Department of Oral Surgery, Pathology and Clinical Dentistry, School of Dentistry, Universidade Federal de Minas Gerais, Av. Pres. Antônio Carlos, 6627, Room 3204, Belo Horizonte, Minas Gerais, CEP: 31.270-910, Brazil.
Department of Periodontics, School of Dentistry, The University of Sydney, Sydney, NSW, Australia.
Odontology. 2024 Jan;112(1):208-220. doi: 10.1007/s10266-023-00811-2. Epub 2023 Apr 14.
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.
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.
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.
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.
牙周炎和冠状病毒病(COVID-19)具有共同的风险因素,并激活类似的免疫病理途径,加剧全身炎症。本研究调查了 COVID-19 患者和对照组个体的临床、免疫和微生物参数,探讨牙周炎驱动的炎症是否导致 COVID-19 终点恶化。
病例(SARS-CoV-2 的 RT-PCR 阳性)和对照组(RT-PCR 阴性)个体接受了临床和牙周评估。在两个时间点分析了唾液中 TNF-α、IL-6、IL-1β、IL-10、OPG、RANKL、中性粒细胞细胞外陷阱和龈下生物膜的水平。从病历中评估与 COVID-19 相关的结局和合并症信息。
共纳入 99 例 COVID-19 病例和 182 例对照组进行分析。牙周炎与更多的住院治疗(p=0.009)、更多的 ICU 住院天数(p=0.042)、半 ICU 住院(p=0.047)和更需要氧疗(p=0.042)相关。调整混杂因素后,牙周炎使住院的可能性增加了 1.13 倍。COVID-19 患者的唾液 IL-6 水平升高(p=0.010)。牙周炎与 COVID-19 后 RANKL 和 IL-1β 的增加相关。牙周病病原体牙龈卟啉单胞菌、伴放线放线杆菌、傅氏密螺旋体和牙髓密螺旋体的细菌负荷没有明显变化。
牙周炎与 COVID-19 结局恶化相关,提示牙周护理对减轻整体炎症负担的重要性。了解 SARS-CoV-2 感染与牙周炎等慢性疾病的相互作用,这些疾病可能影响疾病结局,对于预防 COVID-19 的并发症很重要。