The aim of this talk is review data on genetic and epigenetic factors which may enable individual patient susceptibility to be determined.
Method:
The role of smoking and specific IL-1 and IL-10 gene polymorphisms was investigated in the 5-year University of Queensland Longitudinal Study. Subsequently, focused gene arrays were used to investigate the salivary and peripheral blood transcriptomes and to determine the pattern of growth factor gene expression in gingival fibroblasts of smokers and non-smokers. The EpiTect Methyl II PCR assay (SABioscience) is being used to determine the DNA methylation status of CpG islands in the VEGF-A, HIF-1α, and BMP-2 genes in smokers, former-smokers, and non-smokers.
Result:
There was no direct effect of specific IL-1 and IL-10 gene polymorphisms on the progression of periodontal disease over 5-years while smoking had a direct effect on disease progression and significantly inhibited innate tissue healing. While the level of bacterial DNA contamination was a major issue in determining the salivary transcriptome, BMP8B and IFN-k genes were found to be under-expressed in the peripheral blood of periodontitis subjects. There were significant differences in the pattern of growth factor gene expression in gingival fibroblasts of smokers and non-smokers and the DNA methylation of three specific genes is being investigated.
Conclusion:
Both IL-1 and IL-10 gene polymorphisms are secondary risk factors for periodontal disease progression, while smoking is a primary risk factor. Currently the salivary transcriptome is not suitable to identify patient susceptibility but further longitudinal studies investigating BMP8B and IFN-k gene expression in peripheral blood are warranted. Smoking leads to dysregulation of growth factor genes in the gingival tissues which may be a result of DNA hyper- or hypo- methylation. The relevance of these results to personalised oral health care and the determination of individual patient susceptibility will be discussed.