| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
The relationship between periodontal degradation and smoking has been demonstrated by epidemiological evidence. However, the mechanism of this effect is unknown, and may be related to a host-response reaction. We investigated the effect of smoking on periodontal tissue. Peripheral blood neutrophils are a front line response in the body's defense mechanism, and we exposed these to one of the toxic substances contained in tobacco smoke, nicotine, cotinine (a metabolite of nicotine having a half-life of which ranges from 20 to 40 hours), PMA, and LPS. We then measured the degranulation, elastase activity, total elastase, elastase-alpha-1-antitrypsin complex, alpha-1-antitrypsin and lactoferrin, and the active oxygen production by using cytoenzymology, enzyme assay, and ELISA. The results suggest that nicotine made PMN to hyperactive, but cotinine hypofunctional. We speculate that cotinine was one of the factors in periodontal degradation, because cotinine's half-life ranges from 20 to 40 hours. A relationship between serum cotinine and periodontal degradation has recently been reported, and we are investigating whether there was a correlation between gingival neutrophil activity and saliva cotinine. Furthermore, there is a possibility that the measurement of saliva cotinine may be a convenient biochemical marker. We published the results in the Japanese journal of conservative dentistry, Vol.48, No.6, 891-901, 2005.
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