Osteoclasts are recruited to the subchondral bone in naturally occurring post-traumatic equine carpal osteoarthritis and may contribute to cartilage degradation

Abstract

The role of osteoclasts in osteochondral degeneration in osteoarthritis (OA) has rarely been investigated in spontaneous disease or animal models of OA. The objectives of the current study were to investigate osteoclast density and location in post-traumatic OA (PTOA) and control specimens from racehorses. Cores were harvested from a site in the equine third carpal bone, that undergoes repetitive, high intensity loading. Histological and immunohistochemical (Cathepsin K and Receptor-activator of Nuclear Factor kappa-β ligand (RANKL)) stained sections were scored (global and subregional) and the osteoclast density calculated. The cartilage histological scores were compared with osteoclast density and RANKL scores. There was a greater density of osteoclasts in PTOA samples and they were preferentially located in the subchondral bone plate. RANKL scores positively correlated to the scores of cartilage degeneration and the osteoclast density. The relationship between hyaline articular cartilage RANKL score and osteoclast density was stronger than that of the subchondral bone RANKL score suggesting that cartilage RANKL may have a role in recruiting osteoclasts. The RANKL score in the articular calcified cartilage correlated with the number of microcracks also suggesting that osteoclasts recruited by RANKL may contribute to calcified cartilage degeneration in PTOA. Our results support the hypothesis that osteoclasts are recruited during the progression of spontaneous equine carpal PTOA by cartilage RANKL, contributing to calcified cartilage microcracks and focal subchondral bone loss.