**5. Infectogenomics**

*Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations*

Vitamin D and Vitamin D receptor are important mediators of bone metabolism. SNPs or dysfunction could lead to bone resorption. The gene encoding vitamin D is

Gross et al. in their study found that Fok1 polymorphism was associated with periodontitis. Brett et al. in their study found TaqI, BsmI, FokI and ApaI SNPs were associated with periodontitis [18]. Kaarthikeyan et al. did not find any significant association of VDR Taq1 polymorphism with periodontitis in south Indian population [19]. Mashhadiabbas et al. in their meta-analysis based on 38 studies found an association of vitamin D receptor BsmI, TaqI, FokI, and ApaI polymorphisms with

**2.8 Matrix metalloproteinase and tissue inhibitor of matrix metalloproteinase**

Rhodin et al. in their systematic analysis listed top genes NIN, ABHD12B, WHAMM, AP3B2, CPEB1, HGD, ZNF675, EMK1, TNFRSF10B, HTR4, WDR59, JDP2, OTOF, ANGEL2, etc. that showed evidence of association with severity of periodontitis and colonization of microorganisms [22]. GWAS is a recent development in the field of research. It highlights suggestive loci that could play an important role in periodontitis. However, the method is expensive and technique sensitive. Many GWAS in periodontitis has been carried out and has shown differ-

Epigenetic modifications such as DNA methylation, histone modifications and RNA-associated silencing (micro RNA) play a role in susceptibility to disease. These

Loo et al. in their study showed that methylation of E-Cadherin and COX-2 was observed in periodontitis patients. Nahid et al. demonstrated the expression of miR-146a in infections caused by periodontopathic bacteria. Park et al. in their study observed that miRNA-132 played a major role in pathogenesis induced by P. Gingivalis. Several studies have reported the influence of various microRNAs especially miR-146a, let-7a, miR-196a, miR-499a, and miR-125a in susceptibility to

titis has to be explored with further refined studies.

**3. Genome wide association analysis**

ential expression of varied genes [23–26].

modifications express or repress certain genes.

**4. Epigenetic modifications**

Matrix metalloproteinases (MMPs) are the key enzymes, which play a major role in the destruction of the collagenous and non-collagenous proteins of the connective tissue component. This is essential for maintaining the normal tissue homeostasis. To date, at least 26 members of MMPs have been identified. In periodontitis, this tissue homeostasis is altered with more destruction of connective tissue components and less inhibition by the TIMPs. Elevated levels of MMP-1, MMP-2, MMP-3, MMP-8, and MMP-9 have been detected in gingival crevicular fluid, peri-implant sulcular fluid, and gingival tissue of periodontitis patients. Thus, the genetic changes of the MMPs and TIMPs might play a role in the etiopathogenesis of periodontitis. According to Li et al., there was no significant association of MMP1, 8, 9, 12, 2, or 13 polymorphism with periodontitis. They did a meta-analysis of 17 studies [21]. Thus, the role of MMPs and TIMPs gene polymorphism with periodon-

**2.7 Vitamin D**

located on 12q12-q14.

periodontitis [20].

**44**

Infectogenomics refers to the association of the host genetic variants like single nucleotide polymorphisms with the composition of the microbial complexes in the host body. The recent meta-analysis by Nibali et al. has shown an association of 13 host genetic variants with the red/orange complex bacteria in periodontitis. The study by Divaris et al. has shown an association of two genetic loci (KCNK1 and DAB2IP) with high colonization of red complex bacteria. A more detailed knowledge of the human oral microbiome could provide more information on its association with host genetic variants [31, 32].
