Objective: The primary objective was to investigate the relationship between periodontitis and hypertension in two independent large surveys. The secondary objective was to ascertain whether systemic inflammation had a mediation effect in the association.Methods: This cross‐sectional study analysed representative samples of the US (n = 3460; NHANES 2009/10) and Korean (n = 4539; 2015 KNHANES VI‐3) populations. The association between periodontitis (exposure), hypertension (outcome) and inflammatory markers [C‐reactive protein (CRP) and white blood cell counts (WBC)] (mediators) was assessed using multivariate linear and logistic regression models and mediation analysis.Results: Participants with periodontitis were more likely to have hypertension (NHANES: OR = 1.3, 95% CI: 1.0–1.6, P = 0.025; KNHANES: OR = 1.2, 95% CI: 1.0–1.4, P = 0.041) and actual systolic blood pressure ≥ 140 mmHg (NHANES: OR = 1.6, 95% CI: 1.1–2.3, P < 0.001; KNHANES: OR = 1.3, 95% CI :1.0–1.6, P < 0.031) than those without the disease. These associations were independent of age, gender, BMI, education level, smoking, alcohol consumption, creatinine, physical activity, presence of other comorbidities and confirmed in participants not taking antihypertensive medications. Diagnosis of periodontitis was directly associated with WBC (in both surveys: NHANES: β ± SE = 0.3 ± 0.1, P < 0.004; KNHANES: β ± SE = 0.3 ± 0.1, P < 0.001) and with CRP levels (in one survey: NHANES: β ± SE = 0.1 ± 0.03, P < 0.007; KNHANES: β ± SE = 0.1 ± 0.04, P > 0.213). Mediation analyses confirmed that CRP acted as a mediator in the association between periodontitis and hypertension in both populations (mediated effect: NHANES: β ± SE = 0.010 ± 0.003, P < 0.001; KNHANES: β ± SE = 0.003 ± 0.001, P = 0.015). WBC acted as a mediator in the KNHANES (mediated effect: β ± SE = 0.004 ± 0.001, P = 0.004) whilst in the NHANES, its effect was dependent of CRP inclusion in the model (mediated effect WBC + CRP: β ± SE = 0.002 ± 0.001, P = 0.001).Conclusions: These findings suggest that periodontitis is closely linked to hypertension and systemic inflammation is, in part, a mediator of this association.

Background: Systemic inflammation is implicated in the onset and progression of several chronic diseases. Periodontitis is a potential trigger of systemic inflammation.Purpose: To comprehensively appraise all the evidence on the effects of the treatment of periodontitis on systemic inflammation assessed by serum C‐reactive protein (CRP) levels.Data Sources: Six electronic databases were searched up to 10 February 2022 to identify and select articles in English language only.Study Selection: Twenty‐six randomized controlled clinical trials reporting changes amongst 2579 participants about CRP levels at 6 months or more after treatment.Data Extraction: Two reviewers independently extracted data and rated the quality of studies. Meta‐analyses were performed using random and fixed effect models.Risk of Bias: Risk of bias (RoB 2.0 tool) and quality of evidence (GRADEpro GDT tool) analyses were completed.Data Synthesis: Treatment of periodontitis reduced CRP levels by 0.69 mg/L (95% confidence interval: −0.97 to −0.40) after 6 months, but limited evidence was retrieved from studies with longer follow‐ups. Similar findings were observed in participants with other co‐morbidities in addition to periodontitis. Greatest reductions were observed in participants with concentrations of CRP >3 mg/L at baseline.Limitations: High level of heterogeneity.Conclusions: Treatment of periodontitis reduces serum CRP levels (up to 6 months follow‐up) to a degree equivalent to that observed after traditional lifestyle or drug interventions. This evidence supports a causal association between periodontitis and systemic inflammation.