Meniscal calcification, pathogenesis and implications

Abstract

The purpose of this review is to discuss recent advances in the understanding of the nature of meniscal calcification and its relationships with meniscal degeneration and cartilage lesions in osteoarthritis. Calcium crystals are universally present in hyaline articular cartilage, as well as the meniscus of the knee of end-stage osteoarthritis patients. Osteoarthritis meniscal cells display a distinct gene-expression profile different from normal meniscal cells, have elevated expression of ankylosis progressive analog (ANKH) and ectonucleotide pyrophosphatase/phosphodiesterase1 (ENPP1) and produce more calcium minerals than normal meniscal cells in vitro. Meniscal calcification is positively associated with meniscal degeneration, which is an early event in the development of osteoarthritis and correlates with cartilage lesions and clinical osteoarthritis scores. Phosphocitrate is a potent calcification inhibitor of osteoarthritis meniscal cell-mediated calcium deposition. Its effect on preventing meniscal degeneration and the molecular mechanisms underlying its disease-modifying activity in osteoarthritis remains elusive. Recent findings support a pathogenic role of meniscal calcification in osteoarthritis. Meniscal calcification, similar to meniscal degeneration, is a predisposing factor for cartilage lesions. Meniscal calcification is a new target for the development of therapeutic disease-modifying drugs for osteoarthritis.