Destructive Periodontal Disease and Tobacco and Cannabis Smoking

Hujoel, Philippe P.

doi:10.1001/jama.299.5.574

Cited by 12 publications

(8 citation statements)

References 12 publications

(10 reference statements)

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“…Cigarette smoke is known to dysregulate such host-pathogen interactions, for example, by suppressing pro-inflammatory cytokine production and angiogenesis, helping to explain the dysbiotic microbiota and increased incidence and severity of chronic periodontitis that is consistently noted in tobacco smokers relative to non-smokers (52, 53). Increasing evidence suggests that inhalation of cannabis smoke is also negatively associated with periodontal health (5, 10, 12, 54). The mechanisms of predisposition are unknown, but marijuana has long been attributed anti-inflammatory properties (49, 50).…”

Section: Discussionmentioning

confidence: 99%

Marijuana-Derived Cannabinoids Trigger a CB2/PI3K Axis of Suppression of the Innate Response to Oral Pathogens

Singh

Niyogi

et al. 2019

Front. Immunol.

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Cannabis use is an emergent risk factor for periodontitis, a chronic bacterial-induced disease of the supporting structures of the teeth. However, the mechanisms by which marijuana exposure predisposes to periodontal tissue destruction have yet to be elucidated. Therefore, we examined the influence of physiologically relevant doses of major marijuana-derived phytocannabinoid subtypes (cannabidiol [CBD]; cannabinol [CBN]; and tetrahydrocannabinol [THC], 1.0 μg/ml) on the interactions of three ultrastructurally variant oral pathogens, Porphyromonas gingivalis, Filifactor alocis, and Treponema denticola with the immune system. CBD, CBN, and THC each suppressed P. gingivalis-induced IL-12 p40, IL-6, IL-8, and TNF release while enhancing the anti-inflammatory cytokine, IL-10, from human innate cells. Similar phenomena were observed in F. alocis- and T. denticola-exposed human monocytes and human gingival keratinocytes. Higher phytocannabinoid doses (≥5.0 μg/ml) compromised innate cell viability and inhibited the growth of P. gingivalis and F. alocis, relative to unexposed bacteria. T. denticola, however, was resistant to all cannabinoid doses tested (up to 10.0 μg/ml). Pharmaceutical inhibition and efficient gene silencing indicated that a common CB2/PI3K axis of immune suppression is triggered by phytocannabinoids in vitro. This pathway does not appear to perpetuate through the canonical GSK3β-dependent cholinergic anti-inflammatory pathway, the predominant endogenous inflammatory control system. In a repetitive, transient oral infection model, CBD also suppressed P. gingivalis-induced innate immune markers in wild-type mice, but not in CB2−/− mice. If such phenomena occur in humans in situ, environmental cannabinoids may enhance periodontitis via direct toxic effects on specific oral bacteria; by compromising innate cell vitality; and/or through a suppressed innate response to periodontal pathogens involving a CB2/PI3K signaling lineage.

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Section: Discussionmentioning

confidence: 99%

Marijuana-Derived Cannabinoids Trigger a CB2/PI3K Axis of Suppression of the Innate Response to Oral Pathogens

Singh

Niyogi

et al. 2019

Front. Immunol.

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“…Individuals were excluded from either group if there was evidence of general health issues, chronic inflammatory conditions, pregnancy, use of antibiotics or other mucosal inflammatory disease [ 53 ]. While smoking has been clearly identified as a risk factor in the extent and severity of periodontitis [ 54 , 55 ] it was not included as a feature in the classification approach. Population demographics of the cohorts based on patient-reported information indicated none of the gingivitis patients to be smokers and ~27% of the periodontitis patients as smokers.…”

