Effect of a multinutrient supplement as an adjunct to nonsurgical treatment of periodontitis: A randomized placebo-controlled clinical trial.

BACKGROUND: The aim of this double-blind randomized placebo-controlled clinical trial was to evaluate the efficacy of a multinutrient supplement as an add-on therapy to scaling and root planing for patients with periodontitis. METHODS: Forty-two patients with stage III or IV periodontitis were randomly allocated to a 2-month treatment of either a multinutrient supplement containing vitamin C, vitamin E, zinc, selenium, alpha-lipoic-acid, cranberry extract, grapeseed extract, and coenzyme Q10 or placebo capsules as an adjunct to conservative periodontal therapy. Periodontal parameters, including probing pocket depth, gingival recession, bleeding on probing, approximal plaque index, and papillary bleeding index, were assessed. Clinical attachment loss, periodontal inflamed surface area, periodontal epithelial surface area, and percentages of pocket sites with ≤3, ≤4, ≥5, ≥6, ≥7, and ≥4 mm with bleeding on probing were calculated. RESULTS: All clinical parameters significantly improved from baseline to reevaluation within each group (p < 0.05). Multinutrient intake resulted in a significantly higher reduction of probing-pocket-depth (-0.75 ± 0.42 mm) and bleeding-on-probing (-21.9 ± 16.1%) from baseline to reevaluation compared with placebo (-0.51 ± 0.30 mm, p = 0.040 and -12.5 ± 9.8%, p = 0.046, respectively). All periodontal parameters showed insignificantly higher improvements in patients receiving the supplement compared with those receiving the placebo (p > 0.05). CONCLUSIONS: Multinutrient supplementation as an adjunct to nonsurgical treatment of periodontitis showed some additional benefit regarding probing-pocket-depth and bleeding-on-probing. However, the clinical relevance needs to be further explored.

Periodontitis prevalence in patients with ulcerative colitis and Crohn's disease - PPCC: A case-control study.

AIM: The aim of this questionnaire-based case-control study was to assess whether self-reported oral health and periodontitis in patients with ulcerative colitis (UC) and Crohn's disease (CD) differ from those in matched controls without inflammatory bowel disease (IBD). MATERIALS AND METHODS: A survey including questions on general anamnestic information, IBD diagnosis, and oral health was distributed online. Self-perceived overall health of teeth and gums, severe periodontitis, and tooth loss were defined as outcome parameters. RESULTS: Analyses were based on answers from 1108 patients with IBD and 3429 controls. Patients with IBD reported significantly worse oral health and more periodontal problems compared to controls. Regression analyses corrected for relevant confounders showed significantly increased odds for fair or poor self-perceived overall health of teeth and gums (odds ratio [OR] 2.147 and 2.736, respectively) and for severe periodontitis (OR 1.739 and 2.574, respectively) for patients with UC and CD compared to controls; patients with CD presented additionally 91% higher odds for having <20 remaining teeth. CONCLUSION: Patients with UC and CD have significantly increased odds for worse self-perceived oral health and severe periodontitis compared to controls, with the former being more severely affected and losing more teeth. It is strongly recommended that patients with IBD are kept under close surveillance to prevent periodontitis development and/or mitigate its progression.

Pneumocephalus as result of nonsurgical peri-implantitis treatment with an air-polishing device for submucosal debridement-A case report.

BACKGROUND: A subcutaneous emphysema is an infrequent but potentially life-threatening complication after dental treatment involving instruments functioning with pressurized air. Emphysemata after the use of high-speed handpieces and air-syringes are well documented, however, more recently several reports on emphysemata produced by air-polishing devices during management of peri-implant biological complications have appeared. To the best of our knowledge, direct development of pneumocephalus after a dental procedure has never been reported before. Introduction of air likely contaminated with oral bacteria to the intracranial space bares the risk of developing meningitis. CASE PRESENTATION: This case report describes the spreading of a subcutaneous emphysema into the intracranial space (i.e., development of a pneumocephalus) after treatment of a peri-implantitis lesion with an air-polishing device equipped with the nozzle for submucosal debridement. A subcutaneous emphysema was noticed during the use of an air-polishing device and the subsequent computed tomography (CT) examination revealed a quite unexpected spreading of the emphysema into the intracranial space. The patient was admitted to the hospital for close surveillance, CT follow-up, and intravenous antibiotics to prevent the development of meningitis due to the introduction of air-likely contaminated with oral bacteria-into the intracranial space. After 3 days, the patient was discharged in good condition without any further complications. CONCLUSION: In case of an extensive subcutaneous emphysema as result of a dental procedure, a more extended radiographic examination including the mediastinal and cranial space should be considered, to assess the risk for potentially life-threatening complications.

