Forwood M R, Burr D B, Takano Y, Eastman D F, Smith P N, Schwardt J D
Department of Anatomy and Orthopedic Surgery, Indiana University School of Medicine, Indianapolis 46202, USA.
Bone. 1995 Jun;16(6):643-50. doi: 10.1016/8756-3282(95)00120-3.
Cortical and trabecular bone from the femoral neck of 24 adult female beagle dogs was examined for microdamage following 2 years of treatment with risedronate (NE-58095). Specimens of the femoral neck, sectioned between the femoral head and the intertrochanteric groove, were bulk stained in 1% basic fuchsin in graded alcohols and embedded in methylmethacrylate. Five transverse sections of 100 microns from each specimen were examined for microdamage and measurement of cortical and trabecular area, and three sections from each specimen were measured for calculation of trabecular and cortical bone activation frequency (Ac.f) and bone formation rate (BFR/BV) in the superior and anterior regions of the femoral neck. Although no statistical differences were observed among groups for numerical density or length of microcracks, Kruskal-Wallis analysis showed differences among groups for both cortical and trabecular bone area (p < 0.05). Ac.f was significantly lower in both cortical bone (p < 0.05) and trabecular bone (p < 0.005) of the femoral neck at all dosage levels. No significant difference was observed among groups for trabecular mean wall thickness. The hypothesis that microdamage accumulation increases following reduction in Ac.f was not supported for the canine femoral neck in this experiment. This result could be explained by the fact that microdamage does not accumulate following treatment; that transient increases in microdamage at the beginning of the study period had been repaired; or finally, that the canine femoral neck does not reflect weight-bearing conditions of clinical relevance to humans for assessment of microdamage.
