Alterations in the Oral Microbiome Leading to Inflammatory Periodontal Disease

The oral cavity contains a complex micro-ecosystem of flora inhabiting a variety of different niches. Some of these niches include saliva, shedding surfaces, and non-shedding surfaces. Biofilms in the oral microbiome, colloquially referred to as dental plaque, can accumulate on non-shedding surfaces, such as natural teeth and other artificial hard parts such as braces, dentures, fillings, and implants. These biofilms are made up of many mutualistic bacteria that stick to each other and adhere to hard surfaces. Scientists speculate that at least 700 different species of bacteria inhabit various parts of the mouth. These bacteria occupy different niches in varying amounts to help protect the teeth and body systems from invading pathogens. However, when plaque grows on non-shedding surfaces, the bacteria can over accumulate and cause inflammatory periodontal disease. Inflammatory periodontal disease includes both gingivitis and periodontitis. Gingivitis is an inflammatory disease caused by the overaccumulation of dental plaque in the supragingival area. When this plaque exists for extended periods of time without being removed, the biofilm can spread to the subgingival region of the gum and cause periodontitis. Periodontitis is characterized by tooth loss due to bone resorption and tissue damage. This review aims to discuss the community shifts in the oral microbiome that are associated with the onset of inflammatory periodontal disease, as well as the mechanisms in which these bacteria contribute to disease symptoms

Toward Personalized Oral Diagnosis: Distinct Microbiome Clusters in Periodontitis Biofilms

Periodontitis is caused by pathogenic subgingival microbial biofilm development and dysbiotic interactions between host and hosted microbes. A thorough characterization of the subgingival biofilms by deep amplicon sequencing of 121 individual periodontitis pockets of nine patients and whole metagenomic analysis of the saliva microbial community of the same subjects were carried out. Two biofilm sampling methods yielded similar microbial compositions. Taxonomic mapping of all biofilms revealed three distinct microbial clusters. Two clinical diagnostic parameters, probing pocket depth (PPD) and clinical attachment level (CAL), correlated with the cluster mapping. The dysbiotic microbiomes were less diverse than the apparently healthy ones of the same subjects. The most abundant periodontal pathogens were also present in the saliva, although in different representations. The single abundant species Tannerella forsythia was found in the diseased pockets in about 16–17-fold in excess relative to the clinically healthy sulcus, making it suitable as an indicator of periodontitis biofilms. The discrete microbial communities indicate strong selection by the host immune system and allow the design of targeted antibiotic treatment selective against the main periodontal pathogen(s) in the individual patients