Balance of inflammatory response in stable gingivitis and progressive periodontitis lesions

Abstract

SummaryThe balance between inflammatory mediators and their counter-regulatory molecules may be crucial for determining the outcome of immune pathology of periodontal diseases. Based on clinical and immunological findings, the immune response in stable gingivitis lesion is supposed to be in balance, whereas the response is skewed towards the predominance of proinflammatory reactivity in progressive periodontitis lesion. However, this hypothesis has not been verified. Therefore, the aim of this study was to compare the gene expression profile of inflammatory mediators including proinflammatory cytokines and other inflammatory molecules, and anti-inflammatory cytokines by using quantitative real-time polymerase chain reaction in gingivitis and periodontitis lesions showing distinct clinical entities. For inflammatory mediators, interleukin (IL)-1β β β β , interferon (IFN)-γ γ γ γ and receptor activator of nuclear factor (NF)-κ κ κ κ B ligand tended to be higher in periodontitis, whereas tumour necrosis factor (TNF)-α α α α and IL-12 p40 showed no difference. Heat-shock protein 60 (HSP60) expression was up-regulated significantly in periodontitis. For anti-inflammatory cytokines, transforming growth factor (TGF)-β β β β 1 expression tended to be higher in periodontitis compared with gingivitis, whereas no difference was observed for IL-10 and IL-4. These findings support further our previous finding that autoimmune response to HSP60 may exert in periodontitis lesion, and suggest that perhaps subtle differences in the balance of cytokines may result in different disease expression.

Inflammatory Cytokines and the Pathogenesis of Periodontal Disease

“…Because Th1, Th2, Th17 and monocyte-derived cytokines in periodontal tissues and gingival crevicular fluid (GCF) are involved in periodontal inflammation, even a minimal imbalance of cytokine production may affect induction of bone and collagen destruction in periodontal disease [14][15][16]. As a general rule, immune responses mediated by T cells polarized into a Th1-type phenotype are characteristically cellular and pro-inflammatory; while Th2 cells are associated with humoral immunity and present anti-inflammatory properties [14].…”

“…The local cellular effects of TNF-α include the adhesion of polymorph nuclear leukocytes (PMNs) to endothelial cells, degranulation of PMNs, activation of phagocytosis and intercellular adhesion molecule (ICAM) -1 expression. The amount of TNF-α was demonstrated at high levels in gingival crevicular fluid and diseased periodontal tissues [8,16] and experimental studies have shown a central role for TNF-α in alveolar bone resorption [31,32]. …”

“…Clinical studies have illustrated that the amount of IL-1β is much higher in GCF in periodontal pockets or in the underlying inflamed gingival tissue than at healthy sites. Furthermore, IL-1β levels are higher in active periodontitis sites than in stable sites [16,26,29] It is known that TNF-α induces bone and extracellular matrix resorption by activating the osteoclasts in a similar way with IL-1 [30]. Monocytes and macrophages are the potent cell types producing TNF-α.…”

“…As the other chronic inflammatory diseases inflammatory cytokines are considered to play an important role in the initiation, progression and the host modulation of periodontal disease [12,13] Current knowledge supports that the immunoregulatory properties of T cell derived cytokines can improve or attenuate the progression of periodontal disease [14]. There is evidence that failure to resolve inflammatory periodontal disease may be the result of an imbalance in T helper (Th) 1, Th2 and Th17 response and pro-and anti-inflammatory cytokines [14][15][16][17]. Therefore, in this mini-review, the Th cell subsets and their cytokines which are involved in the host inflammatory response and the destruction of periodontal tissues are summarized.…”

The Role of Chemokines and Cytokines in the Pathogenesis of Periodontal and Periapical Lesions: Current Concepts

“…IFN- is the signature cytokine of Th1-type responses, being considered the main phagocyteactivating cytokine and characteristically associated with the production of inflammatory cytokines and chemokines (Appay et al, 2008, Murphy & Reiner, 2002, Sallusto & Lanzavecchia, 2011, Schroder et al, 2004. Concerning periapical diseases of endodontic origin and periodontitis, IFN- is present at high levels in chronic PLs, and is associated with progressive lesions or higher severity (Colic et al, 2006, Garlet et al, 2003, Honda et al, 2006. In agreement, studies in rodents demonstrated that IFN- is involved in the development of inflammatory reaction and bone resorption in response to A. actinomycetemcomitans and P. gingivalis (Baker et al, 1999, Teng et al, 2005.…”