Reporting Quality of the Abstracts for Randomized Controlled Trials in Pediatric Dentistry.

OBJECTIVES: The purpose of this study is to systematically appraise the reporting quality of abstracts for randomized controlled trials (RCT) published in pediatric dentistry using Consolidated Standards of Reporting Trials (CONSORT) for abstracts and to analyze the relationship between the characteristics of the RCT to the quality of abstracts. MATERIALS AND METHODS: RCTs published in Pediatric Dentistry were retrieved from the PubMed database from 2016 to 2021. The quality of abstracts was appraised using CONSORT for abstracts checklist by two independent reviewers. STATISTICAL ANALYSIS: In descriptive statistics, frequency and percentage analysis were used for categorical variables, whereas mean and standard deviation were used for continuous variables. To find the significant difference between the bivariate samples in independent groups, Mann-Whitney U test was employed. Multivariate analysis was performed using Kruskal-Wallis test and Mann-Whitney U tests. Probability value of p-value less than 0.05 was considered as statistically significant. RESULTS: Two hundred abstracts were included in the study. All the abstracts adequately reported the "objective" item, whereas only 2 and 4% of abstracts adequately addressed "randomization" and "harms" items, respectively. A significant relationship was observed between the continent of first author/corresponding author, number of authors, impact factor, adherence to CONSORT guidelines, word count, focus of study, and a priori protocol registration to the quality of abstracts (p < 0.05). CONCLUSION: The abstracts of the RCT included in the study did not adequately follow the CONSORT for abstract guidelines. Adherence to the reporting guidelines would improve the overall reporting quality of abstracts of RCT published in Pediatric Dentistry. The overall mean score of the abstracts was 6.80 out of 15 indicating that the abstracts did not adequately follow the CONSORT for abstract reporting guidelines.

COMPARING THE CLINICAL AND RADIOGRAPHIC OUTCOMES OF PULPOTOMIES IN PRIMARY MOLARS USING BIOACTIVE ENDODONTIC MATERIALS AND FERRIC SULFATE - A SYSTEMATIC REVIEW AND META-ANALYSIS OF RANDOMIZED CLINICAL TRIALS.

OBJECTIVE: To compare the clinical and radiographic outcomes of pulpotomies in primary molars using bioactive endodontic materials and ferric sulfate. DESIGN: The search was conducted in PubMed, Ebscohost, ProQuest, and Scopus databases till June 2021. Children undergoing pulpotomy therapy in primary molars treated with ferric sulfate (FS) and bioactive endodontic materials were evaluated for clinical and radiographic success. Meta-analysis was performed on a random-effects model to assess the success at 6,12,18, and 24 months. The quality of studies was evaluated using the Cochrane risk of bias tool for randomized trials RESULTS: No significant difference was observed between Mineral trioxide aggregate (MTA) and FS at 24 months for both clinical [RR0.98 (95%CI 0.15,6.34), I2 = 0%] and radiographic [RR0.74 (95%CI: 0.23,2.43), I2 = 0%] success. At 6 months [RR1.36 (95%CI: 0.10,19.34), I2 = 33%], no difference was observed in the clinical [RR1.00 (95%CI: 0.95,1.05), I2 = 0%] and radiographic success [RR0.99 (95%CI: 0.88,1.11), I2 = 51%] between Biodentine (BD), FS and radiographic success of calcium enriched cement and FS [RR0.25 (95%CI: 0.03, 2.22), I2 = 0%]. CONCLUSION: Amongst bioactive materials, MTA and FS demonstrated equal success rates in both clinical and radiographic outcomes with follow-up periods of up to 24 months. Future, high-quality trials are required to verify the result of the current review.

Effect of Low-Level Laser Therapy and Platelet-Rich Fibrin on the Treatment of Intra-bony Defects.

Introduction: Attempts to regenerate the periodontal osseous defect, which is lost as a result of periodontal disease, require the tapping of the innate healing potential of periodontium through appropriately designed therapeutic strategies. A multitude of grafted and non-grafted approaches have been used in the management of Intra-bony defects. However, they do not provide predictable periodontal regeneration. The aim of this study was to evaluate the combined effect of low-level laser therapy (LLLT) and platelet-rich fibrin (PRF), in site modulated intra-bony defects (decortication), which were accessed using a simplified papilla preservation flap (SPPF), on the clinical and radiographic outcomes of periodontal disease. Methods: A total of 30 patients with intra-bony defects were recruited for the study and randomly distributed in two groups (n=15). Test group sites were accessed with SPPF and the defects received intra-marrow Penetration (IMP) following debridement and were irradiated with a low-level laser followed by PRF grafting and suturing done. The control group defects were accessed with SPPF and grafted with PRF before being secured by sutures. The plaque and bleeding score, PPD, CAL, and the position of the gingival margin with radiographic defect depth were recorded and analyzed at baseline and six months post-intervention using the student's t test and Wilcoxon signed rank test. Results: The test group showed a clinically relevant increase in mean PPD reduction, CAL gain, and radiographic bone fill (3.6 ± 1.35 mm, 3.26 ± 1.16 mm and 2.44 ± 1.24 mm) compared to the control group (2.93 ±1.1 mm, 2.267 ± 1.33 mm and 1.26 ± 0.99 mm) six months post-intervention. However, intergroup comparison between the test and control groups did not show any statistically significant difference. Conclusion: These results highlights that test protocol had greater amelioration of the effects of periodontal disease and all the investigated clinical and radiographic parameters showed considerable improvement from baseline to 6 months within test and control group, but intergroup comparison between the test and control groups did not show any statistically significant difference, indicating statistical equivalence between the test and control protocol.

Association of Receptor for advanced glycation end products G82S polymorphism with chronic periodontitis in type II diabetic and non-diabetic South Indians.

