The oral/dental/craniofacial complex as a model for inflammatory disease.
Many inflammatory diseases, including periodontitis, are the result of uncontrolled destruction of host tissues by the host's own inflammatory response. Periodontitis as well as other inflammatory diseases are initiated by bacteria that results from host cell-mediated tissue destruction. The study of inflammation of the oral cavity and craniofacial complex provides an excellent window to the understanding of more complex and difficult to study conditions. In this article, the inflammatory process in periodontitis is reviewed with an emphasis on control pathways that naturally limit inflammation.
Van Dyke
Thomas E
TE
Department of Periodontology and Oral Biology, Boston University, Boston, Massachusetts, USA.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D016905:Gram-Negative Bacterial Infections / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000502:physiology; D008084:Lipoxygenase / Q000378:metabolism; D008563:Membrane Lipids / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D009504:Neutrophils / Q000502:physiology; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D016966:Porphyromonas gingivalis / Q000472:pathogenicity
D001095:Arachidonic Acids; D018836:Inflammation Mediators; D008563:Membrane Lipids; D008084:Lipoxygenase