Exploring the sex-associated differences in molars fused roots.

BACKGROUND: Human sexual dimorphism is associated with many biological characteristics, including dental variables. OBJECTIVES: To investigate if molars fused roots present sex-associated differences. METHODS: Panoramic radiographs were used to investigate the frequency and distribution of permanent molars fused roots. Only patients with all first and second permanent molars were included. Third molars were not investigated. Any molar with roots fused apical to the usual furcal position were considered molar fused roots. Comparisons between males and females were performed using chi-square or Fisher's and Mann-Whitney tests and the established alpha was 5% (p<0.05). Sex-differential liability models were also proposed. RESULTS: A total of 84 males and 86 females were included and 1360 molars were analyzed. Among them, 46 (26.06%) present at least one molar with fused root. Second maxillary molars were the most affected teeth. There was an association between sex and molars with fused roots. Females had a 3.4 higher chance to present fused roots than males (OR=3.4, CI 95% 1.6-6.8; p=0.0008). The female: male ratio of molars with fused roots was 2.5:1. The number of molars with fused roots ranged from 1 to 6 per patient, and the mean number of Females presented more molars with fused roots (mean = 1.01; standard deviation = 1.52) than males (mean = 0.31; standard deviation = 0.85) (p<0.05). CONCLUSIONS: Molar fused root of permanent teeth presents sex-associated differences, in which females are more affected than males. Our results support sex-differential liability models for molars fused roots.

The Complexity of Skeletal Transverse Dimension: From Diagnosis, Management, and Treatment Strategies to the Application of Collaborative Cross (CC) Mouse Model.

This study investigates the significance of skeletal transverse dimension (STD) in orthodontic therapy and its impact on occlusal relationships. The primary goal is to enhance understanding and promote the integration of transverse skeletal diagnostics into routine orthodontic assessments. To achieve this aim, the study employs a comprehensive approach, utilizing model analysis, clinical assessments, radiographic measurements, and occlusograms. The initial step involves a meticulous assessment of deficiencies in the maxilla, mainly focusing on transverse dimension issues. Various successful diagnostic methods are employed to ascertain the type and presence of these deficiencies. Furthermore, the study compares surgically assisted maxillary expansion (SARME) and orthopedic maxillary expansion (OME) in addressing skeletal transverse issues. Stability assessments and efficacy analyses are conducted to provide valuable insights into the superiority of SARME over OME. The findings reveal that proper evaluation of STD is crucial in orthodontic diagnosis, as overlooking transverse dimension issues can lead to complications such as increased masticatory muscle activity, occlusal interferences, and an elevated risk of gingival recession. Surgically assisted maxillary expansion emerges as a more stable solution than orthopedic methods. In conclusion, incorporating skeletal transverse diagnostics into routine orthodontic assessments is imperative for achieving optimal occlusal relationships and minimizing negative consequences on dentition, periodontium, and joints. The study emphasizes the significance of accurate three-dimensional assessments and recommends the consideration of SARME over OME for addressing skeletal transverse deficiencies. Finally, the Collaborative Cross (CC) mouse model is also a novel mouse model for studying complex traits. Exploring the Collaborative Cross mouse model opens avenues for future research, promising further insights into transverse skeletal issues in orthodontics.

Exploring the association between PITX2, third molars agenesis and sella turcica morphology : PITX2, third molars agenesis and sella turcica morphology.

