DNA DAMAGE ACCUMULATION WITH AGING AND OSTEOARTHRITIS IN PRIMARY HUMAN CHONDROCYTES

Abstract

Purpose: Aging is the strongest risk factor for the development of osteoarthritis (OA), but the mechanisms that drive this relationship remain unclear. Previous studies have shown that OA chondrocytes exhibit high levels of DNA damage and that this may contribute to heterogeneous gene expression and dysfunction. However, the degree to which chondrocytes accumulate DNA damage during “normal aging” has not been reported in the literature. It is important to quantify this burden as the presence of unrepaired DNA damage can induce cellular senescence and other age-related phenotypic changes that have been implicated in OA pathophysiology.