Abstract
Osteoporosis affects many patients with celiac disease (CD), representing the consequence of calcium malabsorption and persistent activation of mucosal inflammation. A slight increase of fracture risk is evident in this condition, particularly in those with overt malabsorption and in postmenopausal state. The adoption of a correct gluten-free diet (GFD) improves bone derangement, but is not able to normalize bone mass in all the patients. Biomarkers effective in the prediction of bone response to gluten-free diet are not yet available and the indications of guidelines are still imperfect and debated. In this review, the pathophysiology of bone loss is correlated to clinical aspects, defining an alternative proposal of management for this condition.
Highlights
Osteoporosis is a condition characterized by low bone mass and micro-architectural deterioration of bone tissue resulting in enhanced bone fragility and an increase in fracture risk [1]
Nutrients 2013, 5 celiac disease (CD) patients with an overt malabsorption syndrome at diagnosis suffer from a loss of bone mass [3,4,5,6,7,8,9], and this complication affects about half the patients with subclinical CD, presenting with minimal, transient and apparently unrelated symptoms [3,9], or asymptomatic patients diagnosed because of their first-degree kinship [4]
The pathophysiological role of autoantibodies against OPG is debated, as in a recent paper the presence of these antibodies was detected in a man with CD, high bone turnover and severe osteoporosis not responsive to gluten-free diet (GFD) and to calcium and vitamin D supplementation [36]
Summary
Osteoporosis is a condition characterized by low bone mass and micro-architectural deterioration of bone tissue resulting in enhanced bone fragility and an increase in fracture risk [1]. It affects more than 75 million people in developed countries, causing 8.9 million fractures annually worldwide. There is no doubt that CD is a condition at high risk for secondary osteoporosis, and the evaluation of bone mass and mineral metabolism is very important in the clinical management of these patients. In the last few years, while the mechanisms of bone derangement in CD have been extensively studied, less attention has been paid to the clinical management of this complication: there is very little information available on the timing of the first bone mineral density (BMD) measurement, on follow-up frequency, even on the best treatment options
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
