title: Factors for progression of periodontal diseases.
abstract: Progression factors for periodontal diseases have been suggested by in vitro study of peripheral blood and gingival cells; however, those factors are not established in vivo. This investigation assessed biopsies of three groups of gingival tissues: those adjacent to a 1) < or =3 mm (normal), 2) 4-6 mm, and 3) >6 mm gingival sulcus, to determine changes in the gingival microenvironment coincident to the progression of periodontal disease. Superoxide dismutase (SOD) and catalase activity, and IL-12 and bcl-2 levels, were decreased at >6 mm; total protein and IL-6 concentrations were increased adjacent to >6 mm, as compared to < or =3 and 4-6 mm, sites. Apoptotic cells were evident only within gingiva adjacent to >6 mm sites. These data suggest that IL-12 is an important factor in the shift from a TH1 to TH2 cell profile and that a favorable gingival microenvironment for hyperinflammation may develop coincident to progression of periodontal diseases due to decreased bcl-2 and increased IL-6 concentrations within gingiva. These changes in the gingival microenvironment could impair apoptosis and promote enhanced release of reactive oxygen species (ROS) by phagocytes; decreased catalase and SOD activity could promote accumulation of ROS and result in additional tissue destruction.
authors.affiliation: Department of Periodontics, School of Dentistry, University of Mississippi Medical Center, Jackson 39216-4505, USA.
authors.forename: S D
authors.initials: SD
authors.lastname: Ellis
authors.forename: M A
authors.initials: MA
authors.lastname: Tucci
authors.forename: F G
authors.initials: FG
authors.lastname: Serio
authors.forename: R B
authors.initials: RB
authors.lastname: Johnson
mesh_terms: D000704:Analysis of Variance; D017209:Apoptosis; D002374:Catalase / Q000032:analysis; D018450:Disease Progression; D005881:Gingiva / Q000201:enzymology / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005884:Gingival Hemorrhage / Q000473:pathology / Q000503:physiopathology; D005891:Gingivitis / Q000473:pathology; D006801:Humans; D018664:Interleukin-12 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016014:Linear Models; D010510:Periodontal Diseases / Q000201:enzymology / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010586:Phagocytes / Q000473:pathology; D011506:Proteins / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000032:analysis; D018417:Th1 Cells / Q000473:pathology; D018418:Th2 Cells / Q000473:pathology
chemical_list: D015850:Interleukin-6; D011506:Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D018664:Interleukin-12; D002374:Catalase; D013482:Superoxide Dismutase