The Increase of Maxillary Lateral Expansion Limit by Local Application of Fluvastatin

Abstract

Among hyperlipidemia patients, when total cholesterol and LDL cholesterol are high, arteriosclerosis develops and the risk of inducing myocardial infarction or cerebrovascular disorders increases. In the liver, cholesterol is produced by the action of HMG -CoA reductase, etc., and the cholesterol is transferred to each tissue or expelled in bile. Currently, statins are central among hyperlipidemia medicines. Statins are inhibitors of HMG -CoA reductase in the liver, and by suppressing cholesterol synthesis they have the effect of reducing blood cholesterol (1 -4) .In recent years, it has become clear that the effect of statins is not limited to inhibiting HMG -CoA reductase, but they also cause the promoters of Bone Morphogenetic Proteins -2 (BMP -2) to activate, controlling boneinducing ability by Smad Ubiquitination Regulatory Factor 2 (Smurf2) (5 -7) . In our previous research, we examined the effect of fluvastatin on endochondral ossification. In endochondral tissues, by inhibiting cholesterol modification of Indian Hedgehog (IHH) , statins caused IHH pathways to become active, changing localization of IHH (8) .These resulted in promotion of cell proliferation, increase in the hypertrophic chondrocyte layer, inhibiting apoptosis, and reduction in calcification, proving that it plays a positive role in long bone growth (9, 10) . To summarize, we believe that statins not only inhibit systemic LDL cho-Correspondence to：