An investigation into the association among preterm birth, cytokine gene polymorphisms and periodontal disease
To investigate a putative relationship between preterm delivery and the carriage of polymorphic genes that code for the cytokines interleukin-1β (IL-1β) at codon +3953 and tumour necrosis factor-α (TNF-α) at codon −308 in a group of postpartum women and to elucidate if the concurrent presence of periodontal disease increased the risk of preterm delivery in this group.Design
Postnatal wards at Guy's and St Thomas' Hospital Trust.Population
Postpartum women from southeast London, UK.Methods
Case subjects were defined as those who experienced a birth at less than 37 weeks of gestation. Control subjects gave birth at term. Demographic data were collected and a periodontal examination was performed. Blood samples were collected and analysed by restriction fragment length polymerase techniques for the presence of each of the allelic variants.Main outcome measures
The level of periodontal disease and the carriage of allelic variants of IL-1β+3953 and TNF-α−308 genes.Results
Forty-eight case subjects and 82 control subjects were assessed. There was no statistically significant difference in the carriage of the IL-1β+3953 allelic variant between cases and controls (29%versus 18%, P= 0.112). However, 23 (48%) of the case subjects and 24 (29%) of controls were heterozygous or homozygous for the variant TNF-α−308 gene (odds ratio [OR] 2.2, 95% confidence interval [CI] 1.0–5.0, P= 0.026). There was no association between the carriage of either the polymorphic IL-1β+3953 or TNF-α−308 variant and the severity of periodontal disease. The combination of periodontal disease and the allelic variant did not increase the risk of preterm delivery.Conclusions
In this study, a higher proportion of women who delivered preterm carried the polymorphic TNF-α−308 gene. There did not appear to be any interaction between either of the genotypes and periodontal disease with preterm delivery as has been reported for bacterial vaginosis and the TNF-α−308 polymorphic gene.