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INTRODUCTION: With the popularity of clear aligners, the sequential distalization protocol has been more commonly used for molar distalization. However, the amount of molar distalization that can be achieved, as well as the accompanying side effects on the sagittal dimension, are unclear. METHODS: Registered with PROSPERO (CRD42023447211), relevant original studies were screened from seven databases (MEDLINE [PubMed], EBSCOhost, Web of Science, Elsevier [SCOPUS], Cochrane, LILACS [Latin American and Caribbean Health Sciences Literature], and Google Scholar) supplemented by a manual search of the references of the full-reading manuscripts by two investigators independently. A risk of bias assessment was conducted, relevant data were extracted, and meta-analysis was performed using RStudio. RESULTS: After the screening, 13 articles (11 involving maxillary distalization, two involving mandibular distalization) met the inclusion criteria. All studies had a high or medium risk of bias. The meta-analysis revealed that the maxillary first molar (U6) mesiobuccal cusp was distalized 2.07 mm [1.38 mm, 2.77 mm] based on the post-distalization dental model superimposition, and the U6 crown was distalized 2.00 mm [0.77 mm, 3.24 mm] based on the post-treatment lateral cephalometric evaluation. However, the U6 mesiobuccal root showed less distalization of 1.13 mm [-1.34 mm, 3.60 mm], indicating crown distal tipping, which was validated by meta-analysis (U6-PP angle: 2.19° [1.06°, 3.33°]). In addition, intra-arch anchorage loss was observed at the post-distalization time point (U1 protrusion: 0.39 mm [0.27 mm, 0.51 mm]), which was corrected at the post-treatment time point (incisal edge-PTV distance: -1.50 mm [-2.61 mm, -0.39 mm]). CONCLUSION: About 2 mm maxillary molar distalization can be achieved with the sequential distalization protocol, accompanied by slight molar crown distal tipping. Additional studies on this topic are needed due to the high risk of bias in currently available studies.
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Background: Molar distalization is used to correct molar relationships or to create space for mild anterior crowding. However, whether clear aligners can provide proper vertical control with the sequential distalization strategy has been highly debated. Thus, the current study aimed to systematically review the amount of dentoskeletal changes in the vertical dimension that results from sequential molar distalization in clear aligner therapy without temporary anchorage devices (TADs). Methods: Registered with PROSPERO (CRD42023447211), relevant original studies were screened from seven databases and supplemented by a manual search by two investigators independently. Articles were screened against inclusion and exclusion criteria, and a risk of bias assessment was conducted for each included article. Relevant data were extracted from the included articles and meta-analysis was performed using RStudio. Results: Eleven articles (nine for maxillary distalization and two for mandibular distalization) were selected for the final review. All studies have a high or medium risk of bias. For maxillary molar distalization, the meta-analysis revealed 0.26 mm [0.23 mm, 0.29 mm] of maxillary first molar intrusion based on post-distalization dental model analysis, as well as 0.50 mm [-0.78 mm, 1.78 mm] of maxillary first molar intrusion and 0.60 mm [-0.42 mm, 1.62 mm] of maxillary second molar intrusion based on post-treatment lateral cephalometric analysis. Skeletally, there was a -0.33° [-0.67°, 0.02°] change in the SN-GoGn angle, -0.23° [-0.30°, 0.75°] change in the SN-MP angle, and 0.09° [-0.83°, 1.01°] change in the PP-GoGn angle based on post-treatment lateral cephalometric analysis. There was insufficient data for meta-analysis for mandibular molar distalization. Conclusions: No significant changes in vertical dimension were observed, both dentally and skeletally, after maxillary molar distalization with a sequential distalization strategy. However, further studies on this topic are needed due to the high risk of bias in the currently available studies.
