Osteoarthritis as a marker and potential contributor to cardiovascular risk: a glycocalyx-cartilage axis hypothesis.

Abstract

Osteoarthritis (OA) may be more than simply a reflection of aging; it could represent a symptom of underlying vascular disease processes with serious consequences for health and quality of life. The association of OA with other conditions like cardiovascular disease (CVD) suggests OA may be partially systemic and metabolic in nature. As such, this connection underscores the value of exploring the biochemical parallels between articular joints and the endothelial glycocalyx, the protective lining of blood vessels. N-acetylglucosamine may be central to this link because both articular cartilage and the endothelial glycocalyx depend on N-acetylglucosamine-containing structures. A better understanding of the pathophysiology linking OA and CVD provides the basis for the present hypothesis. Hypothesis: A reduction in available or utilized levels of N-acetylglucosamine results in a parallel degradation of articular cartilage and the endothelial glycocalyx. This would result in a shared glycan-dependent mechanism linking the pathogenesis of OA to increased cardiovascular risk. Implications: OA could serve as an early clinical marker for vascular dysfunction and potentially identify glycocalyx-targeted interventions as a new area of investigation for therapies to reduce both OA and CVD. The novelty of this research hypothesis is based on suggesting that N-acetylglucosamine-dependent glycan insufficiency is a unified mechanism connecting cartilage degeneration with vascular endothelial damage.