Erosive and non-erosive hand osteoarthritis. Use and limitations of two scoring systems

SummaryObjective:To assess the evolution and progression of osteoarthritis (OA) in the finger joints using anatomical changes on standard radiographs.Methods:Data obtained from 85 patients enrolled in a prospective study were used to evaluate systems to score the morbidity and the progression of the disease over 3 years. Posteroanterior (PA) radiographs of the metacarpophalangeal (MCP) and interphalangeal (IP) joints were obtained at entry and after 3 years. Assessment of the progression of OA over time is based on: (1) the increase in incidence of OA in previously normal joints during the study period, (2) the changes in the OA-associated features (osteophyte growth, loss of joint space, subchondral cysts or sclerosis) in the pathological finger joints (anatomical lesion progression score system), and (3) the recognition of consecutive anatomical phases in the course of ‘erosive’ OA (anatomical phase progression score system).Results:Almost 80% of the distal IP and 50% of the proximal IP were affected at study entry. In approximately 40% of the patients, the classical picture of OA of the IP joints was complicated by manifest erosive changes, which were followed by a repair phenomenon in the 'eroded' finger joints. MCP were less affected and showed the non-erosive picture of OA. Numbers of affected DIP, PIP and MCP joints per patient at entry did not differ from those after 3 years of follow-up. Two systems to score the progression of OA (anatomical lesion and anatomical phase progression score system) showed definite progression within 3 years of follow-up, especially in the IP joints. Since changes in both non-erosive and erosive joints were recorded by the anatomical lesion progression system, it was found much more sensitive to change than the anatomical phase progression system which principally recorded the progression through the destructive phases of erosive OA. The results of both progression score systems correlated well.Conclusion:Conventional radiographs can be used to assess the morbidity and progression of hand OA. The existence of non-erosive and erosive forms of OA of the finger joints necessitates the use of two scoring systems: the anatomical lesion progression score system and the anatomical phase progression score system

Exposure to nuclear antigens contributes to the induction of humoral autoimmunity during tumour necrosis factor alpha blockade

OBJECTIVE: Type I interferons and apoptotic particles contribute to antinuclear autoimmunity in experimental models. This study assessed whether similar mechanisms contribute to break peripheral B-cell tolerance in humans by studying the induction of antinuclear antibodies by tumour necrosis factor blockade in spondyloarthritis. METHODS: 40 spondyloarthritis patients treated with infliximab or etanercept and 20 renal cell carcinoma patients treated with sorafenib were studied. Serum antinucleosome IgM and nucleosomes were measured by ELISA. Type I interferon serum activity was measured using a functional reporter cell assay. Synovial apoptosis was assessed by terminal transferase nick end-labelling (TUNEL) assay and anti-active caspase-3 immunostaining. Complement was measured by nephelometry. RESULTS: Despite a similar clinical improvement and reduction of synovial inflammation, antinucleosome IgM were induced by infliximab but not etanercept. This induction did not correlate with type I interferon activity, which was transiently downmodulated by infliximab but persistently upregulated by etanercept. In contrast, antinucleosome IgM levels did correlate with serum nucleosome levels, which were significantly upregulated by infliximab but not by etanercept treatment. This increase in serum nucleosome levels was not directly related to massive cell death, but rather to a decrease of complement 3 and 4 serum levels during infliximab treatment. CONCLUSION: Infliximab and etanercept have a differential effect on both type I interferon activity and nucleosome levels. Only elevated serum nucleosomes relate to the induction of antinucleosome antibodies after infliximab treatmen