Prevalence of stable and successfully treated periodontitis subjects and incidence of subsequent tooth loss within supportive periodontal care: A systematic review with meta-analyses.

AIM: To identify (i) the prevalence of meeting the endpoints of 'stable periodontitis' (probing pocket depth [PPD] ≤ 4 mm, bleeding on probing [BoP] < 10%, no BoP at 4 mm sites), 'endpoints of therapy' (no PPD > 4 mm with BoP, no PPD ≥ 6 mm), 'controlled periodontitis' (≤4 sites with PPD ≥ 5 mm), 'PPD < 5 mm' and 'PPD < 6 mm' at the start of supportive periodontal care [SPC]) and (ii) the incidence of tooth loss in relation to not meeting these endpoints within a minimum of 5 years of SPC. MATERIALS AND METHODS: Systematic electronic and manual searches were conducted to identify studies where subjects, upon completion of active periodontal therapy, entered into SPC. Duplicate screening was performed to find relevant articles. Corresponding authors were contacted to confirm inclusion and retrieve required clinical data for further analyses to assess the prevalence of reaching endpoints and incidence of subsequent tooth loss, if available, within at least 5 years of SPC. Meta-analyses were carried out to evaluate risk ratios for tooth loss in relation to not reaching the various endpoints. RESULTS: Fifteen studies including 12,884 patients and 323,111 teeth were retrieved. Achievement of endpoints at baseline SPC was rare (1.35%, 11.00% and 34.62%, respectively, for 'stable periodontitis', 'endpoints of therapy' and 'controlled periodontitis'). Less than a third of the 1190 subjects with 5 years of SPC data lost teeth-a total of 3.14% of all teeth were lost. Statistically significant associations with tooth loss, at the subject-level, were found for not achieving 'controlled periodontitis' (relative risk [RR] = 2.57), PPD < 5 mm (RR = 1.59) and PPD < 6 mm (RR = 1.98). CONCLUSIONS: An overwhelming majority of subjects and teeth do not achieve the proposed endpoints for periodontal stability, yet most periodontal patients preserve most of their teeth during an average of 10-13 years in SPC.

Accuracy of periodontitis diagnosis obtained using multiple molecular biomarkers in oral fluids: A systematic review and meta-analysis.

AIM: To determine the accuracy of biomarker combinations in gingival crevicular fluid (GCF) and saliva through meta-analysis to diagnose periodontitis in systemically healthy subjects. METHODS: Studies on combining two or more biomarkers providing a binary classification table, sensitivity/specificity values or group sizes in subjects diagnosed with periodontitis were included. The search was performed in August 2022 through PUBMED, EMBASE, Cochrane, LILACS, SCOPUS and Web of Science. The methodological quality of the articles selected was evaluated using the QUADAS-2 checklist. Hierarchical summary receiver operating characteristic modelling was employed to perform the meta-analyses (CRD42020175021). RESULTS: Twenty-one combinations in GCF and 47 in saliva were evaluated. Meta-analyses were possible for six salivary combinations (median sensitivity/specificity values): IL-6 with MMP-8 (86.2%/80.5%); IL-1ß with IL-6 (83.0%/83.7%); IL-1ß with MMP-8 (82.7%/80.8%); MIP-1α with MMP-8 (71.0%/75.6%); IL-1ß, IL-6 and MMP-8 (81.8%/84.3%); and IL-1ß, IL-6, MIP-1α and MMP-8 (76.6%/79.7%). CONCLUSIONS: Two-biomarker combinations in oral fluids show high diagnostic accuracy for periodontitis, which is not substantially improved by incorporating more biomarkers. In saliva, the dual combinations of IL-1ß, IL-6 and MMP-8 have an excellent ability to detect periodontitis and a good capacity to detect non-periodontitis. Because of the limited number of biomarker combinations evaluated, further research is required to corroborate these observations.

The effect of plaque control in the treatment of Oral Lichen Planus with gingival manifestations: a Systematic Review.

