By Andrew E. Horvai (ed.), Thomas Link (ed.)
Store time selecting and diagnosing pathology specimens with excessive Yield Bone and gentle Tissue Pathology, edited through Drs. Andrew Horvai and Thomas hyperlink. a part of the High-Yield Pathology sequence, this name is designed that can assist you evaluate the major pathologic good points of bone and soft-tissue malformations, realize the vintage glance of every ailment, and fast be certain your analysis. Its templated layout, first-class colour pictures, concise bulleted textual content, and authoritative content material can assist you effectively determine greater than a hundred and sixty discrete disorder entities.
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B Fig 5. Anteroposterior radiograph of the pelvis (A) and frog-leg lateral view of the right hip (B) in a patient with osteopetrosis showing diffuse sclerosis of the proximal femur and the pelvis with femoral bowing. The bone-in-bone appearance of the pelvic bones is well visualized. Deformity of the right femoral head suggests remote fracture. Fig 4. Osteopetrotic bone from an adult with calcifying cartilaginous tissue not remodeling into mature bone. OCHRONOSIS Definition and synonyms • Deposition of dark pigment in cartilage and connective tissue due to a metabolic disorder of homogentisic acid oxidase (alkaptonuria) or from exposure to various toxic substances (ochronotic arthropathy) Clinical features Epidemiology • A lkaptonuria is a rare autosomal recessive disease with equal sex distribution • Large peripheral joints are most commonly affected, including knees, shoulders, and hips Presentation • Early degenerative arthritis and tendon insufficiency • Narrowing of the joint spaces and disk calcifications • Spine is affected through degenerative changes of the intervertebral disks • Dark urine and skin pigmentation, particularly the axilla • Gray to brown patch of pigmentation in the sclera, between the margin of the cornea and the outer or inner canthus • Accumulation of pigment in cardiac tissue leads to heart valve dysfunction Prognosis and treatment • No cure is available for alkaptonuria • Diets low in tyrosine and phenylalanine and high in vitamin C may reduce the toxic byproduct homogentisic acid • Ochronotic arthropathy is treated with physiotherapy, analgesia, rest, and prosthetic joint replacement when necessary Fig 1.
Typically, Gaucher cell infiltration is low in signal in T1- and T2-weighted images. B C Fig 3. Scanning magnification of bone involved by Gaucher disease shows infiltration of the marrow space by a uniform population of eosinophilic cells. Fig 4. At higher magnification, Gaucher cells have abundant cytoplasm and small nuclei (A). The cells are filled with abundant crumpled cytoplasm and a single, eccentrically placed nucleus (B and C). The lipids within Gaucher cells are glucocerebroside, a lipid molecule with a single sugar residue that accumulates as a result of the absence of the enzyme.
Sickle cell disease, Gaucher disease, decompression sickness) • Vasculitis • Venous flow obstruction: secondary to trauma and other types of injury • Subcapital femoral neck fracture • A rthritis • Idiopathic (primary) • R isk factors • Corticosteroids, alcoholism, family history • Pediatric syndromes • Usually in preteen-aged or teen-aged athletes with rapidly growing bones, boys more than girls • Thought to be secondary to trauma in genetically susceptible individuals • Legg-Calvé-Perthes (proximal femoral epiphysis) • Osgood-Schlatter disease (tibial tuberosity) Presentation • Variable presentation depending on etiology • Usually joint pain, limited function, may present with a pathologic fracture Prognosis and treatment • May result in fractures through articular surface following collapse of infarcted, necrotic bone or replacement by granulation tissue • A lso may result in detachment of cartilage and secondary degenerative joint disease • Eventually leads to severe arthritis in most cases • Treatment is usually surgical (joint replacement, bone curettage, and stabilization with hardware) • Rarely, a sarcoma may arise in the area of avascular necrosis Radiology • Little if any changes in early stage on radiographs; however, early changes are well visualized on MRI with central fatty necrosis with a margin of granulation tissue (bright on T2-weighted images, low signal on T1-weighted images) and adjacent bone marrow edema pattern • At later stages, radiographs are positive with the following: • Moderately thick calcified serpentine border outlining a central area of radiolucency or wedge-shaped increased sclerosis without deformity • Subchondral collapse (crescent sign) • Flattening of articular surface • Joint narrowing • Advanced degenerative changes Pathology Gross • Early changes • Intact articular cartilage except at edge of necrosis where cartilage may be folded and cracked • Cross section of necrotic subchondral bone is yellow, opaque, and chalky with hyperemic fibrous tissue at margin • Adjacent bone with thickened trabeculae • Late changes • Flattening of joint surface • Detachment and destruction of overlying articular cartilage • Loss of bone and secondary changes of degenerative joint disease Histology • Early changes • Necrosis of bone marrow fat and hematopoietic tissue (easiest to recognize) • Osteocyte lacunae may be enlarged and empty or normal size with pyknotic nuclei • Later changes • Ingrowth of granulation tissue from the lesion periphery with layering of new bone over dead trabeculae (“creeping substitution”), which results in formation of a highly collagenized and, later, calcified rim Main differential diagnosis • Subchondral insufficiency fracture • Osteoarthritis • Calcified enchondroma 43 44 Osteonecrosis A B Fig 1.