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February 1, 2018 | Pathology | By admin | 0 Comments

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

ISBN-10: 1455737909

ISBN-13: 9781455737901

Store time making a choice on and diagnosing pathology specimens with excessive Yield Bone and gentle Tissue Pathology, edited by means of Drs. Andrew Horvai and Thomas hyperlink. a part of the High-Yield Pathology sequence, this name is designed that can assist you evaluate the most important pathologic beneficial properties of bone and soft-tissue malformations, realize the vintage glance of every disorder, and quick verify your analysis. Its templated layout, very good colour pictures, concise bulleted textual content, and authoritative content material might help you effectively determine greater than one hundred sixty discrete disorder entities.

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Fig 2. Necrotic bone (sequestrum) is characterized by the presence of empty lacunae. The surfaces of the bony trabeculae are undergoing destruction, imparting a “chewed” or scalloped configuration. Fig 5. Involucrum, new periosteal bone formation associated with osteomyelitis, develops several days to weeks after infection in a pattern similar to fracture callus. 39 CHRONIC OSTEOMYELITIS Definition • Established (>6 weeks), nonsuppurative bone inflammation arising as a complication of untreated or treatment-refractory acute osteomyelitis or as a result of infection by an indolent pathogen (includes granulomatous osteomyelitis) Clinical features Epidemiology • Fifteen to 30% of acute osteomyelitis (see separate section) go on to chronic disease • Other causes: nonpyogenic bacteria, fungi, and very rarely parasites or viruses • Mycobacterial osteomyelitis • Tuberculous osteomyelitis (Mycobacterium tuberculosis) • One to 3 percent of cases of pulmonary and 10% of extrapulmonary tuberculosis • Usually a solitary bone lesion, frequently multifocal in patients with AIDS • Most frequent sites: spine (Pott disease) usually involves anterior column, T6-L3; hips; knees • Nontuberculous mycobacterial osteomyelitis ­(atypical mycobacteria) • Five to 10 percent of infections have bone ­involvement • R isk factors: immunocompromised state, trauma, surgery • Lepromatous osteomyelitis • Most common sites: facial bones, hands and feet • Treponemal osteomyelitis • Skeletal syphilis (Treponema pallidum) • Congenital • Usually bilateral symmetrical bone involvement with variable severity • Most common in diaphysis of long bones and costochondral junction • Acquired • Usually not before early tertiary stage (2 to 5 years after initial infection) • Most common sites: facial and skull bones, clavicle, tibia • Fungal osteomyelitis • Candida species (most common) • Bone involvement in 1% to 2% of bloodstream Candida species infections • R isk factors: immunosuppression; chronic illness, particularly diabetes; invasive catheters; and parenteral drug use • Most common sites: lumbar spine and long bones, usually single focus • Other fungi: Aspergillus, Cryptococcus, Coccidioides, Paracoccidioides, Histoplasma, Blastomyces species (rare, usually in patients with a primary lung infection); Sporothrix (usually due to penetrating trauma) • Chronic, recurrent multifocal osteomyelitis • Multifocal inflammatory disorder involving skeletal system of children and adolescents • Female preponderance (5:1 female-to-male ratio) • Protracted relapsing course • Cultures typically negative for organisms • Definition evolving, may represent an autoimmune syndrome rather than true infection 40 Presentation • Low-grade fever • Weight loss • Pain over affected area • Swelling, local warmth, erythema Prognosis and treatment • May result in severe disability, pathologic fracture, or extensive soft tissue involvement • Treatment: usually a combination of intravenous antibiotics and surgical debridement Radiology • Compared with acute osteomyelitis, osteopenia and soft tissue swelling are less frequently observed and relatively atypical • Lytic destructive bone lesions with surrounding sclerosis; sclerosis is characteristic and can be abundant • Periosteal reaction is typically solid but can be atypical, including complex, irregular, and layered appearance • Involvement of surrounding soft tissue or sinus tract formation, or both • Bone tumors can have a similar appearance, and differential diagnosis can be difficult • Spine: cortical bone collapse, disk destruction, intervertebral body fusion • Gibbus deformity: kyphosis caused by collapse of vertebral bodies in tuberculous osteomyelitis (Pott disease) Pathology Gross • In curettings, infected bone is discolored ­white-­yellow-gray • In larger specimens, areas of bone destruction are poorly circumscribed and appear as firm white-yellowgray fibroinflammatory tissue • Larger granulomas can sometimes be seen grossly as nodules, often with caseation • Extension through cortex into soft tissue may be present Histology • Variable histology depending on the causal agent and host immune factors • Necrotizing or non-necrotizing granulomatous inflammation (mycobacteria, fungi), or both • Lymphoplasmacytic or histiocytic inflammation (Treponema species, Mycobacterium leprae), or both • May see a component of suppurative inflammation (fungi) • A reas of bone necrosis with osteoclastic activity and bone resorption • Marrow replacement with fibrosis • Reactive bone formation and periosteal reaction at the lesion periphery • Microorganisms are visualized by histochemical stains or routine hematoxylin and eosin staining • Diagnosis relies on presence of diagnostic fungal forms or positive culture, or both Chronic Osteomyelitis Ancillary tests • Culture, Gram, and acid-fast stains from biopsy material • Tissue stains • Acid fast stain (Mycobacteria species) • Warthin-Starry or similar silver stains (Treponema species) • Gomori methenamine silver (fungi) • Immunohistochemical stains • Molecular tests (polymerase chain reaction) • Serology Main differential diagnosis • Subchondral inflammation in severe arthritis • Hematopoietic malignancies (myeloma, lymphoma) • Sarcoidosis (1% to 13% of cases have bone involvement) • Langerhans cell histiocytosis (eosinophilic granuloma) • Plasmacytoma/myeloma A A B Fig 2.

C, The synovial membrane is covered by a fibrinous exudate (at left). D, High magnification of the inflamed synovium shows numerous plasma cells, admixed lymphocytes, and macrophages, without significant neutrophilic component. 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.

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.

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

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