Neutrophil Dysfunction and Host Susceptibility to Periodontal Inflammation: Current State of Knowledge

Sima, Corneliu; Glogauer, Michael

doi:10.1007/s40496-014-0015-x

Cited by 39 publications

(46 citation statements)

References 71 publications

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“…1 ). The subgingival environment is rich in immune and inflammatory mediators and provides unique challenges and opportunities for the bacteria 35-37 . Periodontal health requires a controlled immuno-inflammatory state that can maintain host–microbe homeostasis in the periodontium 38 .…”

Section: Microbial Synergy and Dysbiosismentioning

confidence: 99%

“…Neutrophils are the most common leukocyte recruited to the subgingival crevice or periodontal pockets 35,36 . Individuals with congenital deficiencies in neutrophil numbers or recruitment develop severe periodontitis, suggesting that neutrophils are required for periodontal tissue homeostasis 17,56,57 .…”

Section: Subversion Of Host Immune Responsesmentioning

confidence: 99%

“…Individuals with congenital deficiencies in neutrophil numbers or recruitment develop severe periodontitis, suggesting that neutrophils are required for periodontal tissue homeostasis 17,56,57 . However, hyperactive, supernumerary or dysregulated neutrophils can cause collateral tissue damage through the release of inflammatory and toxic substances or tissue-degrading enzymes 35,58-60 . Indeed, ample clinical evidence show that neutrophils mediate a significant portion of periodontal tissue destruction 61,62 and their local numbers positively correlate with the severity of chronic periodontitis 63 .…”

Section: Subversion Of Host Immune Responsesmentioning

confidence: 99%

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Periodontitis: from microbial immune subversion to systemic inflammation

2014

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Periodontitis is a dysbiotic inflammatory disease with an adverse impact on systemic health. Recent studies have provided insights into the emergence and persistence of dysbiotic oral microbial communities, which can mediate inflammatory pathology at local as well as distant sites. This Review discusses mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extraoral sites.

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Section: Microbial Synergy and Dysbiosismentioning

confidence: 99%

Section: Subversion Of Host Immune Responsesmentioning

confidence: 99%

Section: Subversion Of Host Immune Responsesmentioning

confidence: 99%

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Periodontitis: from microbial immune subversion to systemic inflammation

2014

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“…Briefly stated, the interventional control of inflammation in LAD-I can suppress the local microbiota, despite the absence of the presumed protective effects of neutrophils in the periodontium. In this context, it is of interest to note that individuals with chronic granulomatous disease (CGD) do not have increased susceptibility to periodontitis (as compared to the general population), even though the defective oxygen-dependent bactericidal activity of their neutrophils renders them susceptible to frequent infections, such as pneumonia and abscesses of the skin [5, 41]. Arguably, therefore, defective immune surveillance by neutrophils is not an overriding factor in susceptibility to periodontitis, whereas the extravasation competence of neutrophils is essential for periodontal tissue homeostasis.…”

Section: Lad-i Periodontitis Does Not Involve a Tissue-invasive Inmentioning

confidence: 99%

Role of bacteria in leukocyte adhesion deficiency-associated periodontitis

Hajishengallis

Moutsopoulos

2016

Microbial Pathogenesis

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Leukocyte adhesion deficiency Type I (LAD-I)–associated periodontitis is an aggressive form of inflammatory bone loss that has been historically attributed to lack of neutrophil surveillance of the periodontal infection. However, this form of periodontitis has proven unresponsive to antibiotics and/or mechanical removal of the tooth-associated biofilm. Recent studies in LAD-I patients and relevant animal models have shown that the fundamental cause of LAD-I periodontitis involves dysregulation of a granulopoietic cytokine cascade. This cascade includes interleukin IL-23 (IL-23) and IL-17 that drive inflammatory bone loss in LAD-I patients and animal models and, moreover, foster a nutritionally favorable environment for bacterial growth and development of a compositionally unique microbiome. Although the lack of neutrophil surveillance in the periodontal pockets might be expected to lead to uncontrolled bacterial invasion of the underlying connective tissue, microbiological analyses of gingival biopsies from LAD-I patients did not reveal tissue-invasive infection. However, bacterial lipopolysaccharide was shown to translocate into the lesions of LAD-I periodontitis. It is concluded that the bacteria serve as initial triggers for local immunopathology through translocation of bacterial products into the underlying tissues where they unleash the dysregulated IL-23–IL-17 axis. Subsequently, the IL-23/IL-17 inflammatory response sustains and shapes a unique local microbiome which, in turn, can further exacerbate inflammation and bone loss in the susceptible host.

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“…Neutropenia, altered PMN recruitment into periodontium, and impaired bacterial killing lead to severe forms of periodontitis. 2 On the other hand, hyperresponsiveness and excess reactive oxygen species (ROS) production likely contribute to relapse after CP treatment. Untreated CP is associated with considerable morbidity and represents a risk factor for numerous systemic conditions with underlying low-grade inflammation.…”

mentioning

confidence: 99%

Nuclear Factor Erythroid 2-Related Factor 2 Down-Regulation in Oral Neutrophils Is Associated with Periodontal Oxidative Damage and Severe Chronic Periodontitis

Sima

Aboodi

Lakschevitz

et al. 2016

The American Journal of Pathology

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The balance between reactive oxygen species and antioxidants plays an important role in periodontal health. We previously demonstrated that high reactive oxygen species production by oral polymorphonuclear neutrophils (oPMNs) in chronic periodontitis (CP) refractory to conventional therapy is associated with severe destruction of periodontium. Herein, we show that inhibition of antioxidant production through down-regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in oPMN, despite enhanced recruitment in the oral cavity, is associated with severe CP. Twenty-four genes in the Nrf2-mediated oxidative stress response pathway were down-regulated in PMNs of diseased patients. Downstream of Nrf2, levels of oPMN superoxide dismutase 1 and catalase were decreased in severe CP, despite increased recruitment. Nrf2 À/À mice had more severe loss of periodontium in response to periodontitis-inducing subgingival ligatures compared with wild-types. Levels of 8-hydroxydeoxyguanosine were increased in periodontal lesions of Nrf2 À/À mice, indicating high oxidative damage. We report, for the first time, Nrf2 pathway down-regulation in oPMNs of patients with severe CP. PMNs of CP patients may be primed for low antioxidant response in the context of high recruitment in the oral cavity, resulting in increased oxidative tissue damage. (Am J Pathol 2016 http://dx

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Neutrophil Dysfunction and Host Susceptibility to Periodontal Inflammation: Current State of Knowledge

Cited by 39 publications

References 71 publications

Periodontitis: from microbial immune subversion to systemic inflammation

Periodontitis: from microbial immune subversion to systemic inflammation

Role of bacteria in leukocyte adhesion deficiency-associated periodontitis

Nuclear Factor Erythroid 2-Related Factor 2 Down-Regulation in Oral Neutrophils Is Associated with Periodontal Oxidative Damage and Severe Chronic Periodontitis

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