BACKGROUND: Oral lichen planus (OLP) is a chronic autoimmune disease that frequently affects the oral mucosa. Patients with OLP tend to present with plaque accumulation which may further exacerbate the lichenoid lesion, thus plaque control may improve the quality of life of patients. The aim of this review was to test the effect of plaque control on OLP with gingival manifestations. METHODS: Systematic review following the PRISMA checklist. A search was conducted through Medline, Embase and the Cochrane Library Database up to March 2020 and complemented by a manual search in some relevant journals. Randomised Controlled Trials (RCTs) reporting plaque interventions and their effects in populations with gingival manifestations of OLP, with a follow-up period of at least 3 months were included. Risk of Bias was assessed using the Cochrane Collaboration Tool in Randomised Trials. RESULTS: The initial search generated 89 sources, resulting in final inclusion of three RCTs following full-text reading. The control groups were asked to continue their regular oral hygiene routine, while test groups received additional tailored oral hygiene advice as the intervention. Two of the included papers had sufficiently similar design to be included in meta-analysis. The oral hygiene intervention was associated with improvements in clinical disease status (Escudier index) and patient-reported outcomes (OHIP-14) from baseline compared with the control group. Differences in visual analogue scores for pain between groups were not statistically different between test and control groups. Two studies were judged to have low risk of bias, while one (not included in meta-analysis) had high risk of bias. CONCLUSION: Improvements in disease and patient-reported outcomes can occur as a result of oral hygiene instruction in patients with gingival manifestations of OLP.

Expression of gingival crevicular fluid markers during early and late healing of intrabony defects after surgical treatment: a systematic review.

BACKGROUND: Surgical treatments such as guided tissue regeneration (GTR) and access flap surgery are widely employed for the treatment of intrabony defects. However, little is known regarding the postoperative expression of gingival crevicular fluid (GCF) markers. OBJECTIVE: The aim of this systematic review was to compare the expression of GCF markers following treatment of periodontal intrabony defects with guided tissue regeneration or access surgery. The association of the markers' expression with the clinical outcome was also assessed. METHODS: An electronic literature search was conducted in MEDLINE, EMBASE, OpenGrey, LILACS and Cochrane Library up to December 2018 complemented by a manual search. Human, prospective clinical studies were identified. The changes from baseline up to 30 days (early healing) and 3 months (late healing) were assessed. RESULTS: A total of 164 publications were identified and reviewed for eligibility. Of these, 10 publications fulfilled the inclusion criteria. The included studies evaluated 15 different GCF markers with a follow-up time between 21 and 360 days postoperatively. PDGF, VEGF and TIMP-1 changes were often investigated in the included studies; however, contrasting results were reported. Two studies agreed that both GTR and OFD lead to similar OPG level changes. TGF-ß1 is increased early postoperatively, irrespective of the surgical technique employed. CONCLUSION: There is limited evidence available on the expression of GCF markers after surgical interventions of intrabony periodontal defects. However, OPG and TGF-ß1 tend to increase early post-operatively, irrespective of the surgical technique employed, irrespective of the surgical technique employed. CLINICAL RELEVANCE: More well-designed, powered studies with sampling periods reflecting the regenerative process are needed, and future research should focus on employing standardised protocols for collecting, storing and analysing GCF markers.

Radiographic morphology of intrabony defects in the first molars of patients with localized aggressive periodontitis: Comparison with health and chronic periodontitis.

BACKGROUND AND OBJECTIVE: The aim of this study was to describe the radiographic features of the first molars of patients with localized aggressive periodontitis (LAgP) and of their associated intrabony defects and to compare them with a control sample of chronic periodontitis cases and healthy subjects. METHODS: Data from a total of 93 patients were included in this analysis. First, dental panoramic tomograms of 34 patients with LAgP (131 first molars) and 30 periodontally healthy patients (110 first molars) were compared. Then, periapical radiographs of the first molars of the same patients with LAgP and of 29 patients with chronic periodontitis affected by intrabony defects were analysed. RESULTS: Shorter root trunks were associated with the presence of intrabony defects in patients with LAgP (P = .002 at multilevel logistic regression), also when LAgP molars were compared with healthy subjects (P = .036). Although no difference in defect depth and angle was noted between LAgP and chronic periodontitis intrabony defects, LAgP intrabony defects appeared to be more frequently symmetrical and arch-shaped than in chronic periodontitis (P = .008), with positive predictive value and negative predictive value of for 'wide arch' defect of 87.3% (95% CI = 77.2%-93.3%) and 32.3% (95% CI = 27.7%-37.2%) respectively. CONCLUSION: First molars of patients with LAgP affected by intrabony defects may have some distinct radiographic anatomical characteristics to those of healthy subjects. The shape of intrabony defects seems to differ between LAgP and chronic periodontitis cases. Further studies need to confirm these features and investigate if they are related to the initiation and progression of periodontitis.

