To observe the changes of synovial inflammation score and expression of related molecular markers in patients with rheumatoid arthritis treated with tumor necrosis factor (TNF) antagonist etanercept.
Sixteen patients with rheumatoid arthritis received synovectomy in the knee under arthroscopy, of which 8 patients had been treated with etanercept before surgery (etanercept group) and the other 8 patients were given no etanercept or other biologics (non-biological agent group). The synovial tissues obtained from surgery were subjected to HE staining and immunohistochemical staining respectively, to assess Rooney's inflammation score and detect the expressions of proliferating cell nuclear antigen (PCNA), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and cadherin-11.
Rooney's score in etanercept group was significantly lower than that in non-biological agent group. The expressions of PCNA and cadherin-11 in synovial lining and sublining layers significantly decreased in etanercept group. Expressions of VCAM-1 and ICAM-1 had no significant difference in either synovial lining or sublining layer between the two groups. Clinical inflammatory markers including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelet count (PLT) and disease activity score in 28 joints (DAS28) had no statistical correlation with Rooney's inflammation score.
Etanercept could effectively inhibit proliferation of synoviocytes and infiltration of lymphocytes in synovium of rheumatoid arthritis, and decrease the expressions of proliferation-and adhesion-related molecular markers, which histologically alleviated the synovial inflammation of rheumatoid arthritis. Clinical inflammatory markers might not fully reflect histological changes in the local synovial tissue.