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

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

ISBN-10: 1455737909

ISBN-13: 9781455737901

Keep time picking out and diagnosing pathology specimens with excessive Yield Bone and gentle Tissue Pathology, edited by way of Drs. Andrew Horvai and Thomas hyperlink. a part of the High-Yield Pathology sequence, this name is designed that will help you evaluate the major pathologic good points of bone and soft-tissue malformations, realize the vintage glance of every disorder, and speedy verify your analysis. Its templated structure, first-class colour photos, concise bulleted textual content, and authoritative content material can help you safely establish greater than a hundred and sixty discrete sickness entities.

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E, Russell bodies (arrows) may be present. , AIDS, diabetes) • Prosthetic joint: may be responsible for loosening of prosthesis • Most common pathogens: Staphylococcus aureus (40% to 50%), Streptococcus pyogenes, Streptococcus pneumoniae, gram-negative bacilli (10%, often associated with intravenous drug use) • Gonococcal arthritis (Neisseria gonorrhoeae): most common arthritis due to sexually transmitted bacterial infection • Lyme arthritis (Borrelia burgdorferi) • Acute Lyme arthritis seen in 50% to 60% of cases • Associated with erythema migrans (90% of Lyme cases) • Mycobacterial arthritis (Mycobacterium tuberculosis) • Usually follows infection of the spine and affects hip or knee most commonly • Fungal arthritis • Rare, usually in immunocompromised hosts • Candida species most common Presentation • Symptoms: fever; swollen, warm, erythematous and painful joint • Synovial fluid: gray-green, WBC 20,000 to 200,000 cells/μL, more than 75% neutrophils Prognosis and treatment • Adjacent tendon sheath or bursa may be involved; secondary osteomyelitis in about 8% • May result in severe destruction of musculoskeletal structures, permanent disability (30%), and, very rarely, death • Diagnosis relies on compatible history, physical examination, and synovial fluid Gram stain, microbiology culture, and cell count • Treatment: prompt appropriate antibiotic therapy, joint tap with drainage, debridement in some cases • Loosening of prosthetic joint: intraoperative frozen section and Gram stain to assess for acute inflammation and organisms; if evidence of infection is present, prosthetic replacement delayed until after antibiotic therapy Radiology • Plain films and CT • May be normal in early-stage disease • Joint effusion • Joint space narrowing • Bony erosion and later destruction • Periosteal bone formation • MRI • Synovial thickening and enhancement • Joint effusion, surrounding edema • Bone marrow edema pattern and bony erosions Pathology Gross • Swollen periarticular soft tissue • Thickened or nodular synovial tissue with or without exudate • Cloudy, milky, or thick green joint aspirate • Scarring and erosion of articular cartilage Histology • Suppurative inflammation (pyogenic bacteria, gonococcal arthritis, Lyme arthritis, Candida species) • Synovial edema and dense neutrophilic infiltrate • If not treated promptly, necrosis and destruction of articular cartilage • Eventually, lymphocytes, plasma cells, and histiocytes predominate with development of chronic papillary synovitis, fibrin deposits and thickening of arterial walls (similar to that seen in other inflammatory arthritides) • Organisms can be demonstrated with special histochemical stains (see later) • Granulomatous inflammation (mycobacteria, most fungi) • Acute and chronic synovitis with necrotizing or non-necrotizing granulomas and giant cells • Septic loosening of prosthesis • Neutrophil count on intraoperative frozen section of synovium or prosthetic capsule: • Five neutrophils per high-power field in more than 5 high-power fields (Feldman criteria) • Ten neutrophils per 10 high-power fields (Athanasou criteria) • Neutrophils in fibrinous exudate or blood are not counted Ancillary tests • Gold standard of diagnosis is positive microbiologic culture • Tissue stains • Molecular tests (polymerase chain reaction and reverse-transcriptase polymerase chain reaction techniques) can detect a wide range of microorganisms • Serology (Lyme arthritis, viral arthritides) Main differential diagnosis • R heumatoid arthritis • Gout • Other crystal-induced arthritides • Osteoarthritis 31 32 Septic Arthritis A A B B Fig 1.

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.

S. population is a carrier for type I Gaucher disease, with a prevalence of 1 in 40,000 • Most common among people of Ashkenazi Jewish descent • A ffects men and woman equally Presentation • Three common clinical subtypes; presentation is related to the subtype inherited • Type I: weakness, bone disease, anemia • Type II: rapidly progressive central nervous system damage, hepatosplenomegaly, bone disease • Type III: chronic neuropathy, bone disease, hepatosplenomegaly • Bone involvement includes osteoporosis, bone pain, aseptic necrosis of the femur • Yellow-brown skin pigmentation • MRI can be useful in demonstrating bone marrow infiltration and to calculate bone marrow burden; it also allows differentiation of bone marrow infiltration versus bone marrow infarct Pathology Histology • Accumulation of glucocerebroside (glycosphingolipid) in macrophages (Gaucher cells) replacing bone marrow space • Gaucher cells are large, vacuolated cells with abundant crumpled cytoplasm and small nucleus pushed to one side • Gaucher cells are primarily identified in the spleen, liver, lymph nodes, and bone marrow • Gaucher cells stain positive for periodic acid–Schiff and iron Main differential diagnosis • Storage diseases and macrophage proliferation disorders • Von Gierke disease • Niemann-Pick disease Prognosis and treatment • Prognosis and treatment are related to the subtype • Type I: slight decrease in life expectancy • Type II: rapid progression, fatal by age 2 years • Type III: chronically progressive, death often by age 30 years • Treatment with intravenous enzyme replacement therapy improves outcome, especially in type I • Bone symptoms and deformities can regress after enzyme replacement therapy Radiology • Plain radiographic abnormalities include diffuse osteopenia, osteonecrosis, periosteal reactions, bone erosions, and infarcts • Pathologic fractures commonly affect the distal femur, proximal tibia, and thoracic and lumbar regions of the spine • Erlenmeyer flask deformity (widening of the distal femoral metaphysis) due to defective remodeling and bone marrow expansion • Erlenmeyer flask deformity and epiphyseal osteonecrosis on the same radiograph is suggestive of Gaucher disease Fig 1.

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


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