All cases complained of severe pain and showed massive diaphyseal osteosclerotic lesions in plain radiograms and computed tomography (CT) scans. Cases 2 and 3 were examined using the triphasic bone scan, and a fusiform-shaped intense area of the tracer uptake on delayed bone image was detected in both cases without (Case 2) or slightly increased vascularity (Case 3) on the blood pool image, which was reported as a specific finding of IMOS. -
Upper Limb Development
Upper Limb Development Alphonsus Chong Department of Hand and Reconstructive Microsurgery National University Hospital Why bother? Most congenital limb anomalies are due to: Disorders of embryogenesis or Problems during fetal development Some terminology Embryogenesis 0-8 weeks – new organ systems appear Fetal period Appearance of primary ossification center in humerus Differentiation, maturation and enlargement of existing organs Limb Development Limb Patterning Tissue Differentiation Why is it an arm and not Skeletal a leg? Joint Vascular Nerve Muscle and Tendon Positional Information and Axes of the upper limb Limb Bud in E3 Chick Embryo Limb bud (lateral plate) Loose mesenchymal cells from lateral plate mesoderm Ectodermal epithelial cells Migrating cells Somites --> Muscle Nerves Vasculature Limb Bud Development Limb bud Ectoderm and mesenchyme Not fully differentiated yet but all ingredients there If transplanted ectopic limb Limb Bud Regions AER Progress zone Zone of polarizing activity AER – Proximal to Distal formation Zone of Polarizing Actvity – AP development Morphogen Gradient Model Dorsal / ventral patterning less well understood Separation of Digits Apoptosis (Programmed cell death) of interdigital mesenchyme BMPs important Starts post-axial to pre-axial Mesoderm specifies amount of apoptosis How does this relate to pathogensis? Picture from Greene Learning Points UE development occurs early in embryogenesis – most risk of development congenital anomalies Pattern of limb development follows a body plan Digit formation is by apoptosis Thank You Further Reading Principles of Development 3rd Ed by Lewis Wolpert. Oxford University Press Growing Hand. Amit Gupta and Louisville Group. -
Musculoskeletal Morphing from Human to Mouse
Procedia IUTAM Procedia IUTAM 00 (2011) 1–9 2011 Symposium on Human Body Dynamics Musculoskeletal Morphing from Human to Mouse Yoshihiko Nakamuraa,∗, Yosuke Ikegamia, Akihiro Yoshimatsua, Ko Ayusawaa, Hirotaka Imagawaa, and Satoshi Ootab aDepartment of Mechano-Informatics, Graduate School of Information and Science and Technology, University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan bBioresource Center, Riken, 3-1-1 Takanodai, Tsukuba-shi, Ibaragi, Japan Abstract The analysis of movement provides various insights of human body such as biomechanical property of muscles, function of neural systems, physiology of sensory-motor system, skills of athletic movements, and more. Biomechan- ical modeling and robotics computation have been integrated to extend the applications of musculoskeletal analysis of human movements. The analysis would also provide valuable means for the other mammalian animals. One of current approaches of post-genomic research focuses to find connections between the phenotype and the genotype. The former means the visible morphological or behavioral expression of an animal, while the latter implies its genetic expression. Knockout mice allows to study the developmental pathway from the genetic disorders to the behavioral disorders. Would musculoskeletal analysis of mice also offer scientific means for such study? This paper reports our recent technological development to build the musculoskeletal model of a laboratory mouse. We propose mapping the musculoskeletal model of human to a laboratory mouse based on the morphological similarity between the two mammals. Although the model will need fine adjustment based on the CT data or else, we can still use the mapped musculoskeletal model as an approximate model of the mouse’s musculoskeletal system. -
The Role of Imaging in Tibia Stress Injury
