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Since the earliest cases of COVID-19, Long-COVID (LC) has presented as a multi-system disease/disorder with persistent symptoms in individuals after SARS-CoV-2 infection. SARS-CoV-2 is found in the oral cavity and the periodontium during LC; however, its effects have not been fully investigated. This review proposes LC as a novel risk factor for periodontitis. LC possesses systemic mechanisms of immuno-inflammatory dysregulation, which overlap and thus could enhance periodontitis development. Persistent in-creases in neutrophils, elevated pro-inflammatory cytokine production, complement pro-duction from innate immune system activation are involved in both periodontitis and LC, suggesting the potential for interactions between the two. LC leads to dysbiosis of the GI system and lungs, and we consider here the possibility of oral and periodontal dysbiosis. Gingival epithelium and periodontal ligament cells do express the viral receptor, ACE2, which would allow SARS-CoV-2 entry into these cells. Interestingly, ACE2 is increased during active periodontitis. Additionally, LC has been linked to the re-emergence of herpesvirus infections, especially the Epstein-Barr virus (EBV), which has been associated with both autoimmune diseases and periodontitis. In this review, we comprehensively compile the routes by which LC could act as a systemic risk factor for periodontitis. We aim to provide the theoretical foundation for epidemiologic and mechanistic research that could produce the necessary scientific evidence.