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Background: cytokines that regulate the bone turnover (TNFα, IL-6, etc.) may influence the pathogenesis of skeleton disorders, such as osteoporosis, by stimulating the bone reabsorption and the recruitment and differentiation of osteoclast precursors. Since H. pylori (HP) infection may increase the systemic levels of inflammatory cytokines, we investigated on the possibility that HP infection may affect bone metabolism in a group of male patients with osteoporosis. Material and Methods: we examined 55 male patients with osteoporosis for serum antibodies to HP and the CagA protein (by ELISA tests), and determined the most important biochemical and instrumental parameters of the disease. Proportions were compared in univariate analysis by the chi² tests with the Yates correction, or the Fisher's exact test. P values < 0.05 were considered significant. Results: the mean age of patients was 65 years (range 55-82 years); 37 patients (67.2%) were seropositive for H. pylori infection, and 18 patients (32.7%) were seronegative; 19 infected patients (51.3%) were CagA-positive. No significant difference was found between HP[sup +] and HP[sup -] patients in height, weight, calcium intake, sex hormone and 25 OH vitamin D levels, and femoral BMD. The following parameters showed a trend for difference: IGF-I (ng/ml) (145 ± 102 in HP[sup -] vs. 118 ± 40 in HP[sup +] patients, P = 0.15), serum calcium levels (mg/dl) (9.24 ± 0.37 in HP[sup -] vs. 9.06 ± 0.36 in HP[sup +] patients, P = 0.09) and urinary crosslaps (a marker of bone reabsorption) (µg/mmol) (233.46 ± 130 in HP[sup -] vs. 290.1 ± 108 in HP[sup +] patients, P = 0.14). These differences were even more pronounced in CagA-positive patients, respect to the CagA-negative ones. Discussion: these results suggest that the chronic low inflammatory response stimulated by HP infection may increase the bone turnover, and, in a long run, exacerbate the clinical expression... [ABSTRACT FROM AUTHOR]