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Factors for progression of periodontal diseases
Author(s) -
Ellis S. D.,
Tucci M. A.,
Serio F. G.,
Johnson R. B.
Publication year - 1998
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1998.tb01923.x
Subject(s) - medicine , periodontal disease , dentistry
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) 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 bc1‐2 levels, were decreased at >6 mm; total protein and IL‐6 concentrations were increased adjacent to >6 mm, as compared to <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 T H 1 to T H 2 cell profile and that a favorable gingival microenvironment for hyper‐inflammation 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.