A cross-sectional study from the third National Health and Nutrition Examination Survey in the United States found a significant inverse correlation between Periodontal disease (PD) and serum 25-hydroxyvitamin D [25(OH)D] concentrations1:
Data on periodontal attachment loss (AL) and serum 25(OH)D(3) concentrations from 11 202 subjects aged > or =20 y. Mean AL was modeled in a multiple linear regression with quintile of serum 25(OH)D(3) concentration as an independent variable. 25(OH)D(3) concentrations were significantly and inversely associated with AL in men and women aged >50 y. Compared with men in the highest 25(OH)D(3) quintile, those in the lowest quintile had a mean AL that was 0.39 mm (95% CI: 0.17, 0.60 mm) greater; in women, the difference in AL between the lowest and highest quintiles was 0.26 mm (0.09, 0.43 mm). In men and women younger than 50 y, there was no significant association between 25(OH)D(3) and AL. The bone mass density of the total femoral region was not associated with AL and did not, therefore, mediate the association between 25(OH)D(3) and AL1.
Chronic marginal gingivitis, a chronic inflammation of the gingival tissues that is induced by bacterial dental plaque, is often associated with PD.
In a related study using NHANES III data, Dietrich et al2 found a significant trend for prevalence of bleeding across quintiles of 25(OH)D:
“for the highest (32.4 nmol/L) vs. the lowest (99.6 nmol/L) the odds ratio was 0.90 (0.86-0.95) after adjustment for the same factors as for PD but with the addition of vitamin C, hormone replacement therapy among women, missing teeth, full crown coverage, and frequency of dental visits.”
Much of the action of vitamin D is by the active metabolite of vitamin D, 1,25-dihydroxyvitamin D, through the vitamin D receptor (VDR). VDRs control the expression of several thousand genes, upregulating them in the majority of cases, but also downregulating them in some cases. Thus, observational studies of risk of diseases such as PD with respect to different forms or alleles of the VDRs serves as an indication of whether vitamin D plays a role in affecting risk or progression of that disease.
In a review it was noted that several VDR alleles are associated with early onset, chronic, or aggressive PD3. Additional support for the role of genes and vitamin D receptors playing a role in risk of disease is found in two recent papers:
- Initially thought to play a restricted role in calcium homeostasis, the pleiotropic actions of vitamin D in biology and their clinical significance are only now becoming apparent. However, the mode of action of vitamin D, through its cognate nuclear vitamin D receptor (VDR), and its contribution to diverse disorders, remain poorly understood. We determined VDR binding throughout the human genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After calcitriol (1,25-dihydroxyvitamin D) stimulation, we identified 2776 genomic positions occupied by the VDR and 229 genes with significant changes in expression in response to vitamin D4.
- Participants with a genotype score (combining the three confirmed variants) in the highest quartile were at increased risk of having 25-hydroxyvitamin D concentrations lower than 75 nmol/L (OR 2.47, 95% CI 2.20-2.78, p=2.3×10(-48)) or lower than 50 nmol/L (1.92, 1.70-2.16, p=1.0×10(-26)) compared with those in the lowest quartile5.
There have been several recent papers also reporting an inverse correlation between serum 25(OH)D and PD. One found that pregnant women with periodontal disease “had lower median 25(OH)D levels than controls (59 vs. 100 nmol/L, P<.001) and were more likely to have vitamin D insufficiency (65% vs. 29%, P<.001). The adjusted OR (95%CI) for moderate/severe periodontal disease among women with vitamin D insufficiency was 2.2 (.99-4.5)6.”
PD affects up to 40% of pregnant women7. In addition, “Black women were more likely than white women to have periodontal disease at enrollment (adj. odds ratio 2.9, 95% confidence interval 2.2 to 3.9) and delivery (adj. odds ratio 3.1, 95% confidence interval 2.2 to 4.2), and experience incident disease (adj. odds ratio 2.3, 95% confidence interval 1.6 to 3.4)7.”
An observational study in the U.K. involving post-menopausal women with osteoporosis found PD “is more common in women with osteoporosis and is associated with lower vitamin D and higher concentrations of two cytokines, Receptor Activator for Nuclear Factor κ B Ligand (RANKL) and osteoprotogerin (OPG). Raised cytokines may provide the underlying mechanism that links these two conditions8.”
Page last edited: 17 May 2011
- Dietrich, T. Joshipura, K. J. Dawson-Hughes, B. Bischoff-Ferrari, H. A. Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population. Am J Clin Nutr. 2004 Jul; 80 (1): 108-13.
- Dietrich, T. Nunn, M. Dawson-Hughes, B. Bischoff-Ferrari, H. A. Association between serum concentrations of 25-hydroxyvitamin D and gingival inflammation. Am J Clin Nutr. 2005 Sep; 82 (3): 575-80.
- Amano, Y. Komiyama, K. Makishima, M. Vitamin D and periodontal disease. J Oral Sci. 2009 Mar; 51 (1): 11-20.
- Ramagopalan, S.V. Heger, A. Berlanga, A.J. et al A ChIP-seq defined genome-wide map of vitamin D receptor binding: associations with disease and evolution. Genome Res. 2010; 20 (10): 1352-60.
- Wang, C. Zhao, H. Xiao, L. Xie, C. Fan, W. Sun, S. Xie, B. Zhang, J. Association between vitamin D receptor gene polymorphisms and severe chronic periodontitis in a Chinese population. J Periodontol. 2009 Apr; 80 (4): 603-8.
- Boggess, K. A. Espinola, J. A. Moss, K. Beck, J. Offenbacher, S. Camargo, C. A. Vitamin D Status and Periodontal Disease Among Pregnant Women. J Periodontol. 2010 Sep 1;
- Lieff, S. Boggess, K. A. Murtha, A. P. Jared, H. Madianos, P. N. Moss, K. Beck, J. Offenbacher, S. The oral conditions and pregnancy study: periodontal status of a cohort of pregnant women. J Periodontol. 2004 Jan; 75 (1): 116-26.
- Jabbar, S. Drury, J. Fordham, J. Datta, H. K. Francis, R. M. Tuck, S. P. Plasma vitamin D and cytokines in periodontal disease and postmenopausal osteoporosis. J Periodontal Res. 2010 Aug 20;