Mastering Joint Pathology: Arthritis, OA & Joint Anatomy

JOINT PATHOLOGY Bone & Soft Tissue Pathology MKU Pathology — Dr. Lilian Bosire --- I. JOINT STRUCTURE — OVERVIEW Classification of Joints Solid (Non-synovial) Joints — Synarthroses Lack a joint space; allow minimal movement; provide structural integrity Fibrous synarthroses: Cranial sutures, tooth-jawbone bonds Cartilaginous synarthroses (synchondroses): Symphyses — manubriosternal, pubic symphysis Synovial Joints Have a joint space → wide range of motion Formed at ends of bones via endochondral ossification Strengthened by dense fibrous capsule, ligaments, and muscles Boundary = synovial membrane — anchored to the capsule; does NOT cover the articular surface; forms villous folds near osseous insertion Synovial Membrane Two cell types in 1–4 cell deep layers: Type A synoviocytes — specialized macrophages; phagocytic activity Type B synoviocytes — fibroblast-like; synthesize hyaluronic acid and proteins Lacks a basement membrane → allows efficient exchange of nutrients, gases, and waste between blood and synovial fluid Synovial Fluid Hyaluronic acid-rich plasma filtrate Acts as a viscous lubricant Provides nutrition to avascular articular cartilage Hyaline Cartilage Composition: Water (70%), Type II collagen (10%), Proteoglycans (8%), Chondrocytes Type II collagen → resists tensile stress, transmits vertical loads Water + proteoglycans → limit compression and friction Avascular, alymphatic, aneural Chondrocytes synthesize and digest matrix; half-life of proteoglycans = weeks; type II collagen = years Chondrocytes secrete degradative enzymes in inactive forms + enrich matrix with enzyme inhibitors Disease destroys cartilage by activating degradative enzymes and reducing inhibitor production Key cytokines driving destruction: IL-1, TNF — released by chondrocytes, synoviocytes, fibroblasts, and inflammatory cells --- II. ARTHRITIS Arthritis = inflammation of joints. Major types: Feature Osteoarthritis Rheumatoid Arthritis --- --- --- Primary abnormality Mechanical cartilage injury Autoimmunity Role of inflammation Secondary; exacerbates damage Primary driver Joints involved Weight-bearing (knees, hips) Small joints first; progresses Pathology Cartilage degeneration, osteophytes, subchondral cysts Pannus, ankylosis Serum antibodies None ACPA, rheumatoid factor Other organs No Yes (lungs, heart, vessels) --- III. OSTEOARTHRITIS (OA) Also called degenerative joint disease . Most common joint disease. Definition & Epidemiology Primarily a degenerative disease of cartilage, not primarily inflammatory (despite the name) Primary OA: Idiopathic, aging-related; usually oligoarticular; onset 50 years; ~40% of people 70 years affected Secondary OA: Younger individuals with predisposing factors — joint deformity, prior injury, diabetes, ochronosis, hemochromatosis, marked obesity Knees and hands more common in women; hips more common in men Pathogenesis Principal mechanism: biomechanical stress on articular cartilage Genetic polymorphisms in matrix components and signaling molecules predispose to chondrocyte injury Chondrocytes proliferate and synthesize proteoglycans, but degradation exceeds synthesis Chondrocytes secrete MMPs → degrade type II collagen network Cytokines involved: TGF-β (induces MMPs), TNF, prostaglandins, nitric oxide Chronic low-level inflammation contributes to disease progression Advanced disease: chondrocyte loss + severe matrix degradation Morphology — Sequential Changes Early: Chondrocytes proliferate and form clusters Matrix water content increases; proteoglycan concentration decreases Horizontal collagen fibers in superficial zone are cleaved → surface becomes granular and soft (fibrillation) Progressive: Fissures and clefts form Full-thickness cartilage sloughs → loose bodies (joint mice) in joint space Exposed subchondral bone becomes new articular surface Friction burnishes exposed bone → bone eburnation (ivory-like appearance) Late: Subchondral bone undergoes sclerosis and microfractures Synovial fluid forced into subchondral regions → subchondral cysts Osteophytes — mushroom-shaped bony outgrowths at joint margins, capped by fibrocartilage/hyaline cartilage that gradually ossifies Synovium: mildly congested and fibrotic, minimal inflammation Clinical Features Asymptomatic until 50s in primary OA Deep, achy pain worsening with use Morning stiffness (brief, unlike RA) Crepitus , limited range of motion Osteophytes on spinal foramina → nerve root compression → radicular pain, muscle spasm, neurological deficits Heberden nodes — prominent osteophytes at distal interphalangeal joints; common in women Wrists, elbows, shoulders usually spared Deformities develop but joint fusion does NOT occur (contrast with RA) Radiographic severity does not correlate well with pain/disability Treatment No disease-modifying agents available Pain management, NSAIDs, intraarticular corticosteroids, activity modification Severe cases → arthroplasty --- IV. RHEUMATOID ARTHRITIS (RA) Definition & Epidemiology Chronic