The Bone Cartilage Interface and Osteoarthritis

This review describes results obtained with tissue from prior studies of equine and human osteoarthritis (OA). The main methods considered are scanning electron microscopy, novel methods in light microscopy and X-ray Micro-tomography. The same samples have been re-utilised in several ways. The tissues described are hyaline articular cartilage (HAC; or substitutes), with its deep layer, articular calcified cartilage (ACC), whose deep surface is resorbed in cutting cone events to allow the deposition of subchondral bone (SCB). Multiple tidemarks are normal. Turnover at the osteochondral (ACC-HAC-SCB) junction is downregulated by overload exercise, conversely, during rest periods. Consequent lack of support predisposes to microfracture of the ACC-SCB plate, in the resorption-related repair phase of which the plate is further undermined to form sink holes. The following characteristics contribute to the OA scenario: penetrating resorption canals and local loss of ACC; cracking of ACC and SCB; sealing of cracks with High-Density Mineral Infill (HDMI); extrusion of HDMI into HAC to form High-Density Mineral Protrusions (HDMP) in HAC which may fragment and contribute to its destruction; SCB marrow space infilling and densification with (at first) woven bone; disruption, fibrillation and loss of HAC; eburnation; repair with abnormal tissues including fibrocartilage and woven bone; attachment of Sharpey fibres to SCB trabeculae and adipocyte-moulded extensions to trabeculae (excrescences).

Automated summary

This review summarizes the results of previous studies on equine and human osteoarthritis, focusing on tissue analysis using scanning electron microscopy, light microscopy, and X-ray Micro-tomography. Overload exercise can downregulate the turnover at the osteochondral junction, leading to microfractures and subsequent destruction of the articular cartilage and subchondral bone.