Is periodontitis a comorbidity of COPD or can associations be explained by shared risk factors/behaviors?

被引:66
作者
Hobbins, Stephanie [1 ]
Chapple, Iain L. C. [2 ]
Sapey, Elizabeth [1 ,3 ]
Stockley, Robert A. [4 ]
机构
[1] Univ Birmingham, Inst Inflammat & Aging, Birmingham, W Midlands, England
[2] Univ Birmingham, Sch Dent, Birmingham, W Midlands, England
[3] Queen Elizabeth Hosp, Ctr Translat Inflammat Res, Inst Inflammat & Aging, Mindelsohn Way, Birmingham B15 2GW, W Midlands, England
[4] Univ Hosp Birmingham NHS Fdn Trust, Birmingham, W Midlands, England
基金
英国医学研究理事会;
关键词
inflammation; emphysema; dental health; smoking; neutrophil; OBSTRUCTIVE PULMONARY-DISEASE; PLAQUE ANTISEPTIC DECONTAMINATION; LUNG-FUNCTION DECLINE; AIR-FLOW LIMITATION; SYSTEMIC INFLAMMATION; PERIPHERAL-BLOOD; EXACERBATION FREQUENCY; NOSOCOMIAL INFECTIONS; RESPIRATORY-DISEASE; CIGARETTE-SMOKING;
D O I
10.2147/COPD.S127802
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
COPD is recognized as having a series of comorbidities potentially related to common inflammatory processes. Periodontitis is one of the most common human inflammatory diseases and has previously been associated with COPD in numerous observational studies. As periodontitis and COPD are both chronic, progressive conditions characterized by neutrophilic inflammation with subsequent proteolytic destruction of connective tissue, it has been proposed that they share common pathophysiological processes. The mechanisms proposed to link COPD and periodontitis include mechanical aspiration of oral contents into the respiratory tree, overspill of locally produced inflammatory mediators into the systemic circulation or oral or lung-derived bacteremia activating an acute-phase response and also reactive oxygen species (ROS) and cytokine release by systemic neutrophils at distant sites. Studies of systemic neutrophils in COPD and chronic periodontitis describe altered cellular functions that would predispose to inflammation and tissue destruction both in the lung and in the mouth, again potentially connecting these conditions. However, COPD and periodontitis also share risk factors such as age, chronic tobacco smoke exposure, and social deprivation that are not always considered in observational and interventional studies. Furthermore, studies reporting associations have often utilized differing definitions of both COPD and periodontitis. This article reviews the current available evidence supporting the hypothesis that COPD and inflammatory periodontal disease (periodontitis) could be pathologically associated, including a review of shared inflammatory mechanisms. It highlights the potential limitations of previous studies, in particular, the lack of uniformly applied case definitions for both COPD and periodontitis and poor recognition of shared risk factors. Understanding associations between these conditions may inform why patients with COPD suffer such a burden of comorbid illness and new therapeutic strategies for both the diseases. However, further research is needed to clarify factors that may be directly causal as opposed to confounding relationships.
引用
收藏
页码:1339 / 1349
页数:11
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