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dc.contributor.authorMaddux, William F.
dc.date.accessioned2021-02-23T19:49:12Z
dc.date.available2021-02-23T19:49:12Z
dc.date.issued2002-04
dc.identifier.urien
dc.identifier.urihttp://hdl.handle.net/10675.2/623879
dc.description.abstractResin-based materials have become increasingly popular for use in dentistry. Components of these materials are known to leach out from placement sites, initially at high concentrations and thenafter at relatively lower levels. Available evidence indicates that dental resin components have detrimental effects towards gingival fibroblast and epithelial cells. However, despite the rich vascularity of the oral environment, there is only limited information on the effects of these substances on the responsiveness of vascular tissues. The present investigation was undertaken to determine the effects of the resin components, methyl methacrylate (MMA), hydroxyethyl methacrylate (HEMA), triethylene glycol dimethacrylate (TEGDMA) and dimethylaminoethyl methacrylate (DMAEMA), on vascular reactivity using the isolated rat aorta as a tissue model. In addition, possible vascular effects of the degradation products ofHEMA and DMAEMA, i.e., dimethylethanolamine (DME), methacrylic acid (MAA) and ethylene glycol (EG), were also assessed. In the investigation, isometric tension of aortic rings was measured, and various in vitro conditions were employed to study the mechanisms of resin-induced vascular reactivity. Biochemical assays of tissue levels of prostacyclin (PGh) and thromboxane Az (TXAz) were also carried out to determine if there was a correlation with the mechanical responses. It was found that MMA, HEMA, TEGDMA and DMAEMA caused concentration-dependant relaxation of NE-contracted rat aortic rings with and without endothelium. This finding suggests the existence of both endothelium-dependent and independent components for the vascular responses to these resin components. The endothelium-dependent but not independent responses were inhibited by N-nitro-Larginine methyl ester (L-NAME), indicating the involvement of endothelium-derived nitric oxide. The vasorelaxant effects of MMA, TEGDMA and DMAEMA on the endothelium-intact and denuded aortic rings were attenuated by indomethacin, providing evidence for the role of prostanoids, such as prostacyclin, in these responses. This observation was further supported by the increased production of prostacylin in response to TEGDMA, although this was not well established for MMA and DMAEMA. Glybenclamide selectively inhibited TEGDMA and DMAEMA-induced relaxation of the blood vessels with and without endothelium. However, while the effects of the inhibitor on TEGDMA-induced relaxation were similar in the endothelium intact and denuded aortae, they were greater in the intact tissues relaxed by DMAEMA. These results suggest the activation of vascular smooth muscle KATP channels by both TEGDMA and DMAEMA, and the possible release of endothelium-derived hyperpolarizing factor (EDHF) by DMAEMA. On the other hand, DMAEMA at a relatively high concentration caused contraction of the rat aorta while DME induced concentration-dependant contractile responsiveness at lower concentrations, in both the presence and absence of the endothelium. Endothelium removal did not alter the responses of the tissue to DME. The contractile effe?ts of DME were attenuated by indomethacin, indicating the involvement ofprotanoid metabolite(s) in the vascular action of this degradation product of DMAEMA. In support of this finding, there was enhanced production of TXA2 in aortic rings incubated with DME. Unlike DME, MAA, and EG were without effect on the rat aorta. It is concluded the MMA, HEMA, TEGDMA, and DMAEMA alter the function of blood vessels by causmg relaxation v1a different mechanisms, which, depending upon the substances under consideration, may at least involve the release of nitric oxide and prostacylin, and the activation ofKATP channels. Further, DMAEMA (at high concentration) and its degradation product DME, upon interaction with aortic tissue can cause vasoconstriction; the effect of DME may involve the generation of TXAz. These mechanisms may play a role in tissue homeostasis and certain pathophysiological conditions associated with the use of resin materials in dentistry.en_US
dc.language.isoen_USen_US
dc.publisherAugusta Universityen_US
dc.rightsCopyright protected. Unauthorized reproduction or use beyond the exceptions granted by the Fair Use clause of U.S. Copyright law may violate federal law.en_US
dc.titleAn In vitro investigation of vascular responses to dental resin componenten_US
dc.typeThesisen_US
dc.contributor.departmentDepartment of Oral Biologyen_US
dc.description.advisorAbebe
dc.description.committeeHokett
dc.description.committeeSchuster
dc.description.committeeMozaffari
dc.description.committeeRuggeberg
dc.description.degreeMaster of Scienceen_US
dc.embargoen
refterms.dateFOA2021-02-23T19:49:13Z


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