Abstract
Purpose: The pathological remodeling of the osteochondral junction is thought to be pivotal in osteoarthritis (OA). It includes alterations in the mineralization state of both cartilage and bone. The biomineralization process is orchestrated by protein-mineral interactions. In bone, the peculiar organization of type I collagen fibrils forms gaps between neighboring collagen molecules, which may be the place where CaP crystals nucleate from an amorphous phase and subsequently grow. This intrafibrillar mineralization process may be directed by highly acidic non-collagenous proteins (SIBLING family proteins, Matrix gla protein (MGP) and fetuin A) which stabilize pre-nucleated clusters and inhibit CaP nucleation in the extrafibrillar spaces.
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