ArticlePloS one2016
Associations of Toll-Like Receptor and β-Defensin Polymorphisms with Measures of Periodontal Disease (PD) in HIV+ North American Adults: An Exploratory Study.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Periodontal infectogenomics: a systematic review update of associations between host genetic variants and subgingival microbial detection.Clinical oral investigations · 2022Pooled it
- Systemic Factors Affecting Human Beta-Defensins in Oral Cavity.Pathogens (Basel, Switzerland) · 2024Review
- The Potential Role of Epigenetic Modifications on Different Facets in the Periodontal Pathogenesis.Genes · 2023Review
- Toll-like receptor-1, -2, and -6 genotypes in relation to salivary human beta-defensin-1, -2, -3 and human neutrophilic peptide-1.Journal of clinical periodontology · 2022Article
- Article
- A preliminary assessment ofPapua and New Guinea medical journalArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
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.
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