AIM The current study investigated the association of RAGE G82S polymorphism with chronic periodontitis in South Indians with and without type II Diabetes mellitus. MATERIALS AND METHODS: 405 individuals were enrolled into 3 groups-systemically and periodontally healthy with no attachment loss (n = 135), generalized chronic periodontitis (n = 135)and generalized chronic periodontitis with type II diabetes mellitus(n = 135). Periodontal clinical parameters were recorded. RFLP-PCR was utilized for genotyping. RESULTS: Frequencies of genotype GG, GA and AA were 133, 2, 0 in group I respectively, 131, 4, 0 in group II respectively and 118, 13, 4 in group III respectively. Pearson's Chi squared test demonstrated a significant difference in the genotype distribution between the three groups (χ2 = 19.88,P < 0.001). Fischer exact-test showed that the variant GA/AA genotype was associated with a significantly increased risk for generalized chronic periodontitis in type II diabetics when compared with the GG genotype of systemically and periodontally healthy subjects (OR-9.58, 95% CI 2.168-42.339, P < 0.001) and non-diabetic chronic periodontitis subjects (OR- 4.71, 95% CI: 1.54-14.42, P < 0.05). No association and increased susceptibility to chronic periodontitis was observed in subjects with GA/AA genotype when compared with systemically and periodontally healthy subjects (OR- 2.031, 95% CI: 0.366-11.277 P > 0.05). Furthermore, comparison of clinical parameters based on genotype distribution revealed statistically significant higher mean plaque (P < 0.05) and sulcus bleeding score (P < 0.001) in group-III subjects. CONCLUSION: RAGE G82S gene polymorphism confers susceptibility to generalized chronic periodontitis in type II diabetic subjects of South Indian Tamilian ethnicity.

Estimation of Periostin and Tumour Necrosis Factor-α in Type II Diabetics with Chronic Periodontitis: A case-control study.

BACKGROUND: Periostin, a matricellular protein, is downregulated in chronic inflammatory periodontal disease and is negatively modulated by tumor necrosis factor-α (TNF-α) in human periodontal fibroblast cell culture. The study aimed to estimate the gingival crevicular fluid (GCF) levels of periostin and TNF-α and to discern their relationship in chronic periodontitis (CP) individuals with and without Type II diabetes mellitus (DM). MATERIALS AND METHODS: A total of 60 participants were divided into three groups, with 20 in each group. Group I - systemically and periodontally healthy, Group II - generalized CP, and Group III - generalized CP with Type II DM. Plaque index, gingival index, sulcular bleeding index, probing depth, and clinical attachment level were recorded. GCF periostin and TNF-α were quantified using the enzyme-linked immunosorbent assay. RESULTS: Intergroup comparison was performed using the one-way ANOVA and Kruskal-Wallis. The relationship between the variables was analyzed using the Pearson's and Kendall's Tau correlation. The GCF periostin levels in Groups I, II, and III was 27.52 ± 2.39 ng/mL, 20.18 ± 1.42 ng/mL, and 16.77 ± 3.29 ng/mL, respectively. The GCF TNF-α levels in Groups I, II, and III was 92.41 ± 19.30 ng/L, 118.53 ± 21.93 ng/L, and 147.67 ± 16.35 ng/L, respectively. Periostin decreased, and TNF-α increased in periodontal disease; moreover, periostin level correlated negatively with all the site-specific clinical parameters whereas TNF-α positively correlated (P < 0.001). CONCLUSIONS: TNF-α strongly and negatively downregulates periostin in a chronically inflamed locale leading to compromised integrity of the periodontium.

Evaluation of Association of Vitamin D Receptor Genetic Polymorphism with Severe Chronic Periodontitis in an Ethnic Tamilian Population.

BACKGROUND: Periodontitis is a multifactorial disease characterized by inflammatory responses to increased levels of subgingival pathogens, resulting in connective tissue destruction and alveolar bone loss. The susceptibility of an individual is determined by the complex interplay of the host, genetic, and environmental factors. Vitamin D, a secosteroid hormone, interacts with its nuclear receptor vitamin D receptor (VDR) to regulate crucial biological processes, such as bone metabolism and immune function modulation. Various studies have been conducted in different populations to analyze the association of VDR gene polymorphisms with chronic periodontitis, as these polymorphisms have been demonstrated to play vital roles in the pathogenesis of other diseases. OBJECTIVE: The aim of the present study was to determine the prevalence and association of the VDR TaqI gene polymorphism with severe chronic periodontitis in an Ethnic Tamilian population. MATERIALS AND METHODS: A total of 140 subjects were recruited for the study, of which 70 were diagnosed with severe chronic periodontitis and 70 had healthy gums. Each subject's medical and dental histories were taken, and periodontal examinations were performed. Genomic DNA was extracted and genotyping of the VDR gene at the TaqI site was carried out using polymerase chain reaction/restriction fragment length polymorphism. The frequencies of genotypes and alleles were analyzed between the study groups. RESULTS: The frequency of homozygous TT genotype was 40%, for both the severe chronic periodontitis and the healthy control groups. The distribution of heterozygous Tt genotype was 42.9% in the severe chronic periodontitis group and 47.1% in the healthy control group. The frequency of homozygous tt genotype was 17.1% in the severe chronic periodontitis group and 12.7% in the healthy control group. Although the prevalence of genotype tt and t allele was slightly increased in severe chronic periodontitis patients compared with healthy controls, the frequency of VDR genotype between the study groups was not statistically significant (p-value = 0.751). CONCLUSION: This present study performed in an Ethnic Tamilian population does not support an association between either of the TaqI alleles within the VDR gene and Severe Chronic Periodontitis.