ID de PubMed (PMID): 24436950Páginas 145-151, Idioma: InglésZhou, Shuang Ying / Duan, Xiang Qing / Hu, Rong / Ouyang, Xiang YingObjective: To evaluate the effects of periodontal non-surgical therapy on serum levels of the inflammatory cytokines in chronic periodontitis subjects with stable coronary heart disease.
Methods: Seventy-five subjects with both chronic periodontitis (CP) and stable coronary heart disease (CHD) were enrolled in the study. Forty subjects received periodontal nonsurgical treatment including oral hygiene instruction, scaling and root planing, whereas 35 subjects received oral hygiene instruction only. At baseline and 3 months after completion of periodontal treatment, clinical periodontal parameters were recorded. Serum levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP), lipid profile markers and white blood cell count were assayed. Pearson's correlation analysis was applied to examine the correlation between the change of TNF-α, IL-6 and CRP levels and the change of periodontal parameters after non-surgical periodontal treatment.
Results: At baseline, there were no statistical differences in all clinical, biochemical parameters and cytokine levels between these two groups. Three months later in the treatment group, all clinical parameters improved significantly and the serum levels of TNF-α, IL-6, and CRP reduced significantly. Reduction of TNF-α was significantly positively correlated with the reduction of bleeding index and plaque index; reduction of IL-6 was significantly positively correlated with the reduction of clinical attachment loss; reduction of CRP was significantly positively correlated with the reduction of clinical attachment loss and plaque index. Conclusion: Non-surgical periodontal therapy decreased serum TNF-α, IL-6 and CRP levels in CP subjects with stable CHD, which could help to reduce the inflammatory burden of stable coronary heart disease subjects.
Palabras clave: periodontitis, coronary heart disease, non-surgical periodontal therapy, TNF-α, IL-6, CRP