In turn, during COVID-19 disease, periodontitis facilitates the passage of periodontal–pathogenic bacteria invading the lung, which increase the expression of ACE-2, favoring SARS-CoV-2 infection [131,146], which in turn produces a strong inflammatory response, also characterized by the aberrant production of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) [145,166,172], and the activation of alveolar macrophages, which leads to a cytokine storm, which ultimately induces tissue destruction at the lung level, generating respiratory failure [170]. This evidence concerns the gene IL1B and periodontitis.