title: Sex differences in inflammatory and apoptotic signaling molecules in normal and diseased human gingiva.
abstract: 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.
authors.affiliation: Department of Periodontics and Preventive Sciences, School of Dentistry, University of Mississippi, Jackson, MS.
authors.forename: Roger B
authors.initials: RB
authors.lastname: Johnson
authors.forename: John C
authors.initials: JC
authors.lastname: Wikle
mesh_terms: D000328:Adult; D000367:Age Factors; D051017:Apoptosis Regulatory Proteins / Q000032:analysis*; D053148:Caspase 3 / Q000032:analysis; D053222:Fas Ligand Protein / Q000032:analysis; D005260:Female; D005881:Gingiva / Q000737:chemistry*; D005884:Gingival Hemorrhage / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D051034:Inhibitor of Apoptosis Proteins / Q000032:analysis; D007376:Interleukin-2 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D019950:Mitogen-Activated Protein Kinase 1 / Q000032:analysis; D048308:Mitogen-Activated Protein Kinase 14 / Q000032:analysis; D048052:Mitogen-Activated Protein Kinase 3 / Q000032:analysis; D017622:Periodontal Attachment Loss / Q000378:metabolism; D010510:Periodontal Diseases / Q000378:metabolism*; D010514:Periodontal Pocket / Q000378:metabolism; D012737:Sex Factors; D000077022:Survivin; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000032:analysis
chemical_list: D051017:Apoptosis Regulatory Proteins; C107489:BIRC5 protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C508594:IL2 protein, human; D018836:Inflammation Mediators; D051034:Inhibitor of Apoptosis Proteins; D007376:Interleukin-2; D000077022:Survivin; D053221:TNF-Related Apoptosis-Inducing Ligand; D019950:Mitogen-Activated Protein Kinase 1; D048308:Mitogen-Activated Protein Kinase 14; D048052:Mitogen-Activated Protein Kinase 3; C505407:CASP3 protein, human; D053148:Caspase 3
keywords: Apoptosis; female; gingiva; inflammation; male; periodontal diseases