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Periodontitis and p38 mitogen activated protein kinase pathway:research and development / 中国组织工程研究
Chinese Journal of Tissue Engineering Research ; (53): 7746-7752, 2016.
Article in Chinese | WPRIM | ID: wpr-508673
ABSTRACT

BACKGROUND:

A series of inflammatory signal pathways are activated accompanied by increasing expressions of inflammatory factors after periodontal tissues being stimulated by exogenous substances like bacterium. Inflammation is closely related to periodontal tissue repair and regeneration.

OBJECTIVE:

To il ustrate the correlation of immune response of periodontitis and periodontitis-related inflammatory cytokines to p38 mitogen activated protein kinase (p38MAPK) pathway, and to provide a new idea and method for the treatment of periodontitis in the future.

METHODS:

The related literatures of periodontitis and p38MAPK pathway published from January 1990 to January 2016 were retrieved from the databases of CBM, CNKI, SWIC and PubMed. The research and progress of periodontal tissue repair and regeneration after periodontitis were analyzed. RESULTS AND

CONCLUSION:

Total y 36 literatures were enrol ed final y. Inflammation-regulated and inflammation-associated signaling pathways as wel as subsequent expression of inflammatory mediators can partly control the excessive disease-induced inflammation and immune responses of the host, among which p38MAPK signaling pathway may be involved in the occurrence and development of periodontitis. More studies, however, are needed to validate these findings. The regulation of p38MAPK signaling pathway is stil of great significance in the treatment of periodontal disease, and we hope to provide a new insight and basis for clinical diagnosis and treatment of periodontitis.
Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2016 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2016 Type: Article