Project/Area Number |
17592163
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Periodontal dentistry
|
Research Institution | Meikai University |
Principal Investigator |
HAYASHI Joichiro Meikai University, School of Dentistry, Associate Professor (50337507)
|
Co-Investigator(Kenkyū-buntansha) |
SHIN Kitetsu Meikai University, School of Dentistry, Professor (40187555)
HASEGAWA Akihiko Meikai University, School of Dentistry, Professor (20198708)
GOTO Seiichi Meikai University, School of Dentistry, Lecturer (70306299)
NANBA Nanba Meikai University, School of Dentistry, Assistant Professor (40406393)
|
Project Period (FY) |
2005 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,670,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
Keywords | periodontal disease / diabetes mellitus / mannose-binding lectin / gene polymorphism |
Research Abstract |
Mannose-binding lectin (MBL) plays an important role in aspects of natural immunity such as complement activation and opsonization. It has been reported that MBL deficiency caused by MBL gene polymorphism is related not only to systemic infections, but also to aggressive periodontitis and diabetes mellitus (DM). In this study, we investigated the effect of MBL gene polymorphism and the serum concentration of MBL on the development and progression of type 2 DM, and on the progression of periodontal disease. Sixty-two patients with DM and the same number of healthy subjects (HS) were included in this study. MBL codon 54 gene polymorphism and the serum MBL concentration were investigated in each individual The frequency of the MBL gene mutation was not significantly different between DM patients and HS. The serum MBL concentration was significantly lower in the subjects with the mutated gene (mutations) than in those with the wild-type one (wild-type), in both DM and HS groups. Furthermore, periodontal parameters were investigated in the DM patients. There was a significant difference in bleeding on probing between the mutation and wild-type groups of DM patients, the percentage being higher for the former. Especially in the wild-type group, there was a significant positive correlation between the serum MBL concentration and alveolar bone resorption. In conclusion, our data suggest that MBL gene mutations possibly accelerate inflammation in the periodontal tissue of patients with type 2 diabetes mellitus and that the serum MBL concentration may be a systemic marker of periodontitis.
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