The oral ecosystem is dynamic and changes in response to our diet, physiology, and behavior. Microbiota and human hosts predominantly live in a symbiotic relationship with mutual benefits. [1] Whereas microbes find a safe place with nutrition and convenient biochemical conditions, humans, in return, gain contributions to immune development, digestion, and protection against pathogens, to name just a few. [2] The oral cavity is a unique habitat with very different microenvironments like the hard, nonshedding teeth and the soft epithelial mucosa. More than 1000 species are part of multicellular communities present, whereas composition and microbial diversity vary within the different microenvironments and between human individuals. [3][4][5][6] Over time plaque formation, bioadhesion through biomolecular coverage, and bacterial colonization occur on all soft or hard, natural, or synthetic surfaces in the oral cavity. [7,8] The first step of bioadhesion is a continuously progressing adsorption of salivary proteins and other macromolecules, called pellicles, [2,[9][10][11][12][13] with hundreds of different proteins. [14][15][16] The second step is the initial attachment and subsequent accumulation of bacteria. Long-term plaque accumulation can cause shifts within bacterial composition via increasing proportions of disease-associated species leading to dysbiosis, the basis for many oral diseases. Diets rich in lowmolecular carbohydrates, autoimmune or inflammatory diseases, immunodeficient disorders, and poor oral hygiene can be initiating factors. Metabolic breakdown of sugars by species like Streptococcus mutans leads to acidic conditions, which promote caries formation. [17] Persistent plaque supports the proliferation of Gram-negative anaerobic species, such as Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum. [18][19][20] These species spread virulence factors that trigger inflammatory processes, starting with gingivitis followed by progressive periodontitis, which, if left untreated, can advance into jaw bone loss. Artificial surfaces such as fillings, crowns, dentures, implants, and diverse dental restorations are affected precisely the same way, leading to inflammation and destruction of soft or hard tissue surrounding them. This can be followed by periimplantitis, secondary caries, or cofouling with Candida albicans (mucositis). [21][22][23] Finally, secondary systemic infections like