In studies of osteoporosis, the bone mass is assessed by measuring BMD while the metabolic activity of the bone is assessed by measuring the biochemical markers of bone turnover [21]. These markers have limited utility in individual patients because they have high within-person variability (low precision), and because it is not clear which markers are useful in which clinical situation [21, 22]. In contrast, comparing biochemical markers between groups of patients in clinical studies has been found to be useful in two settings. Firstly, it has been found that high levels of biochemical markers of bone resorption predict fractures independent of BMD [23, 24]. Secondly, early changes in bone markers (at 3-6 months) during anti-resorptive therapy predict later changes in BMD and fracture rates [25-28]. The mechanisms underlying these observations have not been elucidated to date. It is speculated that increased bone resorption, which is reflected in elevation of biochemical markers of bone turnover, increases fragility by weakening trabecular structure prior to or independent of measurable BMD changes. Similarly, decreased bone resorption during pharmacological therapy is likely to improve the trabecular structure before or independent of its effects on BMD. Since the aim of our research is to (indirectly) examine the trabecular structure by performing the radiographic texture analysis, we plan to determine whether the changes in biochemical markers of bone turnover during antiresorptive therapy will correlate with changes in the results of texture analysis.