OBJECTIVES: PITX2 is required for mammalian development and single nucleotide polymorphisms (SNPs) in this gene could be involved in dental agenesis and sella turcica patterns. Thus, the present study evaluated the association between SNPs in PITX2, third molars agenesis and sella turcica phenotypes. MATERIALS AND METHODS: The sample consisted of healthy orthodontic German patients with lateral cephalometric radiographs with clearly visualization of the sella turcica, and dental orthopantomograms. The morphological variations of the sella turcica were evaluated using the lateral cephalograms, while third molar agenesis was evaluated using orthopantomograms. DNA isolated from buccal cells was used for genotyping three SNPs in PITX2 (rs3796902, rs1947187, and rs2595110). The analyzes were performed using a significance of 5%. There was no association between third molar agenesis and sella turcica phenotypes (p > 0.05). SNPs in PITX2 were also not associated with third molars agenesis (p > 0.05). RESULTS: SNPs in PITX2 were associated with sella turcica phenotypes. The rs3796902 was associated with hypertrophic posterior clinoid process (p = 0.013). The rs1947187 and rs2595110 were associated with sella turcica bridge type A (p = 0.013 and p = 0.011, respectively for genotype distribution). Patients that carry the genotypes GG-CC-AG (rs3796902- rs1947187- rs2595110) had 7.2 higher chance to present sella turcica bridge type A (p = 0.002; Odds ratio = 7.2, Confidence interval 95% 2.04-27.04). CONCLUSIONS: Third molar agenesis was not associated with SNPs in PITX2 and sella turcica phenotypes. SNPs in PITX2 may have an important role in sella turcica pattern.

Non-syndromic supernumerary teeth and association with a self-reported family history of cancer.

BACKGROUND: Supernumerary teeth are an alteration of dental developmental and result in the formation of teeth above the usual number. Epidemiologic studies suggested that patients with dentofacial anomalies and their family members may present an increased risk of developing cancer, including female breast cancer and gynecologic cancers. These observations indicate that genetic alterations that result in dental anomalies may be related to cancer development. Thus, the aim of the present study was to evaluate the association between supernumerary teeth and a family history of female breast cancer and gynecologic cancers. METHODS: The diagnosis of supernumerary teeth was based on clinical and radiographic examinations. For data collection, a questionnaire asking for information regarding ethnicity, age, gender, and self-reported family history of cancer up to the second generation was used. Statistical analysis was performed using the Χ2 test and Fisher's exact test with an established α of 5%. RESULTS: A total of 344 patients were included; 47 of them had one or more non-syndromic supernumerary teeth (not associated with any syndrome or cleft lip and palate) and 297 were control patients. Age, ethnicity, and gender distribution were not statistically different between the group with supernumerary teeth and the control group (p > 0.05). The supernumerary teeth were most commonly observed in the incisors area. Breast cancer (n = 17) was the most commonly self-reported type of cancer, followed by uterine cervical (n = 10), endometrial (n = 2), and ovarian (n = 1) cancers. Endometrial cancer was significantly associated with the diagnosis of supernumerary teeth (p = 0.017). CONCLUSION: This study suggests that patients with supernumerary teeth possess a higher risk of having family members with endometrial cancer.

Impact of Mechanical Strain and Nicotinamide on RUNX2-Deficient Osteoblast Mimicking Cleidocranial Dysplasia.

Cleidocranial dysplasia (CCD) is a rare genetic defect caused by a heterozygous mutation of runt-related transcription factor 2 (RUNX2), which is important for osteoblast and skeletal development. RUNX2-deficiency causes extra- and intra-oral malformations that often require orthodontic treatment. Nicotinamide (NAM) affects bone remodelling processes. As these are crucial for orthodontic therapy, NAM could improve orthodontic treatment in CCD patients. This study investigates the effect of NAM in control and RUNX2-deficient osteoblasts under mechanical strain mimicking orthodontic treatment. First, the optimal NAM concentration and the differences in the expression profile of control and RUNX2-deficient osteoblasts were determined. Subsequently, osteoblasts were exposed to tensile and compressive strain with and without NAM, and the expression of genes critically involved in bone remodelling was investigated. NAM increased the expression of bone remodelling genes. RUNX2-deficient osteoblasts expressed more receptor activator of NFkB ligand (RANKL) and interleukin-6 (IL6), but less colony-stimulating factor-1 (CSF1). Most of the positive effects of NAM on bone remodelling genes were impaired by mechanical loading. In conclusion, NAM stimulated osteoblast differentiation by increasing the expression of RUNX2 and regulated the expression of osteoclastogenic factors. However, the positive effects of NAM on bone metabolism were impaired by mechanical loading and RUNX2 deficiency.

