Abstract
Periapical lesions are inflammatory conditions of tooth periapical tissues, triggered by dental pulp infection and characterized by exudation of immune cells to the affected tissues and production of inflammatory mediators such as cytokines. The inflammatory periapical reaction is mainly driven by Th1, Th2, and Th17 responses, and such polarization may modulate progression of the disease and expression of bone proresorptive cytokines. IL-12 is a potent inducer of IFN-γ production, which stimulates Th1 effector cells. Many evidences have shown a positive correlation between the bone resorptive cytokine IL-1β and the production of IL-12 and IFN-γ. Furthermore, IL-12 may have a potential role in the release of bone resorptive mediators and blockade of Th2 cytokines, affecting the progression of periapical bone loss. Nevertheless, IL-12 and IFN-γ have also been described as suppressors of osteoclast differentiation and activation, favoring bone maintenance. This paper focuses on the controversial roles of IL-12 in periapical lesions.
Highlights
Interleukin 12 (IL-12) is an important regulatory cytokine that has a pivotal function in the initiation and regulation of cellular immune responses
When periapical granulomas were categorized into active or inactive based on the RANKL/OPG expression pattern [59], our results demonstrate that the expression of both IL-12 and IFN-γ is significantly higher in active lesions, while Th2- and Th22type cytokines prevail in inactive lesions
IL-12 is related to the differentiation of Th1 cells, and there is evidence that Th cells are directly involved in the progression of periapical lesions and bone resorption
Summary
Interleukin 12 (IL-12) is an important regulatory cytokine that has a pivotal function in the initiation and regulation of cellular immune responses. It can regulate the differentiation of naive T cells, which are crucial in determining resistance and the type of response that will be elicited against a particular pathogen [1]. IL-12 is mainly produced by macrophages, monocytes, dendritic and B cells in response to bacterial products and intracellular parasites. It is primarily responsible for the subsequent production of interferongamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) from NK cells and T helper cells. The aim of this paper is to discuss the mechanisms associated to the IL-12-related immune response in tooth periapical lesions
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