Osteoporosis, Arthritis, and Bone Diseases PDF

Osteoporosis Reduction of bone mass per unit of bone volume Metabolic bone disease Bone displays normal ratio of mineral to matrix Primary and secondary  Primary Osteoporosis Most common Uncertain etiology Postmenopausal women Elderly persons (senil...

Osteoporosis Reduction of bone mass per unit of bone volume Metabolic bone disease Bone displays normal ratio of mineral to matrix Primary and secondary  Primary Osteoporosis Most common Uncertain etiology Postmenopausal women Elderly persons (senile) – Genetic: peak bone mass – Estrogens: decline – Aging – Calcium intake (800mg/day) – Exercise – Environmental factors: smoking leads to estrogen ↓  Primary Osteoporosis Osteopenia Decrease thickness of cortex Reduction in the number and size of trabeculae Fractures can be the first sign Compression fractures of vertebrae  Secondary Osteoporosis Corticosteroids – Inhibition of osteoblastic activity – Impair of vit. D dependant intestinal calcium absorption (secondary hyperparathyroidism) Hematologic malignancies Malabsorption: GI and liver diseases Alcoholism – Inhibition of osteoblasts, – ↓ absorption of calcium  Osteomalacia and rickets Inadequate mineralization of newly formed bone matrix (osteomalacia) Rickets: children, epiphyseal plates open; also problem with cartilage – Beaded appearance of costochondral junctions – Pectus carinatum – Dental abnormalities Vitamin D deficiency (dependent) Phosphate deficiency (resistant) Defects in mineralization process  Osteomalacia and rickets Osteopenia Exaggeration of osteoid seams Poorly localized pain Femoral neck, pubic ramus, spine, ribs  Hyperparathyroidism Parathyroid adenoma, hyperplasia, rare malignancy Parathyroid hormone – Promotes excretion of phosphate in the urine and stimulates osteoclastic activity resulting in hypercalcemia – Stimulates tubular reabsorption of calcium and excretion of phosphate – Stimulates intestinal calcium absorption  Hyperparathyroidism Stones: Kidney Bones: Brown tumors Psychiatric depression GI tract irregularities  Secondary hyperparathyroidism Renal osteodystrophy Chronic renal failure – Decreased filtration of phosphate Hyperphosphatemia – Effect on active vit. D – Decreased Ca absorption in GI Hypocalcemia – Secondary hyperparathyroidism  Osteomyelitis Inflammation of bone caused by an infectious organism Staphylococcus, streptococcus, Escherichia coli, Neisseria gonorrhea, Haemophilus influenza, Salmonella Direct penetration – Wounds, fractures, surgery Hematogenous – Bloodstream, teeth; metaphyses – Knee, ankle, hip  Complications of Osteomyelitis Septicemia Acute bacterial arthritis Pathologic fractures Squamous cell carcinoma Amyloidosis Chronic osteomyelitis  Arthritis - Introduction Inflammation of joints - Common Common site for autoimmune injury – Heart valves & Joints - damage – Exposure of hidden antigens. Infections. Degeneration – Age/Stress/life style  Arthritis – Clinical features: Pain  → Inflammation - capsule, synovium, periosteum. Swelling:  → inflammation, effusion, proliferation. Restricted movement  → pain, fluid, synovial swelling, damage. Deformity  → mal-alignment, erosion, ankylosis  Osteoarthritis Most common joint disease Slow progressive degeneration of articular cartilage Weight bearing joints Fingers Primary: defect in cartilage, not an inflammatory disease Secondary: trauma, crystal deposits, infection Interphalangeal joints, knees, hips, cervical and lumbar spine  Osteoarthritis Narrowing of joint space (loss of disk) Increased thickness of subchondral bone – Eburnated bone Subchondral bone cysts Osteophytes (Haberden nodes) – Fingers, distal interphalangeal joints  Causes Primary Secondary as: Intra articular fracture Previous infective arthritis Rheumatoid Congenital dislocation of hip  Abnormal stresses as Paget’s disease with deformity Chronic overuse Metabolic and endocrine