Abstract
The synovial tissue stands at the epicenter of joint pathology in rheumatoid arthritis (RA). As a primary target of the disease, studies on the synovium have provided invaluable insights into the mechanisms involved in disease pathogenesis. Recent work has, however, revealed the importance of a previously unseen anatomic compartment in direct contact with the joint space, namely the subchondral bone marrow. Bone marrow edema (BME) visible on magnetic resonance imaging (MRI) is clinically meaningful in both early and late RA as it associates with future development of bone erosions and poor functional outcomes. Although the histopathologic correlates of MRI-based BME in early RA remain obscure, studies in advanced disease are consistent in describing lymphocytic inflammatory infiltrates within the subchondral marrow cavity of affected joints. In this review, we discuss the nature of bone marrow lesions in patients with RA, analyze their relationship with synovitis, and explore their potential contribution to the pathological processes of the disease.
Highlights
The synovial tissue stands at the epicenter of joint pathology in rheumatoid arthritis (RA)
Combined with imaging data coming from magnetic resonance imaging (MRI) studies, histopathologic changes described within the subchondral bone marrow (BM) have been postulated to be intimately involved in the pathological processes producing local inflammation and tissue remodeling in RA joints [6,8,9,10]
High cellularity throughout the marrow seen on histologic examination in tumor necrosis factor (TNF)-transgenic mice appears associated with a diffuse bone marrow edema (BME) pattern on MRI, distinct from subchondral Bone marrow edema (BME) coexisting with focal erosions [18]
Summary
The synovial tissue stands at the epicenter of joint pathology in rheumatoid arthritis (RA). Combined with imaging data coming from magnetic resonance imaging (MRI) studies, histopathologic changes described within the subchondral BM have been postulated to be intimately involved in the pathological processes producing local inflammation and tissue remodeling in RA joints [6,8,9,10]. In a similar study of RA subchondral bone removed from a patient undergoing knee replacement surgery, Watson and colleagues [32] described a local inflammatory reaction with nodular lymphocytic infiltrates accompanied by immunoglobulin deposits near areas of destroyed cartilage.
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