Anterior Open Bite Malocclusion: From Clinical Treatment Strategies towards the Dissection of the Genetic Bases of the Disease Using Human and Collaborative Cross Mice Cohorts.

Anterior open bite malocclusion is a complex dental condition characterized by a lack of contact or overlap between the upper and lower front teeth. It can lead to difficulties with speech, chewing, and biting. Its etiology is multifactorial, involving a combination of genetic, environmental, and developmental factors. Genetic studies have identified specific genes and signaling pathways involved in jaw growth, tooth eruption, and dental occlusion that may contribute to open bite development. Understanding the genetic and epigenetic factors contributing to skeletal open bite is crucial for developing effective prevention and treatment strategies. A thorough manual search was undertaken along with searches on PubMed, Scopus, Science Direct, and Web of Science for relevant studies published before June 2022. RCTs (clinical trials) and subsequent observational studies comprised the included studies. Orthodontic treatment is the primary approach for managing open bites, often involving braces, clear aligners, or other orthodontic appliances. In addition to orthodontic interventions, adjuvant therapies such as speech therapy and/or physiotherapy may be necessary. In some cases, surgical interventions may be necessary to correct underlying skeletal issues. Advancements in technology, such as 3D printing and computer-assisted design and manufacturing, have improved treatment precision and efficiency. Genetic research using animal models, such as the Collaborative Cross mouse population, offers insights into the genetic components of open bite and potential therapeutic targets. Identifying the underlying genetic factors and understanding their mechanisms can lead to the development of more precise treatments and preventive strategies for open bite. Here, we propose to perform human research using mouse models to generate debatable results. We anticipate that a genome-wide association study (GWAS) search for significant genes and their modifiers, an epigenetics-wide association study (EWAS), RNA-seq analysis, the integration of GWAS and expression-quantitative trait loci (eQTL), and micro-, small-, and long noncoding RNA analysis in tissues associated with open bite in humans and mice will uncover novel genes and genetic factors influencing this phenotype.

[The importance of guidelines in dentistry and dental education]. / Der Stellenwert von Leitlinien in der Zahnheilkunde und in der zahnmedizinischen Ausbildung.

Evidence-based treatment recommendations are gaining importance within the framework of both medical and dental quality management systems. The scientific findings, which have been evaluated critically by expert committees with regard to their methodological quality, are summarized in easy-to-understand guidelines. All guidelines are evaluated qualitatively in accordance with a balance between consensus and evidence during the drafting process regarding their stages of scientific development. The publication of guidelines and the coordination of guideline development has been carried out by the Association of the Scientific Medical Societies in Germany (AWMF) since its foundation in the 1960s. Forty-four dental guidelines are currently available, which are mostly rated at the highest level (S3) of scientific development. Therefore, recommendations for various treatment protocols are defined for both dental staff at university sites or practices and the implementation of these guidelines into the daily clinical routine is desirable. Poor acceptance and adverse resource requirements are major limitations of the establishment of guidelines with regard to the expansion of evidence-based dentistry. However, these limitations might be overcome by the introduction of basic scientific training within dental universities and increased funding of young researchers in order to ensure high treatment quality and economy in dentistry in the future. Guidelines can facilitate education by providing scientifically validated procedural templates to dental students and assisting educators in meeting the requirements of practical skills.

Narrating the Genetic Landscape of Human Class I Occlusion: A Perspective-Infused Review.

