Articular Cartilage

Articular cartilage is the load-bearing hyaline layer on the ends of bones inside a synovial joint, roughly two to three millimetres thick at the human knee. It is mostly water, held under pressure by a mesh of type II collagen fibrils and the negatively charged proteoglycan aggrecan, which draws water in osmotically and gives the tissue its compressive stiffness. The tissue has no blood vessels, nerves or lymphatics, and chondrocytes are fed only by diffusion from synovial fluid.

That avascularity is why cartilage does not repair itself. A partial-thickness defect never recruits the inflammatory and progenitor response that closes a bleeding wound, so it persists. A defect penetrating the subchondral plate does bleed and does fill, but with fibrocartilage rich in type I collagen, which is softer and prone to breaking down under load. Surgery acknowledges this: marrow stimulation accepts fibrocartilage, while autologous chondrocyte implantation, approved by the FDA in matrix-applied form in 2016, delivers actual chondrocytes into the defect.

This constrains what counts as a claim. Symptom relief in a joint can come from synovium, effusion, bone marrow lesions or the natural fluctuation of pain, none of which requires cartilage to change. Structural claims need structural measurement, and the usual radiographic proxy, joint space width, is confounded by meniscal extrusion and knee positioning as much as by cartilage thickness.

The recurring error is the word regeneration. Filling a defect with repair tissue is not regenerating hyaline cartilage, and quantitative MRI thickness and compositional mapping are the only non-invasive way to say anything about it. No peptide has shown cartilage structural benefit in a controlled human trial; the chondroprotective claims made for several rest on cultured cells and small-animal joints.