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

Retailer time settling on and diagnosing pathology specimens with excessive Yield Bone and tender Tissue Pathology, edited through Drs. Andrew Horvai and Thomas hyperlink. a part of the High-Yield Pathology sequence, this identify is designed that will help you overview the major pathologic positive aspects of bone and soft-tissue malformations, realize the vintage glance of every sickness, and quick make certain your prognosis. Its templated layout, very good colour photos, concise bulleted textual content, and authoritative content material may also help you competently determine greater than a hundred and sixty discrete ailment entities.

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In addition, severe degenerative disease of the patello­ femoral joint is more advanced compared with the other joint compartments, which is a typical finding for CPPD. Fig 4. A and B, Hydroxyapatite (HA) deposition disease, seen here within a tendon (calcific tendonitis), demonstrates dense, basophilic matrix similar to bone. , hypervitaminosis D, renal failure, milk-alkali syndrome) in tumoral calcinosis. 37 ACUTE OSTEOMYELITIS Definition and synonyms • Acute inflammation of the bone resulting from infection by a microbial pathogen (acute bacterial osteomyelitis, acute suppurative osteomyelitis) Clinical features Epidemiology • Most cases are caused by bacteria, less commonly fungi • Three modes of pathogen entry: hematogenous, contiguous spread, and direct inoculation • Osteomyelitis from hematogenous spread (~20% of cases) • Most common in children (1 to 16 years old), maleto-female ratio of 2:1 • R isk factors: indwelling catheters, chronic infections, debilitating conditions, immunocompromised states, nonpenetrating trauma, intravenous drug use • Most common sites: • Children: long bones, usually limited to ­metaphysis • Adults: spine more than pelvis more than long bones • Usually solitary and primary and associated with a single pathogen • Most frequent pathogens: S.

Hyperpara­ thyroidism or Paget disease of bone), particularly if prolonged bed rest • Frequent sites of involvement include kidneys, lungs, cornea, conjunctiva, stomach mucosa, media, and intima of blood vessels • Dystrophic calcification • Not related to disturbances in calcium homeostasis • Common at sites of coagulative necrosis and fat necrosis • May be secondary to trauma • Tumoral calcinosis • Most cases sporadic, some familial cases reported • Usual onset in second decade of life • Characterized by deposition of painless calcific masses around hips, elbows, shoulders, and gluteal areas • Lesions are usually bilateral, affect multiple sites and can be massive • Rarely, intra-articular or intraosseous deposits are present • Serum phosphate is usually elevated • Treatment: excision, low phosphate diet, phosphate binders, diuretics Radiology • CPPD • Radiodense deposits (unlike radiolucent deposits in gout) are characteristically in fibrocartilage in particular menisci (punctate or linear) but may also be in hyaline cartilage (usually parallel subchondral bone end plate) • P unctate deposits may also be seen in synovium • Accelerated degenerative changes, including joint space narrowing and bony sclerosis • Hydroxyapatite deposition, metastatic calcification, dystrophic calcification, tumoral calcinosis • Radiodense soft tissue deposits (calcifications) Pathology Gross • CPPD • Small chalky-white deposits in the affected tissues • Hydroxyapatite deposition • Small calcified soft tissue deposits • Metastatic calcification • Small calcified deposits may not be apparent grossly • Dystrophic calcification • Small calcified deposits may not be apparent grossly • If large enough, may form irregular calcified nod­ ules or masses • Tumoral calcinosis • Irregular calcified soft tissue deposits, masses Histology • CPPD • Crystalline or amorphous deposits composed of small rhomboidal crystals with weak positive bire­ fringence (appear dim blue) • For optimal crystal preservation, ethanol fixation or examination of fresh tissue (smears), or both, may be needed (particularly if gout is in the differential) • In nonvascularized tissue, inflammatory changes are typically not present • Deposits in vascularized tissue may be surrounded by chronic inflammatory and giant cell reaction, often mimicking findings of gout • Hydroxyapatite deposition, metastatic calcification, dystrophic calcification, tumoral calcinosis • Calcified deposits of varying size surrounded by varying, usually mild degree of chronic inflamma­ tion with macrophages and frequently giant cells • No birefringent crystals Ancillary tests • CPPD • Demonstration of sodium pyrophosphate crystals in synovial fluid (see earlier) 35 Other Crystal-Induced Synovitis and Calcium Deposition 36 • Hydroxyapatite deposition, metastatic calcification • Specific testing for associated conditions • Tumoral calcinosis • Serum phosphate is usually elevated A Main differential diagnosis • CPPD • Gout • Osteoarthritis • R heumatoid arthritis • Septic arthritis A B Fig 1.

Fig 4. An infiltrate of neutrophils replaces the marrow space. 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.

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