This review examines a prevalent condition with multifaceted etiology encompassing genetic, environmental, and oral behavioral factors. It stands as a significant ailment impacting oral functionality, aesthetics, and quality of life. Longitudinal studies indicate that malocclusion in primary dentition may progress to permanent malocclusion. Recognizing and managing malocclusion in primary dentition is gaining prominence. The World Health Organization ranks malocclusions as the third most widespread oral health issue globally. Angle's classification system is widely used to categorize malocclusions, with Class I occlusion considered the norm. However, its prevalence varies across populations due to genetic and examination disparities. Genetic factors, including variants in genes like MSX1, PAX9, and AXIN2, have been associated with an increased risk of Class I occlusion. This review aims to provide a comprehensive overview of clinical strategies for managing Class I occlusion and consolidate genetic insights from both human and murine populations. Additionally, genomic relationships among craniofacial genes will be assessed in individuals with Class I occlusion, along with a murine model, shedding light on phenotype-genotype associations of clinical relevance. The prevalence of Class I occlusion, its impact, and treatment approaches will be discussed, emphasizing the importance of early intervention. Additionally, the role of RNA alterations in skeletal Class I occlusion will be explored, focusing on variations in expression or structure that influence craniofacial development. Mouse models will be highlighted as crucial tools for investigating mandible size and prognathism and conducting QTL analysis to gain deeper genetic insights. This review amalgamates cellular, molecular, and clinical trait data to unravel correlations between malocclusion and Class I phenotypes.

Comprehensive Deciphering the Complexity of the Deep Bite: Insight from Animal Model to Human Subjects.

Deep bite is a malocclusion phenotype, defined as the misalignment in the vertical dimension of teeth and jaws and characterized by excessive overlap of the upper front teeth over the lower front teeth. Numerous factors, including genetics, environmental factors, and behavioral ones, might contribute to deep bite. In this study, we discuss the current clinical treatment strategies for deep bite, summarize the already published findings of genetic analysis associated with this complex phenotype, and their constraints. Finally, we propose a comprehensive roadmap to facilitate investigations for determining the genetic bases of this complex phenotype development. Initially, human deep bite phenotype, genetics of human deep bite, the prevalence of human deep bite, diagnosis, and treatment of human deep bite were the search terms for published publications. Here, we discuss these findings and their limitations and our view on future strategies for studying the genetic bases of this complex phenotype. New preventative and treatment methods for this widespread dental issue can be developed with the help of an understanding of the genetic and epigenetic variables that influence malocclusion. Additionally, malocclusion treatment may benefit from technological developments like 3D printing and computer-aided design and manufacture (CAD/CAM). These technologies enable the development of personalized surgical and orthodontic guidelines, enhancing the accuracy and effectiveness of treatment. Overall, the most significant results for the patient can only be achieved with a customized treatment plan created by an experienced orthodontic professional. To design a plan that meets the patient's specific requirements and expectations, open communication between the patient and the orthodontist is essential. Here, we propose to conduct a genome-wide association study (GWAS), RNAseq analysis, integrating GWAS and expression quantitative trait loci (eQTL), micro and small RNA, and long noncoding RNA analysis in tissues associated with deep bite malocclusion in human, and complement it by the same approaches in the collaborative cross (CC) mouse model which offer a novel platform for identifying genetic factors as a cause of deep bite in mice, and subsequently can then be translated to humans. An additional direct outcome of this study is discovering novel genetic elements to advance our knowledge of how this malocclusion phenotype develops and open the venue for early identification of patients carrying the susceptible genetic factors so that we can offer early prevention and treatment strategies, a step towards applying a personalized medicine approach.

The investigation of WNT6 and WNT10A single nucleotide polymorphisms as potential biomarkers for dental pulp calcification in orthodontic patients.

