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Objective To assess in a cross-sectional study the impact of including dental professionals in the multidisciplinary treatment team of head and neck squamous cell carcinoma (HNSCC) patients on the long-term oral health status. Materials and methods Oral health status, dental care behaviours, and oral health–related quality of life were assessed based on a clinical and radiographic examination, interview, and medical records in patients treated for HNSCC ≥ 6 months ago. This patient group (‘cohort 2’) was treated in a multidisciplinary treatment team including dental professionals and compared to a group of HNSCC patients previously treated at the same university, but without dental professionals included in the multidisciplinary treatment team (‘cohort 1’). Results Cohort 2 consisted of 34 patients, who had received a dental check-up and if necessary, treatment by dental professionals prior to the initiation of cancer treatment. This cohort showed significantly improved oral hygiene habits and a better periodontal health status compared to cohort 1. However, cohort 2 still presented high demand for treatment due to active carious lesions; only a few, statistically insignificant improvements were detected compared to cohort 1. Conclusion Including dental professionals in the multidisciplinary treatment team of HNSCC patients has a positive impact on patient oral health status—primarily in terms of periodontal disease—6 months and longer after finishing cancer therapy. Clinical relevance A team-based approach including dental professionals specialised in head and neck cancer improves oral health status.

© 2021 The Authors. Journal of Clinical Periodontology published by John Wiley & Sons Ltd.Aims: Various studies have reported that young European women are more likely to develop early-onset periodontitis compared to men. A potential explanation for the observed variations in sex and age of disease onset is the natural genetic variation within the autosomal genomes. We hypothesized that genotype-by-sex (G × S) interactions contribute to the increased prevalence and severity. Materials and methods: Using the case-only design, we tested for differences in genetic effects between men and women in 896 North-West European early-onset cases, using imputed genotypes from the OmniExpress genotyping array. Population-representative 6823 controls were used to verify that the interacting variables G and S were uncorrelated in the general population. Results: In total, 20 loci indicated G × S associations (P < 0.0005), 3 of which were previously suggested as risk genes for periodontitis (ABLIM2, CDH13, and NELL1). We also found independent G × S interactions of the related gene paralogs MACROD1/FLRT1 (chr11) and MACROD2/FLRT3 (chr20). G × S-associated SNPs at CPEB4, CDH13, MACROD1, and MECOM were genome-wide-associated with heel bone mineral density (CPEB4, MECOM), waist-to-hip ratio (CPEB4, MACROD1), and blood pressure (CPEB4, CDH13). Conclusions: Our results indicate that natural genetic variation affects the different heritability of periodontitis among sexes and suggest genes that contribute to inter-sex phenotypic variation in early-onset periodontitis.

Background Gingival clefts (GCs) develop frequently during orthodontic space closure and may compromise the treatment outcome. This study assessed whether the time‐point of orthodontic space closure initiation, after permanent tooth extraction, affects the incidence of GC. Methods In 25 patients requiring bilateral premolar extraction because of orthodontic reasons, one premolar, chosen at random, was extracted 8 weeks before space closure initiation (“delayed movement,” DM), whereas the contralateral premolar was extracted 1 week before (“early movement,” EM) (“treatment group”). Presence or absence of GC after 3 and 6 months (“time‐point”) was recorded and any association with various parameters (i.e., treatment group, time‐point, gender, jaw, craniofacial growth, gingival biotype, buccal bone dehiscence after extraction, space closure) was statistically assessed. Results Twenty‐one patients contributing with 26 jaws were finally included in the analysis. Overall, GCs were frequent after 3 (DM: 53.9%; EM: 69.2%) and 6 months (DM: 76.9%; EM: 88.5%). EM (P = 0.014) and larger space closure within the study period (P = 0.001) resulted in a significantly higher incidence of GC. Further, there was a tendency for GC development in the presence of buccal bone dehiscence (P = 0.052) and thin gingival biotype (P = 0.054). “Fast movers” (herein cases with a tooth movement ≥1 mm per month) developed a GC in >90% of the cases already after 3 months. “Slow movers” developed a GC in 25% and 70% after 3 months and final evaluation, respectively. Conclusions GC development is a frequent finding during orthodontic space closure and seems to occur more frequently with early tooth movement initiation and in “fast movers.”

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(−9), 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(−9), 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.

