Alendronate transiently decreases bone formation and vascularity in the extraction socket and delays the removal of interdental alveolar bone after tooth extraction in rats.

Yarrow JF, Conover CF, Purandare AV, Bhakta AM, Zheng N, Conrad B, Altman MK, Franz SE, Wronski TJ, Borst SE. Supraphysiological testosterone enanthate administration prevents bone loss and augments bone strength in gonadectomized male and female rats. Am J Physiol Endocrinol Metab 295: E1213-E1222, 2008. First published September 9, 2008 doi:10.1152/ajpendo.90640.2008.-Highdose testosterone enanthate (TE) may prevent hypogonadism-induced osteopenia. For this study, 3-mo-old male and female Fisher SAS rats underwent sham surgery, gonadectomy (GX), or GX plus 28 days TE administration (7.0 mg/wk). GX reduced serum sex hormones (i.e., testosterone, dihydrotestosterone, and estradiol) (P Ͻ 0.05) in both sexes and bone concentrations of testosterone (males only), and estradiol (females only). GX also elevated urine deoxypyridinoline/ creatinine in both sexes and serum osteocalcin (females only), findings that are consistent with high-turnover osteopenia. GX reduced cancellous bone volume (CBV) and increased osteoid surfaces in tibia of both sexes. GX males also experienced reduced trabecular number and width and increased trabecular separation, whereas GX females experienced increased osteoblast and osteoid surfaces. Bone biomechanical characteristics remained unaffected by GX, except that femoral stiffness was reduced in females. In contrast, TE administration to GX rats elevated serum and bone androgens to supraphysiological concentrations in both sexes but altered neither serum nor bone estradiol in males. Additionally, TE did not prevent GX-induced reductions in serum or bone estradiol in females. TE also reduced markers of high-turnover osteopenia in both sexes. In males, TE prevented GX-induced changes in trabecular number and separation, CBV, and osteoid surfaces while diminishing osteoblast and osteoclast surfaces; however, these changes were not fully prevented in females. In both sexes, TE increased femoral length and femoral maximal strength to above that of Sham and GX animals while preventing the loss of femoral stiffness in females. In conclusion, TE administration appears protective of cancellous bone in male rats and augments cortical bone strength in both sexes.androgen; osteoblast; osteoclast; osteoporosis; osteopenia ANDROGENIC [e.g., testosterone and dihydrotestosterone (DHT)] and estrogenic (e.g., estradiol) hormones influence skeletal development and maintenance in both sexes (11,54). In males (16, 48) and females (31), androgen deficiency is associated with reduced bone mineral density (BMD), which reduces skeletal strength and increases fracture risk. Administration of testosterone at a physiological replacement dose appears only modestly effective in improving BMD in hypogonadal males (44) and perhaps hypopituitaric (i.e., androgen-deficient) females (30). However, testosterone exerts dose-dependent anabolic effects on bone (55, 58) and muscle (5, 6), suggesting that administration of higher-than-replacement (supraphysiological) testosterone may be required to completely prevent hypogonadal ...

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As the incidence of cystic fibrosis (CF) bone disease is increasing, we analyzed cystic fibrosis transmembrane conductance regulator (CFTR) deficient mice (CF mice) to gain pathogenic insights. In these studies comparing adult (14 wk) CF and C57BL/6J mice, both bone length and total area were decreased in CF mice. Metaphyseal trabecular & cortical density were also decreased, as well as diaphyseal cortical & total density. Trabecular bone volume was diminished in CF mice. Female CF mice revealed decreased trabecular width and number compared to C57BL/6J, whereas males demonstrated no difference in trabecular number. Female CF mice had reduced mineralizing surface and bone formation rates. Conversely, male CF mice had increased mineralizing surface, mineral apposition and bone formation rates compared to C57BL/6J males. Bone formation rate was greater in males compared to female CF mice. Smaller bones with decreased density in CF, despite absent differences in osteoblast and osteoclast surfaces, suggest CFTR influences bone cell activity rather than number. Differences in bone formation rate in CF mice are suggestive of inadequate bone formation in females, but increased bone formation in males. This pro-anabolic observation in male CF mice is consistent with other clinical sex differences in CF.

We evaluated the effects of trenbolone‐enanthate (TREN) administration on bone turnover and on trabecular bone mineral density (BMD) in order to test the hypothesis that neither the 5alpha reduction nor the aromatization of androgens is required for bone maintenance. 3 month old male Fisher SAS rats received SHAM surgery + vehicle (V), gonadectomy (GNX) + V, GNX + Low (L) TREN (1.0 mg/week), GNX + Moderate (M) TREN (3.5 mg/week), GNX + High (H) TREN (7.0 mg/week), or GNX + supraphysiological testosterone (T) (7.0 mg/week) for 28 days. GNX completely ablated serum T in all groups except GNX + T, where serum T was 18‐fold above SHAM (p < 0.05). Serum trenbolone increased dose‐dependently in response to the graded doses of TREN (L: 8.3 ± 0.5; M: 50.4 ± 3.2; H: 96.6 ± 7.5 ng/ml; p < 0.05). GNX increased serum C‐telopeptide by 13% and osteocalcin by 40% (p < 0.05), indicating high‐turnover osteopenia; while androgen administration prevented this phenomenon. GNX also reduced total and trabecular BMD at the femoral metaphysis by 12% and 15% compared with SHAM, respectively (p < 0.05); while androgen administration prevented this loss similarly across groups, ultimately resulting in 7–16% greater total and trabecular BMD than GNX (p < 0.05). Our results indicate that TREN prevents hypogonadism induced bone loss and suggest that the bone protective effects of androgens can occur independently of the 5alpha reductase and aromatase enzymes.