Section: Methodsmentioning

confidence: 99%

Patient-Specific Variations in Biomarkers across Gingivitis and Periodontitis

et al. 2015

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This study investigates the use of saliva, as an emerging diagnostic fluid in conjunction with classification techniques to discern biological heterogeneity in clinically labelled gingivitis and periodontitis subjects (80 subjects; 40/group) A battery of classification techniques were investigated as traditional single classifier systems as well as within a novel selective voting ensemble classification approach (SVA) framework. Unlike traditional single classifiers, SVA is shown to reveal patient-specific variations within disease groups, which may be important for identifying proclivity to disease progression or disease stability. Salivary expression profiles of IL-1ß, IL-6, MMP-8, and MIP-1α from 80 patients were analyzed using four classification algorithms (LDA: Linear Discriminant Analysis [LDA], Quadratic Discriminant Analysis [QDA], Naïve Bayes Classifier [NBC] and Support Vector Machines [SVM]) as traditional single classifiers and within the SVA framework (SVA-LDA, SVA-QDA, SVA-NB and SVA-SVM). Our findings demonstrate that performance measures (sensitivity, specificity and accuracy) of traditional classification as single classifier were comparable to that of the SVA counterparts using clinical labels of the samples as ground truth. However, unlike traditional single classifier approaches, the normalized ensemble vote-counts from SVA revealed varying proclivity of the subjects for each of the disease groups. More importantly, the SVA identified a subset of gingivitis and periodontitis samples that demonstrated a biological proclivity commensurate with the other clinical group. This subset was confirmed across SVA-LDA, SVA-QDA, SVA-NB and SVA-SVM. Heatmap visualization of their ensemble sets revealed lack of consensus between these subsets and the rest of the samples within the respective disease groups indicating the unique nature of the patients in these subsets. While the source of variation is not known, the results presented clearly elucidate the need for novel approaches that accommodate inherent heterogeneity and personalized variations within disease groups in diagnostic characterization. The proposed approach falls within the scope of P4 medicine (predictive, preventive, personalized, and participatory) with the ability to identify unique patient profiles that may predict specific disease trajectories and targeted disease management.

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“…Smokers are reported to have more plaque, increased signs of dental inflammation, and higher relative risk of teeth loss due to attachment loss compared to non‐smokers . Several reviews discussed the role of tobacco as a common risk factor for both periodontal and systemic diseases . For example, after adjusting for confounders, a significant association between periodontal loss of attachment and a history of heart attack was only found among smokers, suggesting that smoking is a crucial element in this association …”

Section: Discussionmentioning

confidence: 99%

“…74 Several reviews discussed the role of tobacco as a common risk factor for both periodontal and systemic diseases. [75][76][77][78] For example, after adjusting for confounders, a significant association between periodontal loss of attachment and a history of heart attack was only found among smokers, suggesting that smoking is a crucial element in this association. 79 Oral and general health-related habits could account for the epidemiologic associations of the common risk factors theory.…”

Section: Discussionmentioning

confidence: 99%

Where periodontitis meets metabolic syndrome—The role of common health‐related risk factors

Abdalla‐Aslan

Findler

Levin

et al. 2019

J of Oral Rehabilitation

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Objectives To analyse and compare associations between metabolic syndrome (MetS) and its components in periodontitis compared to control patients. Methods This 7‐year cross‐sectional study retrospectively analysed medical records of 504 individuals aged 18‐90 who attended the student dental clinic between 2008 and 2014. Demographics, smoking habits, blood pressure, waist circumference, as well as presence of: periodontitis, MetS, diabetes, hypertension, hyperlipidaemia, stroke, heart disease, cancer and psychiatric disorders were recorded. Results The study population composed of 231 (45.8%) males and 273 (54.2%) females, with an average age of 55.79 ± 16.91 years. A patient profile associated with periodontitis was identified and included male sex, older age, smoking, higher smoking pack‐years, abdominal obesity, higher systolic and diastolic blood pressures, the presence of MetS or its components, hypertension, hyperlipidaemia, diabetes or diseases associated with its consequences such as ischaemic heart disease and stroke. Following multivariate logistic regression analysis, age and smoking retained a significant association with periodontitis, whereas the systemic disorders did not. Conclusions The association between periodontitis and MetS may be explained by shared common profile and risk factors. An appropriate risk factors management approach should be adopted by both dental and general health clinicians and health authorities, to control common high‐risk behaviours.

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Destructive Periodontal Disease and Tobacco and Cannabis Smoking

Cited by 12 publications

References 12 publications

Marijuana-Derived Cannabinoids Trigger a CB2/PI3K Axis of Suppression of the Innate Response to Oral Pathogens

Marijuana-Derived Cannabinoids Trigger a CB2/PI3K Axis of Suppression of the Innate Response to Oral Pathogens

Patient-Specific Variations in Biomarkers across Gingivitis and Periodontitis

Where periodontitis meets metabolic syndrome—The role of common health‐related risk factors

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