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Bone Pathology Normal anatomy • Parts of a long bones: diaphysis (shaft), • physis (growth plate), epiphysis (ends of bone, partially covered by articular cartilage), metaphysis (junction of diaphysis and epiphysis, most common site of primary bone tumors) Cross section: periosteum, cortex (composed of cortical bone or compact bone), medullary space (composed of cancellous or spongy bone) HISTOLOGY • INFECTIONS • BONE TUMORS OSTEOMYELITIS: Denotes inflammation of bones and marrow. • May be a complication of any systemic infection but frequently manifests as a primary solitary focus of disease. • Pyogenic Osteomyelitis. • Tuberculous osteomyelitis • PYOGENIC OSTEOMYELITIS: is almost always caused by bacteria. 1. Hematogenous spread. 2. Extension from a contiguous site. 3. Direct implantation. • E.coli, Klebsiella and Pseudomonas. • Mixed bacterial infections. • Salmonella infections. Sites of involvement: • Influenced by the vascular circulation, which varies with age. • Neonates: the metaphyseal vessels penetrate the growth plate, resulting in frequent infection of the metaphysis, epiphysis or both. • In children: metaphyseal. • Adults: epiphyses and subchondral regions. • Clinical Course: • Fever ,chills, malaise, marked to intense throbbing pain over the affected region. Diagnosis; • Sign/symptoms. • X-ray • Blood cultures • biopsy Complications: • Pathologic fracture. • Secondary amyloidosis • Endocarditis • Sepsis • Squamous cell carcinoma. • Rarely sarcoma in the affected bone Tuberculous osteomyelitis: Routes of entry; • Usually blood borne and originate from a focus of active visceral disease. • Direct extension (e.g. from a pulmonary focus into a rib or from tracheobronchial nodes into adjacent vertebrae) or spread via draining lymphatics. Bone tumors Although the cause of most bone tumors is unknown. Genetic alterations e.g. bone sarcomas in the Li-Fraumeni and hereditary retinoblastoma which are linked to mutations in p53 and Rb genes. Bone infarcts chronic osteomyelitis pagets disease radiation and metal prostheses are also associated with increased incidence of bone neoplasia. Classification of primary tumors involving bones: • Bone Forming tumors. • Cartilage forming tumors. • Fibrous and fibro-osseous tumors. • Miscellaneous tumors. JOINTS/TYPES • Synovial or nonsynovial Synovial joints: also called diarthroses; contain joint space between ends of bones, joints covered by hyaline cartilage, strengthened by dense fibrous capsule continuous with periosteum of bones and an inner synovial membrane; joint is reinforced by ligaments and muscles; presence of joint space allows wide range of motion. JOINTS/TYPES • Nonsynovial joints: also called solid joint or synarthrosis; no joint space present; provides structural integrity and minimal movement Arthritis • SUPPURATIVE ARTHRITIS • TUBERCULOUS ARTHRITIS • OSTEOARTHRITIS • RHEUMATOID ARTHRITIS ARTHRITIS • Suppurative arthritis: • Due to seeding of joint during bacteremia, most • • • • commonly due to Staphylococcus, Streptococcus, gram negative rods; rarely syphilis Also due to postsurgical infection Neonates: often due to osteomyelitis Young women: most commonly due to gonorrhea (gram negative intracellular diplococci, which is associated with multiple joint involvement, including the knee) Sickle cell disease: Salmonella ARTHRITIS • Tuberculous arthritis: • Insidious onset of chronic progressive arthritis, usually • • • monoarticular in knee and hip; usually after osteomyelitis Leads to fibrous ankylosis of joint with obliteration of joint space Can detect from culture and examination of synovial fluid. PCR is sensitive; apparent false positives in clinically negative patients may represent early disease. ARTHRITIS Degenerative joint disease: • Also called osteoarthritis. • Nonneoplastic disorder of progressive erosion of articular cartilage associated with aging, trauma, occupational injury. • Usually age 50+ years (present in 80% at