Objectives The present proof‐of‐principle study assessed whether daily use of a power‐driven water flosser (Sonicare AirFloss; SAF) leads to bacterial colonization in the nozzle and/or the device, resulting in contaminated water‐jet. Material and Methods In five participants, saliva samples at baseline and water‐jet samples of devices used daily with bottled water for 3 weeks (test) were collected. Additionally, water‐jet samples from devices used daily with bottled water extra‐orally for 3 weeks (positive control) and from brand new devices (negative control), as well as samples from newly opened and 1‐ and 3‐week opened water bottles were collected. Colony forming units (CFU) were recorded after 48 h culturing and 20 oral pathogens were assessed by polymerase chain reaction‐based analysis. Results Distinct inter‐individual differences regarding the number of detected bacteria were observed; water‐jet samples of test devices included both aerobic and anaerobic bacterial species, with some similarities to the saliva sample of the user. Water‐jet samples from positive control devices showed limited number of aerobic and anaerobic bacterial species, while the samples from negative control devices did not show any bacterial species. Very few aerobic bacteria were detected only in the 3‐week‐old bottled water samples, while samples of newly and 1‐week opened water bottles did not show any bacterial growth. Conclusions The present proof‐of‐principle study showed that daily use of a power‐driven water flosser for 3 weeks resulted in bacterial colonization in the nozzle and/or device with both aerobic and anaerobic, not only oral, species, that are transmitted via the water‐jet.

AimThe intronic variant rs4252120 in the plasminogen gene (PLG) is known to be associated with aggressive periodontitis (AgP) and atherosclerosis. Here, we examined the chromosomal region spanning PLG for associations with both chronic periodontitis (CP) and AgP. Materials and MethodsThe association of PLG candidate rs4252120 was tested in a German case–control sample of 1,419 CP cases using the genotyping assay hCV11225947 and 4,562 controls, genotyped with HumanOmni BeadChips. The German and Dutch sample of AgP cases (N = 851) and controls (N = 6,836) were genotyped with HumanOmni BeadChips. The North American CP sample (N = 2,681 cases, 1,823 controls) was previously genotyped on the Genome‐Wide Human SNP Array 6.0. Genotypes were imputed (software Impute v2), and association tests were performed using an additive genetic model adjusting for sex and smoking. ResultsRs4252120 was not associated with CP. However, a haplotype block downstream of PLG and not in linkage disequilibrium with rs4252120 (r2 = .08) was associated with both AgP (rs1247559; p = .002, odds ratio [OR] = 1.33) and CP (p = .02, OR = 1.15). That locus was also significantly associated with PLG expression in osteoblasts (p = 6.9 × 10−5). ConclusionsOur findings support a role of genetic variants in PLG in the aetiology of periodontitis.

Periodontitis has low-prevalence, highly severe disease manifestations with an early onset and rapid progression. The diagnosis is based on severe destruction of the alveolar bone in adolescents and young adults. Genetic susceptibility variants and smoking are well-established risk factors, but their interactions in modifying disease susceptibility have not been studied. We aimed to identify genetic risk variants of early-onset periodontitis that unmask their effects on tobacco smoke exposure. To this end, we analyzed 79,780,573 common variants in 741 northwest Europeans diagnosed to have >30% bone loss at >2 teeth before 35 y of age, using imputed genotypes of the OmniExpress BeadChip. Never versus ever smokers were compared in a logistic regression analysis via a case-only approach. To explore the effect of tobacco smoke on the expression of the G×S-associated genes, cultures of primary gingival fibroblasts ( n = 9) were exposed to cigarette smoke extract, and transcripts were quantified by reverse transcription polymerase chain reaction. We identified 16 loci for which our analysis suggested an association with G×S increased disease risk ( P < 5 × 10−5). Nine loci had previously been reported to be associated with spirometric measures of pulmonary function by an earlier G×S genome-wide association study. Genome-wide significant cis expression quantitative trait loci were reported for G×S-associated single-nucleotide polymorphisms at ST8SIA1 and SOST, indicating a causal role of these genes in tobacco-related etiopathology. Notably, SOST is a negative regulator of bone growth, and ST8SIA1 has a role in tissue remodeling. Cigarette smoke extract significantly altered the expression of 2 associated genes: SSH1 ( P = 5 × 10−07), which is required for NF-κB activation and innate immune responses to bacterial invasion, and ST8SIA1 ( P = 0.0048). We conclude that the genetic predisposition to early-onset periodontitis is in part triggered by smoking and that tobacco smoke directly affects the expression of genes involved in bone homeostasis, tissue repair, and immune response.