The impact of a "successfully treated stable periodontitis patient status" on patient-related outcome parameters during long-term supportive periodontal care.

AIM: To assess the importance of achieving a successfully treated stable periodontitis patient status (PPS) during long-term supportive periodontal care (SPC). MATERIALS AND METHODS: This retrospective cohort study included 100 periodontitis patients, who continued for ≥7.5 years after active periodontal treatment with SPC and were judged as overall adherent. The effect of various predictors on three patient-related outcome parameters was assessed: (1) number of diseased teeth at last SPC, (2) number of teeth lost due to periodontitis, and (3) number of teeth lost due to any reason. RESULTS: One-fifth of the patients were classified as stable after active periodontal treatment. After a mean follow-up of 10.77 years, 24 patients lost 38 teeth due to periodontitis. An unstable PPS and a higher number of diseased teeth per patient at first SPC, and inadequate oral hygiene levels over time, significantly increased the risk for a higher number of diseased teeth per patient at last SPC and for more lost teeth due to periodontitis. However, high adherence to SPC appeared to mitigate the negative effect of an unstable PPS, especially regarding tooth loss due to periodontitis. Further, tooth loss due to any reason was about 3 times higher than tooth loss due to periodontitis and was affected by a larger number of predictors. CONCLUSIONS: Successfully treated patients with a stable PPS maintained a small number of diseased teeth and barely lost any teeth during long-term SPC compared to patients who did not achieve a stable PPS after active periodontal therapy.

Including dental professionals in the multidisciplinary treatment team of head and neck cancer patients improves long-term oral health status.

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.

Epigenetic adaptations of the masticatory mucosa to periodontal inflammation.

BACKGROUND: In mucosal barrier interfaces, flexible responses of gene expression to long-term environmental changes allow adaptation and fine-tuning for the balance of host defense and uncontrolled not-resolving inflammation. Epigenetic modifications of the chromatin confer plasticity to the genetic information and give insight into how tissues use the genetic information to adapt to environmental factors. The oral mucosa is particularly exposed to environmental stressors such as a variable microbiota. Likewise, persistent oral inflammation is the most important intrinsic risk factor for the oral inflammatory disease periodontitis and has strong potential to alter DNA-methylation patterns. The aim of the current study was to identify epigenetic changes of the oral masticatory mucosa in response to long-term inflammation that resulted in periodontitis. METHODS AND RESULTS: Genome-wide CpG methylation of both inflamed and clinically uninflamed solid gingival tissue biopsies of 60 periodontitis cases was analyzed using the Infinium MethylationEPIC BeadChip. We validated and performed cell-type deconvolution for infiltrated immune cells using the EpiDish algorithm. Effect sizes of DMPs in gingival epithelial and fibroblast cells were estimated and adjusted for confounding factors using our recently developed "intercept-method". In the current EWAS, we identified various genes that showed significantly different methylation between periodontitis-inflamed and uninflamed oral mucosa in periodontitis patients. The strongest differences were observed for genes with roles in wound healing (ROBO2, PTP4A3), cell adhesion (LPXN) and innate immune response (CCL26, DNAJC1, BPI). Enrichment analyses implied a role of epigenetic changes for vesicle trafficking gene sets. CONCLUSIONS: Our results imply specific adaptations of the oral mucosa to a persistent inflammatory environment that involve wound repair, barrier integrity, and innate immune defense.

Sex-specific genetic factors affect the risk of early-onset periodontitis in Europeans.

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.

Bacterial colonization of a power-driven water flosser during regular use. A proof-of-principle study.

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.

Does the time-point of orthodontic space closure initiation after tooth extraction affect the incidence of gingival cleft development? A randomized controlled clinical trial.

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."

A combined epigenome- and transcriptome-wide association study of the oral masticatory mucosa assigns CYP1B1 a central role for epithelial health in smokers.

