Osteoarthritis is not wear and tear. It is an active, whole-joint disease that begins in the cartilage.

Osteoarthritis is often described as "wear and tear," as if the joint were a mechanical bearing that inevitably fails from use. That metaphor is intuitive but misleading. Modern understanding frames OA as an active disease of the whole joint — involving cartilage, subchondral bone, synovium, ligaments, and the surrounding musculature — with a distinct pathophysiology that goes well beyond surface erosion.

The process begins in articular cartilage — the smooth, avascular, low-friction tissue that caps the ends of long bones. Cartilage is maintained by chondrocytes, which normally balance the synthesis and degradation of the extracellular matrix (primarily type II collagen and aggrecan). In OA, this balance shifts toward catabolism: chondrocytes increase production of matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS), which degrade the matrix faster than it can be replaced. The mechanical properties of the cartilage deteriorate — it becomes softer, more permeable, and eventually fissures and wears away.

What drives that shift is a combination of mechanical and biological factors. Abnormal loading (from obesity, prior injury, malalignment, or muscle weakness) produces shear and compressive stresses that injure chondrocytes directly. Inflammatory cytokines — IL-1β, TNF-α, and IL-6 — produced by the synovium and by the chondrocytes themselves amplify catabolism and further degrade the matrix. Damage-associated molecular patterns released from the degraded matrix perpetuate a low-grade inflammatory state that, while less intense than in rheumatoid arthritis, is enough to drive progression.

As cartilage is lost, the subchondral bone responds. It becomes denser (subchondral sclerosis), develops small cystic areas, and — at the joint margins — grows osteophytes, which are bony outgrowths that the body produces as a compensatory attempt to stabilize the joint. The synovium becomes mildly inflamed, and the joint capsule and ligaments thicken and stiffen. The result is the radiographic signature of OA: joint space narrowing, sclerosis, osteophytes, and subchondral cysts. These findings are what a radiograph actually shows, and they map onto the Kellgren-Lawrence grading system.

The clinical consequences are pain, stiffness, and functional limitation. Pain in OA arises not from cartilage itself — cartilage is avascular and lacks nerve endings — but from the synovium, subchondral bone, joint capsule, and periosteum, all of which are innervated and become sensitized by inflammation. This is why patients with severe radiographic OA can be asymptomatic, and why patients with mild radiographic findings can have significant pain. Imaging and symptoms do not always align.

Most OA medications are generic and inexpensive. Topical diclofenac gel is now available OTC. Oral NSAIDs (naproxen, ibuprofen, meloxicam) and acetaminophen cost a few dollars per month. Duloxetine is generic. The exception is intra-articular hyaluronic acid injections, which remain brand-only and expensive (often $300 to $1,000 per injection) and are covered inconsistently by insurance — the AAOS does not recommend them, while OARSI and some international guidelines do, and coverage varies by plan.

Joint replacement is expensive but widely covered. Total knee and total hip arthroplasty are covered by Medicare and commercial insurance when medically necessary. Costs vary dramatically by facility — a total knee replacement can be $20,000 at an ambulatory surgery center and $60,000 at a hospital. Medicare's bundled payment programs have been an attempt to standardize this. For patients on high-deductible plans, the cost of joint replacement can be a substantial barrier.

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