Osteocyte and vascular network in hip osteoarthritis: A multimodal imaging and histological analysis

Hip osteoarthritis (OA) is characterised by increased remodelling of the subchondral bone, for which the underlying cellular and microvascular mechanisms are unclear. This study investigated alterations in the osteocyte lacunocanalicular network and vascular canal architecture in the femoral head in human hip OA, using a multimodal imaging and histological approach.

Femoral head samples from OA patients (n = 8; 4 female, 4 male; age 69 ± 14) undergoing hip replacement, and healthy controls (n = 8; 5 female, 3 male; age 64 ± 12), were imaged by MRI to assess cartilage volume and subchondral bone pathology. Four trabecular bone cores per femoral head, representing four distinct anatomical sites, were analysed with synchrotron radiation micro-CT to examine osteocyte lacunar morphometry and vascular canal characteristics. Histology was used to evaluate osteocyte viability, senescence, connectivity, and osteoclast activity.

Compared to controls, OA bone showed a significant increase in lacunar volume (p = 0.002) and reduced lacunar sphericity (p = 0.04). OA was also characterised by increased osteocyte loss, reflected by a higher proportion of empty lacunae (p = 0.002), and shorter canaliculi (p = 0.01). Additionally, there was increased vascular canal volume (p = 0.004) and higher vascular canal density (p = 0.002) in OA compared to controls. While some parameters varied across different anatomical regions, most OA-related changes were not region-specific.

Hip OA is characterised by widespread disruption of the osteocyte lacunocanalicular network, associated with reduced bone cell viability, connectivity, and remodelling. Concurrent microvascular alterations further support the hypothesis that osteocyte-vascular network dysfunction contributes to subchondral bone pathology.