Inflammatory and immune pathways in the pathogenesis of periodontal disease

Abstract

The pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis.

TBX21-1993T/C (rs4794067) polymorphism is associated with increased risk of chronic periodontitis and increased T-bet expression in periodontal lesions, but does not significantly impact the IFN-g transcriptional level or the pattern of periodontophatic bacterial infection

“…Periodontitis is initiated by the bacteria harbored in the teeth-attached biofilm that infiltrates the surrounding epithelial and connective periodontal tissues, triggering a host inflammatory immune response that leads to the subsequent lesion development. 1 While any bacteria can essentially trigger a host response, specific Gram negative anaerobic rods have a special capability to elicit and chronically sustain the host inflammatory immune response that mediates periodontal tissue destruction. Most prominent among periodontitis-associated bacteria are the so called red complex cluster (Porphyromonas gingivalis, Tanerella forsytia and Treponema denticola), which has been consistently associated with the occurrence, severity and negative response to treatment of the disease.…”

Ex vivo anti-inflammatory effects of probiotics for periodontal health

“…Moreover, LPS is a principal component of the outer membrane of Gram-negative bacteria, which increase in proportion in plaque during the development of gingivitis [1,2]. Monocytes and gingival fibroblasts were chosen as host cells in the model because both cell types play an important role in maintaining gingival tissue homeostasis and can secrete a variety of inflammatory mediators in response to different stimuli [5]. Since probiotics may have differing immunomodulatory effects on different host cell types, it is relevant to evaluate more than one type of host cell.…”

“…prostaglandin E 2 [PGE 2 ]) secreted by gingival epithelial cells, fibroblasts and resident leukocytes [2–4]. These inflammatory mediators influence various cellular processes, including recruitment and chemotaxis of neutrophils, and promote increased vascular dilation and blood flow in the gingiva [5]. Persistent gingival inflammation can progressively exert selective pressure for the development of a dysbiotic and inflammophilic plaque microbiota [6].…”

Tiyazol-fenilasetik asit bileşiklerinin dual antibakteriyel-COX enzim inhibitörleri olarak sentezleri

“…It has been associated with the pathogeneses of some disorders as arthritis 1 , cancer 2 , neurodegenerative 3 and cardiovascular diseases 4 . The acute stage of inflammation is inevitable and considered by quick influx of blood granulocytes, followed rapidly by monocytes that settled into inflammatory macrophages which subsequently proliferate and affect the functions of resident tissue macrophages.…”