Interactions Between Non-Immune Host Cells and the Immune System During Periodontal Disease: Role of the Gingival Keratinocyte

Abstract

Periodontal disease and inflammatory dermatoses, such as psoriasis, are characterized by the accumulation of dense inflammatory infiltrates immediately beneath the epithelial cell layer of the gingiva and skin, respectively. Dermatologists are increasingly aware that the epidermal keratinocyte probably contributes to inflammatory disease progression by secreting a number of pro-inflammatory cytokines and expressing various adhesion molecules. In psoriatic lesions, it is now believed that epidermal keratinocytes may also act as antigen-presenting cells and participate directly in the superantigenic activation of T-cell clones, some of which may initiate, contribute to, or maintain the disease process. Although the role of the host response in periodontal disease has been extensively studied over the years, very little is known about the contribution of the gingival keratinocyte to the inflammatory response. The available published information is discussed in this review, and we suggest that, like its epidermal counterpart, the gingival keratinocyte may participate actively in the pathogenesis of periodontal disease.

Activation of Human Oral Epithelial Cells by Neutrophil Proteinase 3 Through Protease-Activated Receptor-2

“…The inflamed site is characterized by an infiltration of neutrophils. Infiltration of neutrophils into gingival tissues is an early event in gingival inflammation, and neutrophils are the predominant leukocytes in the gingival crevicular fluid (GCF) (ϳ90%) (48). It is also evident that GCF has neutrophil serine proteinase activities against MeOSuc-Ala-Ala-Pro-Val-pnitroanilide for HLE and Suc-Ala-Ala-Pro-Phe-p-nitroanilide for Cat G (49).…”

Absence of αvβ6 Integrin Is Linked to Initiation and Progression of Periodontal Disease

“…51,52 Although a role for keratinocytes in the immunoregulation of periodontal disease has been proposed, the specific functions of cell surface receptors and their ligands, such as ␣v␤6 integrin and TGF-␤1, have not yet been investigated. 53 It is possible that keratinocytes serve as nonprofessional, antigen-presenting cells to the underlying lymphocytes in a process that is regulated by TGF-␤1. In addition, keratinocytes may inhibit the proliferation of unprimed T cells via a TGF-␤1-mediated mechanism.…”

Activation of human gingival epithelial cells by cell-surface components of black-pigmented bacteria: augmentation of production of interleukin-8, granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor and expression of intercellular adhesion molecule 1

“…IL-8 secreted by gingival epithelial cells might act as a chemo-attractant for neutrophils and T cells [29,30]. These accumulated cells might express LFA-1 on their cell surface and attach to epithelial cells via ICAM-1 and LFA-1 interaction, then in®ltrate into the gingival epithelium [8,27]. In fact, ICAM-1 and IL-8 mRNA expression are topographically associated with the area of neutrophil migration in the junctional epithelium [31].…”

“…The ®rst cells encountered by bacteria are epithelial cells, and the predominant cell type in the gingival epithelium is the keratinocyte [8]. Skin keratinocytes and keratinocytic cell lines produce various cytokines and growth factors [9] and some studies [10,11] have also shown cytokine production by human oral keratinocytes and related cell lines in response to stimulation with oral bacteria.…”