Epiphyseal interfaces

This work explores interconnected articular and growth plate osteochondral interfaces, via complementary anatomical, biomechanical and structural analyses that combine benchtop micro-computed tomography (microCT) and high-resolution synchrotron CT (sCT) imaging approaches. We show that bony sclerosis, well-documented in late-stage OA in humans, and the osteoarthritic STR/Ort mouse model, is preceded by the amplified regionalised expansion of articular calcified cartilage (ACC) where vulnerability load-induced failure is greatest. We further observed marked alterations in the number and size of resident osteocyte lacunae in pre-OA and OA regions in comparison to controls, which age healthily, underscoring the value of CT-based approaches for elucidating early OA-related changes. Notably, our findings imply that excessive ACC formation is an early consequence of disrupted endochondral ossification that precedes and potentially drives OA sclerosis, osteophytosis and indeed, articular cartilage lesions. By applying digital volume correlation (DVC) to sCT images of loaded murine knee joints under physiological conditions, we demonstrate that the joints from a healthy parental control strain of CBA mice efficiently dissipate compressive strain, whereas OA-prone STR/Ort exhibit high strain foci in the epiphyseal compartment prior to cartilage degeneration; suggesting that early strain accumulation may therefore promote early joint vulnerability and subsequently prime degenerative progression with age. Finally, we examined how the cartilaginous growth plate (GP), responsible for all longitudinal bone growth, contributes to mechanical epiphyseal stability for articulation. Analysis of mineralised trans-physeal GP structures (bridges), revealed their dynamic and sexually dimorphic character as well as their regulation by mechanical loading and osteotropic agents. DVC analyses of sCT-imaged murine knee joints subjected to identical physiologically oriented load, identified that regionally heterogeneous load-induced strain patterns in the GP are spatially synchronised to bridge location; a relationship substantiated by finite element simulation. Together, these findings establish intra-physeal GP bridges as regulatable and mechanically sensitive structures that coordinate the transfer of local GP strains, while enhancing epiphyseal stability by distributing compressive and shear strains to thereby permit cessation of longitudinal growth.