Host response in aggressive periodontitis

Abstract

It is critical to understand the underlying host responses in aggressive periodontitis to provide a better appreciation of the risk and susceptibility to this disease. Such knowledge may elucidate the etiology and susceptibility to aggressive periodontitis and directly influence treatment decisions and aid diagnosis. This review is timely in that several widely held tenets are now considered unsupportable, namely the concept that Aggregatibacter actinomycetemycomitans is the key pathogen and that chemotactic defects in polymorphonuclear leukocytes are part of the etiopathology. This review also serves to put into context key elements of the host response that may be implicated in the genetic background of aggressive periodontitis. Furthermore, key molecules unique to the host response in aggressive periodontitis may have diagnostic utility and be used in chairside clinical activity tests or as population screening markers. It is becoming increasingly appreciated that the microbial etiology of aggressive periodontitis and the histopathology of this disease are more similar to than different from that of chronic periodontitis. An important therapeutic consideration from the lack of support for A. actinomycetemycomitans as a critical pathogen here is that the widely held belief that tetracycline had a role in aggressive periodontitis therapy is now not supported and that antibiotics such as those used effectively in chronic periodontitis (metronidazole and amoxicillin) are not contraindicated. Furthermore, A. actinomycetemycomitans-related molecules, such as cytolethal distending toxin and leukotoxin, are less likely to have utility as diagnosis agents or as therapeutic targets.

Gingival crevicular fluid interleukin-36β (-1F8), interleukin-36γ (-1F9) and interleukin-33 (-1F11) levels in different periodontal disease

“…27,29,54 It is known that the quality of the host immuneinflammatory response against bacterial challenge determines the severity and extent of disease. 56,57 CP and G-AgP are different disease entities with different etiology and pathogenesis. 58 Although the initiation of the disease may differ a similar immunopathogenesis in both diseases have been suggested.…”

Familial periodontal disease in the cayo santiago rhesus macaques

“…Existing evidence supports that periodontal disease appears to have an increased prevalence in family units with a member having aggressive periodontitis [Demmer and Papapanou, 2010; Genco and Borgnakke, 2013; Kulkarni and Kinane, 2014]. In addition, various studies have indicated the presence of single nucleotide polymorphisms or specifically mutated genes that occur in patients and populations with increased incidence of periodontitis [Yoshie et al, 2007; Nibali et al, 2009; Divaris et al, 2013].…”

Aggressive Periodontitis: microbes and host response, who to blame?

“…The disease progresses very rapidly, with periodontal attachment and alveolar bone loss but then it often stops even in the absence of therapy, 70 suggesting a possible host response adaptation or the mounting of an effective and 'mature' antibody response to pathogenic bacteria. 71,72 Cementum hypoplasia and a possible role of Cytomegalovirus infection during root formation (causing malformation of attachment apparatus) have been hypothesized as a possible cause of LAgP. 73,74 However, evidence for a possible role of viruses in AgP is still controversial.…”