Agressive early treatment prevents rapid bone loss in rheumatoid arthritis
Rheumatoid arthritis (RA) is a long-term autoimmune disorder of the joints and it is characterized by stiffness, acute swelling and pain in the joints. The International Osteoporosis Foundation (IOF) Chronic Inflammation and Bone Structure (CIBS) Working Group has published its review of bone loss in RA and the role of biologics in bone outcomes - bone mineral density (BMD), bone turnover markers, and fragility fractures. They concluded that early and aggressive treatment with biologics disease-modifying anti-rheumatic drugs (bDMARDs) is crucial to avoid progressive bone loss in patients with RA.
According to Dr. Cristiano Zerbini MD, Co-Author, Director of the Centro Paulista de Investigacao Clinica (CEPIC) in Sao Paolo, Brazil, "Bone loss is one of the most harmful effects induced by chronic inflammation as well as by medications taken to treat RA, such as glucocorticoids. It is therefore important to acquaint a better understanding of medications used to treat chronic inflammation."
Numerous factors may contribute to bone loss, such as anorexia, malnutrition, muscle wasting, cachexia, depression, decreased functional capacity and lack of exercise associated with joint pain, bone damage and progressive bone loss.
Most importantly, corticosteroids used during RA treatment, even a small dose of prednisone of 5mg/day or equivalent for more than 3 months, is linked with rapid and persistent bone loss. One of the studies have shown that continuous treatment with prednisone at 10 mg/day during 90 days or more increased the risk of vertebral fractures 17-fold and hip fractures 7-fold.
The Working Group concluded that:
Early and "aggressive" treatments were more effective in rapidly achieving a low level of inflammation and halting the progressive loss of bone.
Therapies targeting specific cytokines and its signaling pathways with biologic DMARDs may protect the skeleton and should be introduced as soon as possible. However, it should be noted that outcomes in these clinical studies were based mostly on changes in biological markers and only a few reported modifications on BMD or localized osteoporosis. Only three retrospective studies reported reduction in fracture risk after anti- tumour necrosis factors (TNF) therapy.
The TNF blockade studies showed that even in RA patients not responsive to treatment, a protective effect on bone was observed suggesting the possibility that anti-TNF therapy may restore coupling of the bone remodeling independently of its anti-inflammatory action.
Lack of efficacy of TNF blockade on hand bone loss was found, despite its preservation of BMD in lumbar spine and hip. Better results regarding localized bone loss were observed with anti-interleukin (IL6) treatment.
Very few studies reported inhibition of bone loss after rituximab and abatacept treatment.
Anti-RANKL therapy showed beneficial effects in the preservation of bone mass in RA, especially in juxta-articular osteoporosis, although this treatment cannot alter the inflammatory process.
New non-biologic therapies but potent inhibitors of the cytokine network may offer future options for skeleton preservation in RA.
According to Professor Patricia Clark, MD, Co-author, Head of Clinical Epidemiology, Hospital Infantil de Mexico, Mexico City, "Although several studies reported favourable actions of biologic therapies on bone protection, it is clear that there are still unmet needs for research into their actions on the risk of bone fractures in RA patients. In the meantime, we recommend that all physicians treating RA remain vigilant of the high risk of bone loss and fractures in their patients. For many such high risk patients, it is important that osteoporosis treatment be considered to reduce fracture risk."
International Osteoporosis Foundation
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Original title of article:
Biologic therapies for rheumatoid arthritis may protect against rapid bone loss