Abstract

To the Editor: We have examined, in 108 men with low bone mineral density (BMD), the relationships between the BMD, the architectural changes of trabecular bone, and the presence of vertebral fractures.1 Spinal radiographs showed at least one vertebral crush fracture in 62 patients (group II) and none in 46 patients (group I). After adjusting for age, body mass index (BMI), and BMD, there was no significant difference between the two groups in trabecular bone volume (BV/TV), trabecular thickness (Tb, Tn), and star volume of the marrow spaces (Star). In contrast, the mean values of interconnectivity index (ICI), free-end-to-free-end struts, and trabecular separation (Tb.Sp) were significantly higher whereas trabecular number (Tb.N) and node-to-node struts were lower in patients with at least one vertebral fracture. Of these 108 patients, 72 (66.7%) had relevant medical disorders associated with their osteoporosis, and 31 patients had glucocorticosteroid therapy. In group I (patients without vertebral fractures), 17 men were treated with glucocorticoids. In patients with at least one vertebral fracture (group II), 14 men were taking glucocorticoids. Because of this, we believe that in this study, the glucocorticosteroid therapy alone does not explain the differences in trabecular bone connectivity between the men with and without vertebral fractures. In a recent paper, Oleksik et al. have investigated bone structure in transiliac biopsy specimens from 88 postmenopausal women with osteoporosis (T score < −2.5).2 Among these patients, 26 women had at least one vertebral fracture. A lower cortical thickness but also a lower strut length, a lower node-to-loop strut length, and a higher node to terminus strut length were associated with prevalent fracture. These results strongly suggest that bone microarchitecture is also an important determinant of vertebral fracture in osteoporotic women. Recently Dalle Carbonare et al.3 have compared bone remodeling and trabecular bone microarchitecture in postmenopausal women with (n = 22) or without glucocorticosteroid therapy (n = 22). As indicated by a strong increase in ICI, the women taking glucocorticoids has dramatic loss of trabecular connectivity.3 We agree with the hypothesis of Dr. Hordon and Dr. Aaron that the etiology (e.g., idiopathic, steroid, alcohol, hypogonadism) of osteoporosis could influence the rate of bone loss, the quality of bone microarchitecture, and the vertebral fracture risk in men and women.4 We are now evaluating the relationships between risk factors (i.e., age, BMI, steroid, alcohol, tobacco, hypogonadism, chronic disease) and bone microarchitecture on a cohort of 152 men with primary or secondary osteoporosis, and we will submit new histological results to the Journal in 2 months.

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