SPORTS RADIOLOGY THE ROLE OF IMAGING IN TIBIA STRESS INJURY – Written by Keiko Patterson and Bruce Forster, Canada Stress fractures are frequently encountered immediate rehabilitation, rather than to In contrast, an insufficiency fracture occurs injuries in the discipline of sports medi- persist through the pain. when normal stress acts on an already cine, accounting for between 1 and 20% The differential diagnosis between shin abnormal, usually osteoporotic bone. Tibial of all visits to the sports medicine clinic1. splints – also known as medial tibial stress stress fractures are bilateral in 16% of cases Tibial stress fractures account for half of all syndrome (MTSS) – and a true stress fracture and typically occur at the junction of the stress fractures and are especially common is often difficult. MTSS can be thought of as a middle and distal third in adults1. Variants in athletes who are involved in repetitive less advanced version of tibial stress fracture, in tibial stress fractures include the anterior impact sports that are often of high inten- involving pain at the posterior medial border mid-diaphysis known as the ‘dreaded black sity1. Runners and younger participants in during exercise with diffuse periostitis, but line’ (transverse fracture line across entire jumping sports are particularly prone to no cortical break2. The term stress fracture shaft of the tibia) (see Figure 2) found in 5% these injuries due to repetitive submaxi- is therefore not an appropriate label for of cases, and longitudinal stress fractures mal stress on the posterior medial cortex of all stress injuries, as many do not show found usually in the mid- to distal bone1. -
(Osgood- Schlatter Disease): a Review
Open Access Review Article DOI: 10.7759/cureus.780 Apophysitis of the Tibial Tuberosity (Osgood- Schlatter Disease): A Review Raju Vaishya 1 , Ahmad Tariq Azizi 2 , Amit Kumar Agarwal 1 , Vipul Vijay 1 1. Orthopaedics, Indraprastha Apollo Hospitals 2. Orthoapedics, Herat Regional Hospital, Herat, Afghanistan Corresponding author: Amit Kumar Agarwal, [email protected] Abstract Osgood-Schlatter disease (OSD) is a condition in which the patellar tendon insertion on the tibial tuberosity becomes inflamed. It is a well-known condition in late childhood characterized by pain and a bony prominence over the tibial tuberosity. The pain is usually exacerbated by physical activities like running, jumping, and climbing stairs. In the acute stage, the margins of the patellar tendon become blurred in radiographs due to the soft tissue swelling. After three to four months, bone fragmentation at the tibial tuberosity is viewed. In the sub-acute stage, soft tissue swelling resolves, but the bony ossicle remains. In the chronic stage, the bone fragment may fuse with the tibial tuberosity which can appear normal. The primary goal in the treatment of OSD is the reduction of pain and swelling over the tibial tuberosity. The patient should limit physical activities until the symptoms are resolved. In some cases, the patient should restrict physical activities for several months. The presence of pain with kneeling because of an ossicle that does not respond to conservative measures is the indication for surgery. In these cases, the removal of the ossicle, surrounding bursa, and the bony prominence is the treatment of choice. Categories: Orthopedics Keywords: tibial tuberosity, osgood-schlatter disease, apophysitis Introduction And Background Osgood-Schlatter disease (OSD, also called Lannelongue’s disease) is a condition in which the patellar tendon insertion on the tibial tuberosity becomes inflamed [1-2]. -
Homeobox Genes D11–D13 and A13 Control Mouse Autopod Cortical
Research article Homeobox genes d11–d13 and a13 control mouse autopod cortical bone and joint formation Pablo Villavicencio-Lorini,1,2 Pia Kuss,1,2 Julia Friedrich,1,2 Julia Haupt,1,2 Muhammed Farooq,3 Seval Türkmen,2 Denis Duboule,4 Jochen Hecht,1,5 and Stefan Mundlos1,2,5 1Max Planck Institute for Molecular Genetics, Berlin, Germany. 2Institute for Medical Genetics, Charité, Universitätsmedizin Berlin, Berlin, Germany. 3Human Molecular Genetics Laboratory, National Institute for Biotechnology & Genetic Engineering (NIBGE), Faisalabad, Pakistan. 4National Research Centre Frontiers in Genetics, Department of Zoology and Animal Biology, University of Geneva, Geneva, Switzerland. 5Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Charité, Universitätsmedizin Berlin, Berlin, Germany. The molecular mechanisms that govern bone and joint formation are complex, involving an integrated network of signaling pathways and gene regulators. We investigated the role of Hox genes, which are known to specify individual segments of the skeleton, in the formation of autopod limb bones (i.e., the hands and feet) using the mouse mutant synpolydactyly homolog (spdh), which encodes a polyalanine expansion in Hoxd13. We found that no cortical bone was formed in the autopod in spdh/spdh mice; instead, these bones underwent trabecular ossification after birth. Spdh/spdh metacarpals acquired an ovoid shape and developed ectopic joints, indicating a loss of long bone characteristics and thus a transformation of metacarpals into carpal bones. The perichon- drium of spdh/spdh mice showed abnormal morphology and decreased expression of Runt-related transcription factor 2 (Runx2), which was identified as a direct Hoxd13 transcriptional target. Hoxd11–/–Hoxd12–/–Hoxd13–/– tri- ple-knockout mice and Hoxd13–/–Hoxa13+/– mice exhibited similar but less severe defects, suggesting that these Hox genes have similar and complementary functions and that the spdh allele acts as a dominant negative. -
