Vitamin D Deficiency as It Relates to Oral Immunity and Chronic Periodontitis

Khammissa, R A G; Ballyram, R.; Jadwat, Yusuf; Fourie, Jeanine; Lemmer, J; Feller, Liviu

doi:10.1155/2018/7315797

Cited by 49 publications

(71 citation statements)

References 61 publications

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“…While oral supplementation of vitamin D can lead to vitamin D sufficiency in vitamin D‐deficient individuals, including those with chronic periodontitis, the natural feedback mechanism based on the induction of the vitamin D 24‐hydroxylase enzyme guarantees that high concentrations of 1,25(OH) 2 D 3 will not occur in the gingival epithelium. Because of this, hypervitaminosis D and other side effects of high levels of supplementation are rare .…”

Section: Discussionmentioning

confidence: 99%

Activation of vitamin D in the gingival epithelium and its role in gingival inflammation and alveolar bone loss

Menzel

Ruddick

Chowdhury

et al. 2019

J of Periodontal Research

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Background and Objective Both chronic and aggressive periodontal disease are associated with vitamin D deficiency. The active form of vitamin D, 1,25(OH)2D3, induces the expression of the antimicrobial peptide LL‐37 and innate immune mediators in cultured human gingival epithelial cells (GECs). The aim of this study was to further delineate the mechanism by which vitamin D enhances the innate defense against the development of periodontal disease (PD). Materials and Methods Wild‐type C57Bl/6 mice were made deficient in vitamin D by dietary restriction. Cultured primary and immortalized GEC were stimulated with 1,25(OH)2D3, followed by infection with Porphyromonas gingivalis, and viable intracellular bacteria were quantified. Conversion of vitamin D3 to 25(OH)D3 and 1,25(OH)2D3 was quantified by ELISA. Effect of vitamin D on basal IL‐1α expression in mice was determined by topical administration to the gingiva of wild‐type mice, followed by qRT‐PCR. Results Dietary restriction of vitamin D led to alveolar bone loss and increased inflammation in the gingiva in the mouse model. In primary human GEC and established human cell lines, treatment of GEC with 1,25(OH)2D3 inhibited the intracellular growth of P. gingivalis. Cultured GEC expressed two 25‐hydroxylases (CYP27A1 and CYP2R1), as well as 1‐α hydroxylase, enabling conversion of vitamin D to both 25(OH)D3 and 1,25(OH)2D3. Topical application of both vitamin D3 and 1,25(OH)2D3 to the gingiva of mice led to rapid inhibition of IL‐1α expression, a prominent pro‐inflammatory cytokine associated with inflammation, which also exhibited more than a 2‐fold decrease from basal levels in OKF6/TERT1 cells upon 1,25(OH)2D3 treatment, as determined by RNA‐seq. Conclusion Vitamin D deficiency in mice contributes to PD, recapitulating the association seen in humans, and provides a unique model to study the development of PD. Vitamin D increases the activity of GEC against the invasion of periodontal pathogens and inhibits the inflammatory response, both in vitro and in vivo. GEC can convert inactive vitamin D to the active form in situ, supporting the hypothesis that vitamin D can be applied directly to the gingiva to prevent or treat periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Activation of vitamin D in the gingival epithelium and its role in gingival inflammation and alveolar bone loss

Menzel

Ruddick

Chowdhury

et al. 2019

J of Periodontal Research

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“…The maintenance of serum 25(OH)vitD levels within normal range modulates a patient's respond to periodontal treatment 16,31 . Although vitamin D supplementation is associated with decreasing severity of chronic periodontitis, further investigation is required to establish the vitamin's deficiency as an indisputable risk factor 32 . Insufficient calcium intake has been correlated with periodontal disease mainly through its impact on bone metabolism 33 .…”

Section: ) Smokingmentioning

confidence: 99%

Could treating periodontitis prevent osteoporosis? An update of the last decade

Skoufou¹,

Yavropoulou²,

Zafeiris³

2019

JRPMS

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Periodontitis has often been reported as a systematic disease independently associated with a range of AbstractChronic periodontitis and osteoporosis are both systemic diseases, characterized by bone resorption. Over the last decade, their correlation has been examined closely, mainly to investigate whether they present a risk factor or an indicator for each other. It is their pathogenetic similarities, their numerous common risk factors and their frequent concomitant development that initiated researchers' interest in the precise association between these two maladies. The present review is aiming to analyse this correlation, laying emphasis on the effects of periodontal status on the skeletal bone mineral density, as suggested by the latest studies. It will also attempt to clarify whether periodontal management could influence the progression or the onset of osteoporosis.

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“…Periodontitis is associated with imbalanced immune homeostasis in the oral mucosa, with increased bacterial growth and multiplication in the dental plaque. Most of these microorganisms induce an increase in pH and a reduction in the local redox potential, with the upregulation of inflammatory mediators [6] leading to the onset and progression of the disease [7,8]. Immune response in PD is imbalanced, with 70% of B-cell subset dominance and only 30% of the macrophage, neutrophil, and T-cell subset [9,10], in association with an increased level of inflammatory cytokines like interleukin (IL)-1, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, IL-17, and IL-6 [9,11].…”

Section: Introductionmentioning

confidence: 99%

“…The circulating metabolite of vitamin D, 25-hydroxy vitamin D 3 (25(OH)D 3 ), binds the vitamin D receptor [18], playing an important role in oral health maintenance through antibacterial, antiviral, and anti-inflammatory activity. The active form of vitamin D (1,25(OH)2D 3 ) leads to the regulation of both innate and adaptive immunity, modulating inflammatory cytokine production and blocking antigen-presenting dendritic cell maturation with a decrease of antigen-specific T-cell activation and proliferation, associated with regulatory T cell (Treg) activity promotion [7,18,19]. Liu et al [20] have demonstrated the involvement of 25(OH)D 3 and IL-1β in patients with generalized aggressive periodontitis, both in local and systemic evaluation.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Salivary Cytokines and Vitamin D Levels in Periodontopathic Patients

Costantini

Sinjari

Piscopo

et al. 2020

IJMS

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Periodontal disease (PD) is an inflammatory condition of the tissues supporting the teeth, which is widespread among the adult population. Evidence shows a relationship between PD and vitamin D levels, which is involved in the regulation of bone metabolism, mineral homeostasis, and inflammatory response. This study aimed to perform a simultaneous evaluation of inflammatory mediators and vitamin D levels in saliva in periodontopathic patients to better understand their role in periodontal disease. In this observational study, clinical periodontal parameter examination was performed for each patient. Moreover, the saliva levels of 25(OH)D3, TGFβ, IL-35, IL-17A, and MMP9 were evaluated using an ELISA assay. An increase in TGFβ, IL-35, MMP9, and IL-17A salivary levels and a reduction in 25(OH)D3 levels were observed in periodontopathic patients with respect to the healthy controls. The present study revealed significant positive correlation between cytokines and highly negative correlation between 25(OH)D3 and salivary cytokine levels. Further studies are needed to better understand if salivary cytokines and vitamin D evaluation may represent a new approach for detection and prevention of progressive diseases, such as PD.

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Vitamin D Deficiency as It Relates to Oral Immunity and Chronic Periodontitis

Cited by 49 publications

References 61 publications

Activation of vitamin D in the gingival epithelium and its role in gingival inflammation and alveolar bone loss

Activation of vitamin D in the gingival epithelium and its role in gingival inflammation and alveolar bone loss

Could treating periodontitis prevent osteoporosis? An update of the last decade

Evaluation of Salivary Cytokines and Vitamin D Levels in Periodontopathic Patients

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