Leukocyte receptor expression in chronic periodontitis.

BACKGROUND AND OBJECTIVE: Microbial recognition in the periodontium through specific leukocyte receptors gives rise to the response which in susceptible individuals can lead to periodontal diseases. The aim of this study was to explore the expression of leukocyte receptors in the gingival tissues of chronic periodontitis patients and to analyse differences between diseased and control sites (sites with probing pocket depth <4 mm). MATERIAL AND METHODS: Thirty-seven chronic periodontitis patients were included in the study. Gingival biopsies were harvested from diseased and control sites and processed by flow cytometry for the determination of the expression of 16 leukocyte receptors (CD4, CD8, CD11b, CD14, CD16, CD19, CD25, CD28, CD49d, CD49e, CD62, CD71, CD80, CCR7, Ly6G and HLA-DR). RESULTS: Expression of all studied receptors was higher in test compared with control sites (p < 0.005). Sampled sites with less bleeding on probing exhibited higher expression of CD16 and CD14 receptors (p = 0.020 and 0.011, respectively). CONCLUSIONS: This study points towards considerable differences in the expression of leukocyte receptors between diseased and control sites in the same periodontal patients.

Lipid subclasses profiles and oxidative stress in aggressive periodontitis before and after treatment.

BACKGROUND AND OBJECTIVE: Associations between dyslipidaemia, oxidative stress and periodontitis have emerged in recent years. However, there is a lack of studies investigating these associations in aggressive periodontitis (AgP) cases. The aim of this study was to investigate the lipid and oxidative stress profiles in patients with AgP, and to relate them to clinical variables and interleukin (IL)-6 genetic variants. MATERIAL AND METHODS: Twelve non-smoking Caucasian patients with AgP selected based on their IL6 haplotypes underwent periodontal non-surgical and surgical treatment. Peripheral blood samples taken at baseline and at six different time-points after treatment were processed to determine IL-6 circulating levels, lipid profiles (cholesterol, triglycerides, high-density lipoprotein [HDL] and low-density lipoprotein [LDL] subclasses) and oxidative stress markers (glutathione and total lipid hydroperoxide levels). RESULTS: HDLs were the most prevalent lipoproteins, followed by intermediate-density lipoprotein, very-low-density lipoprotein and LDL. The LDL subclasses consisted mainly of the less atherogenic large LDL. The lipid profile did not consistently change after treatment up to 3 mo after surgery. Periodontal disease severity was associated with LDL levels and size. The IL6 haplotypes were associated with total cholesterol, triglycerides, HDL and LDL subclasses after adjusting for confounders. IL-6 circulating levels were associated with both very-low-density lipoprotein and lipid hydroperoxide levels. CONCLUSION: Based on these data, we conclude that both periodontal disease severity and IL6 haplotypes may influence lipid profiles in AgP.

Linkage analysis confirms heterogeneity of hereditary gingival fibromatosis.

OBJECTIVES: Hereditary Gingival Fibromatosis (HGF) is a rare benign fibrous lesion of the gingival tissues presumably caused by single gene defects. The aim of this study was to identify the genetic defect leading to HGF in an extended pedigree. MATERIALS AND METHODS: We report the clinical features and genetic analysis of a family affected by HGF. A total of 17 subjects were assessed clinically and had blood samples taken for DNA extraction. Multipoint parametric linkage analysis was performed to identify the possible chromosomal location responsible for HGF in this family. RESULTS: Presence of severe HGF associated with tooth impaction was confirmed for seven members of this three-generation family. Linkage analysis revealed that loci on chromosomes 7, 10, 13, 15, 16, 17, 19 and 20 were linked to this trait. Previously found mutations in the SOS1 and GINGF loci were therefore excluded by this analysis. CONCLUSIONS: This study brings further evidence for genetic heterogeneity of HGF and points towards the existence of different, not-yet-identified genes linked to this condition.

Influence of IL-6 haplotypes on clinical and inflammatory response in aggressive periodontitis.