Knee Pain in Children, Part II: Limb- and Life-Threatening Conditions, Hip Pathology, and Effusion
Knee Pain in Children, Part II: Limb- and Life-threatening Conditions, Hip Pathology, and Effusion Michael Wolf, MD* *Pediatrics and Orthopedic Surgery, St Christopher’s Hospital for Children, Philadelphia, PA. Practice Gap Clinicians who evaluate knee pain must be able to recognize limb- and life-threatening conditions, hip pathology, or joint effusion and pursue the appropriate management. Objectives After reading the article, the reader should be able to: 1. Describe the presentation and treatment of common limb- and life-threatening conditions that can cause knee pain in children. 2. Delineate how hip pathology can contribute to knee pain in children and how such conditions should be diagnosed and treated. 3. Explain the diagnosis and treatment of conditions that may cause effusion in conjunction with knee pain in children. INTRODUCTION As noted in the first part of this three-part review of knee pain in children, the clinician can use the information gained from the history and physical examination in an algorithm to establish a working diagnosis and direct subsequent evaluation and management. The initial priorities are to identify emergent limb- and life-threatening conditions, hip pathology, or effusion (Table). LIMB- AND LIFE-THREATENING CONDITIONS Bacterial Infections Septic Arthritis. The knee is the most common site of septic arthritis in children. Usually, septic arthritis is characterized by the acute onset of steadily progressive knee pain with fever and a physical examination demonstrating effusion, warmth, AUTHOR DISCLOSURE Dr Wolf has disclosed fi erythema, and limited motion. Concern for septic bacterial arthritis in children no nancial relationships relevant to this article. This commentary does not contain a warrants emergent evaluation, including knee radiographs (anteroposterior [AP] discussion of an unapproved/investigative and lateral) and laboratory studies (complete blood cell [CBC] count with use of a commercial product/device. -
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 -
Hyperostosis Corticalis Infantalis (Caffey's Disease)* J
754 S.A. TYDSKRIF VIR GENEESKU DE 14 Junie 1969 HYPEROSTOSIS CORTICALIS INFANTALIS (CAFFEY'S DISEASE)* J. M. WAGNER, M.B., B.CH., M.R.e.p., Senior Paediatrician, Edenvale Hospital, AND A. SoLOMON, M.B., B.CH., DIP.MED., D.M.R.(D.), Radiologist, Pneumoconiosis Research Unit, CSIR, Baragwanath Hospital, Johannesburg Infantile cortical hyperostosis is a disorder affecting the skeleton and some of its contiguous fascias and muscles. It is suggested that infantile cortical hyperostosis is a pre natal collagen disease.' The early stage is of acute inflammation and loss of the periosteal and subperiosteal definition. There is a fibrous and osteoblastic reaction and overlying tissue including muscle is involved. No bacteria are seen. Later, there is subperiosteal new lamellar bone formation. The peri osteum is thickened and hyperplastic and the overlying soft tissues are oedematous and sections show round-cell infiltration. The subacute phase re-establishes periosteum as an entity. The later remodelling stage removes the extraperipheral bone from within, resulting in dilatation of the medullary cavity. There is evidence to suggest that infantile cortical hyper ostosis had been recognized in 1930.' Caffey and Silver man first described the disease in 1946." Smyth et al.' also recorded cases in 1946. Altogether 102 cases have been reported, Sidbury and Sidbury' contributing 69 reports and Holrnan' describing 33 cases. Infantile cortical hyper ostosis has been described in Negroes but seems rare in the South African Bantu. CASE REPORT The patient, a 3-year-old Bantu male, had a normal birth weight. Two siblings were in good health. The mother stated that the child's jaw was swollen and that he had Fig.