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INTRODUCTION: Over the past decades, a trend of increasing obesity among children has emerged. This study aimed to evaluate and summarize the impacts of overweight and obesity on children's and adolescents' skeletal and dental developmental advancement that may influence orthodontic management. METHODS: Registered with the Prospective Register of Systematic Reviews (registration no. CRD42022347488), this study complies with the 2020 Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline. Particularly, relevant original studies on skeletal or dental age evaluation were screened from accessible electronic databases and supplemented by hand-searching. Meta-analysis was recruited to calculate differences (and their 95% confidence interval [CI]) between subjects with overweight or obese and normal-weight counterparts. RESULTS: After applying the inclusion and exclusion criteria, 17 articles were selected for the final review. Two of the 17 selected studies were found to have a high risk of bias and moderate the other 15. A meta-analysis detected no statistically significant difference in skeletal age between children and adolescents with overweight and normal-weight counterparts (P = 0.24). However, the dental age of children and adolescents with overweight was found to be 0.49 years (95% CI, 0.29-0.70) advanced in comparison with normal-weight counterparts (P <0.00001). In contrast, children and adolescents with obesity were found to have advanced skeletal age by 1.17 (95% CI, 0.48-1.86) years (P = 0.0009) and dental age by 0.56 (95% CI, 0.37-0.76) years (P <0.00001) compared with their normal-weight counterparts. CONCLUSION: Because the orthopedic outcomes of the orthodontic intervention are closely tied to the skeletal age of the patients, these results suggest that the orthodontic evaluation and treatment of children and adolescents with obesity might occur earlier than that of the normal-weight population.
Subject(s)
Overweight , Pediatric Obesity , Humans , Adolescent , Child , Infant , Overweight/epidemiology , Overweight/therapy , Pediatric Obesity/epidemiologyABSTRACT
Background: The mechanism of tumorigenicity potentially evolved in mesenchymal stem cells (MSCs) remains elusive, resulting in inconsistent clinical application efficacy. We hypothesized that subclones in MSCs contribute to their tumorgenicity, and we approached MSC-subclones at the single-cell level. Methods: MSCs were cultured in an osteogenic differentiation medium and harvested on days 12, 19, and 25 for cell differentiation analysis using Alizarin Red and followed with the single-cell transcriptome. Results: Single-cell RNA-seq analysis reveals a discrete cluster of MSCs during osteogenesis, including differentiation-resistant MSCs (DR-MSCs), differentiated osteoblasts (DO), and precursor osteoblasts (PO). The DR-MSCs population resembled cancer initiation cells and were subjected to further analysis of the yes associated protein 1 (YAP1) network. Verteporfin was also used for YAP1 inhibition in cancer cell lines to confirm the role of YAP1 in MSC--involved tumorigenicity. Clinical data from various cancer types were analyzed to reveal relationships among YAP1, OCT4, and CDH6 in MSC--involved tumorigenicity. The expression of cadherin 6 (CDH6), octamer-binding transcription factor 4 (OCT4), and YAP1 expression was significantly upregulated in DR-MSCs compared to PO and DO. YAP1 inhibition by Verteporfin accelerated the differentiation of MSCs and suppressed the expression of YAP1, CDH6, and OCT4. A survey of 56 clinical cohorts revealed a high degree of co-expression among CDH6, YAP1, and OCT4 in various solid tumors. YAP1 inhibition also down-regulated HeLa cell viability and gradually inhibited YAP1 nuclear localization while reducing the transcription of CDH6 and OCT4. Conclusions: We used single-cell sequencing to analyze undifferentiated MSCs and to discover a carcinogenic pathway in single-cell MSCs of differentiated resistance subclones.
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An increasing number of reports indicate that mesenchymal stem cells (MSCs) play an essential role in promoting tumorigenesis and progression of head and neck squamous cell carcinoma (HNSCC). However, the molecular mechanisms underlying this process remain unclear. Using the MSC model system, this study analyzes the molecular pathway by which differentiation resistant MSCs promote HNSCC. MSCs were cultured in osteogenic differentiation media and harvested on days 12 and 19. Cells were stained for cell differentiation analysis using Alizarin Red. The osteogenesis-resistant MSCs (OR-MSCs) and MSC-differentiation-derived osteoblasts (D-OSTBs) were identified and subjected to the single-cell transcriptome analysis. Gene-specific analyses of these two sub-populations were performed for the patterns of differential expression. A total of 1 780 differentially expressed genes were determined to distinguish OR-MSCs significantly from D-OSTB. Notably, AJUBA, ß-catenin, and CDH4 expression levels were upregulated considerably within the OR-MSCs compared to D-OSTBs. To confirm their clinical relevance, a survey of a clinical cohort revealed a high correlation among the expression levels of AJUBA, ß-catenin and CDH4. The results shed new light that OR-MSCs participate in the development of HNSCC via a pathway mediated by AJUBA, ß-catenin, CDH4, and CTNNB1, thereby implying that MSC-based therapy is a promising therapeutic approach in the management of HNSCC.
