Periodontitis and hypertension are linked through systemic inflammation: A 5‐year longitudinal study

Abstract

AimTo investigate the associations between periodontitis and hypertension and potential mediation via systemic inflammation through a 5‐year longitudinal study.Materials and MethodsThe severity and extent of periodontitis were determined using probing depth (PD). Oral hygiene was assessed using plaque scores. The associations between periodontal variables and 5‐year blood pressure changes or incident hypertension were analysed using linear or Poisson regression, adjusting for potential confounders. Mediation analysis of two systemic inflammatory biomarkers, namely white blood cell count (WBC) and C‐reactive protein (CRP) levels, was performed.ResultsThe study population included 901 hypertension‐free participants, aged 50–73 years. Greater mean PD, higher percentage of sites with PD ≥ 6 mm and poor oral hygiene were associated with elevated systolic blood pressure and increased hypertension risk (relative risks = 1.17 [95% confidence interval [CI]: 1.02–1.34], 1.13 [95% CI: 1.02–1.26] and 1.08 [95% CI: 1.03–1.13], respectively). Periodontitis and poor oral hygiene were associated with higher WBC and CRP levels (p < .05), which, in turn, were associated with increased hypertension risk (p < .05). WBC and CRP jointly mediated 14.1%–26.9% of the associations between periodontal variables and incident hypertension.ConclusionsPeriodontitis and poor oral hygiene were associated with increased hypertension risk, and systemic inflammation was, in part, a mediator of these associations.

Systemic Impact of Subgingival Infection Control in Periodontitis Patients with Cardiovascular Disease: A Narrative Review

“…CRP and S100A8 were chosen as relevant markers of systemic inflammation associated with both periodontitis and CVD. Increased circulating levels of CRP have been reported in periodontitis [73][74][75] as well as in CVD patients [61,76]. Subclinical inflammation, as indicated by plasma CRP levels, was associated not only with the presence of coronary atherosclerosis but also with the severity of coronary plaque burden and the clinical manifestation of ischemia [77].…”