Department of Surgical Sciences, C.I.R. Dental School, University of Turin, Turin, Italy.
Unit of Periodontology, Endodontology and Restorative Dentistry, Department of Medical Biotechnologies, University of Siena, Siena, Italy.
J Dent Res. 2022 Nov;101(12):1430-1440. doi: 10.1177/00220345221104725. Epub 2022 Jun 30.
Since the beginning of 2020, the entire global health care system has been severely challenged by the outbreak of coronavirus 2019 disease (COVID-19). Robust evidence has demonstrated a more severe course of COVID-19 in the presence of several comorbidities, such as cardiovascular diseases, diabetes mellitus, and obesity. Here, we critically appraise the recent research discoveries linking periodontitis to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and to severe COVID-19, with a special focus on the associated biological mechanisms and the available epidemiological evidence. SARS-CoV-2 main receptors and coreceptors (ACE2, TMPRSS2, furin, CD147) are overexpressed in periodontal tissues of periodontitis patients, with inflammation, periodontal pathogens, and damage-induced pyroptosis triggering a positive feedback loop. However, meta-analyses of epidemiological studies only indicated a nonstatistically significant tendency for an increased risk of SARS-CoV-2 infection in subjects with periodontitis (odds ratio [OR] = 1.69; 95% CI, 0.91-3.13, = 0.09). Furthermore, periodontitis may worsen clinical COVID-19 courses through multiple direct and indirect pathways, including damage to lower airways due to aspiration of periodontal pathogens, exacerbation of the cytokine storm via the low-grade chronic systemic inflammation, and SARS-CoV-2 dissemination through the ulcerated gingival epithelium with consequent induced pulmonary vessels vasculopathy. Indeed, meta-analyses of epidemiological studies indicated that periodontitis subjects are more likely to experience a more severe course of COVID-19. Specifically, periodontitis was associated with a 4-fold increased odds of hospitalization (OR = 4.72; 95% CI, 1.11-20.03, = 0.04), 6-fold of requiring assisted ventilation (OR = 6.24; 95% CI, 2.78-14.02, = 0.00), and more than 7-fold of death due to COVID-19 complications (OR = 7.51; 95% CI, 2.16-26.10, = 0.00). The breakthrough analyzed here emphasizes the relevance of the mouth-systemic connection as a target to mitigate the current COVID-19 emergency and the future predicted coronavirus pandemics.
自 2020 年初以来，全球整个医疗保健系统都受到了 2019 年冠状病毒病（COVID-19）爆发的严重挑战。大量证据表明，患有心血管疾病、糖尿病和肥胖症等多种合并症的 COVID-19 患者病情更严重。在这里，我们批判性地评估了将牙周炎与严重急性呼吸系统综合征冠状病毒 2（SARS-CoV-2）感染和严重 COVID-19 联系起来的最新研究发现，特别关注相关的生物学机制和现有的流行病学证据。牙周炎患者的牙周组织中过度表达了 SARS-CoV-2 的主要受体和辅助受体（ACE2、TMPRSS2、弗林蛋白酶、CD147），炎症、牙周病原体和损伤诱导的细胞焦亡引发了正反馈循环。然而，对流行病学研究的荟萃分析仅表明，牙周炎患者感染 SARS-CoV-2 的风险有增加的非统计学趋势（比值比 [OR] = 1.69；95%置信区间，0.91-3.13， = 0.09）。此外，牙周炎可能通过多种直接和间接途径使 COVID-19 的临床病程恶化，包括由于牙周病原体吸入而导致下呼吸道受损、通过低度慢性全身炎症加重细胞因子风暴以及通过溃疡牙龈上皮传播 SARS-CoV-2 进而引起肺部血管病变。事实上，对流行病学研究的荟萃分析表明，牙周炎患者更有可能经历 COVID-19 的更严重病程。具体而言，牙周炎与住院的可能性增加 4 倍相关（OR = 4.72；95%置信区间，1.11-20.03， = 0.04）、需要辅助通气的可能性增加 6 倍（OR = 6.24；95%置信区间，2.78-14.02， = 0.00）以及因 COVID-19 并发症而死亡的可能性增加 7 倍以上（OR = 7.51；95%置信区间，2.16-26.10， = 0.00）。这里分析的突破强调了口腔-系统连接作为减轻当前 COVID-19 紧急情况和未来预测的冠状病毒大流行的目标的相关性。
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