Infliximab in spondylarthropathy: Influence on bone density

O s t e o p o rosis is fre q u e n t ly associat e d with Ankylosing Spondylitis (AS). Bone mineral density (BMD) decreased pr e dominantly in patients with active dis ease. Moreover, conventional therapy, i.e. NSAID seems to have no influence in the bone loss. It has been suggested t h at local or systemic infl a m m at o ry cytokine release might be implicated in bone loss. Monoclonal antibody to TNF in patients with AS demonstrat ed significant clinical response with significant reduction in the acute-phase reactants ESR and CRP. We evaluated the changes in bone min e ral density (BMD) in patients with Spondylarthropathy (SpA) treated with infliximab (a human/mouse neutralising chimeric monoclonal antibody). We included 29 patients. In 6 months,there was a statistically significant increase in BMD both at the spine and total hip. There was an increase in osteocalcin b e t ween baseline and week 6. Th e s e d ata suggest a benefit of anti-TNF therapy on BMD in patients with SpA, may be through an uncoupling ef fect on bone cells. It has been recognized for a long time that osteoporosis is frequently associated with Ankylosing Spondylitis (AS). Two longitudinal studies in ear ly AS have shown that spine and hip bone mineral density (BMD) decreased predominantly in patients with active dis ease (1, 2). More ove r, c o nventional therapy, i.e. NSAID seems to have no influence in the bone loss (1). The etiolo gy of SpA-associated osteoporosis remains controversial. Among p o s s i b le mech a n i s m s , i n fl a m m at o r y mediators released during the course of AS, and decreased mobility of patients, might play a role in the occur rence of osteoporosis, by directly affecting bone remodeling. It has been suggested that local or sys temic infl a m m at o ry cytokine re l e a s e might be implicated in bone loss. This bone loss could be related to an in