Background Previous studies have shown an increased prevalence of synovitis and tenosynovitis in systemic sclerosis (SSc) as detected by magnetic resonance imaging (MRI) or musculo-skeletal ultrasound (US). It was assumed that MRI and US can accurately describe synovitis and tenosynovitis in these patients. However, histological examination was not available in these studies.

Objectives To assess the histologic pattern of synovium in SSc patients suffering from synovitis detected by MRI or US.

Methods Seven synovial biopsies from 4 different SSc patients were analyzed by immunohistochemistry (IC). Three patients underwent a second synovial biopsy one year later. Imaging studies (US, MRI, radiographs) were performed prior to biopsies. The histologic pattern in synovium from SSc patients was compared with that observed in patients suffering from lupus arthritis (LA, n:5), rheumatoid arthritis (RA, n:7), spondylarthritis (SPA, n:10) and osteoarthritis (OA, n:6).

Results In all SSc patients, imaging studies confirmed the presence of joint effusion and active synovitis with increased vascularisation (Figure). In addition, in one SSc patient, intra-articular calcifications were observed by US. Microscopic examination of the SSc synovium revealed altered global architecture with marked angiogenesis, inflammatory cell infiltrates, increased collagen density and extracellular deposits (Figure). The increased thickness of the synovium was due both to increased deposition of extracellular matrix (collagen) and infiltrates of inflammatory cells. These changes paralleled those observed by imaging and were more severe in patients with longer duration of the disease. Furthermore, IC revealed an increased density of T lymphocytes and macrophages (Figure), with low density of B-cells and plasmocytes. Perivascular T-cell infiltrates and T-cell aggregates were present around inflammatory nodules, the latter being associated with marked deposits of extracellular, amorphous material. Angiogenesis consisted mainly in increased density of immature vessels, as detected by WT1 immunostaining. Arteriolar onion-skin like lesions were present in biopsies from two patients with more severe patients. Paired synovial biopsies confirmed the persistence of abnormal synovial findings at one year. This histologic pattern was distinct from that observed in LA, RA, SPA and OA. One SSc patient had joint infection and delayed wound healing after biopsy, leading us to stop recruiting SSc patients.

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Conclusions SSc-related synovitis is characterized by the presence of both inflammatory and non-inflammatory changes, including increased vascularity, inflammatory cells infiltrates, fibrosis and collagen deposits within the synovium. Furthermore, we present here the first histologic data suggesting that US and MRI can accurately describe synovitis and tenosynovitis in SSc patients. Larger studies including more synovial biopsies are ethically difficult to justify in view of the increased probability of infections and delayed wound healing in SSc patients.

Disclosure of Interest None declared