COVID-19作为一种泛流行病正在减弱,但有必要了解病毒与口腔组织和口腔炎性疾病的相互作用。我们回顾了牙周病(PD),一种常见的炎症性口腔疾病,作为COVID-19和口服急性后遗症(PASC)的驱动因素。口服PASC与PD鉴别,牙齿脱落,熟食症,口干症,唾液质-唾液质,和粘膜炎。我们认为,与PD相关的口腔微生物菌群失调涉及较高的牙周病菌负担,为严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染提供了最佳的微环境。这些病原体与口腔上皮细胞相互作用,激活促进病毒粘附的分子或生化途径,条目,以及在口腔中的持久性。一系列不同的分子确定了这种关系,包括脂质,碳水化合物和酶。SARS-CoV-2的S蛋白与ACE2受体结合,并被切割S蛋白亚基以促进病毒进入的宿主弗林蛋白酶或TRMPSS2的蛋白酶活性激活。然而,PD病原体通过诱导病毒进入受体ACE2/TRMPSS提供模拟furin和增强SARS-CoV-2粘附的额外酶辅助,在口腔上皮细胞上表达不良。我们讨论了涉及促进SARS-CoV-2感染和免疫抵抗的牙周病原体和宿主因子的机制,这些机制导致不完全清除和具有PASC特征的“远程”口腔健康问题的风险。最后,我们提出了减轻口服PASC的潜在诊断标志物和治疗途径.
COVID-19 as a pan-epidemic is waning but there it is imperative to understand virus interaction with oral tissues and oral inflammatory diseases. We review periodontal disease (PD), a common inflammatory oral disease, as a driver of COVID-19 and oral post-acute-sequelae conditions (PASC). Oral PASC identifies with PD, loss of teeth, dysgeusia, xerostomia, sialolitis-sialolith, and mucositis. We contend that PD-associated oral microbial dysbiosis involving higher burden of periodontopathic bacteria provide an optimal microenvironment for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. These pathogens interact with oral epithelial cells activate molecular or biochemical pathways that promote viral adherence, entry, and persistence in the oral cavity. A repertoire of diverse molecules identifies this relationship including lipids, carbohydrates and enzymes. The S protein of SARS-CoV-2 binds to the ACE2 receptor and is activated by protease activity of host furin or TRMPSS2 that cleave S protein subunits to promote viral entry. However, PD pathogens provide additional enzymatic assistance mimicking furin and augment SARS-CoV-2 adherence by inducing viral entry receptors ACE2/TRMPSS, which are poorly expressed on oral epithelial cells. We discuss the mechanisms involving periodontopathogens and host factors that facilitate SARS-CoV-2 infection and immune resistance resulting in incomplete clearance and risk for \'long-haul\' oral health issues characterising PASC. Finally, we suggest potential diagnostic markers and treatment avenues to mitigate oral PASC.