Pathogenesis of Periodontal Diseases by Nagihan Bostanci & Georgios N. Belibasakis

Author:Nagihan Bostanci & Georgios N. Belibasakis
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

6.2.2 The Parallels Between Acute Inflammation and Innate Immune Response

At the early host response phase, the predominant immune cell type in the periodontium is the polymorph nuclear neutrophil [6, 31]. Even in healthy conditions, a stable influx of neutrophils (3 × 105 cells/min) permeates the connective tissue in transit to the sulcus though the junctional epithelium, attracted by a constant gradient of IL-8/CXCL8 permanently secreted from keratinocytes and gingival fibroblast in response to the recognition of PAMPs by TLRs [32–34]. Once inside the tissue, neutrophil leukocytes become activated by the interaction of their own TLRs with PAMPs. After their activation, the neutrophils produce and secrete molecular mediators to amplify the inflammation; also, their phagocytic activity is enhanced, as well as the production of reactive oxygen species (ROS) used to kill the phagocyted microorganism. These ROS affect the oxidative status of the periodontal tissue, activating and sustaining a pervasive inflammatory response that amplifies the initial signaling, and when uncontrolled promotes the spreading of the inflammation to the surrounding tissues [15, 35, 36].

While neutrophils exert a very important anti-infective role in the periodontal environment, it is also important to consider that most of the periodontal microorganisms have evolved complex and elegant strategies of immune evasion and have the capacity to use the immune/inflammatory response to their own benefit, modulating the periodontal microenvironment to adjust it to their specific metabolic needs [37]. For example, the recognized periodontopathogen Porphyromonas gingivalis is capable of downregulating the initial immune response of periodontium resident cells, completely abolishing the secretion of the neutrophil-attractant chemokine IL-8/CXCL8 by a gingipain-dependent mechanism [19, 38], facilitating its survival and growth within the periodontal connective tissue. Interestingly, despite the initial dampening of inflammatory cell migration over time will ultimately result in an exacerbated, but inefficient in microbial control terms, host response. Indeed, as previously mentioned, in the development of periodontitis, infecting microorganism resists eradication in part due to the particular anatomy of the periodontal sulcus/pocket and in part due to their proprietary virulence and evasion mechanism along the additional protection conferred by the biofilm structure, eliciting a sustained chronic inflammatory response.

At this point, neutrophils may have or have not succeeded in eliminating the agent that elicited the inflammatory response. If not, additional cell types with different antimicrobial strategies and weapons may be able to achieve the task, but even if neutrophils are successful in eliminating infecting agents, additional cell recruitment is required to repair the damage (even if minimal) inflicted at the response site. To achieve this objective, a special polarized subpopulation of macrophages with regulatory and reparative functions may be recruited to the damaged tissue. This distinctive subpopulation of macrophages possesses the capacity to potentiate the repair, and in some instances, the fibrosis of the tissue as required [39].

Additionally, monocytes also play a relevant role during the early stages of the acute inflammatory process and initial innate immune response, and readily infiltrate the periodontal tissue in the first hours post infection [12, 40]. Monocytes are attracted from the circulation to the periodontal tissues following gradients of chemokines, such as monocyte chemoattractant protein 1 (MCP-1, a.

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