Objective: The aim of this study was to gain insight into the pathogenesis of bone mass loss and weakening affecting patients with celiac disease, according to the new concepts of bone structure/strength and muscle/bone interrelationships.
Methods: We studied serum variables and tomographic indicators of bone structure and strength and regional muscle masses in a series of patients at diagnosis and after 1 yr on a gluten-free diet and in gender- and age-matched controls.
Results: At diagnosis, serum levels of calcium and vitamin D were low, and indicators of parathyroid hormone activity and bone formation and resorption were increased. All these parameters were normalized by treatment. Peripheral quantitative CT scans of the distal radius revealed that cortical bone was generally more affected than trabecular bone. The cross-sectional area (CSA) and the volumetric mineral content and density of cortical bone (indicators of cortical tissue mass and mechanical quality), and moments of inertia (CSMI, indicator of the bone architectural design) were in the lower end of normal range in men, and below that in 50% of women. In men, the CSMI/CSA ratio (indicator of the architectural efficiency of distribution of the available cortical tissue) was lower than expected and remained unchanged after treatment. In women, the baseline ratio was normal, but both the ratio and the CSMI were low at diagnosis and normalized after treatment. Both baseline values and the treatment-induced changes of cortical and trabecular bone in the radius and the axis (L3) correlated inversely with serum parathyroid hormone levels. Baseline values or changes in the mineral content of the vertebral bone correlated with the CSA of psoas and spine-extensor muscles. Multiple regression analyses showed that metabolic and mechanical parameters were independent determinants of different aspects of the vertebral bone weakening.
Conclusions: Our results show that bone weakening in celiac disease might result from both 1) a metabolic disturbances of bone remodeling affecting trabecular and cortical bone masses and the mechanical quality of the bone material, and 2) a reduction of muscle strength impairing the modeling-dependent optimization of bone architectural design and mass of cortical bone. Dietary treatment seems to correct almost exclusively the metabolically induced disturbances, which were predominant in women.