The oral cavity is a diverse and dynamic environment. The three domains of life (Archaea, Bacteria, and Eukarya) along with viruses constitute the human oral microbiome. The ratio of prokaryotic organisms to human cells is reported to range from 1:1 to 10:1 while viral-like particles surpass this prokaryotic ratio and lie closer to 100:1. 1 The formation of our commensal microbiome begins shortly after birth and develops continuously throughout our lifetimes. 2 Within this ecological unit, there is compositional variation of the human microbiota between body sites as a result of distinct selective pressures. For example, the taxonomic and genomic composition of a microbial community on the coronal portion of a tooth is more similar among individuals than those of the same individuals' tongues. 3 Coexistence with our diverse microbiome equips us with crucial biological functions and traits to protect us from invasion by transient or pathogenic microorganisms. Despite how stable the oral landscape may be, rupture of this symbiosis contributes to oral diseases, such as dental caries, periodontitis, and oral mucosal diseases, and is implicated in a number of systemic diseases. [4][5][6][7] Traditionally, investigations describing these oral diseases have focused on a bacterial or fungal etiology despite the advancement of viral metagenomics and cultivation methods, which have demonstrated viruses to be drivers of oral blisters, ulcers, and tumors. 8 More recently, extensive reviews have detailed the intimate topographic relationship between common herpesviruses and known periodontopathogens and their potential role in the development of periodontal diseases. 9
| Periodontal inflammationWithin clinical dental practices, treatment is generally centered on dental and periodontal diseases. Periodontitis continues to be a leading chronic polymicrobial inflammatory condition that affects over 30% of the adult population. Periodontal health can be disrupted when there are shifts in the complex interactions between the microbiota in a biofilm state and the host immune defenses. This dysbiosis can arise from modifications of biological, social, and environmental factors, such as diabetes, alimentary habits, or smoking.Although bacteria are considered the primary etiologic factors in the initiation of periodontitis, host factors influence the progression of periodontitis. Thus, although plaque is necessary for the development of periodontal disease, on its own it is insufficient to drive all the destructive processes that are seen.Viruses as potential drivers of periodontal disease have been implicated in studies using murine models of disease and human oral subgingival plaque, where virome composition and diversity differ with disease progression. 10,11 Additionally, characterizing the oral virome cannot be limited to eukaryotic viruses without taking into account the most abundant entity, namely, prokaryotic viruses.Prokaryotic viruses, more commonly known as bacteriophages, are the natural predators of bacteria. After utili...