Inflammatory mediators in the pathogenesis of periodontitis

Abstract

Periodontitis is a chronic inflammatory condition of the periodontium involving interactions between bacterial products, numerous cell populations and inflammatory mediators. It is generally accepted that periodontitis is initiated by complex and diverse microbial biofilms which form on the teeth, i.e. dental plaque. Substances released from this biofilm such as lipopolysaccharides, antigens and other virulence factors, gain access to the gingival tissue and initiate an inflammatory and immune response, leading to the activation of host defence cells. As a result of cellular activation, inflammatory mediators, including cytokines, chemokines, arachidonic acid metabolites and proteolytic enzymes collectively contribute to tissue destruction and bone resorption. This review summarises recent studies on the pathogenesis of periodontitis, with the main focus on inflammatory mediators and their role in periodontal disease.

Periodontal and inflammatory bowel diseases: Is there evidence for complex pathogenic interactions?

“…As a result, inflammatory mediators, including cytokines, chemokines and proteolytic enzymes, are produced and contribute to tissue degradation and bone resorption. Neutrophils are the first cells to arrive at the inflammatory inflitrate and predominate within the junctional epithelium and gingival crevice [18] . Previous studies from our group have shown that neutrophils from periodontitis patients are hyper-reactive and contribute to tissue destruction [3,19,20] .…”

“…When the resolution of inflammation is not achieved, antigen-presenting cells are activated by bacterial pro-ducts and interact with naïve T helper cells (Th0), driving their differentiation into several subsets, such as Th1, Th2, Th17, and Treg. These subsets are characterized according to the cytokines they produce [18] . For a long time, periodontitis lesions were conceptually defined based on a Th1/Th2 paradigm, with inconclusive studies pointing to both Th1 and Th2 responses as characterizing disease progression [23] .…”

“…In conjunction with infiltrating inflammatory cells, gingival fibroblasts take part in the inflammatory process in the periodontium and contribute to the disease persistence [18] . These cells are able to produce cytokines, chemokines and matrix metalloproteinases [26][27][28] .…”

“…As a consequence of the unresolved inflammation and an increased concentration of inflammatory mediators, tissue destruction occurs. Matrix metalloproteinases (MMPs) are proteolytic enzymes involved in the homeostasis of connective tissue and the balance between MMPs and their endogenous inhibitors (tissue inhibitor of matrix metalloproteinases -TIMPs) controls the MMP activity [18,31] . MMPs play an important role in tissue degradation observed in periodontitis and there is strong evidence of their increased activity in periodontitis [32,33] , as well as of an imbalance between MMPs and TIMPs [34] .…”

Inflammatory Cytokines and the Pathogenesis of Periodontal Disease

“…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.…”