Abstract
The goal of the present study was to record changes in bone mineral density (BMD) and markers of bone turnover in patients with rheumatoid arthritis (RA) who were treated with methotrexate combined (or not combined) with infliximab. Included were 90 patients with RA who required anti-TNF-α therapy with infliximab because of persistent active disease despite treatment with methotrexate. The historical control group included 99 patients with RA who were treated with methotrexate at a time when anti-TNF-α treatment was not yet available. Lumbar and femoral neck BMD was measured using dual energy X-ray absorptiometry at baseline and 1 year later. Osteocalcin, C-terminal cross-linked telopeptide of type I collagen, parathyroid hormone and 25-hydroxycholecalciferol were measured in plasma at baseline and 1 year later. At 1 year BMD had decreased in the control group at spine (P < 0.01) and femoral neck (P < 0.001). In contrast, BMD at spine and femoral neck did not change after 1 year of infliximab treatment. At the same time point, no change in bone remodelling markers was observed. No association was observed between clinical response and changes in BMD, indicating that even those who did not respond clinically did not lose bone over a 1-year period. These data confirm the BMD decrease observed in RA patients treated with methotrexate alone. This bone loss was prevented by infliximab therapy. Importantly, this beneficial effect was also observed in apparent nonresponders.
Highlights
Rheumatoid arthritis (RA) is a chronic disease that is characterized by joint inflammation and local bone erosion
The goal of the present study was to record changes in bone mineral density (BMD) and markers of bone turnover in patients with rheumatoid arthritis (RA) who were treated with methotrexate combined with infliximab
Among the factors that can influence bone resorption and osteoclast activity, tumour necrosis factor (TNF)-α plays a central role in the destructive process of RA and has been shown to increase bone resorption in systemic osteoporosis related to oestrogen deficiency [4]
Summary
Rheumatoid arthritis (RA) is a chronic disease that is characterized by joint inflammation and local bone erosion. Generalized bone loss has been demonstrated in RA patients [1,2]. This could be due to the disease itself, to reduced exercise activity, or to treatment with steroids [3], but it could result from common postmenopausal osteoporosis. Among the factors that can influence bone resorption and osteoclast activity, tumour necrosis factor (TNF)-α plays a central role in the destructive process of RA and has been shown to increase bone resorption in systemic osteoporosis related to oestrogen deficiency [4]. In transgenic mice expressing soluble TNF receptor to neutralize TNF-α, animals were protected from oestrogen deficiency-related bone loss [5]. TNF-α is a powerful inhibitor of bone formation [6]
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