The potential of p38 MAPK inhibitors to modulate periodontal infections.
Periodontal disease initiation and progression occurs as a consequence of the host immune inflammatory response to oral pathogens. The innate and acquired immune systems are critical for the proper immune response. LPS, an outer membrane constituent of periodontal pathogenic bacteria, stimulates the production of inflammatory cytokines IL-1beta, TNFalpha, IL-6 and RANKL either directly or indirectly. In LPS-stimulated cells, the induction of cytokine expression requires activation of several signaling pathways including the p38 MAPK pathway. This review will discuss the significance of the p38 MAPK pathway in periodontal disease progression and the potential therapeutic consequences of pharmacological antagonism of this pathway in the treatment of periodontal diseases.
Kirkwood
Keith L
KL
Department of Craniofacial Biology, Center for Oral Health Research, Medical University of South Carolina, Charleston, SC 29425, USA. klkirk@musc.edu
Rossa
Carlos
C
D000818:Animals; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism; D010510:Periodontal Diseases / Q000188:drug therapy* / Q000382:microbiology / Q000503:physiopathology; D015398:Signal Transduction / Q000187:drug effects; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors*
D016207:Cytokines; D004791:Enzyme Inhibitors; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D048051:p38 Mitogen-Activated Protein Kinases