Degenerative and inflammatory joint diseases

1. Degenerative Joint Disease → Osteoarthritis (OA)

Definition

• Most common joint disorder.
• Part of aging (“wear and tear”) → degeneration of articular cartilage.

Classification

• Primary OA: appears with aging, no apparent cause.
• Secondary OA: in younger people; associated with:
  • Previous traumatic injury
  • Developmental deformity
  • Marked obesity
• Distribution:
  • Women: knees, hands.
  • Men: hips.

Morphology

• Superficial cartilage degraded → fibrillation + cracking of matrix.
• Cartilage contains more water + less proteoglycans.
• Bone eburnation: exposed bone plate polished by friction.
• Reactive bone outgrowths (osteophytes).
• Small fractures → subchondral cysts.

Pathogenesis

• Stimulus: genetic factors, mechanical stress, aging.
• Cartilage → ↑ water + ↓ collagen/proteoglycan → strength compromised.
• Chondrocyte apoptosis → chondromalacia (soft + granular cartilage).

Clinical Course

• Affects 50s–60s.
• Main joints: hip, knees, DIP + PIP of fingers.
• Sx: aching pain, morning stiffness (< 30 min), crepitus, ↓ ROM.
• Bony outgrowth in spinal foramina → nerve root compression → muscle spasms, atrophy, neurologic deficits.
• Heberden nodes: DIP swelling from osteophytes.
• Bouchard nodes: PIP swelling.

2. Inflammatory Joint Disease

A) Infectious (Suppurative) Arthritis

• Rapid joint destruction + permanent deformities.
• Routes: hematogenous (bacteremia), direct inoculation, contiguous spread from osteomyelitis.
• Pathogens:
  • H. influenzae in children < 2 yr (now rare due to Hib vaccine).
  • S. aureus in adults (most common overall).
  • N. gonorrhoeae — sexually active young adults; #1 in sexually active; migratory arthritis, tenosynovitis, dermatitis.
  • Salmonella — sickle cell.
• Sudden onset of pain, redness, swelling of joint; fever.
• Tx: arthrocentesis + IV antibiotics; emergency.

B) Rheumatoid Arthritis (RA)

Overview

• Systemic chronic inflammatory autoimmune disease; mainly joints.
• Non-suppurative proliferative synovitis in small joints → destruction of articular cartilage + underlying bone.
• F : M = 5:1; peak 40–50 yr.
• HLA-DR4 association.

Pathogenesis

• Autoimmune: CD4⁺ T cells secrete cytokines (IFN-γ, TNF, IL-1) → inflammation (loss of self-tolerance).
• Anti-CCP (cyclic citrullinated peptide) antibodies → cause joint lesions; most specific marker.
• Rheumatoid factor (RF): autoantibody (IgM) against Fc portion of own IgG → immune complex (2 antibodies bound) → deposited in joints → inflammation + tissue damage.

Morphology — Synovitis → Pannus → Ankylosis

• Symmetric arthritis in small joints of hands, feet, ankles (MCP, PIP; spares DIP).
• Chronic synovitis:
  • Synovial cell hyperplasia.
  • Neutrophils + fibrin aggregates in joint space.
  • ↑ Osteoclast activity → synovial penetration + bone erosion.
• Pannus: synovial membrane becomes frond-like + edematous, invades cartilage.
• Ankylosis: fibrosis + calcification → permanent joint stiffness; destroys tendons, ligaments, capsule → deformities.

Clinical Features

• Aching pain + morning stiffness > 1 hr (improves with use).
• Joint enlargement → ↓ ROM → complete ankylosis (“craw-like position”, ulnar deviation, swan-neck, boutonnière).
• Extra-articular: rheumatoid nodules (subcutaneous over extensor surfaces), vasculitis, ILD, pericarditis, Sjögren overlap.
• Felty syndrome: RA + splenomegaly + neutropenia.

C) Gout

Overview

• Inflammatory arthritis with recurrent attacks of red, tender, hot, swollen joint.
• Cause: excessive uric acid (end product of purine metabolism).
• Low uric acid = anti-inflammatory; high uric acid = pro-inflammatory.

Types

• Primary gout: unknown cause / inborn metabolic defect → hyperuricemia (e.g., HGPRT deficiency — Lesch-Nyhan).
• Secondary gout: known cause:
  • ↑ Nucleic acid turnover: tumor lysis, leukemia, psoriasis (↑ production).
  • ↓ Renal excretion: chronic renal disease, thiazides, alcohol.

Pathogenesis + Morphology

• Acute arthritis: neutrophilic infiltration of synovium with monosodium urate crystals.
  • Needle-shaped, negatively birefringent under polarized light (yellow when parallel).
• Chronic arthritis: repetitive urate precipitation → synovial thickening → cartilage destruction + bone erosion.
• Tophi (hallmark of gout): aggregates of urate surrounded by inflammatory cells → in articular cartilage, soft tissue, helix of ear.
• Gout nephropathy: renal complications from urate deposition.

Clinical Features (4 stages)

1. Asymptomatic hyperuricemia.
2. Acute gouty arthritis: sudden, excruciating pain (typically 1st MTP joint = podagra); resolves.
3. Intercritical gout: between attacks; recurrent.
4. Chronic tophaceous gout: tophi, juxta-articular bone erosion, loss of joint space.

Triggers

• Alcohol (beer), red meat, seafood (purine-rich); diuretics; surgery.

Treatment

• Acute: NSAIDs, colchicine, glucocorticoids.
• Chronic: allopurinol/febuxostat (xanthine oxidase inhibitors), probenecid (uricosuric).

3. Comparison Table

Feature	Osteoarthritis	Rheumatoid Arthritis	Gout
Mechanism	Wear/tear, cartilage degen	Autoimmune synovitis	Urate crystal deposition
Age	50–60s	40–50	Middle-aged men
Joints	DIP/PIP, knees, hips	MCP/PIP, wrists (spares DIP)	1st MTP (podagra), big toe
Stiffness	< 30 min, AM	> 1 hr, AM	Sudden severe attacks
Distribution	Asymmetric	Symmetric	Mono/oligoarticular
Crystals	None	None	Needle-shaped, negatively birefringent (yellow ∥)
Labs	Normal	RF, anti-CCP, ↑ ESR	↑ Uric acid
Nodes / nodules	Heberden (DIP), Bouchard (PIP)	Rheumatoid nodules	Tophi

💡 High-yield: OA = wear & tear; DIP/PIP/knees/hips; Heberden (DIP) + Bouchard (PIP) nodes; osteophytes + bone eburnation + chondromalacia; morning stiffness < 30 min. RA = autoimmune, F 5:1, MCP/PIP (spares DIP); anti-CCP (most specific) + RF; synovitis → pannus → ankylosis; ulnar deviation + swan-neck; rheumatoid nodules. Septic arthritis: S. aureus #1 adults, Hib < 2 yr (rare), gonococcus in sexually active; Salmonella in sickle cell. Gout = uric acid; podagra (1st MTP), needle-shaped negatively birefringent crystals, tophi (hallmark), Lesch-Nyhan; Tx allopurinol.