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The relationship of oral disturbances of diabetes mellitus patients with paraoxonase gene polymorphisms
The relationship of oral disturbances of diabetes mellitus patients with paraoxonase gene polymorphisms
The relationship of oral disturbances of diabetes mellitus patients with paraoxonase gene polymorphisms
Diabetes Mellitus (DM) is a multisystemic disorder with serious complications and these patients may also have serious problems with their oral cavity probably because of the microangiopathic and neuropathic complications. In diabetic patients, there may be several problems of the oral cavity such as gingivitis, periodontitis, candidiasis, glossitis, oral ulcerations, loss of taste sensations, opportunistic infections and several other conditions dependent on these. One of the recent theories about complications in DM is the contribution of reactive oxygen radicals. Paraoxonase (PON1) is an enzyme that is synthesized in liver and having the capability of hydrolasing the active metabolite of an insectisid, parathion. Previously it was shown that there are two polymorphic areas on the PON1 gene: one causing a Leu [rarr] Met substitution at 55th position, the other causing Gln [rarr] Arg at the 192nd position. We investigated the differences in PON activities related to the oral lesions in Type 2 diabetics and control subjects to see their relationships with PON1 activity levels and the two main gene polymorphisms of PON1 genes, PON1 192 and PON1 55. We had 51 patients and 53 healthy subjects used in the study. PON activity was significantly decreased in Type 2 DM group compared to the control group. Neither PON1 192 nor PON1 55 genotypes had any differential effect on PON1 enzyme activity levels in either group. However, we found that PON1 55 M allele carriers had greater risk for general periodontal and/or gingival problems. Copyright © 2008 John Wiley & Sons, Ltd.
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Cell Biochemistry and Function
By John Wiley & Sons, Inc - Copyright © 2008 John Wiley & Sons, Ltd. - version: v1.5 build A
By John Wiley & Sons, Inc - Copyright © 2008 John Wiley & Sons, Ltd. - version: v1.5 build A