Menopause is the most prevalent cause of accelerated bone loss in women. Biochemical markers of bone resorption can be used clinically to predict future bone loss. This study aimed to determine the level of bone resorption markers in healthy pre and postmenopausal Malay women and determine their association with the risk. A total of 150 healthy women were recruited for this study (51 pre and 99 postmenopausal subjects). Data on socioeconomic, lifestyle habit and clinical were gained by personal interview. Fasting serum was collected to measure both C-telopeptide (CTx) and N-telopeptide (NTx) of type 1 collagen. Both markers were highly correlated with each other (r=0.568, p<0.001). Both intra- and inter-assay coefficient of variations (CV) of NTx were higher than those of CTx (8% and 12% vs 6% and 5%). The mean CTx values of pre and postmenopausal subjects were comparable with the expected values (0.2833 (0.1769) ng/mL and 0.4323 (1.851) ng/mL compared with 0.287 and 0.438 ng/mL, respectively). The NTx value for premenopausal subjects were higher than the expected values (15.2 (8.10) compared to 12.6 (3.20) nM BCE). The median was 19.929 nM BCE. The mean CTx and NTx levels of postmenopausal subjects were significantly lower than premenopausal subjects (p<0.05). The risk factors for bone resorption in this population were duration of menopause, marital status, body mass index (BMI), physical activity and education level. In conclusion, postmenopausal women showed a higher bone resorption, indicating higher bone loss. Increasing education and physical activity intervention might be effective to ensure better health in Malaysian older population.
This study was conducted to determine the effectiveness of three forms of vitamin E supplements following nicotine treatment on bone histomorphometric parameters in an adult male rat model. Rats were divided into seven groups: baseline (B, killed without treatment), control (C, normal saline for 4 months), nicotine (N, nicotine for 2 months), nicotine cessation (NC), tocotrienol-enhanced fraction (TEF), gamma-tocotrienol (GTT), and alpha-tocopherol (ATF). Treatments for the NC, TEF, GTT, and ATF groups were performed in two phases. For the first 2 months they were given nicotine (7 mg/kg), and for the following 2 months nicotine administration was stopped and treatments with respective vitamin E preparations (60 mg/kg) were commenced except for the NC group, which was allowed to recover without treatment. Rats in the N and NC groups had lower trabecular bone volume, mineral appositional rate (MAR), and bone formation rate (BFR/BS) and higher single labeled surface and osteoclast surface compared to the C group. Vitamin E treatment reversed these nicotine effects. Both the TEF and GTT groups, but not the ATF group, had a significantly higher trabecular thickness but lower eroded surface (ES/BS) than the C group. The tocotrienol-treated groups had lower ES/BS than the ATF group. The GTT group showed a significantly higher MAR and BFR/BS than the TEF and ATF groups. In conclusion, nicotine induced significant bone loss, while vitamin E supplements not only reversed the effects but also stimulated bone formation significantly above baseline values. Tocotrienol was shown to be slightly superior compared to tocopherol. Thus, vitamin E, especially GTT, may have therapeutic potential to repair bone damage caused by chronic smoking.
Vitamin E is beneficial in restoring bone histomorphometric parameters in nicotine-treated rats. This study determined the effectiveness of 3 forms of vitamin E in restoring bone metabolism in nicotine-treated rats.