Vitamin D Receptor Gene Polymorphism and Smoking in the Risk of Chronic Periodontitis
Journal of Periodontology, Posted online on August 4, 2016. (doi:10.1902/jop.2016.160222)
Soranun Chantarangsu,* Thanyachai Sura,† Sanutm Mongkornkarn,‡ Kobkiat Donsakul,§ and Kitti Torrungruang? Kitti.T at Chula.ac.th.
*Department of Oral Pathology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
†Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
‡Department of Periodontology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
§Health Division, Medical and Health Department, Electricity Generating Authority of Thailand, Nonthaburi, Thailand.
?Department of Microbiology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
Risk Factors - VDR alone:1.8, Smoking alone: 2.5; Multipled: 4.5 but if coexisting: 9.6
This is the first time I can recall a more than multiplicative combination of two vitamin D risk factors
Note: Receptor problems ARE NOT noticed by Vitamin D tests
See also VitaminDWiki
- Smoking reduces vitamin D starts with:
Two pathways often proposed for smoking decreasing vitamin D
1. Smoking decreases Calcium. and Vitamin D is used up in replacing the Calcium
2. Smoking injures the body, and vitamin D is used up in repairing the body
- Vitamin D Receptor category listing has
198 items along with related searches
The items in both categories of Dental and Vitamin D Receptor are listed here:
See also web
"Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that is caused by accumulation of profuse amounts of dental plaque"
Background: Polymorphisms of the vitamin D receptor (VDR) gene have been implicated in the susceptibility to infections and bone-related diseases. However, their relationship with periodontal disease remains unclear. This cross-sectional study investigated whether the susceptibility to chronic periodontitis (CP) in a Thai population is associated with VDR polymorphisms.
Methods: Genomic DNA was obtained from 1,460 subjects, aged 39-66. Genotyping of VDR polymorphisms (FokI, BsmI, ApaI, and TaqI) was performed using real-time polymerase chain reaction. Subjects were categorized into three groups: no/mild, moderate, and severe CP. Multinomial logistic regression was used to determine the degree of association between VDR polymorphisms and periodontal status adjusted for known confounders.
Results: The CC+CT genotypes of FokI polymorphism were associated with severe CP with an odds ratio (OR) of 1.9 (95% CI:1.3-2.8). Compared with genotype-negative (TT) non-smokers, positivity for the risk genotypes (CC+CT) alone and current smoking alone were associated with severe CP with ORs of 1.8 (95% CI:1.1-3.2) and 2.5 (95% CI:1.0-6.2), respectively.
The combination of being genotype positive and smoking further increased the OR to 9.6 (95% CI:4.5-20.4). This combined effect was 3.7 times (95% CI:1.2-11.1) greater than what would be expected from the sum of their individual effects, indicating a synergistic interaction. No significant association was observed between other polymorphisms and CP.
Conclusion: The FokI CC+CT genotypes were associated with increased susceptibility to severe CP, which was aggravated further when combined with smoking.
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