关键词: COVID-19 Cytokines Periodontal diseases Periodontitis SARS-CoV-2

Mesh : Humans Porphyromonas gingivalis Interleukin-6 Case-Control Studies COVID-19 SARS-CoV-2 Periodontitis / epidemiology microbiology Inflammation Treponema denticola Chronic Periodontitis / microbiology

来  源:   DOI:10.1007/s10266-023-00811-2   PDF(Pubmed)

Abstract:
OBJECTIVE: Periodontitis and coronavirus disease (COVID-19) share risk factors and activate similar immunopathological pathways, intensifying systemic inflammation. This study investigated the clinical, immunological and microbiological parameters in individuals with COVID-19 and controls, exploring whether periodontitis-driven inflammation contributes to worsening COVID-19 endpoints.
METHODS: Case (positive RT-PCR for SARS-CoV-2) and control (negative RT-PCR) individuals underwent clinical and periodontal assessments. Salivary levels of TNF-α, IL-6, IL-1β, IL-10, OPG, RANKL, neutrophil extracellular traps, and subgingival biofilm were analyzed at two timepoints. Data on COVID-19-related outcomes and comorbidity information were evaluated from medical records.
RESULTS: Ninety-nine cases of COVID-19 and 182 controls were included for analysis. Periodontitis was associated with more hospitalization (p = 0.009), more days in the intensive care unit (ICU) (p = 0.042), admission to the semi-ICU (p = 0.047), and greater need for oxygen therapy (p = 0.042). After adjustment for confounders, periodontitis resulted in a 1.13-fold increase in the chance of hospitalization. Salivary IL-6 levels (p = 0.010) were increased in individuals with COVID-19 and periodontitis. Periodontitis was associated with increased RANKL and IL-1β after COVID-19. No significant changes were observed in the bacterial loads of the periodontopathogens Porphyromona gingivalis, Aggregatibacter actinomycetemcomitans, Tanerella forsythia, and Treponema denticola.
CONCLUSIONS: Periodontitis was associated with worse COVID-19 outcomes, suggesting the relevance of periodontal care to reduce the burden of overall inflammation. Understanding the crosstalk between SARS-CoV-2 infection and chronic conditions such as periodontitis that can influence disease outcome is important to potentially prevent complications of COVID-19.
摘要:
目的:牙周炎和冠状病毒病(COVID-19)具有共同的危险因素,并激活相似的免疫病理途径,加剧全身炎症。这项研究调查了临床,COVID-19患者和对照组的免疫学和微生物学参数,探讨牙周炎驱动的炎症是否导致COVID-19终点恶化。
方法:病例(SARS-CoV-2RT-PCR阳性)和对照(RT-PCR阴性)个体接受临床和牙周评估。唾液TNF-α水平,IL-6,IL-1β,IL-10,OPG,RANKL,中性粒细胞胞外诱捕网,在两个时间点分析龈下生物膜。从病历中评估COVID-19相关结局的数据和合并症信息。
结果:纳入99例COVID-19和182例对照进行分析。牙周炎与更多的住院相关(p=0.009),在重症监护病房(ICU)的天数增加(p=0.042),进入半ICU(p=0.047),和更大的需要氧疗(p=0.042)。在对混杂因素进行调整后,牙周炎导致住院机会增加1.13倍.患有COVID-19和牙周炎的个体的唾液IL-6水平升高(p=0.010)。COVID-19后,牙周炎与RANKL和IL-1β升高有关。在牙周病菌牙龈卟啉单胞菌的细菌负荷中未观察到显着变化,放线菌聚集杆菌,连翘油菌,和Denticola密螺旋体.
结论:牙周炎与COVID-19预后较差相关,提示牙周护理与减轻整体炎症负担的相关性。了解SARS-CoV-2感染与可能影响疾病预后的牙周炎等慢性疾病之间的串扰,对于潜在预防COVID-19并发症非常重要。
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