Osteoarthritis

•RCT evidence— Symptomatic treatment well-established; DMOADs still elusive

What it is

OA is a whole-joint disease, not just "cartilage wear and tear". Cartilage loss is accompanied by subchondral bone changes (sclerosis, cysts, osteophytes), synovial inflammation, and meniscal degeneration. Pain is poorly correlated with imaging severity — many adults with severe radiographic OA have minimal pain, and vice versa.

What works

• Exercise: structured strengthening and aerobic conditioning is the most-evidence-based intervention. Effect sizes comparable to NSAIDs.
• Weight loss: each kg lost reduces knee load multifold; symptoms improve substantially with 5–10% weight loss in obese.
• NSAIDs: oral or topical (topical preferred when feasible).
• Acetaminophen / paracetamol: modest effect; better safety profile.
• Intra-articular corticosteroid: short-term symptom benefit; repeated injections raise structural-progression concerns.
• Hyaluronic acid injections: small effects, limited evidence.
• Platelet-rich plasma: mixed evidence.
• Total joint replacement: highly effective for end-stage hip and knee OA.

What doesn’t work as advertised

• Glucosamine and chondroitin: large RCTs (GAIT) negative or marginal.
• Stem cell injections: weak evidence.
• Most "supplements for joints".

Emerging

• Sprifermin (FGF18): cartilage thickness preservation in trials.
• Cathepsin K inhibitors.
• Wnt-pathway modulators (lorecivivint).
• Senolytics (UBX0101 trial was negative; the senescence-OA hypothesis remains active).

Related entries

Curcumin, Cellular senescence, Frailty.