Osteoarthritis
A wear-and-tear condition where the cartilage protecting the ends of bones wears down, causing pain, stiffness, and bone-on-bone friction in joints like the knees and hips.
Emergency Management: OA itself rarely causes emergencies. A ruptured Baker's cyst can cause acute calf swelling and pain, requiring ultrasound to rule out DVT.
Osteoarthritis is a chronic, degenerative joint disease characterized by the progressive loss of articular cartilage, subchondral bone remodeling, osteophyte (bone spur) formation, and synovial inflammation. It is the most common form of arthritis and primarily affects weight-bearing joints and the hands.
Detailed Overview
Once thought to be simple 'wear and tear', OA is now recognized as an active disease process involving defective cartilage repair and low-grade inflammation. Chondrocytes undergo phenotypic changes, producing proteases that degrade the extracellular matrix. As cartilage thins, bone rubs on bone, causing severe pain and functional disability. It is a leading cause of mobility impairment worldwide.
Epidemiology & Demographics
Affects over 32 million adults in the US. Prevalence rises exponentially after age 50. Women are more frequently affected than men, particularly for hand and knee OA.
Etiological Mechanism
A combination of mechanical stress on the joint and biochemical alterations in the articular cartilage and subchondral bone.
Primary Causes
Primary OA is age-related and idiopathic. Secondary OA results from prior joint trauma (e.g., ACL tear), congenital joint malformations (e.g., hip dysplasia), or metabolic disorders (e.g., hemochromatosis).
Mechanical stress and aging alter chondrocyte function. Chondrocytes release matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS) that degrade type II collagen and aggrecan in the extracellular matrix. Cartilage fibrillates and eventually ulcerates. The denuded subchondral bone undergoes sclerosis and microfractures, forming subchondral cysts. At the joint margins, endochondral ossification creates osteophytes. The synovium thickens and produces excess fluid containing inflammatory cytokines (IL-1b, TNF-a).
Diagnostic Criteria & Guidelines
Primarily a clinical and radiographic diagnosis. American College of Rheumatology criteria for knee OA: Knee pain plus at least 3 of: Age > 50, stiffness < 30 mins, crepitus, bony tenderness, bony enlargement, no palpable warmth. X-rays confirm findings.
Non-pharmacologic: Weight loss (goal >5% body weight), targeted physical therapy (quadriceps strengthening for knee OA), and supportive braces/canes. Pharmacologic: Topical NSAIDs (Diclofenac 1% gel QID) and/or Oral NSAIDs (Naproxen 500 mg BID or Celecoxib 200 mg daily) taken with PPIs if GI risk is high.
Second-Line & Adjunctive Therapy
Intra-articular glucocorticoid injections (e.g., Triamcinolone 40 mg) for acute flares (up to 3-4 times per year). Duloxetine (30-60 mg PO daily) for chronic pain management. Intra-articular hyaluronic acid injections (controversial efficacy).
Surgical & Procedural Management
Total Joint Arthroplasty (e.g., Total Knee Replacement or Total Hip Replacement) is definitively indicated for severe disease refractory to conservative management with unacceptable quality of life.
Patient Counseling & Advice
Educate that X-ray severity does not perfectly correlate with pain levels. Advise that paracetamol/acetaminophen is no longer considered first-line due to lack of efficacy. Reassure that appropriate exercise will not 'wear out' the joint faster.
Follow-Up & Monitoring Schedule
Clinical reassessment every 6-12 months for pain control, functional status, and side effects of chronic NSAID use (monitor blood pressure, creatinine, and hemoglobin).
Preventive Strategies
Maintaining an optimal body weight and preventing traumatic joint injuries during sports.
Progressive and irreversible, but the rate of progression varies. Most patients can maintain good quality of life with conservative management and eventual joint replacement.