Survival of periodontal ligament myofibroblasts after short-term mechanical strain in rats and in vitro: Could myofibroblasts contribute to orthodontic relapse?

Objectives: To investigate in vivo whether myofibroblasts formed in the PDL after exposure to short-term high experimental orthodontic forces in rats survive. To study in vitro whether human PDL fibroblasts can differentiate into myofibroblasts and survive when chemical or mechanical stimuli are removed.

Design: Nine 6-week-old male Wistar rats were used in this experiment.

foxe1 mutant zebrafish show indications of a hypothyroid phenotype and increased sensitivity to ethanol for craniofacial malformations.

Background: FOXE1 mutations in humans are associated with cleft palate and hypothyroidism. We previously developed a foxe1 mutant zebrafish demonstrating mineralization defects in larvae. In the present study, we investigate the thyroid status and skeletal phenotype of adult foxe1 mutants.

Stem cells and extracellular vesicles to improve preclinical orofacial soft tissue healing.

Orofacial soft tissue wounds caused by surgery for congenital defects, trauma, or disease frequently occur leading to complications affecting patients' quality of life. Scarring and fibrosis prevent proper skin, mucosa and muscle regeneration during wound repair. This may hamper maxillofacial growth and speech development.

A potential osteogenic role for microRNA-181a-5p during palatogenesis.

Background: In a previous study, we found that the highly conserved hsa-miR-181a-5p is downregulated in palatal fibroblasts of non-syndromic cleft palate-only infants.

Objectives: To analyze the spatiotemporal expression pattern of mmu-miR-181a-5p during palatogenesis and identify possible mRNA targets and their involved molecular pathways.

Material And Methods: The expression of mmu-miR-181a-5p was analyzed in the developing palates of mouse embryos from E11 to E18 using qPCR and ISH.

Disruption of the gene in zebrafish reveals conserved functions in development of the craniofacial skeleton and the thyroid.

Mutations in the FOXE1 gene are implicated in cleft palate and thyroid dysgenesis in humans. To investigate whether zebrafish could provide meaningful insights into the etiology of developmental defects in humans related to FOXE1, we generated a zebrafish mutant that has a disruption in the nuclear localization signal in the foxe1 gene, thereby restraining nuclear access of the transcription factor. We characterized skeletal development and thyroidogenesis in these mutants, focusing on embryonic and larval stages.

Targeting fibroblast growth factor receptors causes severe craniofacial malformations in zebrafish larvae.

Background And Objective: A key pathway controlling skeletal development is fibroblast growth factor (FGF) and FGF receptor (FGFR) signaling. Major regulatory functions of FGF signaling are chondrogenesis, endochondral and intramembranous bone development. In this study we focus on , as mutations in this gene are found in patients with craniofacial malformations.

Excess vitamin a might contribute to submucous clefting by inhibiting WNT-mediated bone formation.

Objectives: Cleft lip and/or palate (CLP) is a common craniofacial birth defect caused by genetic as well as environmental factors. The phenotypic spectrum of CLP also includes submucous clefts with a defect in the palatal bone. To elucidate the contribution of vitamin A, we evaluated the effects of the vitamin A metabolite all-trans retinoic acid (ATRA) on the osteogenic differentiation and mineralization of mouse embryonic palatal mesenchymal cells (MEPM).

Effect of niche components on masseter satellite cell differentiation on fibrin coatings.

In skeletal muscles, niche factors stimulate satellite cells to activate and induce muscle regeneration after injury. In vitro, matrigel is widely used for myoblast differentiation, however, is unsuitable for clinical applications. Therefore, this study aimed to analyze attachment and differentiation of satellite cells into myotubes on fibrin coatings with selected niche components.

Corrigendum: Zebrafish Models of Craniofacial Malformations: Interactions of Environmental Factors.

[This corrects the article DOI: 10.3389/fcell.2020.

Functional analysis of the rat soft palate by real-time wireless electromyography.

Objective: The aim of this study was to analyze the function of the palatal muscles in vivo by real-time wireless electromyography in rats. The effects of palatal wounding were also analyzed.

Methods: Microelectrodes were implanted six rats; in the masseter muscle (two-rats) for comparison, in the unwounded soft palate (two-rats) and the soft palate that received a surgical wound (two-rats).

Zebrafish Models of Craniofacial Malformations: Interactions of Environmental Factors.

The zebrafish is an appealing model organism for investigating the genetic (G) and environmental (E) factors, as well as their interactions (GxE), which contribute to craniofacial malformations. Here, we review zebrafish studies on environmental factors involved in the etiology of craniofacial malformations in humans including maternal smoking, alcohol consumption, nutrition and drug use. As an example, we focus on the (cleft) palate, for which the zebrafish ethmoid plate is a good model.