OBJECTIVES: The aim of this study was to investigate the inflammatory response in aggressive periodontitis (AgP) patients after periodontal therapy and associate these changes to subjects' interleukin-6 (IL-6) genetic variants. MATERIALS AND METHODS: Twelve non-smoking UK Caucasian patients with AgP were selected based on their IL6 haplotypes (six haplotype positive and six haplotype negative based on polymorphisms rs 2069827 and rs 2069825) and underwent full mouth non-surgical periodontal therapy, followed by open flap surgery. Gingival crevicular fluid (GCF) and peripheral blood samples were taken at baseline and at six different time points after treatment. Gingival biopsy samples were harvested during surgery and underwent immunohistochemical analysis for identification of IL-6. RESULTS: An overall improvement in clinical periodontal parameters was observed following periodontal therapy. Haplotype status was associated with clinical presentation, Aggregatibacter actinomycetemcomitans counts in subgingival plaque samples, white cell count, neutrophils, red cell count and haemoglobin. GCF IL-6 concentrations increased dramatically 1 day after surgery and IL-6 haplotype-positive subjects exhibited a higher magnitude in this increase. CONCLUSIONS: IL6 haplotypes may have an effect on clinical presentation and magnitude and kinetics of local and systemic inflammatory responses following non-surgical and surgical periodontal therapy in aggressive periodontitis. CLINICAL RELEVANCE: Detecting IL-6 haplotype-positive periodontitis patients might become helpful in identifying subjects prone to excessive inflammatory response and increased periodontal breakdown.

Host Genotype Links to Salivary and Gut Microbiota by Periodontal Status.

Limited evidence describing how host genetic variants affect the composition of the microbiota is currently available. The aim of this study was to assess the associations between a set of candidate host genetic variants and microbial composition in both saliva and gut in the TwinsUK registry. A total of 1,746 participants were included in this study and provided stool samples. A subset of 1,018 participants also provided self-reported periodontal data, and 396 of those participants provided a saliva sample. Host DNA was extracted from whole-blood samples and processed for Infinium Global screening array, focusing on 37 selected single-nucleotide polymorphisms (SNPs) previously associated with periodontitis. The gut and salivary microbiota of participants were profiled using 16S ribosomal RNA amplicon sequencing. Associations between genotype on the selected SNPs and microbial outcomes, including α diversity, ß diversity, and amplicon sequence variants (ASVs), were investigated in a multivariate mixed model. Self-reported periodontal status was also compared with microbial outcomes. Downstream analyses in gut microbiota and salivary microbiota were carried out separately. IL10 rs6667202 and VDR 2228570 SNPs were associated with salivary α diversity, and SNPs in IL10, HSA21, UHRF2, and Fc-γR genes were associated with dissimilarity matrix generated from salivary ß diversity. The SNP that was associated with the greatest number of salivary ASVs was VDR 2228570 followed by IL10 rs6667202, and that of gut ASVs was NPY rs2521364. There were 77 salivary ASVs and 39 gut ASVs differentially abundant in self-reported periodontal disease versus periodontal health. The dissimilarity between saliva and gut microbiota within individuals appeared significantly greater in self-reported periodontal cases compared to periodontal health. IL10 and VDR gene variants may affect salivary microbiota composition. Periodontal status may drive variations in the salivary microbiota and possibly, to a lesser extent, in the gut microbiota.

Interleukin-6 in oral diseases: a review.

Interleukin-6 (IL-6) is a pleomorphic cytokine involved in a number of physiologic and pathologic processes including response to trauma and infection and development and progression of inflammation and malignancy. IL-6 is emerging as an important mediator and novel therapeutic target for chronic inflammatory diseases and cancer. The present study reviews the available evidence regarding the association between IL-6 and a range of oral diseases including infections (periodontal disease and endodontic infections), immunologically mediated disorders (oral lichen planus and Sjögren's syndrome) and malignancy (oral cancer and precancer). The role of common genetic variants of IL-6 in determining individual susceptibility to certain oral diseases, as well as novel therapeutic strategies based on IL-6 inhibition are also discussed.

Patterns of subgingival microbiota in different periodontal phenotypes.