Background Periodontal diseases are responsible for a vast burden of disease globally and are associated with other severe illnesses such as cardiovascular diseases or diabetes. Tests for early diagnosis of periodontal diseases and effective treatments are available. The effectiveness of screening for periodontal diseases to detect periodontal diseases at an early stage during periodic health examinations at primary care facilities, however, is unclear. The objective of this systematic review is to assess the benefits and risks of screening for periodontal diseases in adults during the periodic health examinations. Methods We will use two methodological approaches: (1) a systematic review to assess the effectiveness and risk of harms of screening for periodontal diseases during periodic health examinations and (2) an overview of systematic reviews to determine the effectiveness of treatment approaches for early periodontal disease. We will search electronic databases (Ovid MEDLINE, Embase.com, the Cochrane Library, Epistemonikos, Centre for Reviews and Dissemination databases, PubMed (non-MEDLINE content)) for published studies as well as sources for grey literature to detect unpublished studies. Two authors will independently screen abstracts and full texts using pre-defined eligibility criteria, select studies, extract data, and assess the risk of bias of included studies or reviews. In general, we will conduct a systematic narrative synthesis. Criteria for conducting meta-analyses were defined a priori. Our primary outcomes of interest are tooth loss, loosening of teeth, and depletion of bone tissue. Secondary outcomes are gingivitis/gum inflammation, pocket depths, dental hygiene, lifestyle modifications (e.g., smoking, alcohol, nutrition), and toothache. We consulted a panel of experts and patient representatives to prioritize these outcomes. Two investigators will assess independently the certainty of the evidence for each outcome using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Discussion We anticipate that our review will highlight the gaps in the available evidence about the effectiveness of screening for periodontal diseases during periodic health examinations. Implications for screening programs may be based on linked evidence about the validity of available screening tools and the effectiveness of early treatment. Systematic review registration PROSPERO CRD42017081150 Electronic supplementary material The online version of this article (10.1186/s13643-019-0977-9) contains supplementary material, which is available to authorized users.

Objectives The present randomized controlled trial aimed to assess the effect of hyaluronan (HY) injections to augment deficient interproximal papillae at implant-supported crowns in the anterior maxilla. Methods Twenty-two patients with a deficient papilla in the anterior maxilla next to an implant-supported crown were randomly assigned to receive twice either HY (test) or saline solution (control) injection. The following parameters were recorded prior to injection (baseline) and 3 and 6 months after injection: distance between the papilla tip and contact point (PT-CP), modified papilla index score (MPIS), and standard clinical periodontal parameters. Pain level after injection was recorded on a visual analogue scale (VAS). The deficient area was evaluated on clinical photographs, and the esthetic appearance was recorded on a VAS. Differences in mucosal volume were assessed after 3 months by intraoral scans. The bone level was assessed on periapical radiographs. Results No differences were observed between groups, neither at baseline nor at 3 and 6 months post-treatment. Mean PT-CP ranged between 1.8 mm and 2.3 mm without significant differences between groups or over time within groups; MPIS was 2 for all patients at all time points. Similarly, insignificant differences between groups or time points were observed for deficient area, gingival volume changes, bone level, and esthetic appearance. There were no differences in pain level between groups during injection, but discomfort after injection lasted longer in the test group. Conclusions Injection of HY adjacent to maxillary anterior implant-supported crowns did not result in any clinical conspicuous volume augmentation of deficient papillae.

Objectives To report two cases of adverse reaction after mucosal hyaluronan (HY) injection around implant-supported crowns, with the aim to augment the missing interdental papilla. Material and Methods Two patients with single, non-neighbouring, implants in the anterior maxilla, who were treated within the frames of a randomized controlled clinical trial testing the effectiveness of HY gel injection to reconstruct missing papilla volume at single implants, presented an adverse reaction. Injection of HY was performed bilaterally using a 3-step technique: (i) creation of a reservoir in the mucosa directly above the mucogingival junction, (ii) injection into the attached gingiva/mucosa below the missing papilla, and (iii) injection 2–3 mm apically to the papilla tip. The whole-injection session was repeated once after approximately 4 weeks. Results Both patients presented with swelling and extreme tenderness with a burning sensation on the lip next to the injection area, after the second injection session. In one of the cases, a net-like skin discoloration (livedo reticularis) was also noted. The symptoms lasted for up to 7 days, and in both cases, symptoms resolved without any signs of skin or mucosal necrosis or any permanent damage. Conclusion Most likely, water attraction over time by the highly hygroscopic HY, exerted progressively an external vascular compression and at least partial occlusion of neighbouring blood vessels. An infection or an allergic reaction seems unlikely, since all symptoms gradually disappeared within a week irrespective use of antimicrobials, while an allergic reaction most likely would not have been restricted to one side.

