Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms | Science Publications

American Journal of Immunology

Júlia Faria Nunes¹  André Cruz de Sousa¹  Maria do Carmo Machado Guimarães¹  Anne Carolina Eleutério Leite¹  Valéria Martins de Araújo Carneiro¹  Maria Imaculada Muniz-Junqueira¹ 

关键词: Transforming Growth Factor Beta;    T Helper Cell;    Periodontal Diseases;    RANKL/RANK;   

DOI  :  10.3844/ajisp.2015.125.138

学科分类：过敏症与临床免疫学

来源: Science Publications

【 摘 要 】

Periodontal Diseases (PD) are characterized by pathologicalmanifestation of host immune response to bacterial infection at thetooth/gingival interface. Evidences points periodontitis as a risk factor forpathological systemic conditions, such as, cardiovascular diseases anddiabetes. The identification of host factors that determine theirsusceptibility to immune subversion can provide useful information in thepathogenesis of periodontitis. Protective acute inflammatory response fails toremove inflammatory cells, especially neutrophils, evolving to chronic,destructive and pathological lesions. T and B cells actively participate inpathogenesis of the disease. CD4+ naive T cells are activated by antigenicstimulation and differentiate into subpopulations of distinct effector cells,characterized by its specific cytokine production profiles and functions. Inperiodontal infection, activated Th17 and regulatory T lymphocytes (Tregs) playantagonistic roles as effector and suppressor cells, respectively. In presenceof Tregs, there is a decrease in the levels of pro-inflammatory cytokines, suchas, Interferon gamma (IFN-γ), Interleukin (IL) -17, Tumor Necrosis Factor (TNF)and IL-1 β, at sites of disease. Absence of Tregs may cause a variety ofdisorders, such as, periodontitis. The RANKL/RANK system and Osteoprotegerin (OPG)are modulators of bone resorption in periodontitis. The balance betweenperiodontal bone resorption by osteoclasts and bone formation by osteoblastscontrols bone mass. RANKL induces osteoclast differentiation and maturation andOPG inhibits RANK/RANKL interaction and prevents bone resorption. RANKL mRNAand the RANKL/OPG mRNA ratio were enhanced in chronic periodontitis.Furthermore, the role of NF-kB, FoxP3 and T-bet transcription factors wereexplored. Therapies for periodontitis involving cellular and molecular biologyare not specific and have many side effects. Current therapies to successfullycontrol the PD reduces clinical signs of inflammation at local sites of thedisease; however, new treatments for periodontitis should address thecontribution of immune cells in bone resorption, particularly in the naturalcourse of the disease, considering its periods of remission and progression.

【 授权许可】

Unknown