Pathogenesis

Animal models of joint instability suggest that the first change in the articular cartilage is an increase in water content. This may cause loss of the matrix proteoglycans. In humans it is thought that loss of proteoglycans is due to a failure of the internal collagen network which normally restrains the matrix gel (1).

The cartilage becomes less stiff and durable and may be damaged. Release of cellular enzymes leads to further cartilage breakdown.

Cartilage deformation puts more stress on the collagen network which perpetuates the problem.

Defects in the articular surface act to concentrate the forces of joint loading over a very small area. The result is:

• focal trabecular degeneration
• cyst formation
• increased vascularity and reactive sclerosis

Regenerative cartilage formation at the edge of the joint becomes ossified, resulting in osteophytes (2).

Reference:

1. 1. Heinemeier KM et al. Radiocarbon dating reveals minimal collagen turnover in both healthy and osteoarthritic human cartilage. Sci Transl Med. 2016 Jul 6;8(346):346ra90.
2. 2. Glyn-Jones S, Palmer AJ, Agricola R, et al. Osteoarthritis. Lancet. 2015 Jul 25;386(9991):376-87.