Background The aim of the present study was to evaluate the validity of the German version of the Oral Health Impact Profile (OHIP-G) in comparison with the Visual Analogue Scale (VAS) and to evaluate whether gender has a potential influence on OHIP scores and dimensions in oral lichen planus (OLP) patients.

AIM: To evaluate the effect of hyaluronan (HY) application as monotherapy or as adjunct to non-surgical and/or surgical periodontal therapy. METHODS: Literature search was performed according to PRISMA guidelines with the following main eligibility criteria: (a) English or German language; (b) preclinical in-vivo or human controlled trials; (c) effect size of HY evaluated histologically or clinically. RESULTS: Two preclinical in-vivo studies on surgical treatment and 12 clinical trials on non-surgical and/or surgical treatment were included. Most of the studies were highly heterogeneous, regarding with HY product used and application mode, and of high risk of bias, thus not allowing meta-analysis. The majority of clinical studies described a beneficial, occasionally statistically significant, effect of HY on bleeding on probing (BoP) and pocket depth (PD) reduction (2.28-19.5% and 0.2-0.9mm, respectively), comparing to controls; no adverse effects were reported. CONCLUSIONS: HY application as adjunct to non-surgical and surgical periodontal treatment seems to have a beneficial, generally moderate, effect on surrogate outcome variables of periodontal inflammation, i.e., BoP and residual PD, and appears to be safe. The large heterogeneity of included studies, does not allow recommendations on the mode of application or effect size of HY as adjunct to non-surgical and surgical periodontal treatment. (Less)

This commentary is intended to: 1) honor Gottlieb’s discovery of “periodontosis;” 2) “review Gottlieb's influence on our understanding of periodontal pathogenesis”; and 3) stimulate interest in unresolved questions.

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.

Aim: Periodontitis (PD) is influenced by genetic as well as lifestyle and socio-economic factors. Epidemiological studies show that men are at greater risk of severe forms of PD, suggesting interplay between sex and genetic factors. We aimed to systematically analyse patients with aggressive periodontitis (AgP) for gene–sex interactions. Materials and Methods: Three hundred and twenty-nine German AgP cases and 983 controls were genotyped with Affymetrix 500K Arrays and were analysed by logistic regression analysis. The most significant gene–sex interaction was replicated in an independent sample of 382 German/Austrian AgP cases and 489 controls. Results: Ten single-nucleotide polymorphisms (SNPs) in strong linkage disequilibrium (r 2 > 0.85) upstream the gene neuropeptide Y (NPY) suggested gene–sex interaction (p < 5 9 10 � 5 ). SNP rs198712 showed the strongest association in interaction with sex (p = 5.4 9 10 � 6 ) with odds ratios in males and females of 1.63 and 0.69 respectively. In the replication, interaction of sex with rs198712 was verified with p = 0.022 (pooled p = 4.03 9 10 � 6 ) and similar genetic effects. Analysis of chromatin elements from ENCODE data revealed tissue-specific transcription at the associated non-coding region. Conclusion: This study is the first to observe a sexually dimorphic role of alleles at NPY in humans and support previous genome-wide findings of a role of NPY in severe PD.

AimIdentification of variants within genes SLC23A1 and SLC23A2 coding for vitamin C transporter proteins associated with aggressive (AgP) and chronic periodontitis (CP).Material and MethodsEmployment of three independent case-control samples of AgP (I. 283 cases, 979 controls; II. 417 cases, 1912 controls; III. 164 cases, 357 controls) and one sample of CP (1359 cases, 1296 controls).ResultsStage 1: Among the tested single-nucleotide polymorphisms (SNPs), the rare allele (RA) of rs6596473 in SLC23A1 showed nominal significant association with AgP (p = 0.026, odds ratio [OR] 1.26, and a highly similar minor allele frequency between different control panels. Stage 2: rs6596473 showed no significant association with AgP in the replication with the German and Dutch case-control samples. After pooling the German AgP populations (674 cases, 2891 controls) to significantly increase the statistical power (SP = 0.81), rs6596473 RA showed significant association with AgP prior to and upon adjustment with the covariates smoking and gender with padj = 0.005, OR = 1.35. Stage 3: RA of rs6596473 showed no significant association with severe CP.ConclusionSNP rs6596473 of SLC23A1 is suggested to be associated with AgP. These results add to previous reports that vitamin C plays a role in the pathogenesis of periodontitis.

