Grouping patients for masseter muscle genotype-phenotype studies

Moawad, Hadwah Abdelmatloub; Sinanan, Andrea; Lewis, Mark P.; Hunt, NP

doi:10.2319/122810-750.1

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…Several MYH genes were previously associated with both types of malocclusions ( Table 1 and Table 4 ). In particular, higher expression levels of MYH3 , MYH6 , and MYH7 were detected in patients with mandibular retrognathism than in those with mandibular prognathism, while no significant difference was found between these two populations in regard to MYH1 , MYH2 , and MYH8 expression levels [ 44 ]. Thus, it is safe to say that the MYH proteins could be future research targets for craniofacial skeletal sagittal growth prediction and modification.…”

Section: Discussionmentioning

confidence: 99%

Genes and Pathways Associated with Skeletal Sagittal Malocclusions: A Systematic Review

Gershater

et al. 2021

IJMS

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Skeletal class II and III malocclusions are craniofacial disorders that negatively impact people’s quality of life worldwide. Unfortunately, the growth patterns of skeletal malocclusions and their clinical correction prognoses are difficult to predict largely due to lack of knowledge of their precise etiology. Inspired by the strong inheritance pattern of a specific type of skeletal malocclusion, previous genome-wide association studies (GWAS) were reanalyzed, resulting in the identification of 19 skeletal class II malocclusion-associated and 53 skeletal class III malocclusion-associated genes. Functional enrichment of these genes created a signal pathway atlas in which most of the genes were associated with bone and cartilage growth and development, as expected, while some were characterized by functions related to skeletal muscle maturation and construction. Interestingly, several genes and enriched pathways are involved in both skeletal class II and III malocclusions, indicating the key regulatory effects of these genes and pathways in craniofacial development. There is no doubt that further investigation is necessary to validate these recognized genes’ and pathways’ specific function(s) related to maxillary and mandibular development. In summary, this systematic review provides initial insight on developing novel gene-based treatment strategies for skeletal malocclusions and paves the path for precision medicine where dental care providers can make an accurate prediction of the craniofacial growth of an individual patient based on his/her genetic profile.

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Section: Discussionmentioning

confidence: 99%

Genes and Pathways Associated with Skeletal Sagittal Malocclusions: A Systematic Review

Gershater

et al. 2021

IJMS

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“…DNA is bundled with histone proteins in eukaryotic cells to create nucleosomes, which are then condensed into chromatin fibers [42]. Acetylation of histones in masseter muscle genes can boost the production of type IIX MHC, which is involved in fast-twitch muscle fibers [43,44]. On the other hand, histone deacetylation can cause chromatin closure, lowering the expression of type I MHC, which regulates slow-twitch muscle fibers [45].…”

Section: Epigenetic and Skeletal Class III Malocclusionmentioning

confidence: 99%

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

Zohud

Lone

Midlej

et al. 2023

JCM

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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.

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