Abstract
IntroductionOsteoporosis is characterized by low bone mass and density, as well as change in microarchitecture of bone tissue leading to decreased bone strength. In vitro research shows nicotine can increase osteoblast activity and proliferation, also suppress osteoclast activity. Therefore we explore nicotine anti-resorptive property by in vivo true experimental and randomized posttest only controlled group research that was conducted in 18-20 weeks old Rattus norvegicus.MethodsTwenty-five female rats were divided into five groups, with 5 rats per group. The first group represented normal rats (Sham), while the second to fifth group underwent bilateral ovariectomy. The second group serves as positive control group (ovariectomy-only/OVX). The third to fifth group serve as dose 1 (P1-0.25mg/kg), dose 2 (P2-0.5 mg/kg), and Dose 3 (P3-0.75 mg/kg) treatment group receiving daily per-oral nicotine for 28 days, started 3 weeks post- ovariectomy. After 28 days treatment, the serum was checked.ResultsNicotine has dose-dependent manner on serum osteocalcin and serum DPD level. Level of osteocalcin in P2 group was significantly lower (Mann-Whitney, p = 0.008) compared to OVX group (59.4% lower). Level of DPD in all group was not significantly different (ANOVA, p < 0.05) but shows lowest level in P2 group. For serum calcitonin level, there's no significant different between groups.ConclusionNicotine at right low-dose might be able to inhibit osteoclast activity, thus open a possibility of anti-resorptive property of nicotine.
Highlights
Osteoporosis is a disease of bone characterized by low bone mass and density, as well as change in microarchitecture of bone tissue that leads to decreased of bone strength
The statistically significant decrement was achieved by P2 group (p = 0,008), and the trend suggest that nicotine administration lower the serum osteocalcin level (Figure 1)
Serum calcitonin level was highest in Sham group with 12.1% higher level compared to OVX group
Summary
Osteoporosis is a disease of bone characterized by low bone mass and density, as well as change in microarchitecture of bone tissue that leads to decreased of bone strength This disease increases the bone fragility to fracture [1]. There is an imbalance between the activity of osteoclasts (resorption agent) and osteoblasts (bone-forming agent). This imbalance can increase bone fragility [3]. The potency of nicotine as an anti-resorptive agent for osteoporosis is still poorly studied. We wanted to see the effectiveness of nicotine as a preventive agent for osteoporosis by examining bone turnover marker: serum osteocalcin, serum deoxypyridinoline (DPD) and serum calcitonin in ovariectomized wistar strain rats as model of postmenopausal osteoporosis
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