Osteoarthritis

Etiology

• Risk Factors
  • Age: Most significant risk factor.
  • Obesity: Increases mechanical stress on weight-bearing joints (knees, hips).
  • Female gender: More common in women, especially post-menopause.
  • Joint Trauma/Overuse: Previous injuries or occupations with repetitive stress can predispose to OA.
  • Genetics: A family history plays a role, particularly in OA of the hand and hip.

---

Clinical Features

• History:
  • Pain: Deep, aching; worse with activity/weight-bearing, relieved by rest (advanced disease may have pain at rest/night).
  • Stiffness: Morning stiffness < 30 minutes; “gelling” phenomenon (transient stiffness after brief inactivity).
  • Distribution: Asymmetric or symmetric; weight-bearing joints (knees, hips), spine (cervical/lumbar), and hands.
  • Hand involvement: DIP joints and PIP joints, 1st CMC joint (spares MCP joints and wrists).
  • Absence of constitutional symptoms (no fever, weight loss, or fatigue).
• Physical Examination:
  • Bony enlargement & joint line tenderness.
  • Crepitus on active/passive ROM.
  • Decreased active and passive ROM.
  • Heberden nodes (osteophytes at DIP joints).
  • Bouchard nodes (osteophytes at PIP joints).
  • “Squaring” of the hand (1st CMC joint osteophytes/subluxation).
  • Minimal/cool joint effusion without prominent warmth or erythema.

Diagnosis

• Initial / Best Initial Test: Clinical diagnosis (often sufficient based on age, typical hx, and PE findings).
• Imaging:
  • Plain Radiographs (X-ray): Weight-bearing views (knee/hip).
  • Classic 4 Radiographic Findings:
    1. Asymmetric joint space narrowing (loss of articular cartilage).
    2. Subchondral sclerosis (bone thickening/hardening).
    3. Osteophyte formation (bony spurs at margins).
    4. Subchondral cysts (geodes).
• Key Labs:
  • ESR / CRP: Normal (rules out systemic inflammatory arthritides).
• Synovial Fluid Analysis (Arthrocentesis):
  • Indicated only if diagnosis is uncertain or to exclude infection/crystals during an acute effusion.
  • Findings: Non-inflammatory (clear/yellow, WBC < 2,000/mm³, < 25% PMNs, negative Gram stain/crystals).

---

Differential diagnosis

---

• Traditionally, osteoarthritis (OA) has been classified as a non-inflammatory or “wear-and-tear” arthritis
  • The inflammation is generally less pronounced
  • It doesn’t typically feature systemic inflammation markers
  • It doesn’t involve autoimmune mechanisms as its primary cause
  • Morning stiffness is typically shorter in duration

Osteoarthritis (OA) vs Rheumatoid Arthritis (RA)

Feature	Osteoarthritis (OA)	Rheumatoid Arthritis (RA)
Mechanism	Mechanical “Wear & Tear”	Autoimmune (Pannus)
Stiffness	< 30 min (Worse w/ use)	> 1 hr (Better w/ use)
Symmetry	Asymmetric	Symmetric
Key Joints	DIP (Heberden), PIP, Knees	MCP, PIP, Wrist (Spares DIP)
Labs	Normal	+Anti-CCP (Specific), +RF, ↑ ESR
X-ray	Osteophytes, Sclerosis	Marginal Erosions, Osteopenia
Treatment	NSAIDs, Acetaminophen	DMARDs (Methotrexate)

1. Stiffness

• OA (<30m): “Gelling.” Synovial fluid gets thick at rest. Movement quickly warms and lubricates it.
• RA (>1h): Edema. Inflammatory fluid pools during sleep. Takes time to mechanically pump/drain the boggy joint.

2. Pain

• OA (Worse w/ use): Mechanical. Bone-on-bone friction compresses exposed nerve endings.
• RA (Better w/ use): Washout. Movement flushes out stagnant inflammatory cytokines and fluid, relieving pressure.

3. Pathology

• OA (Osteophytes): Construction. Bone grows spurs to widen surface area and stabilize the failing joint.
• RA (Erosions): Destruction. Pannus (granulation tissue) releases enzymes/RANKL that eat into the bone.

Link to original

Management

1. First-line (Non-Pharmacologic - Foundational for all patients):
   • Weight loss (reduces mechanical load, particularly for knee/hip OA).
   • Physical therapy / low-impact exercise (e.g., quadriceps strengthening, swimming, cycling). c
   • Biomechanical interventions: Contralateral cane use, lateral wedge insoles, shock-absorbing footwear.
2. First-line (Pharmacologic - Symptom Relief):
   • Topical NSAIDs (e.g., topical diclofenac): Preferred initial medication, especially for knee OA and elderly patients (minimal systemic SEs). c
   • Oral NSAIDs (e.g., celecoxib, naproxen, ibuprofen): Most effective oral pharmacotherapy. Use lowest effective dose; add PPI in patients at high risk for GI bleeding. Monitor renal function and BP/CV risk.
   • Note: Acetaminophen has limited efficacy compared to NSAIDs; topical capsaicin is a secondary adjuvant.
3. Second-line / Refractory to First-Line Oral/Topical Agents:
   • Intra-articular (IA) corticosteroid injections: Short-term relief (weeks to months) for acute moderate-to-severe exacerbations/effusions.
   • Duloxetine: SNRI effective as adjunctive therapy for chronic OA pain (especially with comorbid depression or central sensitization).
4. Refractory / Advanced Disease (Definitive):
   • Total Joint Arthroplasty (TJA) (e.g., total knee/hip replacement).
   • Indication: Severe pain, refractory to conservative therapy, leading to significant impairment in activities of daily living (ADLs) with radiographic evidence of advanced disease.

Tip

Pharmacotherapy should only be used as a short-term treatment in symptomatic patients; long-term therapy is associated with many adverse effects.