*4.2.1 Fc*γ *receptor polymorphisms*

The phagocytes harbour the Fc-gamma receptor which attaches to IgG. There are three broad classes of FcR: FcãRI (CD 64), FcãR II (CD 32), FcãR III (CD 16) in chromosome 1. Of which FcãR IIIa and FcãR IIIb, is found to be frequently associated with chronic periodontitis. FcãR IIIb has a NA1-NA2 polymorphism. NA1 is a more efficient opsono-phagocytic agent than NA2 [58].

When one or several of FcγR-mediated leukocyte functions are less or over efficient due to polymorphisms, it is likely that vulnerability or severity of periodontal disease is seen [46, 47].

#### *4.2.2 Toll-like receptors (TLR-2,-4) gene polymorphism*

These are signal molecules essential for the cellular response to bacterial cell wall components. TLR 2 exhibits polymorphism (Arg to Thr at 677, Arg to Gly at 753) which alters their ability to respond to cell wall components. Polymorphism of TLR4 (Asp 299 Arg 677 Trp; Arg753 Gln) have been known to be linked with impaired Lipopolysaccharide (LPS) signal transduction. Their relationship has still not been established [48].

#### *4.2.3 CD14 gene polymorphism*

The transcriptional activity of the CD 14 gene is enhanced by the presence of R-allele in the promoter region at position −260(−159). Research in Caucasian population revealed CD14–260 polymorphism in chronic periodontitis with no major link. A higher frequency of the N –allele and the N/N genotype of CD14–1359 polymorphism were observed in patients with aggressive periodontitis and in subjects with severe periodontal disorder [37, 41].

#### *4.2.4 CARD 15 gene polymorphisms*

The 3020insC and 2104 C > T polymorphisms seen in CARD15 (NOD2) gene results in decreased stimulation of nuclear factor-kappa B, thereby leads to alteration in the gene expression of pro inflammatory cytokine genes and diminished production of cytokines. However there has been no further established role for CARD 15 from studies in Caucasians [52].

#### *4.2.5 Polymorphism of RANK gene*

RANKL and its receptor RANK are the key elements reported to cause increased bone resorption in periodontal disease through osteoclast differentiation and activation of nuclear factor-B (RANK), RANK ligand (RANKL), and osteoprotegrin (OPG). Association studies show no significant link of the SNPs with AgP in Japanese population.

*Genetics and Periodontal Disease: An Explicit Insight DOI: http://dx.doi.org/10.5772/intechopen.99266*

### *4.2.6 N-formyl peptide receptor polymorphism*

FMLP receptor has a high affinity variant (FPR1) which binds with FMLP receptors of microbial cells triggering chemotaxis, degranulation and superoxide production which are found to be disrupted in genetically modified periodontitis. Polymorphisms were noted at the nt329T-C (codon 110 phenylalanine-serine), and at the nt378C-G (codon 126 cysteine-tryptophan) in the 583 bp interval of FMLP receptor gene. Coincidentally this is found to be significantly linked to the Agp phenotype in Afro-American patients [17, 18].
