Sex Differences in Inflammatory and Apoptotic Signaling Molecules In Normal and Diseased Human Gingiva
- Autores: Roger B.Johnson, John C. Wikle
- Localización: Journal of periodontology, ISSN 0022-3492, Vol. 85, Nº. 11, 2014, págs. 1612-1619
- Idioma: inglés
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Resumen
Background: The purpose of this study is to determine whether sex dimorphism exists in the expression of inflammatory and apoptotic mediators in gingiva obtained from normal and diseased sites of periodontal disease.
Methods: Gingival papillae were obtained from individuals (56 males and 62 females) who required extraction of adjacent teeth. Gingival samples were grouped by adjacent sulcus depth: 1 to 3 mm (normal), 3 mm with bleeding on probing (slight disease), 3 to 6 mm (moderate disease), and >6 mm (severe disease). The tissue concentrations of cysteine-requiring aspartate-directed protease 3 (caspase-3), interleukin-2, tumor necrosis factor–related apoptosis-inducing ligand, Fas ligand, p38α mitogen-activated protein kinase, extracellular signal-related kinase 1/2, and survivin were determined by enzyme-linked immunosorbent assay. These mediator concentrations, age of donor, sex of donor, and gingival sulcular depth were the outcome variables. Data were compared by factorial analysis of variance, post hoc Tukey, and Pearson correlation test. P <0.05 was used to indicate significant differences among the outcome variables.
Results: The mean gingival sulcular depth was significantly greater in male than in female groups (P <0.05). The majority of the tested mediators were significantly correlated with both sex and sulcular depth and with caspase-3 (P <0.05). The concentration of caspase-3 in female gingiva at all diseased sites was significantly greater than in gingiva derived from male sites (P <0.05).
Conclusions: These data suggest sex dimorphism in the presence of gingival apoptosis at sites of periodontal disease, with females having the highest incidence of apoptosis. Because apoptosis clears inflammatory cells and promotes healing, this phenomenon could provide a mechanism for sex dimorphism for the incidence of periodontal disease.
