Host-Pathogen Interactions in Progressive Chronic Periodontitis

Abstract

Periodontitis is an infection characterized by the occurrence of supporting tissue destruction with an episodic nature. Disease progression is often determined by the loss of attachment level or alveolar bone, and sequential probing of periodontal attachment remains the most commonly utilized method to diagnose progressive destruction of the periodontium. The tolerance method has been the most extensive clinical method used in recent years to determine site-specific attachment level changes. There is abundant evidence that major tissue destruction in periodontal lesions results from the recruitment of immune cells. Considerable effort has been made to study the host cell and mediator profiles involved in the pathogenesis of chronic periodontitis, but the definition of active sites, where current periodontal breakdown occurs, and consecutive characterization of the mediators involved are still among the main concerns. In the present review, we summarize periodontopathic bacteria and host factors, including infiltrating cell populations, cytokines, and host matrix metalloproteinases, associated with under-going episodic attachment loss that could partly explain the mechanisms involved in destruction of the supporting tissues of the tooth.

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

“…14 While the immune response pattern associated with a clear disease outcome seems to vary significantly, the common point among progressive lesions (in both periodontitis and periapical lesions) seems to be the presence of recognized pathogens. [40][41][42][43] Therefore, the data presented herein demonstrates a disproportionate large effect of the presence/absence of red complex bacteria with the disease status and the periodontitis subrogate variable PD. Even though the T-allele carriers were enriched in the diseased group, and the TT and CT genotypes were overrepresented in the CP patients group (indicating an association of the SNP with the disease status); the environmental microbiological covariate obscures this association in the logistic regression model.…”

The subgingival microbiome in health and periodontitis and its relationship with community biomass and inflammation

“…The oral cavity represents an easily accessible niche to study such community dynamics and the community-host interactions that result in dysbiosis. Periodontitis affects the supporting structures of teeth and it is characterized by accumulation of bacterial deposits at the gingival margin with formation of an inflammatory infiltrate resulting in destruction of connective tissue attachment to the tooth, alveolar bone resorption and tooth loss (Hernandez et al, 2011). Periodontitis is diagnosed clinically by measuring the level of attachment of periodontal tissues to the tooth root, together with radiographic evidence of bone loss (Armitage, 1995).…”

Porphyromonas gingivalis-derived Lysine Gingipain Enhances Osteoclast Differentiation Induced by Tumor Necrosis Factor-α and Interleukin-1β but Suppresses That by Interleukin-17A

“…Among the various proinflamma- tory cytokines, TNF-␣, IL-1␤, IL-6, and IL-17A are especially considered to be major causative factors of inflammatory bone destruction in periodontitis (33,34). Bone loss after infection with P. gingivalis was found to be reduced in TNF-␣ receptordeficient mice (35).…”