The aim of this study is to evaluate if single nucleotide polymorphisms (SNPs) in WNT6 and WNT10A are associated with the risk of dental pulp calcification in orthodontic patients. This cross-sectional study followed the "Strengthening the Reporting of Genetic Association Studies" (STREGA) guidelines. Panoramic radiographs (pre- and post-orthodontic treatment) and genomic DNA from 132 orthodontic patients were studied. Dental pulp calcification (pulp stones and/or pulp space narrowing) was recorded in upper and lower first molars. The SNPs in WNT6 and WNT10A (rs7349332, rs3806557, rs10177996, and rs6754599) were assessed through genotyping analysis using DNA extracted from buccal epithelial cells. The association between pulp calcification and SNPs were analyzed using allelic and genotypic distributions and haplotype frequencies (p<0.05). Prevalence of dental pulp calcification was 42.4% in the 490 studied molars. In the genotypic analysis, the SNPs in WNT10A showed a statistically significant value for molar calcification (p = 0.027 for rs1017799), upper molar calcification (p = 0.040 for rs1017799) (recessive model), and molar calcification (p = 0.046 for rs3806557) (recessive model). In the allelic distribution, the allele C of the SNP rs10177996 in WNT10A was associated with molar calcifications (p = 0.042) and with upper first molar calcification (p = 0.035). Nine combinations of haplotypes showed statistically significant value (p<0.05). The findings of this study indicates that SNPs in WNT10A and WNT6 are associated with dental pulp calcification in molars after orthodontic treatment and may be considered as biomarkers for dental pulp calcification.

Skeletal Class II Malocclusion: From Clinical Treatment Strategies to the Roadmap in Identifying the Genetic Bases of Development in Humans with the Support of the Collaborative Cross Mouse Population.

Depending on how severe it is, malocclusion, which may involve misaligned teeth, jaws, or a combination of the two, can hurt a person's overall facial aesthetics. The maxillary molar develops before the mandibular molar in class II malocclusion, which affects 15% of the population in the United States. With a retrusive mandible, patients typically have a convex profile. The goal of this study is to classify the skeletal and dental variability present in class II malocclusion, to reduce heterogeneity, present the current clinical treatment strategies, to summarize the previously published findings of genetic analysis, discuss these findings and their constraints, and finally, propose a comprehensive roadmap to facilitate investigations aimed at determining the genetic bases of malocclusion development using a variety of genomic approaches. To further comprehend the hereditary components involved in the onset and progression of class II malocclusion, a novel animal model for class II malocclusion should be developed while considering the variety of the human population. To overcome the constraints of the previous studies, here, we propose to conduct novel research on humans with the support of mouse models to produce contentious findings. We believe that carrying out a genome-wide association study (GWAS) on a large human cohort to search for significant genes and their modifiers; an epigenetics-wide association study (EWAS); RNA-seq analysis; integrating GWAS and the expression of quantitative trait loci (eQTL); and the testing of microRNAs, small RNAs, and long noncoding RNAs in tissues related to the skeletal class II malocclusion (SCIIMO) phenotype, such as mandibular bone, gum, and jaw in humans and the collaborative cross (CC) mouse model, will identify novel genes and genetic factors affecting this phenotype. We anticipate discovering novel genetic elements to advance our knowledge of how this malocclusion phenotype develops and open the venue for the early identification of patients carrying the susceptible genetic factors so that we can offer early prevention treatment strategies.

Prevalence and local causes for retention of primary teeth and the associated delayed permanent tooth eruption.

BACKGROUND: This study aimed to evaluate the prevalence of retained primary teeth (RPT) associated with delayed permanent tooth eruption and the factors associated with this condition in German children. METHODS: This is a cross-sectional retrospective study that evaluated panoramic radiographs from orthodontic patients. The diagnosis of RPT was established according to Nolla developmental stage. The primary tooth was considered retained when its successor permanent tooth was in Nolla stage 8, 9, or 10. Statistical analysis was performed with an α of 5% (p < 0.05). RESULTS: A total of 102 children (48 girls and 54 boys), and 574 primary teeth and their respective permanent successor teeth were evaluated. We classified 192 teeth as RPT. Sixty-one (59.8%) children presented one or more RPT. Gender was not significantly different between RPT and control teeth (p = 0.838; odds ratio 0.95, confidence interval 95% 0.44-2.16). In the majority of the RPT cases (68.7%), no clear cause to explain the prolonged retention was identified. The pathological problems most commonly observed with RPT were dental fillings (19.3%), followed by dental caries (4.6%), and ectopic tooth eruption (2.1%). CONCLUSIONS: The incidence of RPT associated with delayed permanent tooth eruption in German children was high and the most common pathological condition associated with RPT was dental caries.

Validation of a mathematical-geometrical model to calculate the length of an individual anterior arch.

PURPOSE: For resolving anterior dental crowding or spacing, it is of key interest in personalised orthodontic diagnostics and treatment planning to predict the extent of space gained or lost in the anterior dental arch by changing incisor inclination or position. To facilitate the determination of anterior arch length (AL) and to predict its alterations following tooth movements, a mathematical-geometrical model, based on a third-degree parabola, was established. The aim of this study was to validate this model and assess its diagnostic precision. METHODS: This retrospective diagnostic study evaluated 50 randomly chosen dental casts taken before (T0) and after (T1) orthodontic treatment with fixed appliances. Plaster models were digitally photographed, allowing two-dimensional digital measurements of arch width, depth and length. A computer programme based on the mathematical-geometrical model to be validated was created to calculate AL for any given arch width and depth. Mean differences and correlation coefficients as well as Bland-Altman plots were used to compare the measured and the calculated (predicted) AL, evaluating the precision of the model. RESULTS: Inter- and intrarater reliability tests showed reliable measurements of arch width, depth and length. Measured and calculated (predicted) AL revealed high concordance according to concordance correlation coefficient (CCC), intraclass correlation coefficient (ICC), and Bland-Altman analyses and negligible differences between the mean values. CONCLUSIONS: The mathematical-geometrical model calculated anterior AL without significant difference to the measured AL, indicating its validity. The model can thus be used clinically for predicting alterations of AL following therapeutic changes of incisor inclination/position.

Impact of genetic variations in the WNT family members and RUNX2 on dental and skeletal maturation: a cross-sectional study.

BACKGROUND: This study evaluated if genetic variations in the WNT family members and RUNX2 are associated with craniofacial maturation, investigating dental and skeletal maturity in children and teenagers. METHODS: Radiographs from pre-orthodontic treatment of Brazilian patients (7 to 17 years-old) were used to assess dental (panoramic radiographs) and skeletal maturity (cephalometric radiographs). The chronological age (CA) was calculated based on the date of birth and the time the radiographs were performed. For the dental maturity analysis, the Demirjian (1973) method was used and a delta [dental age - chronological age (DA-CA)] was calculated. For the skeletal maturity analysis, the Baccetti et al. (2005) method was used and the patients were classified as "delayed skeletal maturation", "advanced skeletal maturation" or "normal skeletal maturation". DNA isolated from buccal cells was used for genotyping of two genetic variations in WNT family genes: rs708111 (G > A) in WNT3A and rs1533767 (G > A) in WNT11; and two genetic variations in RUNX2: rs1200425 (G > A) and rs59983488 (G > T). A statistical analysis was performed and values of p < 0.05 indicated a significant difference. RESULTS: There were no associations between dental maturity and genotypes (p > 0.05). In the skeletal maturity analysis, the allele A in the rs708111 (WNT3A) was statistically more frequent in patients with delayed skeletal maturation (Prevalence Ratio = 1.6; 95% Confidence Interval = 1.00 to 2.54; p-value = 0.042). CONCLUSIONS: The rs708111 in the WNT3A gene impacts on skeletal maturation.

Association between craniofacial patterns and third molar agenesis in orthodontic patients.

PURPOSE: Third molar agenesis (TMA) is the most common craniofacial anomaly and has been associated with craniofacial patterns in different populations. Therefore, the aim of this retrospective cross-sectional study was to assess a possible association between craniofacial patterns and TMA in German orthodontic patients. METHODS: Patients undergoing orthodontic treatment with dental records including anamnesis, pretreatment lateral cephalograms and orthopantomograms were evaluated. Cephalometric analyses were conducted digitally and lines, angles and proportions were measured to investigate craniofacial morphology. Skeletal classes were determined by the individualised Wits appraisal and ANB angle. The TMA was identified with the help of orthopantomograms. Patients showing agenesis of at least one third molar were included in the TMA group. Statistical analysis was performed to assess the association between TMA and craniofacial patterns (α of p ≤ 0.05). RESULTS: A total of 148 patients were included, 40 (27.0%) presented at least one missing tooth (TMA group) and 108 (73.0%) showed full dentition (control group). Skeletal class determined by the individualised Wits appraisal revealed statistical significance between the TMA and control groups (p = 0.022), in which TMA patients were 11 times more likely to present with an individualised skeletal class III (odds ratio 11.3, 95% confidence interval 1.7-139.5). Skeletal cephalometric analysis revealed no statistical differences between TMA and control groups for any further angular, linear and proportional parameters. CONCLUSION: Third molar agenesis was associated with skeletal class III determined by the individualised Wits appraisal.

Advancing oral immunology for improving oral health.

Although substantial progress has been made in dentistry in terms of diagnosis and therapy, current treatment methods in periodontology, orthodontics, endodontics, and oral and maxillofacial surgery, nevertheless, suffer from numerous limitations, some of which are associated with a dramatic reduction in the quality of life. Many general mechanisms of inflammation and immunity also apply to the oral cavity and oral diseases. Nonetheless, there are special features here that are attributable, on the one hand, to developmental biology and, on the other hand, to the specific anatomical situation, which is characterized by a close spatial relationship of soft and hard tissues, exposure to oral microbiota, and to a rapid changing external environment. Currently, a comprehensive and overarching understanding is lacking about how the immune system functions in oral tissues (oral immunology) and how oral immune responses contribute to oral health and disease. Since advances in translational immunology have created a game-changing shift in therapy in rheumatology, allergic diseases, inflammatory bowel disease, and oncology in recent years, it is reasonable to assume that a better understanding of oral immunology might lead to practice-changing diagnostic procedures and therapies in dentistry and thereby also profoundly improve oral health in general.

Impact of polishing system on surface roughness of different ceramic surfaces after various pretreatments and bracket debonding.

OBJECTIVE: Evaluating various polishing methods after bracket debonding and excessive attachment material removal for different ceramics and pretreatments. MATERIAL AND METHODS: Zirconia (ZrO2), leucite (LEU) and lithium disilicate (LiSi) specimens were pretreated with a) silica coated alumina particles (CoJet); LEU and LiSi additionally with b) hydrofluoric acid (HF), c) Monobond Etch&Prime (MEP), d) silicium carbide grinder (SiC) before bracket bonding, shearing off, ARI evaluation, excessive attachment material removal and polishing with i) Sof-Lex Discs (Soflex), ii) polishing paste (Paste), iii) polishing set (Set). Before/after polishing surface roughness (Ra) was measured with a profilometer. Martens hardness parameter were also assessed. RESULTS: Irrespective of pretreatment Ra of LEU increased the most, followed by LiSi and ZrO2 (p < 0.001, SiC: p = 0.012), in accordance with the measured Martens hardness parameter. CoJet/SiC caused greater roughness as HF/MEP (p < 0.001). The ZrO2 surface was rougher after polishing with Paste/Set (p < 0.001; p = 0.047). Ra improved in the LEU/CoJet, LEU/SiC and LiSi/SiC groups with Soflex/Set (p < 0.001), in the LiSi/CoJet and LEU/HF groups by Soflex (p = 0.003, p < 0.001) and worsened by Paste (p = 0.017, p < 0.001). Polishing of HF or MEP pretreated LiSi with Set increased Ra (p = 0.001, p < 0.001), so did Paste in the LEU/MEP group (p < 0.001). CONCLUSIONS: Paste couldn't improve the surfaces. Soflex was the only method decreasing Ra on rough surfaces and not causing roughness worsening. Polishing of LEU/LiSi after MEP, LEU after HF pretreatment doesn´t seem to have any benefit. CLINICAL RELEVANCE: To avoid long-term damage to ceramic restorations, special attention should be paid to the polishing method after orthodontic treatment.

Towards Genetic Dissection of Skeletal Class III Malocclusion: A Review of Genetic Variations Underlying the Phenotype in Humans and Future Directions.

INTRODUCTION: Skeletal abnormalities and malocclusions have varied features that impact populations globally, impairing aesthetics and lowering life quality. The prevalence of the Skeletal Class III disease is the lowest among all angle malocclusions, with varied prevalence across nations. Environmental, genetic, and societal factors play a role in its numerous etiologies. In this study, we conducted a thorough search across the published data relating to quantitative trait loci (QTL) and the genes associated with Class III progression in humans, discussed these findings and their limitations, and proposed future directions and strategies for studying this phenotype. METHODS: An inclusive search of published papers in the PubMed and Google Scholar search engines using the following terms: 1. Human skeletal Class III; 2. Genetics of Human skeletal Class III; 3. QTL mapping and gene associated with human skeletal Class III; 4. enriched skeletal Class-III-malocclusion-associated pathways. RESULTS: Our search has found 53 genes linked with skeletal Class III malocclusion reported in humans, genes associated with epigenetics and phenomena, and the top 20 enriched pathways associated with skeletal Class III malocclusion. CONCLUSIONS: The human investigations yielded some contentious conclusions. We conducted a genome-wide association study (GWAS), an epigenetics-wide association study (EWAS), RNA-seq analysis, integrating GWAS and expression quantitative trait loci (eQTL), micro- and small-RNA, and long non-coding RNA analysis in tissues connected to skeletal Class III malocclusion phenotype in tissues connected with the skeletal phenotype. Finally, we invite regional, national, and international orthodontists and surgeons to join this effort by contributing human samples with skeletal Class III malocclusion following the accepted Helsinki ethical protocol to challenge these phenomena jointly.

Effect of genetic polymorphisms rs2301113 and rs2057482 in the expression of HIF-1α protein in periodontal ligament fibroblasts subjected to compressive force.

OBJECTIVE: Many genes and signaling molecules are involved in orthodontic tooth movement, with mechanically and hypoxically stabilized HIF-1α having been shown to play a decisive role in periodontal ligament signaling during orthodontic tooth movement. Thus, this in vitro study aimed to investigate if genetic polymorphisms in HIF1A (Hypoxia-inducible factor α-subunits) influence the expression pattern of HIF-1α protein during simulated orthodontic compressive pressure. METHODOLOGY: Samples from human periodontal ligament fibroblasts were used and their DNA was genotyped using real time Polymerase chain reaction for the genetic polymorphisms rs2301113 and rs2057482 in HIF1A . For cell culture and protein expression experiments, six human periodontal ligament fibroblast cell lines were selected based on the patients' genotype. To simulate orthodontic compressive pressure in fibroblasts, a 2 g/cm2 force was applied under cell culture conditions for 48 hours. Protein expression was evaluated by Western Blot. Paired t-tests were used to compare HIF-1α expression with and without compressive pressure application and unpaired t-tests were used to compare expression between the genotypes in rs2057482 and rs2301113 (p<0.05). RESULTS: The expression of HIF-1α protein was significantly enhanced by compressive pressure application regardless of the genotype (p<0.0001). The genotypes in the genetic polymorphisms rs2301113 and rs2057482 were not associated with HIF-1α protein expression (p>0.05). CONCLUSIONS: Our study confirms that compressive pressure application enhances HIF-1α protein expression. We could not prove that the genetic polymorphisms in HIF1A affect HIF-1α protein expression by periodontal ligament fibroblasts during simulated orthodontic compressive force.