- Osteoarthritis (OA): A degenerative joint disease characterized by progressive loss of articular cartilage, subchondral bone sclerosis, and osteophyte formation. Risk factors include age, obesity, joint trauma, and genetic predisposition. OA typically affects weight-bearing joints such as knees, hips, and spine.
- Rheumatoid Arthritis (RA): An autoimmune inflammatory disorder where the synovial membrane becomes inflamed, leading to pannus formation and joint destruction. It often presents symmetrically in small joints of hands and feet and can involve extra-articular systems like lungs and heart.
- Psoriatic Arthritis (PsA): Associated with psoriasis, this seronegative spondyloarthropathy causes inflammation in the entheses and joints. It can manifest as oligoarticular or polyarticular patterns, with potential for spinal involvement resembling ankylosing spondylitis.
- Gout: A crystal arthropathy resulting from monosodium urate deposition due to hyperuricemia. Acute flares are intensely painful, often in the first metatarsophalangeal joint. Chronic tophaceous gout can lead to joint deformity.
- Pathophysiology Overview: Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-1, IL-6) drive synovitis and cartilage degradation in RA. OA involves mechanical stress and enzymatic breakdown of collagen. Understanding these pathways guides treatment selection.
- Clinical Presentation Variations: OA pain worsens with activity and improves with rest; RA presents with morning stiffness lasting more than 30 minutes. PsA may include dactylitis (sausage digit) and nail changes. Gout flares are acute, often triggered by alcohol or purine-rich foods.
- Diagnostic Criteria: For RA, the 2010 ACR/EULAR criteria use joint involvement duration and acute-phase reactants. OA diagnosis is primarily clinical with radiographic evidence of joint space narrowing. Gout requires synovial fluid analysis for urate crystals.
- Impact on Patient Function: Chronic arthritis reduces mobility, independence, and quality of life. Pain and fatigue contribute to work disability and psychological distress. Early intervention and coordinated management are essential to preserve function.
- Pharmacologic Management of OA: Initial treatment includes acetaminophen and topical NSAIDs for mild pain. Oral NSAIDs with gastroprotection are used for moderate to severe pain, while intra-articular corticosteroids provide short term relief. Adjunctive therapies like duloxetine may help centralized pain. Avoid chronic opioid use due to risks.
- Disease Modifying Antirheumatic Drugs for RA: Methotrexate is the cornerstone of RA treatment, often combined with sulfasalazine or hydroxychloroquine. Biologic DMARDs such as TNF inhibitors, abatacept, and tocilizumab target specific inflammatory pathways. Janus kinase inhibitors offer oral alternatives. Early aggressive treatment improves long term outcomes.
- Nonpharmacologic Interventions: Physical therapy strengthens periarticular muscles and improves joint stability. Occupational therapy assists with adaptive techniques to reduce joint stress. Weight loss significantly decreases pain and disability in knee OA. Patient education on joint protection and energy conservation is essential for all arthritis types.
- Surgical Options: Total joint arthroplasty is indicated when conservative measures fail and pain severely limits function. Arthroscopic procedures may benefit select cases of mechanical symptoms but are not routinely recommended for OA. Synovectomy can reduce synovitis in RA. Postoperative rehabilitation is critical for recovery.
- Synovitis
- Inflammation of the synovial membrane lining a joint.
- Pannus
- Abnormal granulation tissue in RA that invades and destroys cartilage.
- Enthesitis
- Inflammation at the site where tendon or ligament attaches to bone.
- Hyperuricemia
- Elevated serum uric acid level, predisposing to gout.
- Major arthritis types include OA, RA, PsA, and gout, each with distinct pathophysiology.
- OA is degenerative; RA is autoimmune; PsA involves enthesitis; gout is crystal-induced.
- Inflammatory cytokines drive RA; mechanical stress and enzymes drive OA.
- Diagnosis relies on clinical presentation, laboratory markers, and imaging.
- Chronic arthritis significantly impacts function and quality of life.
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