OBJECTIVES: To compare the subgingival microbiota of patients with aggressive (AgP) or chronic periodontitis (CP) to healthy (H), non-periodontitis patients as well as to explore their relevant associations to different host genetic variants. METHODS: Following clinical examination, blood and subgingival plaque sampling of 471 study participants (125 AgP, 121 CP, 225 H), subgingival community analysis was performed by next generation sequencing of the 16S rRNA. Microbial data from 266 participants (75 AgP, 95 CP, 98 H) were available for analysis. SNPs in the IL6, IL6R and FTO gene were selected for genetic marker analyses. RESULTS: Combined periodontitis patients (AgP + CP), particularly those classified with AgP, exhibited lower alpha- and beta- diversity. Several genera (including Peptostreptococcaceae, Filifactor, Desulfobulbus, Tannerella and Lachnospiracee) and species were over-abundant in combined periodontitis vs. healthy individuals, while other genera such as Prevotella or Dialister were found to be more abundant in healthy cases. The only genus with difference in abundance between AgP and CP was Granulicatella. No associations between IL6, IL6RA and FTO genetic variants and microbial findings were detected. CONCLUSION: This study suggests that limited microbial differences existed between AgP and CP and challenges the current notion that periodontitis is associated with increased subgingival microbial diversity compared with periodontal health. CLINICAL SIGNIFICANCE: The findings of this study cast some doubts on the notion that the dysbiosis characteristic of periodontal disease is expressed as increased microbial diversity.

IL6 -174 genotype associated with Aggregatibacter actinomycetemcomitans in Indians.

AIM: Genetic factors have recently been associated with presence of Aggregatibacter actinomycetemcomitans subgingivally in populations living in industrialized countries. The aim of this study was to analyse associations between Interleukin-6 (IL6) single nucleotide polymorphisms and presence and levels of A. actinomycetemcomitans and other subgingival microbes in a rural Indian population. SUBJECTS AND METHODS: A total of 251 individuals from a rural village in India with a periodontal phenotype ranging from healthy to severe periodontitis were included. Checkerboard DNA-DNA analysis was performed to detect 40 periodontal taxa in subgingival plaque samples. Genomic DNA was extracted to genotype five polymorphisms in the IL6 promoter region. RESULTS: The IL6-74 GG genotype was associated with high (above median) counts of A. actinomycetemcomitans (both in all subjects and in periodontally healthy only) and with presence and counts of Capnocytophaga sputigena. Differences in detection of several other bacteria were noted between periodontitis and healthy subjects. CONCLUSIONS: These findings support the influence of genetic factors on the subgingival microbiota.

Subgingival periodontal pathogens in Down syndrome children without periodontal breakdown. A case-control study on deciduous teeth.

AIM: Down syndrome is the most common form of aneuploidia compatible with a long survival. The affected subjects are more susceptible to severe early-onset periodontal disease and show a lower risk to develop dental caries than the non-affected population. This study investigated the prevalence of periodontal pathogens in the subgingival plaque of deciduous teeth in children with Down syndrome without signs of periodontal breakdown. METHODS: Thirty children suffering from Down syndrome and 46 matched healthy subjects were studied. A total of 228 subgingival plaque samples from deciduous teeth were separately collected and evaluated by polymerase chain reaction assays. CONCLUSION: In absence of periodontal impairment, Down syndrome children display a clear presence of periodontal pathogens already in the deciduous dentition. The hypothesis of an intrinsic predisposing condition is here supported.

Application of label-free absolute quantitative proteomics in human gingival crevicular fluid by LC/MS E (gingival exudatome).

Periodontal disease is perhaps the most common infectious disease in humans. Gingival crevicular fluid (GCF) is a local inflammatory exudate of the periodontal tissues. Its composition greatly varies between health and periodontal disease. GCF collection is rapid and noninvasive, but previous approaches aiming to analyze its composition have mainly involved single protein biomarkers. The aim of this study was to perform analysis of the GCF exudatome from healthy and periodontally diseased sites by LC/MS(E), a label-free mass spectrometry method that enables simultaneous protein identification and absolute quantification in biological fluids. In total, 154 proteins of human, bacterial, and viral origin were identified in the 40 GCF samples obtained from the 10 subjects (five healthy and five generalized aggressive periodontitis). The proportion of bacterial, viral, and yeast protein was increased in disease, compared to health. The presence of host defense-related proteins, such as Cystatin-B and defensins, was confirmed to be present only in health. Among the newly identified GCF proteins were L-plastin detected only in disease (15.6 +/- 12.1 fmol) and Annexin-1 detected in 5-fold higher levels in health. Nevertheless, pro-inflammatory cytokines or periodontal pathogen proteins were rarely detected. Conclusively, the LC/MS(E) technology may facilitate characterization of GCF proteome in periodontal health and disease, thus conferring prognostic and diagnostic value. Larger cohort studies are required to characterize the complete GCF proteome in health and disease.

