Impact of Oral Commensal Bacteria on Degradation of Periodontal Connective Tissue in Mice

Abstract

These results indicate that commensal bacteria induced a low-grade inflammatory state in JE and that such conditions may contribute to degradation of collagen in PCT in mice.

Differences in the paranasal sinuses between germ‐free and pathogen‐free mice

“…The sterility of GF animals was examined by aerobic and anaerobic culture of oral swabs and fecal pellets on nonselective media and by polymerase chain reaction (PCR) using universal 16S primers. Studies further describing the sterility of this GF colony and which bacteria have been isolated from the SPF mice have been published …”

Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells

“…Are the present findings clinically relevant? To answer that question, it is worth mention that the commensal bacteria that induce a low-grade inflammatory state in the junctional epithelium are likely the triggers of ICAM-1 expression and neutrophils migration [7]. Thus, there is strong ICAM-1 staining of the junctional epithelium in both clinically healthy and inflamed tissue [2], even though soluble ICAM-1 shed into the gingival crevicular fluid was higher in patients with inflammation [63].…”

“…Thus, the increase of adhesion molecules by inflammatory mediators has to be counterbalanced by local cues to control an excessive influx of cells of the innate immune system.The influx of cells is controlled by intercellular adhesion molecule-1 (ICAM-1), allowing the transmigration of leucocytes which express the corresponding lymphocyte function-associated antigen-1 and macrophage adhesion ligand-1 [4]. ICAM-1, being induced by inflammatory cues such as interleukin-1-beta (IL1β) and tumor necrosis factor-α (TNFα) [5], is expressed by the vascular endothelium and by the junctional epithelium [6], thus, facilitating transmigration of leukocytes across vascular endothelia and the invasion of the extracellular matrix [7]. Although ICAM-1 is consistently expressed by junctional epithelial cells in healthy gingiva and in pocket epithelium, it is not detectable on the majority of keratinocytes in the external gingival epithelium [6,8].…”

Impact of commensal flora on periodontal immune response to lipopolysaccharide

“…Microbial stimulation by commensal flora plays a crucial role in the development of an appropriate immune system in periodontal tissues, including the junctional epithelium (JE) and connective tissues subjacent to the JE . A previous study demonstrated that the area of the JE in specific‐pathogen‐free (SPF) mice was significantly greater than that in germ‐free (GF) mice . Further, commensal flora stimulate the innate defense system of the periodontium, upregulating not only the number of neutrophils but also the expression of fibroblast growth factor receptor‐1 and matrix metalloproteinases‐1 and 8 in the JE, while also yielding decreased collagen density in periodontal connective tissue (PCT) .…”

“…A previous study demonstrated that the area of the JE in specific‐pathogen‐free (SPF) mice was significantly greater than that in germ‐free (GF) mice . Further, commensal flora stimulate the innate defense system of the periodontium, upregulating not only the number of neutrophils but also the expression of fibroblast growth factor receptor‐1 and matrix metalloproteinases‐1 and 8 in the JE, while also yielding decreased collagen density in periodontal connective tissue (PCT) . The degradation of PCT may allow the host to homeostatically regulate the inflammatory response of healthy periodontal tissue in response to immune surveillance of commensal flora colonization.…”