Bone and Soft Tissue Pathology by Andrew E. Horvai (ed.), Thomas Link (ed.)

By Andrew E. Horvai (ed.), Thomas Link (ed.)

Keep time opting for and diagnosing pathology specimens with excessive Yield Bone and delicate Tissue Pathology, edited by way of Drs. Andrew Horvai and Thomas hyperlink. a part of the High-Yield Pathology sequence, this identify is designed that can assist you overview the foremost pathologic beneficial properties of bone and soft-tissue malformations, realize the vintage glance of every ailment, and fast be sure your prognosis. Its templated structure, first-class colour images, concise bulleted textual content, and authoritative content material might help you safely establish greater than a hundred and sixty discrete sickness entities.

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Anteroposterior radiograph of the pelvis demonstrating severe left hip osteoarthritis with superolateral joint space narrowing, osteophytes, subchondral sclerosis, and a subchondral cyst in the femur. Mild to moderate right hip osteoarthritis with osteophytes at the femoral head and os acetabuli is visible. Osteoarthritis A B C D E Fig 4. Microscopic changes of osteoarthritis. A, Cartilage necrosis with scattered ghost chondrocytes (arrows) and loss of ­proteoglycan matrix density. B, Reduplication and irregularity of tidemark (arrows).

Microscopic changes of osteoarthritis. A, Cartilage necrosis with scattered ghost chondrocytes (arrows) and loss of ­proteoglycan matrix density. B, Reduplication and irregularity of tidemark (arrows). C, Cartilage cracking and clefting. D, Exposure and sclerosis of bone at a site of eburnation. E, Subchondral cysts. S. 1% to 5% (~1% of whites) • Women affected two to three times more than men, about 5% of women older than 65 years affected • Peak onset between 30 and 55 years of age • R isk factors: female gender, nulliparity, smoking, HLA-DR β gene variant (“shared epitope”), gene polymorphisms in TNF-α, STAT4, PTPN, TCR • A ffected joints: typically symmetrical peripheral polyarthritis; classically metacarpophalangeal, metatarsophalangeal, and proximal interphalangeal joints of hands and feet; also wrist, elbow, knee; less commonly axial joints or monoarthritis Presentation • Symptoms: morning stiffness; swelling of joints with redness, pain, deformities, limited range of motion, subcutaneous nodules, fatigue, muscle weakness • Extra-articular manifestations: anemia, subcutaneous rheumatoid nodules, myositis, vasculitis, neutrophilic dermatitis, pericarditis or myocarditis, interstitial lung disease • Laboratory findings: 50% to 70% have rheumatoid factor (immunoglobulin M [IgM] autoantibodies to Fc portion of IgG), which has low specificity; autoantibodies to cyclic citrullinated peptides (CCPs) both sensitive and more than 90% specific • Synovial fluid: leukocytosis with neutrophil predominance (particularly in acute stage) but WBC lower than in septic arthritis (<75,000 cells/µL), protein approaching plasma concentration, low glucose, low C3 and C4 Prognosis and treatment • Variable clinical course—most patients have periodic flares, some have unabating activity, remissions are possible; structural damage is cumulative and irreversible over years; if untreated may progress to destruction of articular cartilage and joint ankylosis • Treatment: nonsteroidal anti-inflammatory drugs (NSAIDs), immunosuppressive drugs, surgery (joint replacement, synovectomy) Radiology • Joint effusions and soft tissue swelling • Juxta-articular osteopenia • Bone and cartilage erosions, typically at marginal joint regions • Narrowing of joint space • Joint deformities: radial wrist deviation, ulnar deviation of digits, swan-neck finger deformities 28 • A ffects typically metacarpophalangeal joints and carpal region at the hand and metatarsophalangeal joints at the foot Pathology Gross • Joint destruction and joint deformities • Little or no reparative tissue, proliferative cartilage, bone sclerosis, or osteophytes (unlike osteoarthritis) • Joints have edematous, thick, hyperplastic synovium covered by delicate and bulbous fronds Histology • Hypertrophic and hyperplastic synovium • Chronic inflammation, uncommonly with lymphoid follicles and germinal centers cuffed by a dense population of plasma cells • Hyperplasia of synovial cells may result in multinucleation (Grimley-Sokoloff giant cells) • Focal fibrinoid exudate and neutrophils at the synovial surface • Organizing fibrin may float into joint space as rice bodies • Reactive synovium extends from periphery to cover entire articular surface forming a pannus with destructions of underlying cartilage characterized by enlarged and often empty chondrocyte lacunae (Weichselbaum lacunae) • Wall thickening and onion-skin appearance of synovial arteries • Chronic inflammation also often involves subchondral bone • Synovitis typically less pronounced in advanced disease with little remaining cartilage or following joint replacement but typically recurs following synovectomy • R heumatoid nodules in about 25% of cases • Usually in subcutaneous tissue along extensor surfaces of forearm, elbow, and shin • Less commonly in visceral organs (heart, lungs, intestinal tract) or in joint synovium • Characterized by central fibrinoid necrosis rimmed by palisaded histiocytes and giant cells and a cuff of lymphocytes and plasma cells Cytology • Joint aspirate may have inflammatory exudate with neutrophils, which may suggest septic arthritis Ancillary tests • Serology (rheumatoid factor, CCPs) used as one of the diagnostic criteria Main differential diagnosis • Osteoarthritis • Crystal-induced arthritis • Septic arthritis, particularly if monoarticular disease • R heumatoid nodule: infection, epithelioid sarcoma Rheumatoid Arthritis A B A B C Fig 1.

A B C D Fig 2. Microscopic changes of osteonecrosis. A, Low magnification showing the periphery of the lesion with ingrowth of granulation tissue (center) and necrosis (right). B, Intermediate magnification showing bone marrow fat necrosis and necrotic bone with empty lacunae. C, High magnification of granulation tissue adjacent to necrotic bone with empty lacunae. D, Irregular calcifications and granulation tissue at the edge of a well-established lesion. , neoplasm, osteomyelitis, osteoporosis) help establish the etiology 45 46 Bone Fracture and Fracture Callus A C B Fig 1.

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