age 65 years) • Cartilage degradation may be mediated by IL-1. • Sites: men-hips, women-knees and hands; also first metatarsophalangeal joint, lumbar spine; usually one joint or same joint bilaterally, at least initially Osteoarthritis • Symptoms: pain worse with use of joint, • crepitus, limited range of motion, nerve root compression; Heberden nodes in fingers of women only (osteophytes at DIP joints) Secondary degenerative joint disease: younger patients with predisposing condition (trauma, congenital, diabetes, obesity, ochronosis, hemochromatosis), such as knees of basketball players Osteoarthritis • Gross: early changes are even degeneration of hyaline • cartilage of articular surface, with fragmentation later thinning of cartilage and articular surface is often soft and granular with altered shape, sloughing of cartilage . cysts: (synovial fluid forced into fractures via ball valvelike mechanism), osteophytes: (bony outgrowths at margins of articular surface) Osteoarthritis • Loose bodies: may form if portion of articular cartilage breaks off; normally loose body is nourished by synovium and continues to grow. GOUT • Gout and gouty arthritis • Transient attacks of acute arthritis initiated by • • crystallization of urates and neutrophils, followed by chronic gouty arthritis with tophi in joints and urate nephropathy Causes 2-5% of chronic joint disease Sites: 50% have initial attack in first metatarsophalangeal joint; also ankles, heels, knees, wrists, fingers, elbows GOUT • Primary gout (90%): idiopathic (85%) with • overproduction of uric acid or known enzyme defects. Secondary gout (10%): increased nucleic acid turnover due to leukemia/lymphoma, chronic renal disease. GOUT • Gout is due to hyperuricemia and deposition of • • monosodium urate crystals in joints and viscera and uric acid kidney stone formation. Need serum urate > 7 mg/dl for deposition (saturation threshold for urate at 98.6 F) Risk factors for gout with hyperuricemia are age > 30 years, familial history of gout, alcohol use, obesity, thiazide administration, lead etc. Rheumatoid arthritis • Chronic systemic inflammatory disorder affecting • • • synovial lining of joints, bursae and tendon sheaths; also skin, blood vessels, heart, lungs, muscles Produces nonsuppurative proliferative synovitis, may progress to destruction of articular cartilage and joint ankylosis 75% are women, peaks at ages 10-29 years; also menopausal women Sites: small bones of hand affected first (MCP, PIP joints of hands and feet), then wrist, elbow, knee Rheumatoid arthritis • Xray: joint effusions, erosions • narrowing of joint space; destruction of tendons, ligaments and joint capsules produce radial deviation of wrist, ulnar deviation of digits, swan neck finger abnormalities Rheumatoid arthritis • Diagnosis: morning stiffness, arthritis in 3+ joint areas • arthritis in hand joints, • symmetric arthritis, • rheumatoid nodules, rheumatoid factor, typical radiographic changes OSTEOPOROSIS Is a term that denotes increased porosity of the skeleton resulting from reduction in the bone mass. It may be localized →disuse osteoporosis of a limb. or may involve the entire skeleton, as a metabolic bone disease. OSTEOPOROSIS • Primary • Secondary PRIMARY: post menopausal Senile OSTEOPOROSIS • Secondary: • Endocrine Disorders OSTEOPOROSIS Pathophysiology: • AGING • ↓ replicative activity of the osteoprogenitorcells • ↓ synthetic activity of the osteoblasts. • ↓ activity of the matrix bound growth factors. OSTEOPOROSIS • Menopause: • ↓ serum estrogen • ↑ IL-1,IL-6 levels • ↑ osteoclast activity Genetic factors Nutritional effects OSTEOPOROSIS Prevention Strategies • The best long-term approach to osteoporosis is prevention. • children and young adults, particularly women, with a good diet (with enough calcium and vitamin D) and get plenty of exercise, will build up and maintain bone mass. • This will provide a good reserve against bone loss later in life. Exercise places stress on bones that builds up bone mass