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