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Research in both mice and humans on the pathogenesis of osteoarthritis (OA) has begun to coalesce recently. In children, bone growth occurs through extension of cartilage at the growth plate combined with conversion of cartilage to bone at the junction point — endochondral ossification. In adults with healthy nongrowing bone, forces that build and degrade cartilage are balanced.
Two new Asian studies show that many of the genes that are involved in endochondral ossification during childhood are reactivated in adulthood by various joint stressors — particularly mechanical stress, oxidative stress, and inflammatory mediators — in a futile attempt to repair damaged cartilage. The result is hypertrophy of chondrocytes, cartilage destruction, and…