Abstract
Polymorphisms in toll-like receptor (TLR) and β-defensin (DEFB) genes have been recognized as potential genetic factors that can influence susceptibility to and severity of periodontal diseases (PD). However, data regarding associations between these polymorphisms and PD are still scarce in North American populations, and are not available in HIV+ North American populations. In this exploratory study, we analyzed samples from HIV+ adults (n = 115), who received primary HIV care at 3 local outpatient HIV clinics and were monitored for PD status. We genotyped a total of 41 single nucleotide polymorphisms (SNPs) in 8 TLR genes and copy number variation (CNV) in DEFB4/103A. We performed regression analyses for levels of 3 periodontopathogens in subgingival dental plaques (Porphyromonas gingivalis [Pg], Treponema denticola [Td], and Tannerella forsythia [Tf]) and 3 clinical measures of PD (periodontal probing depth [PPD], gingival recession [REC], and bleeding on probing [BOP]). In all subjects combined, 2 SNPs in TLR1 were significantly associated with Td, and one SNP in TLR2 was significantly associated with BOP. One of the 2 SNPs in TLR1 was significantly associated with Td in Caucasians. In addition, another SNP in TLR1 and a SNP in TLR6 were also significantly associated with Td and Pg, respectively, in Caucasians. All 3 periodontopathogen levels were significantly associated with PPD and BOP, but none was associated with REC. Instrumental variable analysis showed that 8 SNPs in 6 TLR genes were significantly associated with the 3 periodontopathogen levels. However, associations between the 3 periodontopathogen levels and PPD or BOP were not driven by associations with these identified SNPs. No association was found between DEFB4/103A CNV and any periodontopathogen level or clinical measure in all samples, Caucasians, or African Americans. Our exploratory study suggests a role of TLR polymorphisms, particularly TLR1 and TLR6 polymorphisms, in PD in HIV+ North Americans.
Highlights
Periodontal diseases (PD) modified by HIV, together with other oral infections, is considered to be among serious complications of HIV infection, and may have implications for oral health but possibly for systemic health as well [1,2,3]
We found that a total of 5 single nucleotide polymorphisms (SNPs) in TLR1, TLR2, and TLR6 were significantly associated with 2 periodontopathogen levels and one clinical measure of PD
Linear regression analysis using a binary (CNV ! 5, copy number variation (CNV) < 5) or categorical (CNV < 5, CNV = 5, CNV > 5) model did not show any association between CNV and any periodontopathogen level or clinical measure in all samples, Caucasians, or African Americans (p>0.05, data not shown). In this exploratory study, utilizing samples from HIV+ North American subjects, we found that a total of 5 SNPs in TLR1 (n = 3), TLR2 (n = 1), and TLR6 (n = 1) were significantly associated with 2 periodontopathogen levels (Table 2) and one clinical measure of PD (Table 3)
Summary
Periodontal diseases (PD) modified by HIV, together with other oral infections, is considered to be among serious complications of HIV infection, and may have implications for oral health but possibly for systemic health as well [1,2,3]. The components of innate immunity in PD include toll-like receptors (TLRs) [12,13] and β-defensins [14,15,16,17] It is, not surprising that polymorphisms in these innate immune response genes (TLR and DEFB, respectively) have been extensively studied as potential genetic factors that may influence susceptibility to and severity of PD [12,18,19,20,21,22,23,24,25,26,27,28]. The present study takes the first step toward closing these gaps
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