title: The potential role of chemokines and inflammatory cytokines in periodontal disease progression.
abstract: Inflammation is regulated by the expression of mediators that cause a number of pleiotropic events culminating in the recruitment of inflammatory cells and release of biologic mediators by leukocytes. If the inflammation is transient in nature, it can protect the host by activating defense mechanisms and initiating wound repair. However, if the inflammation is inappropriate, it can lead to considerable tissue damage. My colleagues and I have investigated the role of chemokines, particularly monocyte chemoattractant protein 1, in various pathological processes and the role of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF) in experimental periodontitis. I will discuss first the studies on chemokines and then the use of IL-1 and TNF blockers in inhibiting inflammation and bone loss in the periodontium.
authors: Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Massachusetts, USA. dgraves@acs.bu.edu
authors: D T
authors: DT
authors: Graves
mesh_terms: D018932:Chemokine CCL2 / Q000378:metabolism*; D018450:Disease Progression; D005881:Gingiva / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009000:Monocytes / Q000502:physiology; D010006:Osteoblasts / Q000378:metabolism; D010518:Periodontitis / Q000276:immunology / Q000503:physiopathology* / Q000517:prevention & control; D012867:Skin / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D018932:Chemokine CCL2; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha