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Background Molar-incisor hypomineralization (MIH) is a systemic condition characterized by a qualitative defect in the dental enamel. It primarily affects the first permanent molars and is often associated with the permanent incisors. Resin restorations in MIH-affected teeth consistently show worse results than those in normal teeth because of the ultrastructure of hypomineralized enamel, which compromises adhesion. The incorporation of bioactive particles into adhesives is a promising option for inducing remineralization. This study protocol describes a randomized clinical trial evaluating restorative treatment using an adhesive system containing 45S5 bioactive glass for MIH-affected teeth. Methods Restorations will be performed on the upper or lower first permanent molars in children with MIH aged 6–12 years. The inclusion criteria will include MIH teeth with post-eruptive enamel fractures that compromise the middle third of the dentin, with at least two surfaces of hypomineralized enamel near the cavity, without caries, pulpal, or periradicular involvement. Before treatment, children will complete the Child Perceptions Questionnaire 8–10 and 11–14 (CPQ8–10 and CPQ11–14). The teeth will be divided into two groups: a control group (commercial self-etching adhesive system: Clearfil SE Bond (CF) Primer + Bond) and an experimental group (CF Primer + experimental Bond using 10% 45S5 bioglass [Bond 45S5 10%]). Restorations will be made using composite resin, and quality will be assessed using digital radiographs (interproximal and periapical), intraoral photographs, and epoxy resin replicas. Clinical evaluation of the restorations will be performed immediately following the procedure (baseline) and after 1, 3, 6, and 12 months using the World Dental Federation (FDI) criteria. The impact of the treatment on the quality of life will be assessed after 3, 6, and 12 months through the re-administration of CPQ8–10 and CPQ11–14. Discussion 45S5 bioactive glass is capable of enhancing the effect of materials on bone and dental structures, promoting remineralization. The results of this study may aid in the clinical management of patients with MIH, given the challenges of treating sensitive and compromised teeth and the difficulty in achieving long-term restorative success while addressing the individual patient needs. Trial registration Rebec, U1111-1259-1738. Registered on January 10, 2021.

To assess the long term effects of zinc oxide (ZnO) nanoparticle coated elastomeric modules on S. mutans concentration and enamel mineralization among orthodontic patients over a period of one year. A total of 16 patients were recruited for this study. Either the left or right maxillary lateral incisor received the coated module. Group I : ZnO coated elastomeric modules (N = 16); Group II: Non-coated elastomeric modules (N = 16). S. mutans in plaque was assessed at the end of 3 months and one year using Rt -PCR. Enamel mineralization was assessed by laser fluorescence at the end of one year. Integrity of the ZnO nanoparticle coating over a period of one month on a weekly basis was also assessed. Independent t-test was done to find the significant difference between the bivariate samples and intra-group comparison was done using paired t-test. Pearson’s correlation was done to determine the relationship between the variables. For all the statistical tests, p < 0.05 was considered to be statistically significant. S. mutans concentration at the end of three months and one year was higher in the non-coated group compared to the coated group but it was statistically significant only at the end of one year (p value = 0.032). Laser fluorescence values was higher for the non-coated group compared to the coated group which showed statistical significance (p = 0.020). ZnO coating of the modules showed evidence of disintegration of the coating after two weeks, with further deterioration of the coating at the end of one month. As elastomeric modules are changed periodically, this appears to be a viable option, especially since the nanoparticle release would be around the most common area of plaque retention.

The sequencing of ancient DNA has enabled the reconstruction of speciation, migration and admixture events for extinct taxa 1 . However, the irreversible post-mortem degradation 2 of ancient DNA has so far limited its recovery—outside permafrost areas—to specimens that are not older than approximately 0.5 million years (Myr) 3 . By contrast, tandem mass spectrometry has enabled the sequencing of approximately 1.5-Myr-old collagen type I 4 , and suggested the presence of protein residues in fossils of the Cretaceous period 5 —although with limited phylogenetic use 6 . In the absence of molecular evidence, the speciation of several extinct species of the Early and Middle Pleistocene epoch remains contentious. Here we address the phylogenetic relationships of the Eurasian Rhinocerotidae of the Pleistocene epoch 7 – 9 , using the proteome of dental enamel from a Stephanorhinus tooth that is approximately 1.77-Myr old, recovered from the archaeological site of Dmanisi (South Caucasus, Georgia) 10 . Molecular phylogenetic analyses place this Stephanorhinus as a sister group to the clade formed by the woolly rhinoceros ( Coelodonta antiquitatis ) and Merck’s rhinoceros ( Stephanorhinus kirchbergensis ). We show that Coelodonta evolved from an early Stephanorhinus lineage, and that this latter genus includes at least two distinct evolutionary lines. The genus Stephanorhinus is therefore currently paraphyletic, and its systematic revision is needed. We demonstrate that sequencing the proteome of Early Pleistocene dental enamel overcomes the limitations of phylogenetic inference based on ancient collagen or DNA. Our approach also provides additional information about the sex and taxonomic assignment of other specimens from Dmanisi. Our findings reveal that proteomic investigation of ancient dental enamel—which is the hardest tissue in vertebrates 11 , and is highly abundant in the fossil record—can push the reconstruction of molecular evolution further back into the Early Pleistocene epoch, beyond the currently known limits of ancient DNA preservation. Palaeoproteomic analysis of dental enamel from an Early Pleistocene Stephanorhinus resolves the phylogeny of Eurasian Rhinocerotidae, by enabling the reconstruction of molecular evolution beyond the limits of ancient DNA preservation.

Molar Incisor Hypomineralisation (MIH) is defined as a qualitative demarcated enamel hypomineralisation defect of tooth enamel affecting at least one first permanent molar (FPM), often affecting permanent incisors. More recently, the term Hypomineralised Second Primary Molar (HSPM) was used to describe similar defects affecting second primary molars. Our observational study aimed at determining HSPM and MIH frequencies in a medieval and early-modern-age population population (Sains-en-Gohelle, France, 7th − 17th centuries) and compare it to the current worldwide and French prevalence values. To date, there are no other studies on this subject in France. European studies have been published, but the diagnosis of these pathologies is based solely on a visual examination. Our study differs from others by using objective diagnostic. microtomography and X-ray fluorescence. The use of these diagnostic methods allows differentiation between hypomineralised and taphonomic lesions. The frequencies of MIH and HSPM were, respectively, 12.3% and 13.3%. In fact, there were 10 individuals with at least one first permanent molar affected by MIH amongst the 81 individuals with at least one first permanent molar present, and 15 individuals with at least one second primary molar affected by HSPM among the 113 individuals with at least one second primary molar present.The presence of MIH and HSPM in ancient populations with frequencies respectively equivalent and higher than current worldwide averages renews the debate and questioning about the aetiological factors of these pathologies.

ObjectivesTo define an expert Delphi consensus on when to intervene in the caries process and on existing carious lesions using non- or micro-invasive, invasive/restorative or mixed interventions.MethodsNon-systematic literature synthesis, expert Delphi consensus process and expert panel conference.ResultsCarious lesion activity, cavitation and cleansability determine intervention thresholds. Inactive lesions do not require treatment (in some cases, restorations will be placed for reasons of form, function and aesthetics); active lesions do. Non-cavitated carious lesions should be managed non- or micro-invasively, as should most cavitated carious lesions which are cleansable. Cavitated lesions which are not cleansable usually require invasive/restorative management, to restore form, function and aesthetics. In specific circumstances, mixed interventions may be applicable. On occlusal surfaces, cavitated lesions confined to enamel and non-cavitated lesions radiographically extending deep into dentine (middle or inner dentine third, D2/3) may be exceptions to that rule. On proximal surfaces, cavitation is hard to assess visually or by using tactile methods. Hence, radiographic lesion depth is used to determine the likelihood of cavitation. Most lesions radiographically extending into the middle or inner third of the dentine (D2/3) can be assumed to be cavitated, while those restricted to the enamel (E1/2) are not cavitated. For lesions radiographically extending into the outer third of the dentine (D1), cavitation is unlikely, and these lesions should be managed as if they were non-cavitated unless otherwise indicated. Individual decisions should consider factors modifying these thresholds.ConclusionsComprehensive diagnostics are the basis for systematic decision-making on when to intervene in the caries process and on existing carious lesions.Clinical relevanceCarious lesion activity, cavitation and cleansability determine intervention thresholds. Invasive treatments should be applied restrictively and with these factors in mind.

As the hardest tissue formed by vertebrates, enamel represents nature’s engineering masterpiece with complex organizations of fibrous apatite crystals at the nanometer scale. Supramolecular assemblies of enamel matrix proteins (EMPs) play a key role as the structural scaffolds for regulating mineral morphology during enamel development. However, to achieve maximum tissue hardness, most organic content in enamel is digested and removed at the maturation stage, and thus knowledge of a structural protein template that could guide enamel mineralization is limited at this date. Herein, by examining a gene-modified mouse that lacked enzymatic degradation of EMPs, we demonstrate the presence of protein nanoribbons as the structural scaffolds in developing enamel matrix. Using in vitro mineralization assays we showed that both recombinant and enamel-tissue–based amelogenin nanoribbons are capable of guiding fibrous apatite nanocrystal formation. In accordance with our understanding of the natural process of enamel formation, templated crystal growth was achieved by interaction of amelogenin scaffolds with acidic macromolecules that facilitate the formation of an amorphous calcium phosphate precursor which gradually transforms into oriented apatite fibers along the protein nanoribbons. Furthermore, this study elucidated that matrix metalloproteinase-20 is a critical regulator of the enamel mineralization as only a recombinant analog of a MMP20-cleavage product of amelogenin was capable of guiding apatite mineralization. This study highlights that supramolecular assembly of the scaffold protein, its enzymatic processing, and its ability to interact with acidic carrier proteins are critical steps for proper enamel development.

This study aimed to investigate the effect of enamel matrix derivatives (EMD) on the early healing biomarkers’ expression following flapless treatment. Thirty-eight patients with residual deep intrabony defects after steps 1 and 2 of periodontal therapy were randomly assigned to the test (flapless with EMD) or control group (flapless alone). Periodontal parameters were recorded at baseline and 6 months after treatment. Gingival crevicular fluid (GCF) was collected at baseline and 2 weeks after treatment to quantify the levels of biomarkers related to epithelial healing (epidermal growth factor, EGF), connective tissue healing (matrix metalloproteinase-8 [MMP-8], fibroblast growth factor [FGF], transforming growth factor-β [TGF-β]), and bone formation (osteoprotegerin [OPG]). The test group showed a significant reduction in MMP-8 levels (p = 0.039), along with significant increases in EGF (p < 0.01), FGF (p < 0.01), and OPG (p < 0.01). The control group demonstrated a significant decrease in MMP-8 (p = 0.010). No significant changes in TGF-β levels were observed in either group. At 6 months, the test group exhibited significantly greater reductions in probing pocket depth and clinical attachment level compared to the control group. This study is the first to characterize the biochemical changes following flapless treatment with EMD. These preliminary findings suggest that EMD may enhance early wound healing by modulating the expression of key regenerative biomarkers.

Cleft lip with or without cleft palate (CLP) is considered the most frequent congenital malformations of the head and neck, with cleft individuals exhibiting more chances of presenting abnormalities such as developmental defects of enamel (DDE). Matrix metallopeptidase 2 ( MMP2 ) is a membrane-bound protein with collagen-degrading ability and has important roles in tooth formation and mineralization. The aim of this study was to evaluate the frequency, location, severity and extent of DDE found in the maxillary incisors for groups of individuals born with CLP, as well as understanding their relationship with the cleft side. Besides, this study addresses the hypothesis that DDE can be influenced by variation in the MMP2 genes (rs9923304). Individual samples, clinical history, intraoral photographs and panoramic radiographs were obtained from 233 patients under treatment at the Cleft Lip and Palate Service of the University Hospital Lauro Wanderley at the Federal University of Paraíba. Digital images were examined by the same evaluator using the Classification of Defects According to the Modified DDE Index, and then loaded into the Image Tool software, where two measurements were made: total area of the buccal surface (SA) and the area of the DDE (DA), obtaining the percentage of the surface area affected (%SAD) (ICC = 0.99). Genomic DNA was extracted from saliva samples from 124 participants. Genotyping was carried out using TaqMan chemistry for one marker in MMP2 (rs9923304). Statistical analyses were performed by The Jamovi Project software. The Shapiro-Wilk test was applied, followed by the Student’s t-test and the Mann-Whitney test. Chi-square and Fisher’s exact tests, and odds ratio (OR) with 95% confidence interval (CI) calculations were used to determine Hardy-Weinberg equilibrium and statistically significant differences with an alpha of 0.05. No significant differences in the prevalence and extent of enamel defects were found between male and female individuals born with CLP (p = 0.058256). The frequency of individuals presenting teeth with DDE, in relation to the cleft and non-cleft side, was statistically different (p <0.001; OR = 7.15, CI: 4.674> 7.151> 10.942). However, the averages of %SAD were similar (p = 0.18). The highest means of the %SAD were found in individuals with bilateral cleft lip with or without cleft palate (BCLP) when compared to individuals with unilateral cleft lip with or without cleft palate (UCLP), for the teeth inside (IA) and outside the cleft area (OA) (p <0.001). Regardless of the cleft side, individuals with BCLP were 7.85 times more likely to have more than one third of the tooth surface affected, showing more frequently defects in the three thirds (OA: p <0.001) (IA: p = 0.03), as well as a higher frequency of more than one type of defect (OA: p = 0.000358) (IA: p = 0.008016), whereas in UCLP, defects were isolated and restricted to only one third, more frequently, the incisal third (OA: p = 0.009) (IA: p = 0.001), with greater frequency of milder defects, such as demarcated (p = 0.02) and diffuse (p = 0.008) opacities. A higher frequency of the T allele, less common, was observed in the group of CLP individuals who had all the affected teeth or at least two teeth with %SAD greater than 20% (p = 0.019843). Our results suggest that MMP2 may have a role in the cases that presented DDE and genotyping rs9923304 could serve as the basis for a genomic approach to define risks for individuals born with CLP. Frequency and severity of DDE is strongly related to the CLP phenotype, since the highest values were found for BCLP. However, the extent of the DDE is independent of its relationship with the side of the cleft.

The phylogenetic relationships between hominins of the Early Pleistocene epoch in Eurasia, such as Homo antecessor , and hominins that appear later in the fossil record during the Middle Pleistocene epoch, such as Homo sapiens , are highly debated 1 – 5 . For the oldest remains, the molecular study of these relationships is hindered by the degradation of ancient DNA. However, recent research has demonstrated that the analysis of ancient proteins can address this challenge 6 – 8 . Here we present the dental enamel proteomes of H. antecessor from Atapuerca (Spain) 9 , 10 and Homo erectus from Dmanisi (Georgia) 1 , two key fossil assemblages that have a central role in models of Pleistocene hominin morphology, dispersal and divergence. We provide evidence that H. antecessor is a close sister lineage to subsequent Middle and Late Pleistocene hominins, including modern humans, Neanderthals and Denisovans. This placement implies that the modern-like face of H. antecessor —that is, similar to that of modern humans—may have a considerably deep ancestry in the genus Homo , and that the cranial morphology of Neanderthals represents a derived form. By recovering AMELY-specific peptide sequences, we also conclude that the H. antecessor molar fragment from Atapuerca that we analysed belonged to a male individual. Finally, these H. antecessor and H. erectus fossils preserve evidence of enamel proteome phosphorylation and proteolytic digestion that occurred in vivo during tooth formation. Our results provide important insights into the evolutionary relationships between H. antecessor and other hominin groups, and pave the way for future studies using enamel proteomes to investigate hominin biology across the existence of the genus Homo . Analyses of the proteomes of dental enamel from Homo antecessor and Homo erectus demonstrate that the Early Pleistocene H. antecessor is a close sister lineage of later Homo sapiens , Neanderthal and Denisovan populations in Eurasia.

Molar-Incisor Hypomineralization (MIH) is a qualitative defect of enamel of unknown etiology, affecting one or more permanent molars and may include incisors. This condition is a clinical challenge and its prevalence is still uncertain given the recent increase in research. Thus, we aimed to comprehensively estimate the overall prevalence of MIH and associated characteristics. This systematic review is reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA). We searched articles using PubMed, MEDLINE, CENTRAL, Web of Science, SciELO, LILACS and TRIP databases, until July 2021. Heterogeneity and publication bias were computed via I 2 test statistics and Egger’s significance test, respectively. Random-effects meta-analysis of prevalence were processed. We used the Strength of Recommendation Taxonomy [SORT] to grading the strength of evidence. Overall, 116 observational studies were included, with one study with moderate methodological quality and the remaining of high methodological quality. Subgroup analysis confirmed an influence of not using the 2003 MIH case definition (p = 0.0066). The pooled prevalence of MIH was 13.5% (95% CI 12.0–15.1, I 2  = 98.0%). Affected incisors were seen in 36.6% (95% CI 30.0–43.7, I 2  = 92.5%) of the cases. Lastly, the prevalence of hypomineralization of the second primary molars was observed in 3.6% of the MIH cases (95% CI 1.9–6.8, I 2  = 96.3%). America was the continent with highest prevalence (15.3, 95% CI 12.8–18.3, p < 0.001, I 2  = 96.3%) and Asia had the lowest prevalence (10.7, 95% CI 8.5–13.5, p < 0.001, I 2  = 98.7%), however no continental differences were found. Sample size and year of publication were slight contributing factors to the heterogeneity in the analysis. Overall, these results were classified with a SORT A recommendation.