Introduction: Structural, cellular, and molecular changes within subchondral bone are causal of osteoarthritis initiation and progression. Despite osteocytes being the most abundant cell type within the bone, their association in OA pathogenesis, particularly hip OA, remains unknown. Overall, hip OA's osteocyte viability, density, and connectivity are largely unexplored. This study aimed to comprehensively characterise osteocyte metabolic and functional state in human subchondral bone of hip OA.
Method: Femoral heads were collected from 8 patients undergoing total hip replacement surgery (4 females, aged 69 14 years) and 8 human cadavers (5 females, 64 12 years). Two bone core biopsies were sampled per subject, imaged by synchrotron micro-CT to obtain osteocyte lacunar properties, and then processed for histological assessment and evaluation of osteocyte density, viability, and connectivity.
Results: Compared to control, subchondral bone in OA tissue were characterised by larger (p=0.0003) and more spheric (p=0.03) osteocyte lacunae, decreased osteocyte cell density (p=0.020, p<0.0001), decreased canalicular number (p=0.003, p=0.002) and decreased canalicular length (p=0.01, p=0.003) but significantly increased percentage of empty lacunae (p=0.0009, p<0.0001) and apoptotic osteocytes (p=0.02, p=0.04) in both plate and trabeculae respectively. Osteocyte senescence assessed by Sudan Black B staining was not significantly different between control and OA.
Discussion: These data demonstrate that osteocyte viability and connectivity is compromised within OA subchondral bone implicating a direct role for osteocytes in hip OA pathogenesis. The results from this study have the potential to identify a specific target for the development of effective therapies to prevent OA progression in suffering patients. However, further investigation is necessary to identify osteocyte molecular mechanisms involved in the pathogenesis in hip OA.