Aim To evaluate the periodontal status of single-rooted endodontically treated teeth (ET), correcting for patient- and tooth-related factors. Methods Clinical parameters (BoP,PD,CAL) of 240 ET and 240 contralateral vital teeth (VT), before and after non-surgical periodontal treatment, were extracted retrospectively from the journals of 175 patients. Possible patient-related (age, gender, smoking status) and tooth-related (interproximal restoration, root canal filling's extent, post, tooth type) confounders were tested. Results At baseline, frequency of BoP at an interproximal site at ET versus VT was 70.4% versus 65.0%, respectively. The frequency of teeth with interproximal PD ≥5 mm and CAL ≥5 mm was 47.9% versus 42.9% and 54.6% versus 49.6% at ET and VT, respectively. Interproximal PD and CAL at ET versus VT were 3.86 versus 3.61 mm and 4.11 versus 3.95 mm. After correcting for tooth-related factors, no significant differences were observed between ET and VT. An improper restoration had a significant (p

Background— Genetic studies demonstrated the presence of risk alleles in the genes ANRIL and CAMTA1/VAMP3 that are shared between coronary artery disease (CAD) and periodontitis. We aimed to identify further shared genetic risk factors to better understand conjoint disease mechanisms. Methods and Results— In-depth genotyping of 46 published CAD risk loci of genome-wide significance in the worldwide largest case–control sample of the severe early-onset phenotype aggressive periodontitis (AgP) with the Illumina Immunochip (600 German AgP cases, 1448 controls) and the Affymetrix 500K array set (283 German AgP cases and 972 controls) highlighted ANRIL as the major risk gene and revealed further associations with AgP for the gene PLASMINOGEN ( PLG ; rs4252120: P =5.9×10 −5 ; odds ratio, 1.27; 95% confidence interval, 1.3–1.4 [adjusted for smoking and sex]; 818 cases; 5309 controls). Subsequent combined analyses of several genome-wide data sets of CAD and AgP suggested TGFBRAP1 to be associated with AgP (rs2679895: P =0.0016; odds ratio, 1.27 [95% confidence interval, 1.1–1.5]; 703 cases; 2.143 controls) and CAD ( P =0.0003; odds ratio, 0.84 [95% confidence interval, 0.8–0.9]; n=4117 cases; 5824 controls). The study further provides evidence that in addition to PLG , the currently known shared susceptibility loci of CAD and periodontitis, ANRIL and CAMTA1/VAMP3 , are subjected to transforming growth factor-β regulation. Conclusions— PLG is the third replicated shared genetic risk factor of atherosclerosis and periodontitis. All known shared risk genes of CAD and periodontitis are members of transforming growth factor-β signaling.

Miller's is the most commonly used classification of gingival tissue recessions, defined as the displacement of the soft tissue margin apical to the cemento-enamel junction. However, data on the reliability of this classification are missing so far, although reliability, which reflects the consistency of repeated measurements, is regarded as a prerequisite for judging the utility of a classification. The aim of the present study was to evaluate inter- and intra-observer agreement on Miller's classification of gingival tissue recessions. Two hundred photographs (50 of each region: maxillary/mandibular anterior/posterior teeth) of gingival tissue recessions were evaluated twice by four observers with different degrees of experience in Miller's classification, gingival phenotype, tooth shape, and identifiability of the cemento-enamel junction. The following inter- and intra-observer agreements were found: Miller's classification, 0.72 and 0.73-0.95; gingival phenotype, 0.29 and 0.45-0.58; tooth shape, 0.39 and 0.44-0.59; and identifiability of the cemento-enamel junction, 0.21 and 0.30-0.59. A higher agreement was detected for anterior teeth. Further, gingival phenotype (thin-high scalloping) significantly correlated with tooth shape (long-narrow) (ρ = 0.662, p0.001). Miller's classification of gingival tissue recessions was evaluated by four examiners using 200 clinical photographs and yielded substantial to almost perfect agreement, with higher agreement for anterior teeth. Although limited to photographic assessment, the present study offers the so far missing proof on the sufficient inter- and intra-observer agreement of this classification.