as : Hemochromatosis Gout Calcium phosphate deposition  Neuropathic disorders as : Peripheral neuropathy as in diabetes mellitus Intraarticular corticosteroid in excess  Osteoarthritis: Degenerative end result - (ageing) >80% in >65y. Progressive erosion & fibrillation of articular cartilage → forms Loose bodies. Large weight bearing joints. Hardened articular bone – eburnation. & Subarticular cyst formation in bone. Periarticular osteophyte formation. Mild inflammation but painful, morning stiffness. Limited range of movements Heberden nodes (F)  Radiologic Features: no uniform joint space loss, osteophyte formation, cyst formation subchondral sclerosis Sclerosis, ankylosis & deformity.  Rheumatoid arthritis Systemic chronic inflammatory disease Autoimmune disease Diarthrodial joints bilaterally STARTS AS SYNOVIAL DISEASE 3:1 women Remissions and exacerbations Heredity; EBV(?)  Theory of Pathogenesis Genetically susceptible patient Infection ? Formation of Abs Abs act as new antigens Production of rheumatoid factor Deposits of immune complexes in the synovium Activation of complement cascade Inflammation Activation of macrophages Homing of T cells Secretion of cytokines  RA - Definition: Chronic Multisystem autoimmune inflammatory disorder primarily affecting joints producing a proliferative synovitis that often progresses to destruction of the articular cartilage and ankylosis.  Etiology: Genetic Susceptibility: – HLA DR4, or DR1 in 65% to 80% cases. Microbial inciting agent: – Epstein-Barr virus, Borrelia & Mycoplasma Autoimmunity: – IGM anti IgG – RA Factor. – Helper T cell (CD4) against type II collagen & cartilage glycoprotein-39  Pathology Inflammation of the joint and hyperplasia of the synovium followed by destruction of the articular structures The synovium infiltrated with lymphocytes and plasma cells Fibrin exudation on the synovial fluid forming sometimes soft loose bodies called Rice bodies Neutrophil polymorphs are present  All previous changes are reversible When granulation tissue grows over the surface of the articular cartilage Pannus interfere with the nutrition of the cartilage leads to permanent joint damage.  Histopathological features Rice bodies Hyperplastic synovium Pannus Allison-Ghormley bodies Rheumatoid nodules  Extra articular manifestation Rheumatoid nodule Vasculitis Cardiac disease Pulmonary disease Serosal inflammation Amyloidosis Anemia Eye involvement  Morphology: Proliferative synovitis with lymphocytes (CD4), plasma cell & macrophages Pannus. Organizing fibrin (rice bodies). Neutrophils on the joint surface and fluid. Juxta-articular erosions, cysts & osteoporosis Fibrous ankylosis. Skin - Rheumatoid nodules Vasculitis (commonly of digital arteries)  RA - Clinical Features: 1. Morning stiffness. 2. Arthritis in 3 or more joint areas. 3. Arthritis of small hand joints. 4. Symmetric arthritis. 5. Rheumatoid nodules. 6. Serum rheumatoid factor. 7. Typical radiographic changes At least 4 features for diagnosis.  Extra-Articular RA Rheumatoid Nodules Vasculitis Pleuritis Pericarditis Tendonitis  Rheumatoid arthritis osteoarthritis Age Any age 25- 55 Elderly Affected joint Symetrical artheritis Hip metacarbophalangeal Knee inerphalangeal wrist Ankle shoulder Synovium Hyperplasia dense Mild secondary inflammation inflammation Articular cartilage Eroded by pannus loss of weigh bearing surface Systemic disease Yes No Pathogenesis Autoimmune disease degenerative  Juvenile rheumatoid artheritis Starts below 16 years Most common 1- 3 years High spiking fever daily or twice daily Hepatosplenomegaly Serosal inflammation ( pericarditis ) Generally involve knee, wrist, elbow, small joints of hands and feet.  Juvenile Rheumatoid Arthritis: Before age 16 Multisystem involvement - Splenomegaly, Starts with systemic involvement unlike RA. No serum RA Factor – Seronegative Antinuclear Antibody (ANA) +ve → autoimmune.