The perceived impact of Covid-19 on periodontal practice in the United Kingdom: A questionnaire study.

INTRODUCTION: COVID-19 has impacted dentistry in unprecedented ways. OBJECTIVE: The following research aimed to investigate the impact of the COVID-19 pandemic on periodontal practice in the United Kingdom using the COM-B (Capability Opportunity Motivation-Behaviour) model as the basis for a questionnaire. BASIC RESEARCH DESIGN: An online survey link was sent to all members of the British Society of Periodontology and Implant Dentistry. A total of 358 responses were received and analysed. RESULTS: The great majority of participants thought that the pandemic had an impact on their profession, while only 4.7 % had no concerns. The main worries related to financial concerns and ability to provide appropriate levels of care. More than 80 % of respondents agreed that their establishment was compliant with infection control procedures. Some participants felt benefits mainly in terms of more time for CPD activities. It was felt that some of the changes needed will need to be sustained long-term. CONCLUSIONS: Respondents were generally worried. However, they perceived they had the physical and psychological ability to effect changes to their practice, higher than the physical and social opportunities that they were afforded. Although the COVID-19 pandemic is causing profound changes and worries for the profession of Periodontology, clinicians are clear about their capability to control the situation and feel they have the motivation to make the required changes. CLINICAL SIGNIFICANCE: COVID-19 has presented clinicians with novel challenges. Investigating the professional response to change and expected impact is of interest in the current climate as we navigate the 'new normal'. Assessing the results could be useful in informing support strategies moving forward.

Heritability of periodontitis: A systematic review of evidence from animal studies.

OBJECTIVE: The aim of this study was to quantify the heritability of periodontitis via a systematic appraisal of the existing evidence derived from animal studies. DESIGN: A search was conducted through the electronic databases MEDLINE, Embase, LILACS, Cochrane Library, Open Grey, Google Scholar and ResearchGate, complemented by a hand search, for studies reporting measures of heritability of periodontitis. After full-text reading, 7 studies conducted on animal models met the inclusion criteria. Six studies carried out experimental periodontitis models in mice, while one study assessed bone loss in dry skulls of baboons with known pedigrees. RESULTS: Heritability of 'naturally-occurring bone loss' (3 studies, non-experimental conditions) was estimated at 0.39 (95% confidence interval: 0.13-0.64) with virtually no heterogeneity (I2 = 0%, p = 0.97). Heritability of experimental periodontitis in mice (6 studies) was 0.43 (0.28-0.58) with considerable heterogeneity (I2 = 96%, p < 0.01). There was no evidence of publication bias. CONCLUSIONS: Over a third of the phenotypic variance of periodontitis in animal studies is due to genetic factors, somewhat higher than the estimate from human studies. It can be argued that, under the strictly-controlled experimental conditions of laboratory-induced periodontitis, the relative role of heritable factors predisposing to periodontitis and bone loss may be stronger compared with human studies.

Association between periodontitis and common variants in the promoter of the interleukin-6 gene.

