Impact of Oral Microbiome in Periodontal Health and Periodontitis: A Critical Review on Prevention and Treatment

Abstract

The skin, oral cavity, digestive and reproductive tracts of the human body harbor symbiotic and commensal microorganisms living harmoniously with the host. The oral cavity houses one of the most heterogeneous microbial communities found in the human organism, ranking second in terms of species diversity and complexity only to the gastrointestinal microbiota and including bacteria, archaea, fungi, and viruses. The accumulation of microbial plaque in the oral cavity may lead, in susceptible individuals, to a complex host-mediated inflammatory and immune response representing the primary etiological factor of periodontal damage that occurs in periodontitis. Periodontal disease is a chronic inflammatory condition affecting about 20-50% of people worldwide and manifesting clinically through the detection of gingival inflammation, clinical attachment loss (CAL), radiographic assessed resorption of alveolar bone, periodontal pockets, gingival bleeding upon probing, teeth mobility and their potential loss in advanced stages. This review will evaluate the changes characterizing the oral microbiota in healthy periodontal tissues and those affected by periodontal disease through the evidence present in the literature. An important focus will be placed on the immediate and future impact of these changes on the modulation of the dysbiotic oral microbiome and clinical management of periodontal disease.

Keywords: Microbiome; Periodontal Health; Periodontal defects; dysbiosis; oral disease; oral health; oral microbiome; periodontal disease; periodontal treatment; periodontitis.

Figure 1

The hypothesis proposed by [27] suggests that the acquisition of antigen information by the Fetal Antigen Presenting Cells (APCs) through the placental tissue during pregnancy inducesthe development of fetal tolerance toward the oral microbiome of the mother and the consequent safe acquisition of a normal microbiome by the newborn. Under the terms of the Creative Commons Attribution License (CC BY).

Figure 2

A diagram by Jiang et al. [49]. (A) In periodontal tissue, the dental plaque stimulates local inflammatory and immune responses. (B) LPS and other plaque PAMPs as well as DAMPs activate the HEVs leading to vascular hyperpermeability and leakage PMN transmigration. (C) APCs interact with naive T helper cells, driving their differentiation into several subsets. (D) The amplification of local immune response leads to the development of inflammation and results in the progression of periodontal destruction and bone resorption. Under the terms of the Creative Commons Attribution License (CC BY).