Vertebral fractures (VFX) are caused by low bone mass and microstructural deterioration of bone tissue. The latter is not well defined. We investigated bone structure in transiliac biopsy specimens from 88 volunteers. Biopsy specimens were obtained at baseline in the Multiple Outcomes of Raloxifene Evaluation trial, a prospective study in osteoporotic (BMD ≤ −2.5 T score) postmenopausal women without or with VFX on standardized lateral spinal radiographs. Bone biopsy specimens were embedded in methylmethacrylate (MMA). Histomorphometry was done in 8 μm (U.S.A.) or 5 μm (Europe) Goldner stained sections. Vertebral fracture status (yes/no) was the outcome variable in logistic regression models adjusted for age and biopsy specimen origin (U.S.A. vs. Europe). Patients with and without VFX (26/62) were similar regarding age (69.2 ± 5.2 years vs. 67.3 ± 6.7 years), bone volume (BV/TV; 17.7 ± 4.7% vs. 19.0 ± 5.8%), and bone surface (BS/TV; 2.7 ± 0.6 mm²/mm³ vs. 2.8 ± 0.6 mm²/mm³). A lower cortical thickness (C.Th; 652 ± 267 μm vs. 822 ± 325 μm), total strut length (TSL; 826 ± 226 μm/mm² vs. 922 ± 256 μm/mm²), node‐to‐loop (Nd‐Lp) strut length (10.1 ± 10.3% vs. 15.0 ± 13.6%), together with a higher node‐to‐terminus (Nd‐Tm) strut length (45.6 ± 9.7% vs. 39.1 ± 9.3%) were each associated with prevalent VFX (0.01 < p < 0.10). Differences in BV/TV did not explain these associations. In conclusion, cortical thinning and disruption of trabecular lattice are possible pathogenic mechanisms in patients with VFX.
Keywords: cancellous bone structure; strut analysis; cortical thickness; prevalent vertebral fractures; postmenopausal osteoporosis