Osteoarthritis (OA) is a common joint disease characterised by articular cartilage degeneration. Although the etiology of OA is unknown, it has long been thought of as a condition affecting the extracellular matrix (ECM) of articular cartilage. However, it is now well accepted that chondrocytes, the only cell type present in normal cartilage, also play a role in the catabolic and anabolic processes that drive the degenerative process. Just how the process of degeneration in OA is initiated (via the ECM, the cell or both) remains unknown.

Chondrocyte clusters at the eroding articulating surface in severe osteoarthritic articular cartilage. Top row: DIC images of osteoarthritic cell cluster. Bottom row: Confocal z-projections of primary cilia (arrows). Cilia (arrows) are oriented toward the centre of the cluster within the expanding chondron. Scale bars = 5 um.

We speculate that changes in primary cilia-mediated signalling may play a role in the onset of OA.

Our lab has examined the incidence and morphology of primary cilia in chondrocytes during joint degeneration using a naturally occurring bovine model of OA. Our preliminary findings have shown that in normal cartilage cilia number and length were lowest in the superficial zone and increased with distance from the articular surface, whereas in OA tissue the incidence and length of cilia increased at the eroding articulating surface, resulting in an overall increased proportion of cilia.

Our research is now focused on functional studies to understand the mechanisms of these OA-related changes.

People involved:

Dr Sue McGlashan (PI)
Assoc Professor Tony Poole (PI)
Assoc Professor Cynthia Jensen
Mrs Sarah Kennedy
Emma Cluett (Summer student, 2004)

Partially funded by:

HOPE Foundation for Aging, NZ