Abstract

Although non-surgical periodontal treatment is considered the gold standard, a subgroup of patients displays recurrence/progression of periodontitis after treatment. The aim of the present prospective study was to assess the effect of IL-6 -572 G/C and IL-10 -592 C/A gene polymorphisms on the risk of disease recurrence/progression at 3 years following non-surgical periodontal treatment. Thirty-seven patients diagnosed with chronic periodontitis received oral hygiene instructions and non-surgical periodontal treatment and were monitored for 3 years. All individuals were clinically evaluated for PPD, CAL and BOP at baseline and 3 years. Based on the clinical findings at 3 years, all subjects were considered either "at risk" or "not at risk" of periodontal disease progression based on specific criteria. Blood samples were collected at baseline and genotyping of the polymorphisms in IL-6 (rs1800796) and IL-10 (rs1800872) genes were performed by PCR. Following DNA separation and genotyping, 70.3% of the patients were homozygous carriers of the IL-6 -572G and 45.9% were carriers of the IL-10 -592A allele. Individuals at risk of disease progression ranged from 16.2% to 56.8% based on the criteria used. IL-6 -572 G/C and IL-10 -592 C/A polymorphisms were not associated with an increased risk of further disease progression (P>0.05) when the three criteria were examined. All examined periodontal clinical measures were significantly improved (P<0.05) after treatment. Males showed a significantly higher risk of disease progression than females when full-mouth BOP ≥30% was considered (P=0.008). Within the limitations of this 3-year prospective study, individuals susceptible to periodontal disease as determined by the presence of the IL-6 -572GG genotype or the IL-10 -592A allele were not associated with an increased risk of further disease progression and the potential need for further treatment following non-surgical periodontal treatment. Males were more prone to be at risk of disease progression than females.

Full Text
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