Summary

Vitamin D, a secosteroid hormone synthesised in the skin under ultraviolet radiation or obtained through dietary sources, plays a central role in calcium homeostasis, bone metabolism and immune regulation. In the periodontium, active vitamin D metabolites regulate osteoblastic and osteoclastic activity within alveolar bone, modulate matrix metalloproteinase expression in gingival tissues and enhance the innate immune barrier by upregulating antimicrobial peptides. Epidemiological evidence links low serum 25-hydroxyvitamin D levels with increased prevalence and severity of gingival inflammation and chronic periodontitis, with periodontal attachment loss correlating inversely with vitamin D status. Early deficiency may result in impaired tooth mineralisation and enamel hypoplasia, while in adults it can compromise postoperative healing and outcomes of regenerative procedures. Mechanistic studies demonstrate that vitamin D influences periodontal ligament cells, gingival epithelial function and local immune cell responses to curb tissue destruction and promote repair. Moreover, vitamin D may modulate host–microbiome interactions by restricting colonisation of periodontopathic bacteria. Given the global burden of vitamin D insufficiency and periodontitis, integrating routine assessment of vitamin D status into periodontal care protocols holds promise for improving therapeutic outcomes and mitigating the systemic health risks associated with chronic inflammation.

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Vitamin D Influence on Periodontal Health publication trend

The graph below shows the total number of articles in vitamin d influence on periodontal health across all publications each year (not limited to Nature Index journals).

Technical terms

25-hydroxyvitamin D3 (25(OH)D3): The primary circulating form of vitamin D measured to assess status.

Calcitriol (1,25-dihydroxyvitamin D3): The active hormonal form of vitamin D that binds to cellular receptors.

Periodontal Ligament-Derived Mesenchymal Stromal Cells (hPDL-MSCs): Multipotent cells in the periodontal ligament that contribute to tissue repair and immune regulation.

LL-37: A cathelicidin antimicrobial peptide induced by vitamin D that defends against oral pathogens.

Autophagy: A regulated intracellular degradation process involved in cell homeostasis and modulation of inflammation.

HDAC Inhibitors: Compounds that alter chromatin structure by inhibiting histone deacetylases, enhancing gene expression.

References

  1. 25-hydroxyvitamin D3 generates immunomodulatory plasticity in human periodontal ligament-derived mesenchymal stromal cells that is inflammatory context-dependent. Frontiers in Immunology (2023).
  2. The Role of Vitamin C and Vitamin D in the Pathogenesis and Therapy of Periodontitis—Narrative Review. International Journal of Molecular Sciences (2023).
  3. Calcitriol-enhanced autophagy in gingival epithelium attenuates periodontal inflammation in rats with type 2 diabetes mellitus. Frontiers in Endocrinology (2023).
  4. Enhancement of innate immunity in gingival epithelial cells by vitamin D and HDAC inhibitors. Frontiers in Oral Health (2024).
  5. Vitamin D and Periodontitis: A Systematic Review and Meta-Analysis. Nutrients (2020).
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