Tobacco smoke exacerbates <i>Filifactor alocis</i> pathogenicity

Iskander, Mina M. Z.; Lamont, Gwyneth; Tan, Jinlian; Pisano, M. Michele; Uriarte, Silvia M.; Scott, David A.

doi:10.1111/jcpe.13729

Cited by 4 publications

(3 citation statements)

References 67 publications

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“…Cigarette smoke contains toxic substances that dissolve in oral epithelial linings and spread throughout the body, interfering in biological events involved in redox homeostasis, immune responses, bone metabolism and tissue repair ( 38 , 39 ). Tobacco-rich conditions facilitate proliferation of Filifactor alocis and enhance its pathogenicity ( 40 ). The detrimental effect of smoking on periodontal health persists long even after quitting.…”

Section: Discussionmentioning

confidence: 99%

The association of composite dietary antioxidant index with periodontitis in NHANES 2009–2014

Meng,

Zheng,

Meng

et al. 2024

Front. Immunol.

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BackgroundTo date, evidence is rare regarding whether and how dietary antioxidants are associated with the risk of periodontitis. This study aimed to investigate the association of composite dietary antioxidant index (CDAI) with periodontitis and tooth loss, using data from the National Health and Nutrition Examination Survey (2009–2014).MethodsA cross-sectional analysis was conducted using data from 10,067 adults aged ≥30 years who underwent assessments of periodontal health and the 1st day dietary recall. Based on a crude model and three adjusted models, multivariate regressions were used to examine the relationship between CDAI and periodontitis-related measurements including probing pocket depth, clinical attachment loss and tooth loss. Subgroup analyses and the restricted cubic splines plots were applied to examine the association between CDAI ingredients and periodontitis.ResultsFor the subjects with high CDAI scores, increased CDAI was associated with significant (P < 0.05) reduction of severe periodontitis (odd ratio = 0.663, 95% confidence interval: 0.491–0.896) and increased number of remaining teeth (weighted β[SE] = 1.167[0.211]). However, the protective effect of CDAI on periodontitis vanished (P > 0.05) in active smokers and former smokers. There were threshold levels for β-carotene, Vitamin A, C and E intakes where the risk of periodontitis significantly decreased (P < 0.05) above these levels.ConclusionIncreased CDAI was associated with reduced risk of periodontitis and tooth loss for non-smokers. It was recommendable that proper dietary intakes of β-carotene, Vitamin A, C and E would be of benefit for preventive dental care and adjuvant therapies for periodontitis.

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Section: Discussionmentioning

confidence: 99%

The association of composite dietary antioxidant index with periodontitis in NHANES 2009–2014

Meng,

Zheng,

Meng

et al. 2024

Front. Immunol.

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“…Filifactor alocis ATCC 35896 was cultured in brain heart infusion as previously described in ( 36 ). Porphyromonas gingivalis ATCC 33277 was cultured in Tryptic soy broth, supplemented with 5 μg/ml hemin, 250 μg/ml L-cysteine and 1 μg/ml menadione as described previously ( 37 ).…”

Section: Methodsmentioning

confidence: 99%

Enhancement of innate immunity in gingival epithelial cells by vitamin D and HDAC inhibitors

Figgins,

Arora,

Gao

et al. 2024

Front. Oral. Health

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IntroductionThe human host defense peptide LL-37 is a component of the innate immune defense mechanisms of the oral cavity against colonization by microbes associated with periodontal disease. We have previously shown that the active form of vitamin D, 1,25(OH)2D3, can induce the expression of LL-37 in gingival epithelial cells (GEC), and prevent the invasion and growth of periopathogenic bacteria in these cells. Further, experimental vitamin D deficiency resulted in increased gingival inflammation and alveolar bone loss. Epidemiological studies have shown associations between vitamin D deficiency and periodontal disease in humans, suggesting application of vitamin D could be a useful therapeutic approach. Further, since we have shown the local activation of vitamin D by enzymes expressed in the GEC, we hypothesized that we could observe this enhancement with the stable, and inexpensive inactive form of vitamin D, which could be further increased with epigenetic regulators.MethodsWe treated 3-dimensional primary cultures of GEC topically with the inactive form of vitamin D, in the presence and absence of selected histone deacetylase (HDAC) inhibitors. LL-37 mRNA levels were quantified by quantitative RT-PCR, and inhibition of invasion of bacteria was measured by fluorescence microscopy.ResultsVitamin D treatment led to an induction of LL-37 mRNA levels, as well as an inhibition of pro-inflammatory cytokine secretion. This effect was further enhanced by HDAC inhibitors, most strongly when the HDAC inhibitor, phenyl butyrate (PBA) was combined with Vitamin D3. This was observed both in solution and in a prototype gel formulation using sodium butyrate. Finally, this combination treatment led to an increase in the antimicrobial activity against infection by Porphyromonas gingivalis and Filifactor alocis, bacteria associated with periodontal lesions, as well as herpes simplex virus, which has also been shown to be associated with periodontal lesions.ConclusionsOur results demonstrate that a combination of inactive vitamin D and sodium butyrate could be developed as a safe treatment for periodontal disease.

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“…Cigarette smoke contains toxic substances that dissolve in oral epithelial linings and spread throughout the body, interfering in biological events involved in redox homeostasis, immune responses, bone metabolism and tissue repair (38,39). Tobacco-rich conditions facilitate proliferation of Filifactor alocis and enhance its pathogenicity (40). The detrimental effect of smoking on periodontal health persists long even after quitting.…”

Section: Discussionmentioning

confidence: 99%

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Tobacco smoke exacerbates Filifactor alocis pathogenicity

Cited by 4 publications

References 67 publications

The association of composite dietary antioxidant index with periodontitis in NHANES 2009–2014

The association of composite dietary antioxidant index with periodontitis in NHANES 2009–2014

Enhancement of innate immunity in gingival epithelial cells by vitamin D and HDAC inhibitors

Table_2.docx

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