AimEpidemiological and clinical studies indicated a relationship of periodontitis with rheumatoid arthritis (RA). We aimed to identify shared genetic susceptibility loci of RA and periodontitis.Materials and MethodsForty-seven risk genes of genome-wide significance of RA and SLE were genotyped in a German case-control sample of aggressive periodontitis (AgP), using Immunochip genotyping arrays (Illumina, 600 cases, 1440 controls) and Affymetrix 500 K Genotyping Arrays (280 cases and 983 controls). Significant associations were replicated in 168 Dutch AgP cases and 679 controls and adjusted for the confounders smoking and sex.ResultsVariants at IRF5 and PRDM1 showed association with AgP. Upon covariate adjustment for smoking and sex, the most strongly associated variant at IRF5 was the rare variant rs62481981 (ppooled = 0.0012, odds ratio [OR] = 3.1, 95% confidence interval [95% CI] = 1.6-6.1; 801 cases, 1476 controls).Within PRDM1 it was rs6923419 (ppooled = 0.004, OR = 0.7, 95% CI = 0.6-0.9; 833 cases, 1440 controls). The associations lost significance after correction for multiple testing in the replication. Both genes are implicated in beta-interferon signalling and are also genome-wide associated with SLE and inflammatory bowel disease.ConclusionThe study gives no definite evidence for a pathogenic genetic link of periodontitis and RA but suggests IRF5 and PRDM1 as shared susceptibility factors.

AimMany studies investigated the role of genetic variants in periodontitis, but few were established as risk factors. We aimed to validate the associations of recent candidate genes in aggressive periodontitis (AgP).Material and MethodsWe analysed 23 genes in 600 German AgP patients and 1441 controls on the Illumina custom genotyping array Immunochip. We tested a suggestive association in a Dutch and German/Austrian AgP case-control sample, and a German chronic periodontitis (CP) case-control sample using Sequenom iPlex assays. We additionally tested the common known risk variant rs1333048 of the gene ANRIL for its association in a Turkish and Italian population.ResultsNone of the analysed genes gave statistical evidence for association. Upon covariate adjustment for smoking and gender, in the pooled German-Austrian AgP sample, IL10 SNP rs6667202 was associated with p = 0.016, OR = 0.77 (95% CI = 0.6-0.95), and in the Dutch AgP sample, adjacent IL10 SNP rs61815643 was associated with p = 0.0009, OR = 2.31 (95% CI = 1.4-3.8). At rs61815643, binding of the transcription factor PPARG was predicted. ANRIL rs1333048 was associated in the Turkish sample (pallelic = 0.026, OR = 1.67 [95% CI = 1.11-2.60]).ConclusionsPrevious 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.

Background: There is an increasing demand from patients for highly esthetic outcomes of implant restorations. Open gingival embrasures – also called ‘black triangles’ – may occur after tooth replac ...

The aim of this study was to test in vitro the effect of enamel matrix derivative (EMD) on the proliferation/viability, migration, and expression of angiogenic factor and adhesion molecules in human umbilical vein endothelial cells (HUVECs). To date, discussions on angiogenic effects of EMD are rather controversial.The effect of EMD on the proliferation/viability of HUVECs after 24 hours was measured using 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl tetrazolium bromide (MTT) assay and direct cell counting. Cell migration was observed in an especially adapted in vitro monolayer wound-healing model. The expression of angiogenic factor angiopoietin-2 (ang-2) and adhesion molecules intercellular adhesion molecule (ICAM)-1 and vascular endothelium-selectin (E-selectin) was quantified with real-time polymerase chain reaction (PCR).The proliferation/viability of HUVECs measured in MTT assay was stimulated by 0.1 microg/ml EMD and inhibited by higher doses (50 to 100 microg/ml), but the total number of cells was not affected. Cell migration in the wound-healing assay was promoted by EMD at doses of 0.1 to 50 microg/ml and inhibited at 100 microg/ml. The highest expression level of all three tested genes (ICAM-1, E-selectin, and ang-2) was observed at 50 microg/ml EMD.The results of the present in vitro study show the potential influence of EMD on the angiogenic activity of HUVECs, which may play an important role in periodontal tissue regeneration and wound healing.