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Osteoarthritis
The most common type of joint disease characterized by the progressive erosion of articulating cartilage, resulting in breakdown due to biochemical and metabolic alterations.
Pathogenesis
The development of osteoarthritis is attributed to aging, mechanical stresses, and predisposing conditions like joint deformity, previous joint injury, diabetes, ochronosis, hemochromatosis, or obesity.
Genetic Factors
Genetic components play a role in osteoarthritis, leading to changes in cartilage composition, mechanical properties, decreased collagen synthesis, and increased cartilage breakdown.
Morphology
Osteoarthritis manifests as fibrillation, cracking of cartilage, bone eburnation, subchondral bone cysts, and osteophytes developing at the margins of the articular surface.
Clinical Course
Symptoms of osteoarthritis typically appear in the fifties, including deep pain, morning stiffness, crepitus, and joint limitation, with management involving pain control, activity modification, and arthroplasty for severe cases.
Purine Metabolism
The process involving the synthesis and breakdown of purine nucleotides like adenine and guanine.
Gout
A form of arthritis characterized by sudden, severe attacks of pain, redness, and tenderness in joints.
Chronic Tophaceous Arthritis
Advanced stage of gout where tophi deposits lead to joint damage and deformity.
Pseudogout
A condition similar to gout but caused by calcium pyrophosphate crystal deposits in the joints.
Suppurative Arthritis
Joint infection caused by bacteria, leading to pain, swelling, and fever.