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Is systemic inflammation a missing link between periodontitis and hypertension? Results from two large population‐based surveys
Author(s) -
Muñoz Aguilera E.,
Leira Y.,
Miró Catalina Q.,
Orlandi M.,
CzesnikiewiczGuzik M.,
Guzik T. J.,
Hingorani A. D.,
Nart J.,
D’Aiuto F.
Publication year - 2021
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.13180
Subject(s) - national health and nutrition examination survey , medicine , periodontitis , c reactive protein , logistic regression , cross sectional study , blood pressure , population , systemic inflammation , inflammation , pathology , environmental health
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.