Aim: Periodontitis is a relapsing–remitting disease. Compared with bleeding on probing (BoP), expression of disease activity, periodontal inflamed surface area (PISA), incorporates chronic disease parameters. We tested the association of PISA and BoP with blood pressure (BP) in NHANES III. Materials and methods: A total of 8,614 subjects (≥30 years) with complete periodontal and BP examinations were enrolled. PISA was derived from periodontal probing depth and BoP. The association of PISA and BoP with high/uncontrolled BP was examined by multiple-adjusted models. Inflammatory markers were tested as possible mediators. A machine learning (ML) approach was used to define the relative importance of PISA and BoP and estimate the power of BP status prediction. Results: Compared to no inflammation, severe PISA and BoP were associated with 43% (p <.001) and 32% (p =.006) higher odds of high/uncontrolled BP (≥130/80 mmHg), and with higher systolic BP by ≈4 (p <.001) and 5 (p <.001) mmHg, respectively. Inflammatory markers appeared to mediate this association with various extents, without threshold effect. BoP predicted high/uncontrolled BP more efficiently than PISA using ML. Conclusion: PISA and BoP describe the association of periodontal inflammation and hypertension with subtle differences. The contribution of local inflammation to the global inflammatory burden might explain the observed findings.

Association between periodontal inflammation and hypertension using periodontal inflamed surface area and bleeding on probing

Pietropaoli D.
;
Del Pinto R.;Ferri C.;Marzo G.;Giannoni M.;Ortu E.;Monaco A.
2019-01-01

Abstract

Aim: Periodontitis is a relapsing–remitting disease. Compared with bleeding on probing (BoP), expression of disease activity, periodontal inflamed surface area (PISA), incorporates chronic disease parameters. We tested the association of PISA and BoP with blood pressure (BP) in NHANES III. Materials and methods: A total of 8,614 subjects (≥30 years) with complete periodontal and BP examinations were enrolled. PISA was derived from periodontal probing depth and BoP. The association of PISA and BoP with high/uncontrolled BP was examined by multiple-adjusted models. Inflammatory markers were tested as possible mediators. A machine learning (ML) approach was used to define the relative importance of PISA and BoP and estimate the power of BP status prediction. Results: Compared to no inflammation, severe PISA and BoP were associated with 43% (p <.001) and 32% (p =.006) higher odds of high/uncontrolled BP (≥130/80 mmHg), and with higher systolic BP by ≈4 (p <.001) and 5 (p <.001) mmHg, respectively. Inflammatory markers appeared to mediate this association with various extents, without threshold effect. BoP predicted high/uncontrolled BP more efficiently than PISA using ML. Conclusion: PISA and BoP describe the association of periodontal inflammation and hypertension with subtle differences. The contribution of local inflammation to the global inflammatory burden might explain the observed findings.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/140094
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