Background/Objectives: Dental plaque is a significant contributor to various prevalent oral health conditions, including caries, gingivitis, and periodontitis. Consequently, its detection and management are of paramount importance for maintaining oral health. Manual plaque assessment is time-consuming, error-prone, and particularly challenging in uncooperative pediatric patients. These limitations have encouraged researchers to seek faster, more reliable methods. Accordingly, this study aims to develop a deep learning model for detecting and segmenting plaque in young permanent teeth and to evaluate its diagnostic precision. Methods: The dataset comprises 506 dental images from 31 patients aged between 8 and 13 years. Six state-of-the-art models were trained and evaluated using this dataset. The U-Net Transformer model, which yielded the best performance, was further compared against three experienced pediatric dentists for clinical feasibility using 35 randomly selected images from the test set. The clinical trial was registered on under the ID NCT06603233 (1 June 2023). Results: The Intersection over Union (IoU) score of the U-Net Transformer on the test set was measured as 0.7845, and the p-values obtained from the three t-tests conducted for comparison with dentists were found to be below 0.05. Compared with three experienced pediatric dentists, the deep learning model exhibited clinically superior performance in the detection and segmentation of dental plaque in young permanent teeth. Conclusions: This finding highlights the potential of AI-driven technologies in enhancing the accuracy and reliability of dental plaque detection and segmentation in pediatric dentistry.

The present study aimed to (1) investigate biocompatibility and cytotoxicity of pulp-capping materials on viability of human dental pulp stem cells (hDPSCs); (2) determine angiogenic, odontogenic, and osteogenic marker mRNA expressions; and (3) observe changes in surface morphology of the hDPSCs using scanning electron microscopy (SEM). Impacted third molars were used to isolate the hDPSCs, which were treated with extract-release fluids of the pulp-capping materials (Harvard BioCal-Cap, NeoPUTTY MTA, TheraCal LC, and Dycal). Effects of the capping materials on cell viability were assessed using 3-(4,5-di-methyl-thiazol-2-yl)-5-(3-carboxy-methoxy-phenyl)-2-(4-sulfo-phenyl)-2H-tetrazolium (MTS) assay and the apoptotic/necrotic cell ratios and reactive oxygen species (ROS) levels from flow cytometry. Marker expressions (alkaline phosphatase [ALP], osteocalcin [OCN], collagen type I alpha 1 [Col1A], secreted protein acidic and rich in cysteine [SPARC], osteonectin [ON], and vascular endothelial growth factor [VEGF]) were determined by quantitative reverse-transcription polymerase chain reaction. Changes in surface morphology of the hDPSCs were visualised by SEM. The MTS assay results at days 1, 3, 5, and 7 indicated that Harvard BioCal-Cap, NeoPUTTY MTA, and TheraCal LC did not adversely affect cell viability when compared with the control group. According to the MTS assay results at day 14, no significant difference was found amongst Dycal, Harvard BioCal-Cap, NeoPUTTY MTA, and TheraCal LC affecting cell viability. Dycal was the only capping material that increased ROS level. High levels of VEGF expression were observed with Harvard BioCal-Cap, TheraCal LC, and NeoPUTTY MTA. NeoPUTTY MTA, and Dycal upregulated OCN expression, whereas TheraCal LC upregulated Col1A and SPARC expression. Only Dycal increased ALP expression. HDSCs were visualized in characteristic spindle morphology on SEM when treated with TheraCal LC and Harvard BioCal-Cap. NeoPUTTY MTA and Harvard BioCal-Cap showed suitable biocompatibility values; in particular, these pulp-capping materials were observed to support the angiogenic marker.

Kök malformasyonları çeşitli genetik ve çevresel faktörlerin bir sonucu olarak ortaya çıkabilmektedir. Kök gelişimi sırasında meydana gelen problemler enfeksiyon, travma, kemoterapi veya radyasyon tedavisine bağlı oluşabilmektedir. Yakın zamanda tanımlanan bir dental anomali olan molar keser malformasyonu veya molar keser kök malformasyonu, daimi birinci molar dişlerin köklerinde görülen gelişim bozuklukları ile karakterizedir. Aynı zamanda süt ikinci molar ve maksiller daimi santral keser dişleri etkileyebilmektedir. Molar keser kök malformasyonu veya molar keser malformasyonu, erken çocukluk döneminde maruz kalınan farklı çevresel faktörler sebebiyle diş köklerinin anormal oluşumu ile ilişkilendirilmiştir. Bu anomalinin görüldüğü dişlerden, molar dişler normal kron morfolojisine sahip olup ancak radyografi ile teşhis edilebilirken, keser dişler de kron morfoloji etkilenmiştir. Bu dişlerde herhangi bir çürük veya kron deformitesi olmaksızın enfeksiyon ve periodontal hastalık görülebilmektedir. Tedavi için ilk seçenek, doğru zamanda dişlerin çekimi ve ikinci daimi molar dişlerin oluşan boşluğuna doğru sürdürülmesi olabilmektedir. Malforme kökler ve kalsifiye pulpa dokusu sebebi ile endodontik tedavinin çok zor olduğu belirtilmektedir. Güncel klinik ve radyografik teşhis ve tedavi yöntemlerinin uygulandığı farklı vaka raporları bulunmaktadır. Bu derlemenin amacı, ‘Molar Keser Malformasyonu’ olarak adlandırılan anomalinin güncel literatür ışığında değerlendirilmesidir.

Background/Objectives: Early childhood caries (ECC) is a chronic inflammatory condition that may impose a systemic burden in pediatric patients. This study aimed to evaluate the association between dental caries severity, classified by dmft (decayed, missing, and filled teeth for primary dentition) scores, and preoperative systemic inflammatory markers derived from routine complete blood counts (CBC). Methods: This retrospective study included 159 children aged 36–71 months. Participants were categorized into three groups based on dmft scores: low (0–3), medium (4–8), and high (≥9). Hematological parameters and inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII), were analyzed using one-way ANOVA with post hoc comparisons. Results: Significant differences were observed among dmft groups for neutrophil and lymphocyte percentages (p = 0.026 and p = 0.027) and lymphocyte count (p = 0.020). The medium severity group demonstrated higher neutrophil levels and lower lymphocyte values compared to the high severity group (p < 0.05). Although overall group differences for NLR and SII were not statistically significant (p > 0.05), both markers were significantly higher in the medium group than in the high group (p < 0.05). No significant differences were found in hemoglobin, RDW, or platelet parameters. Conclusions: A non-linear trend was observed, with relatively elevated inflammatory markers in the moderate dmft group. These findings suggest that systemic inflammation in ECC is more closely related to disease characteristics than to caries burden alone. CBC-derived parameters may provide supportive but limited value for assessing systemic inflammatory status in pediatric dental patients.