There are a number of ways in which vascular disease may contribute to either the initiation or structural progression of osteoarthritis (OA). We should keep in mind that atherosclerotic vascular disease, like OA, occurs with increasing frequency as people age and consequently understanding their inter-relationship and any potential causal relationship is dificult. Of interest is the suggested epidemiological links between cardiovascular mortality and OA, though again this is difficult to discern the casual part of the relationship. Links between vascular disease and osteoarthritis may of course be mediated through a common disease association, obesity. One hypothesis is that osteoarthritis is a differentiation disorder involving altered lipid metabolism.

It should also be remembered that articular cartilage is avascular, and it receives much of its nutrition from the subchondral bone or synovial fluid. Vascular disease in the subchondral bone may accelerate structual progression through alterations in cartilage nutrition or through direct ischaemic effects on bone. Imaging plays a key role in hypotheses about vascular involvement in OA, since it is commonly used for diagnosis and assessing progression. It has been suggested that the MRI subchondral bone changes typical of OA (termed bone marrow lesions) are similar to those seen in avascular necrosis, especially in the hip.

How might vascular changes effect OA? Certainly OA structural changes have been proposed because of secondary vascular changes in the high-pressure subchondral bone environment. These have been described in terms such as ‘venous outflow obstruction’ and also ‘localised hypercoagulabilities’, and have been described in animal and human studies. Venous outlet syndrome in the subchondral region can result in ischaemia of bone and the adjacent cartilage. Dynamic contrast enhanced (DCE-)MRI and positron emission tomography (PET) have demonstrated that venous outflow obstruction results in decreased perfusion and that venus staus is associated with trabecular remodelling, in animal OA models.

Another potential role for vascular perturbation is in the synovitis commonly seen in OA. Given the frequency of synovitis in (especially knee) OA, it is possible that a patchy distribution of reduced blood flow (local ischaemia) happens in areas of greater inflammation. Greater levels of synovial inflammation have been associated with OA progression.

Another hypothesis is that atheromatous disease might directly effect OA pathology progression. Computered tomography (CT) has been used in the spine to demonstrate an association between arterial calcification and the degree of disc degeneration, and there has also been shown to be a relationship between disc degeneration and adjacent bony end plate damage. These spinal changes are similar to OA joint pathologies. Another study demonstrated an association between hand osteoarthritis imaging findings and aortic calcification.

References

1. Aaron RK, Racine J, Dyke J. Contribution of circulatroy disturbances in subchondral bone to the pathophysiology of osteoarthritis. Curr Rheumatol Rep 2017;19:49.
2. Conaghan PG, Vanharanta H, Dieppe PA. Is progressive osteoarthritis an atheromatous vascular disesase? Ann Rheum Dis 2005;64:1539–41.

Disclosure of Interest: None declared

DOI: 10.1136/annrheumdis-2018-eular.7854