Previous candidate genes carry no susceptibility factors for AgP. Association of IL-10 rs61815643 with AgP is suggested. ANRIL is associated with periodontitis across different populations.
Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. It is classified into the widespread moderate form chronic periodontitis (CP) and the rare early-onset and severe phenotype aggressive periodontitis (AgP). These different disease manifestations are thought to share risk alleles and predisposing environmental factors. To obtain novel insights into the shared genetic etiology and the underlying molecular mechanisms of both forms, we performed a two step-wise meta-analysis approach using genome-wide association studies of both phenotypes. Genotypes from imputed genome-wide association studies (GWAS) of AgP and CP comprising 5,095 cases and 9,908 controls of North-West European genetic background were included. Two loci were associated with periodontitis at a genome-wide significance level. They located within the pseudogene MTND1P5 on chromosome 8 (rs16870060-G, P = 3.69 × 10, OR = 1.36, 95% CI = [1.23-1.51]) and intronic of the long intergenic non-coding RNA LOC107984137 on chromosome 16, downstream of the gene SHISA9 (rs729876-T, P = 9.77 × 10, OR = 1.24, 95% CI = [1.15-1.34]). This study identified novel risk loci of periodontitis, adding to the genetic basis of AgP and CP.
Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome. Previous genome-wide association studies (GWAS) have reported several suggestive susceptibility loci. Here, we conducted a GWAS using a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare but highly severe and early-onset form of periodontitis, validated the associations in a German sample of severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls). Positive findings were replicated in a Turkish sample of AgP (223 cases, 564 controls). A locus at SIGLEC5 (sialic acid binding Ig-like lectin 5) and a chromosomal region downstream of the DEFA1A3 locus (defensin alpha 1-3) showed association with both disease phenotypes and were associated with periodontitis at a genome-wide significance level in the pooled samples, with P = 1.09E-08 (rs4284742,-G; OR = 1.34, 95% CI = 1.21-1.48) and P = 5.48E-10 (rs2738058,-T; OR = 1.28, 95% CI = 1.18-1.38), respectively. SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling. Alpha defensins are antimicrobial peptides with expression in neutrophils and mucosal surfaces and a role in phagocyte-mediated host defense. This study identifies the first shared genetic risk loci of AgP and CP with genome-wide significance and highlights the role of innate and adaptive immunity in the etiology of periodontitis.
Objectives: To determine the effects of a probiotic milk drink consumed over a period of 28 days, regarding the expression of clinical inflammatory parameters of the oral gingiva during various phases of plaque-induced gingivitis. Methods: Twenty-eight adults with healthy gingiva took part in a prospective and clinical-controlled study. The test group was advised to consume a probiotic milk drink (Yacult) daily during a period of 4 weeks; the control group did not receive any probiotic food or drink. After 2 weeks of consumption of the probiotic drink, participants were advised not to brush their teeth for 14 days. Subsequently, at baseline as well as on days 1, 3, 5, 7 and 14, the following clinical parameters were assessed: plaque index (PI), gingival index (GI), gingival crevicular fluid (GCF) volume and bleeding on probing (BOP). Results: At baseline, the PI was significantly higher in the test group compared with controls (0.44±0.50 vs 0.09±0.24 PI; P ¼ 0.0001). The termination of oral hygiene increased clinical inflammatory parameters in both groups. At day 14, the parameters PI, GI, GCF volume and BOP were significantly higher compared with baseline values (P ¼ 0.0001). At day 14, BOP levels (18.75 ± 12.32 vs 36.88 ± 12.54%) and GCF volume (18.78 ± 16.7 vs 35.72 ± 16.1 Periotron units) were significantly lower in the test group compared with the control group (P ¼ 0.005). Conclusion:The results of our study indicate that a daily consumption of a probiotic milk drink reduces the effects of plaqueinduced gingival inflammation associated with a higher plaque score due to the high-carbohydrate content of the probiotic milk beverage.
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