Tonetti Maurizio S, Van Dyke Thomas E
European Research Group on Periodontology, Genova, Italy.
The Forsyth Institute, Cambridge, MA, USA.
J Periodontol. 2013 Apr;84 Suppl 4S:S24-S29. doi: 10.1902/jop.2013.1340019.
This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue.
This report examined biological plausibility, epidemiology and early results from intervention trials. Plausibility: Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation.
In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for ACVD was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective.
There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C-reactive protein (CRP) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles - supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to ACVD. There are no periodontal intervention studies on primary ACVD prevention and there is only one feasibility study on secondary ACVD prevention.
It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well-designed intervention trials on the impact of periodontal treatment on prevention of ACVD hard clinical outcomes are needed.
本共识报告关注牙周炎与动脉粥样硬化性心血管疾病（ACVD）之间的关联。牙周炎是一种由微生物引起的慢性多因素炎症性疾病，其特征是牙齿支持组织逐渐破坏导致牙齿脱落；因此，它是一个重大的公共卫生问题。
本报告研究了生物学合理性、流行病学以及干预试验的早期结果。合理性：牙周炎导致细菌进入血流。这些细菌通过多种机制激活宿主炎症反应。宿主免疫反应有利于动脉粥样硬化的形成、成熟和加重。
在评估心血管事件发生率的纵向研究中，报告显示牙周炎患者发生ACVD的风险在统计学上显著增加。这与已确定的心血管危险因素无关。调整后的额外风险量因心血管结局类型以及不同人群的年龄和性别而异。鉴于牙周炎的高患病率，从公共卫生角度来看，即使是低至中度的额外风险也很重要。
有中等证据表明牙周治疗：（i）可降低全身炎症，如C反应蛋白（CRP）降低以及内皮功能的临床和替代指标改善所证明；但（ii）对血脂谱没有影响——支持特异性。有限的证据表明牙周治疗后凝血、内皮细胞激活生物标志物、动脉血压和亚临床动脉粥样硬化有所改善。现有证据一致，表明牙周炎对ACVD有促成作用。目前尚无关于原发性ACVD预防的牙周干预研究，仅有一项关于继发性ACVD预防的可行性研究。
得出以下结论：（i）有一致且有力的流行病学证据表明牙周炎会增加未来心血管疾病的风险；（ii）虽然体外、动物和临床研究确实支持这种相互作用和生物学机制，但迄今为止的干预试验不足以得出进一步结论。需要设计良好的干预试验来研究牙周治疗对预防ACVD硬临床结局的影响。
