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Vitamin D and Health

SACN_Vitamin_D_and_Health_report

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<strong>and</strong> tooth wear that spread rapidly through the enamel <strong>and</strong> underlying thinned dentine to expose the<br />

dental pulp, which results in early pulp death. These changes in the structure of enamel <strong>and</strong> dentine<br />

occur during tooth development from intra-uterine development up to around 18y of age. Any<br />

change in serum 25(OH)D concentration after the age of 18y will not affect the structure of the teeth.<br />

6.337 In children with rickets, there is also increased susceptibility to periodontal disease or periodontitis, an<br />

inflammatory disease of the attachment apparatus of the tooth to the jaws. The supporting structures<br />

make up the periodontium <strong>and</strong> comprise the gingiva (or gum), the ligament that attaches the tooth to<br />

the bone <strong>and</strong> the alveolar bone that supports the tooth (Margvelashvili et al., 2014).<br />

6.338 A bacterial biofilm (dental plaque) forms on the surface of teeth throughout their life. The bacteria in<br />

mature plaque produce metabolites that irritate the gingival tissues around the margin of the tooth<br />

causing a localised inflammatory response or gingivitis. This initial lesion can remain confined to the<br />

gingiva or it can progress to the periodontium resulting in periodontitis. This is characterised by<br />

progressive loss of attachment of the tooth to its supporting bone. The bone destruction is thought to<br />

be a consequence of the host inflammatory response removing bone in an inflamed environment.<br />

The bone does not regrow <strong>and</strong> loss of support is permanent. The end stage of this pattern of disease<br />

progression is that the tooth becomes detached from the bone <strong>and</strong> is lost to function. This process is<br />

often accelerated by a dentist extracting the tooth when it becomes loose <strong>and</strong> sensitive. There is<br />

some evidence suggesting beneficial effects of anti-inflammatory agents in preventing periodontal<br />

bone loss in active teeth (Chapple et al., 2012). It is possible, therefore, that vitamin D could affect<br />

periodontal disease by modifying the rate of progression of bone loss or through anti-inflammatory<br />

effects.<br />

6.339 IOM Report: The IOM did not consider vitamin D in relation to oral health.<br />

Evidence considered<br />

RCTs<br />

6.340 No RCTs on vitamin D <strong>and</strong> oral health could be identified.<br />

Observational studies<br />

6.341 Cross sectional studies have reported an association between higher serum 25(OH)D concentration<br />

<strong>and</strong> reduced risk of gingival inflammation (Dietrich et al., 2005), periodontitis (Millen et al., 2013) <strong>and</strong><br />

tooth loss (Jimenez et al., 2014). A large cross-sectional analysis of NHANES data (n=11,202; age<br />

≥ 20y) reported a significant <strong>and</strong> inverse association between serum 25(OH)D concentration <strong>and</strong><br />

periodontal tooth loss in men <strong>and</strong> women aged ≥ 50 y (Dietrich et al., 2004); however no association<br />

was found between BMD of the total femoral region <strong>and</strong> tooth loss (Dietrich et al., 2004).<br />

6.342 A prospective cohort study in Germany, with 5 years follow-up (n=1904; age, 20-79y), reported that<br />

higher serum 25(OH)D concentration at baseline was associated with a lower risk of tooth loss (Zhan<br />

et al., 2014). Compared with participants in the 1st quintile of serum 25(OH)D concentration (mean,<br />

12.5 nmol/L), those in the 5 th quintile (mean, 67.6 nmol/L) had a 23% lower risk of tooth loss (RR=0.77;<br />

95% CI: 0.60-0.99). Since serum 25(OH)D concentration was only measured once at baseline<br />

information was not available on whether concentrations changed during the follow-up period.<br />

Genetic studies<br />

6.343 It has been suggested that associations between vitamin D <strong>and</strong> periodontal disease progression may<br />

be independent of it role in terms of bone metabolism <strong>and</strong> relate more to the role of VDR receptors in<br />

regulating inflammatory disease (Dietrich et al., 2004; Amano et al., 2009). A number of studies have<br />

95

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