Highly variable rate of orthodontic tooth movement measured by a novel 3D method correlates with gingival inflammation.

Objectives: Individual orthodontic treatment duration is hard to predict. Individual biological factors are amongst factors influencing individual rate of orthodontically induced tooth movement (OTM). The study aim is to determine the rate of OTM by a novel 3D method and investigate parameters that may predict the rate of tooth movement.

Deregulated Adhesion Program in Palatal Keratinocytes of Orofacial Cleft Patients.

Orofacial clefts (OFCs) are the most frequent craniofacial birth defects. An orofacial cleft (OFC) occurs as a result of deviations in palatogenesis. Cell proliferation, differentiation, adhesion, migration and apoptosis are crucial in palatogenesis.

Retinoic acid disrupts osteogenesis in pre-osteoblasts by down-regulating WNT signaling.

The skull bones are formed by osteoblasts by intramembranous ossification. WNT signaling is a regulator of bone formation. Retinoic Acid (RA) act as a teratogen affecting craniofacial development.

Tissue engineering strategies combining molecular targets against inflammation and fibrosis, and umbilical cord blood stem cells to improve hampered muscle and skin regeneration following cleft repair.

Cleft lip with or without cleft palate is a congenital deformity that occurs in about 1 of 700 newborns, affecting the dentition, bone, skin, muscles and mucosa in the orofacial region. A cleft can give rise to problems with maxillofacial growth, dental development, speech, and eating, and can also cause hearing impairment. Surgical repair of the lip may lead to impaired regeneration of muscle and skin, fibrosis, and scar formation.

Muscle fibrosis in the soft palate: Delivery of cells, growth factors and anti-fibrotics.

The healing of skeletal muscle injuries after major trauma or surgical reconstruction is often complicated by the development of fibrosis leading to impaired function. Research in the field of muscle regeneration is mainly focused on the restoration of muscle mass while far less attention is paid to the prevention of fibrosis. In this review, we take as an example the reconstruction of the muscles in the soft palate of cleft palate patients.

Thermosensitive biomimetic polyisocyanopeptide hydrogels may facilitate wound repair.

Changing wound dressings inflicts pain and may disrupt wound repair. Novel synthetic thermosensitive hydrogels based on polyisocyanopeptide (PIC) offer a solution. These gels are liquid below 16 °C and form gels beyond room temperature.

Differential microRNA expression in cultured palatal fibroblasts from infants with cleft palate and controls.

Background: The role of microRNAs (miRNAs) in animal models of palatogenesis has been shown, but only limited research has been carried out in humans. To date, no miRNA expression study on tissues or cells from cleft palate patients has been published. We compared miRNA expression in palatal fibroblasts from cleft palate patients and age-matched controls.

MicroRNAs in Palatogenesis and Cleft Palate.

Palatogenesis requires a precise spatiotemporal regulation of gene expression, which is controlled by an intricate network of transcription factors and their corresponding DNA motifs. Even minor perturbations of this network may cause cleft palate, the most common congenital craniofacial defect in humans. MicroRNAs (miRNAs), a class of small regulatory non-coding RNAs, have elicited strong interest as key regulators of embryological development, and as etiological factors in disease.

Novel mutations in LRP6 highlight the role of WNT signaling in tooth agenesis.

Purpose: We aimed to identify a novel genetic cause of tooth agenesis (TA) and/or orofacial clefting (OFC) by combining whole-exome sequencing (WES) and targeted resequencing in a large cohort of TA and OFC patients.

Methods: WES was performed in two unrelated patients: one with severe TA and OFC and another with severe TA only. After deleterious mutations were identified in a gene encoding low-density lipoprotein receptor-related protein 6 (LRP6), all its exons were resequenced with molecular inversion probes in 67 patients with TA, 1,072 patients with OFC, and 706 controls.

Retinoic acid signalling in the development of the epidermis, the limbs and the secondary palate.

Retinoic acid (RA), the active derivative of vitamin A, is one of the major regulators of embryonic development, including the development of the epidermis, the limbs and the secondary palate. In the embryo, RA levels are tightly regulated by the activity of RA synthesizing and degrading enzymes. Aberrant RA levels due to genetic variations in RA metabolism pathways contribute to congenital malformations in these structures.

Visualisation of newly synthesised collagen in vitro and in vivo.

Identifying collagen produced de novo by cells in a background of purified collagenous biomaterials poses a major problem in for example the evaluation of tissue-engineered constructs and cell biological studies to tumor dissemination. We have developed a universal strategy to detect and localize newly deposited collagen based on its inherent association with dermatan sulfate. The method is applicable irrespective of host species and collagen source.