BACKGROUND: The oral mucosa has an important role in maintaining barrier integrity at the gateway to the gastrointestinal and respiratory tracts. Smoking is a strong environmental risk factor for the common oral inflammatory disease periodontitis and oral cancer. Cigarette smoke affects gene methylation and expression in various tissues. This is the first epigenome-wide association study (EWAS) that aimed to identify biologically active methylation marks of the oral masticatory mucosa that are associated with smoking. RESULTS: Ex vivo biopsies of 18 current smokers and 21 never smokers were analysed with the Infinium Methylation EPICBeadChip and combined with whole transcriptome RNA sequencing (RNA-Seq; 16 mio reads per sample) of the same samples. We analysed the associations of CpG methylation values with cigarette smoking and smoke pack year (SPY) levels in an analysis of covariance (ANCOVA). Nine CpGs were significantly associated with smoking status, with three CpGs mapping to the genetic region of CYP1B1 (cytochrome P450 family 1 subfamily B member 1; best p = 5.5 × 10-8) and two mapping to AHRR (aryl-hydrocarbon receptor repressor; best p = 5.9 × 10-9). In the SPY analysis, 61 CpG sites at 52 loci showed significant associations of the quantity of smoking with changes in methylation values. Here, the most significant association located to the gene CYP1B1, with p = 4.0 × 10-10. RNA-Seq data showed significantly increased expression of CYP1B1 in smokers compared to non-smokers (p = 2.2 × 10-14), together with 13 significantly upregulated transcripts. Six transcripts were significantly downregulated. No differential expression was observed for AHRR. In vitro studies with gingival fibroblasts showed that cigarette smoke extract directly upregulated the expression of CYP1B1. CONCLUSION: This study validated the established role of CYP1B1 and AHRR in xenobiotic metabolism of tobacco smoke and highlights the importance of epigenetic regulation for these genes. For the first time, we give evidence of this role for the oral masticatory mucosa.

Screening for periodontal diseases by non-dental health professionals: a protocol for a systematic review and overview of reviews.

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.

Meta-analysis of genome-wide association studies of aggressive and chronic periodontitis identifies two novel risk loci.

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.

Genome-wide association meta-analysis of coronary artery disease and periodontitis reveals a novel shared risk locus.

Evidence for a shared genetic basis of association between coronary artery disease (CAD) and periodontitis (PD) exists. To explore the joint genetic basis, we performed a GWAS meta-analysis. In the discovery stage, we used a German aggressive periodontitis sample (AgP-Ger; 680 cases vs 3,973 controls) and the CARDIoGRAMplusC4D CAD meta-analysis dataset (60,801 cases vs 123,504 controls). Two SNPs at the known CAD risk loci ADAMTS7 (rs11634042) and VAMP8 (rs1561198) passed the pre-assigned selection criteria (PAgP-Ger < 0.05; PCAD < 5 × 10-8; concordant effect direction) and were replicated in an independent GWAS meta-analysis dataset of PD (4,415 cases vs 5,935 controls). SNP rs1561198 showed significant association (PD[Replication]: P = 0.008 OR = 1.09, 95% CI = [1.02-1.16]; PD [Discovery + Replication]: P = 0.0002, OR = 1.11, 95% CI = [1.05-1.17]). For the associated haplotype block, allele specific cis-effects on VAMP8 expression were reported. Our data adds to the shared genetic basis of CAD and PD and indicate that the observed association of the two disease conditions cannot be solely explained by shared environmental risk factors. We conclude that the molecular pathway shared by CAD and PD involves VAMP8 function, which has a role in membrane vesicular trafficking, and is manipulated by pathogens to corrupt host immune defense.

A haplotype block downstream of plasminogen is associated with chronic and aggressive periodontitis.

AIM: The 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 METHODS: The 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. RESULTS: Rs4252120 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 ). CONCLUSIONS: Our findings support a role of genetic variants in PLG in the aetiology of periodontitis.

A genome-wide association study identifies nucleotide variants at SIGLEC5 and DEFA1A3 as risk loci for periodontitis.

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.

Can hyaluronan injections augment deficient papillae at implant-supported crowns in the anterior maxilla? A randomized controlled clinical trial with 6 months follow-up.

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.

Adverse reaction after hyaluronan injection for minimally invasive papilla volume augmentation. A report on two cases.

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.

A root canal filling per se does not have a significant negative effect on the marginal periodontium.

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 < 0.001) negative effect on BoP [OR 3.49 (95%CI: 1.95-6.27)], PD [36.81% (95%CI: 18.52-57.92)] and CAL [27.01% (95%CI: 12.67-43.18)]. No significant differences between ET and VT were observed regarding clinical outcome of non-surgical periodontal therapy. CONCLUSIONS: Presence of a root canal filling per se does not have a significant negative influence on the marginal periodontium, when correcting for the quality of the interproximal restoration.