BACKGROUND: Recently, an association between the severity of periodontitis and specific variations in the interleukin-1 (IL1) alpha and beta genes has been demonstrated. AIM: : The purpose of this study was to evaluate the relationship of the IL1 genotype to the development of experimental gingivitis. MATERIALS AND METHODS: Twenty young adult subjects presenting with healthy gingival conditions participated after giving their informed consent. The group included 10 risk genotype positive (P+) and 10 risk genotype negative (P-) individuals. The IL1 genotypes were determined on DNA samples from peripheral blood using PCR-RFLP analyses for the IL1alpha and IL1beta polymorphisms. Experimental gingivitis was allowed to develop in two posterior sextants per subject. Bleeding on probing (BOP%) and gingival crevicular fluid volume (GCF) were assessed at baseline and days 2, 7, 9, 14, 16 and 21. The day 21 results for BOP and GCF as well as the rate of increase of these parameters - mean area under the curve (AUC) and mean increase per day (slope) - were evaluated using risk analyses for IL1 genotype, smoking status and gender. RESULTS: Experimental gingivitis developed with a gradual increase in BOP scores and GCF values (expressed as Periotron units=PU) from baseline to day 21 (BOP, P+: 0.5 to 26.0%; P-: 1.0 to 28.1%; GCF, P+: 36.8 to 138.5 PU, P-: 43.1 to 143.4 PU). No significant risk was associated with P+ and P- for day 21 results, AUC or slope. CONCLUSION: The results of this study failed to provide evidence that the IL1 risk genotype was associated with higher GCF volume and percentage BOP during the development of experimental gingivitis.
BACKGROUND: Recently, an association between the severity of periodontitis and specific variations in the interleukin-1 (IL1) alpha and beta genes has been demonstrated. AIM: : The purpose of this study was to evaluate the relationship of the IL1 genotype to the development of experimental gingivitis. MATERIALS AND METHODS: Twenty young adult subjects presenting with healthy gingival conditions participated after giving their informed consent. The group included 10 risk genotype positive (P+) and 10 risk genotype negative (P-) individuals. The IL1 genotypes were determined on DNA samples from peripheral blood using PCR-RFLP analyses for the IL1alpha and IL1beta polymorphisms. Experimental gingivitis was allowed to develop in two posterior sextants per subject. Bleeding on probing (BOP%) and gingival crevicular fluid volume (GCF) were assessed at baseline and days 2, 7, 9, 14, 16 and 21. The day 21 results for BOP and GCF as well as the rate of increase of these parameters - mean area under the curve (AUC) and mean increase per day (slope) - were evaluated using risk analyses for IL1 genotype, smoking status and gender. RESULTS: Experimental gingivitis developed with a gradual increase in BOP scores and GCF values (expressed as Periotron units=PU) from baseline to day 21 (BOP, P+: 0.5 to 26.0%; P-: 1.0 to 28.1%; GCF, P+: 36.8 to 138.5 PU, P-: 43.1 to 143.4 PU). No significant risk was associated with P+ and P- for day 21 results, AUC or slope. CONCLUSION: The results of this study failed to provide evidence that the IL1 risk genotype was associated with higher GCF volume and percentage BOP during the development of experimental gingivitis.