HMGCo-A reductase inhibitors increase bone formation

Abstract

Statin, a HMG-CoA reductase inhibitor, was shown to turn on the gene for bone formation, by blocking the mevalonate pathway in cholesterol production. Naringin is a flavonoid available commonly in citrus fruits which is also a HMG-CoA reductase inhibitor. Objective: To compare the amount of new bone produced by HMG-CoA reductase inhibitors, statin and naringin, in collagen matrix carrier to that of collagen matrix carrier alone. Methods: Twenty bone defects were created in the parietal bone of 12 New Zealand White rabbits. In the experimental groups, 5 defects were grafted with statin solution mixed with collagen matrix carrier, 5 defects were grafted with naringin solution mixed with collagen matrix carrier. In the control groups, 5 defects were grafted with collagen matrix carrier alone (positive control) and 5 were left empty (negative control). Animals were killed on day 14 and the defects were dissected and prepared for histological assessment. Serial sections were cut across each defect. Quantitative analysis of new bone formation was made on 150 sections (50 sections for each group) using image analysis. Results: A total of 308% and 490% more new bone was present in defects grafted with statin in collagen matrix carrier, naringin in collagen matrix carrier, respectively, than those grafted with collagen matrix carrier. No bone was formed in the passive control group. Conclusions: HMGCo-A Reductase Inhibitors like statin and naringin in collagen matrix carriers have the effect of increasing new bone formation locally and can be used as bone graft materials. This has tremendous potential as statin is a commonly prescribed cholesterol-lowering drug whereas naringin is available commonly in edible fruits.