We recently reported an association between interleukin-6 (IL6) polymorphisms (SNPs) and haplotypes and aggressive periodontitis (AgP). The aim of this study was to investigate this association in a larger cohort of subjects, affected by either aggressive or chronic periodontitis. Five IL6 SNPs were analyzed in 765 subjects (167 generalized aggressive periodontitis, 57 localized aggressive, 310 chronic periodontitis and 231 periodontally healthy). Among Caucasians (n=454) there were moderate associations for -1363T allele (p=0.011) and for -174GG and -1363GG genotypes with diagnosis of periodontitis (respectively, p=0.044, OR=1.6, 95% CI=1.0-2.4, and p=0.017, OR=1.8, 95% CI=1.1-2.8, adjusted for age, gender and smoking). Haplotypes containing the -174G>C, -1363G>T and -1480C>G polymorphisms were associated with diagnosis of periodontitis (p=0.02). Subgroup analysis by disease phenotype showed associations for the localized AgP (LAgP) group and -1480C>G and -6106A>T SNPs (p=0.007 and 0.010, respectively). Among Caucasians the genotypes IL6 -1480 CC and -6106 TT increased the adjusted OR for LAgP (OR=3.09 and 2.27, respectively). This study supports the hypothesis that IL6 polymorphisms and haplotypes are moderately associated with periodontitis, possibly acting through influencing tissue levels of IL6. This association is stronger for LAgP than for other periodontal disease phenotypes.

Minimally invasive non-surgical vs. surgical approach for periodontal intrabony defects: a randomised controlled trial.

BACKGROUND: Periodontal intrabony defects are usually treated surgically with the aim of increasing attachment and bone levels and reducing risk of progression. However, recent studies have suggested that a minimally invasive non-surgical therapy (MINST) leads to considerable clinical and radiographic defect depth reductions in intrabony defects. The aim of this study is to compare the efficacy of a modified MINST approach with a surgical approach (modified minimally invasive surgical therapy, M-MIST) for the treatment of intrabony defects. METHODS: This is a parallel-group, single-centre, examiner-blind non-inferiority randomised controlled trial with a sample size of 66 patients. Inclusion criteria are age 25-70, diagnosis of periodontitis stage III or IV (grades A to C), presence of ≥ 1 'intrabony defect' with probing pocket depth (PPD) > 5 mm and intrabony defect depth ≥ 3 mm. Smokers and patients who received previous periodontal treatment to the study site within the last 12 months will be excluded. Patients will be randomly assigned to either the modified MINST or the M-MIST protocol and will be assessed up to 15 months following initial therapy. The primary outcome of the study is radiographic intrabony defect depth change at 15 months follow-up. Secondary outcomes are PPD and clinical attachment level change, inflammatory markers and growth factors in gingival crevicular fluid, bacterial detection, gingival inflammation and healing (as measured by geometric thermal camera imaging in a subset of 10 test and 10 control patients) and patient-reported outcomes. DISCUSSION: This study will produce evidence about the clinical efficacy and potential applicability of a modified MINST protocol for the treatment of periodontal intrabony defects, as a less invasive alternative to the use of surgical procedures. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03797807. Registered on 9 January 2019.

What Is the Heritability of Periodontitis? A Systematic Review.

The aim of this study was to systematically appraise the existing literature on the yet-unclear heritability of gingivitis and periodontitis. This review was conducted following the PRISMA guidelines. A search was conducted through the electronic databases Medline, Embase, LILACS, Cochrane Library, Open Grey, Google Scholar, and Research Gate, as complemented by a hand search, for human studies reporting measures of heritability of gingivitis and periodontitis. A total of 9,037 papers were initially identified from combined databases and 10,810 on Google Scholar. After full-text reading, 28 articles met the inclusion criteria and were carried forward to data abstraction. The reviewed data included information from >50,000 human subjects. Meta-analyses were performed by grouping studies based on design and outcome. Heritability ( H2) of periodontitis was estimated at 0.38 (95% CI, 0.34 to 0.43; I2 = 12.9%) in twin studies, 0.15 (95% CI, 0.06 to 0.24; I2 = 0%) in other family studies, and 0.29 (95% CI, 0.21 to 0.38; I2 = 61.2%) when twin and other family studies were combined. Genome-wide association studies detected a lower heritability estimate of 0.07 (95% CI, -0.02 to 0.15) for combined definitions of periodontitis, increasing with disease severity and when the interaction with smoking was included. Furthermore, heritability tended to be lower among older age groups. Heritability for the self-reported gingivitis trait was estimated at 0.29 (95% CI, 0.22 to 0.36; I2 = 37.6%), while it was not statistically significant for clinically measured gingivitis. This systematic review brings forward summary evidence to confirm that up to a third of the periodontitis variance in the population is due to genetic factors. This seems consistent across the different studied populations and increases with disease severity. In summary, up to a third of the variance of periodontitis in the population is due to genetic factors, with higher heritability for more severe disease.