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Chronic inflammatory intestinal diseases and bone loss
  1. M T Bardella1,
  2. M L Bianchi2,
  3. A Teti3
  1. 1Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, IRCCS, Milano, Italy
  2. 2Bone Metabolism Unit, Istituto Auxologico Italiano, IRCCS, Milano, Italy
  3. 3Department of Experimental Medicine, University of L’Aquila, L’Aquila, Italy
  1. Correspondence to:
    Dr M T Bardella
    University of Milan, Mangiagalli e Regina Elena, IRCCS, Via Francesco Sforza, 35 Milano, Italy;

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We were very interested in the recent article by Moschen et al on activation of the RANKL/OPG system in inflammatory bowel disease (IBD) (Gut 2005;54:479–87). Until recently, osteoporosis secondary to gastrointestinal diseases was mainly considered a direct consequence of malabsorption.1,2 The article of Moschen et al and a previous one of our group on bone loss in coeliac disease,3 a disorder similarly characterised by intestinal inflammation, offer a new perspective on the pathogenesis of bone loss and reveal a more complex picture. Moschen et al demonstrated overproduction of OPG in the cells of colonic mucosa in IBD whereas Taranta and colleagues3 showed the direct role of the soluble cytokines in the serum of coeliac patients on bone cells. In fact, they found an increased RANKL/OPG ratio in untreated coeliac patients and different effects of the sera of untreated coeliac patients with respect to those on a gluten free diet, on cultured bone cells. These effects included increased in vitro osteoclastogenesis, and lower interleukin 18 and OPG expression in osteoblasts.

In both studies, these biochemical observations were translated in a reduction of bone mass. Moschen et al found a negative correlation between OPG plasma levels and spine and femoral neck bone mineral density (BMD). Taranta and colleagues3 observed a significant negative correlation between BMD z score and interleukin 6 levels and RANKL/OPG ratio. In the discussion, Moschen et al observed that “studies of OPG/RANKL and BMD are required to validate” his model.

We believe that our study may be a first step towards understand, at least in part, the relative contribution of inflammation to bone loss in intestinal diseases. These results are also in accordance with recent studies on primary osteoporosis, which are beginning to show a relevant role of local and systemic factors on bone cell activity.4–6 Finally, these studies may also open the way to different therapeutic approaches—namely, drugs specifically acting on cytokines release and/or activity—for bone loss secondary to “inflammatory intestinal diseases”.


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  • Conflict of interest: None declared.

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