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The Thymic Defect
Published in Miroslav Holub, Immunology of Nude Mice, 2020
Cortical epithelial cells in the obviously specialized subcapsular area contain keratin and the thymic hormones thymopoietin, thymosin α1, β3, and β4.11 The latter two polypeptides are missing in medullary endocrine cells. Also, another thymic hormone, the FTS of French workers, seems to be associated with keratin-positive epithelial cells in the murine thymic cell cultures.15 Human subcapsular epithelial cells, forming a dense mesh, express neuronal gangliosides on their surface; they may be derived from the neural crest and they belong to a family of neuroendocrine cells found in many organs11 and in all species, including mice (Section V). It cannot be excluded that neural crest mesenchyme (ectomesenchyme), also suggested as playing an inductive role in the epithelial anlage differentiation, may be directly involved in the subcapsular area. Thy-1-positive cells of epithelial appearance have been described in this layer11 where Thy-1-positive immature, large lymphoid cells are stuffed among the epithelial cell processes.13 Thy 1 antigen was suggested as triggering cell-stroma adhesions and interactions.16,17 Almost all mouse, rat, or human thymic epithelial cells exhibiting tonofilaments and growing in culture can be shown to express Thy-1 or Thy-1-analogous antigens.18,19
Anatomy and Embryology of the Mouth and Dentition
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
As the neural plate of the embryo invaginates to form the neural tube, neural crest cells (ectomesenchyme) at the margins proliferate and migrate from this site to various parts of the body. There, interacting with the overlying epithelium (epithelial/mesenchymal interactions), the neural crest plays a significant role in normal development, contributing to many systems, such as the nervous system, soft and hard connective tissues. In addition, the cells play a major role in tooth development and give rise to melanocytes.
Prenatal Development of the Facial Skeleton
Published in D. Dixon Andrew, A.N. Hoyte David, Ronning Olli, Fundamentals of Craniofacial Growth, 2017
As one example, part of a sophisticated series of experiments, Hörstadius and Sellman (1946) transplanted neural crest in Ambystoma larvae to find out if neural crest cells are preprogrammed to reach their destination or if they are influenced by other cells during their migration. Part of the crest was removed on one side, stained with Nile blue, and implanted in the ventral side of the head. Ectomesenchyme from the contralateral crest, stained with neutral red, migrated ventrally on the operated side to intermingle with blue-stained columns of transplanted cells that grew dorsally in the opposite direction to normal. But they still found their way into each of the gill arches, a phenomenon also observed later for transplanted avian trunk crest (Weston, 1963; Erickson, 1980).
Dental and dentoalveolar dimensions in individuals with osteogenesis imperfecta
Published in Acta Odontologica Scandinavica, 2021
Janna Waltimo-Sirén, Henri Tuurala, Ella Säämäki, Petteri Holst, Marjut Evälahti, Heidi Arponen
Genetic defects, such as OI, that are associated with disturbance of mesenchymal matrix deposition can be speculated to also affect tooth morphogenesis, which is regulated by reciprocal interaction between dental epithelium and the underlying tooth mesenchyme. Dentine is of ectomesenchymal origin and rich in type I collagen. During tooth morphogenesis, formation of a layer of type I collagen-containing predentin precludes final differentiation of epithelium-derived ameloblasts and deposition of enamel. Disturbances in tooth morphogenesis due to mutations in several regulatory signalling genes are known to cause hypodontia and oligodontia, but quantitative factors may also be involved [20]. In OI patients with the DI phenotype, the abnormal dentine displays significantly less than normal dentinal tubules with varying shape and size [2,21,22]. DI is present in approximately one fourth of OI patients [15,16]. However, normally coloured teeth and absence of radiographic signs of DI do not necessarily indicate absence of dentine anomalies [4,22,23]. Individuals with OI have twice as many missing teeth as the general population [14]. Tooth agenesis has been noted to be slightly more common in OI patients with a mutation leading to qualitative defect in collagen type I and the severe disorder type than in those with quantitative mutations [24]. Presence of dentine abnormality has been shown to increase the risk of hypodontia in individuals with OI [21], and the diminished amount or structural abnormality of predentin might have an effect on tooth size [2,22]. This study supports evidence from a previous observation reporting smaller than normal tooth size in several teeth of patients with OI [25]. The exact mechanism of hypodontia in OI is thus far unknown, but the diminished tooth size and hypodontia may be of shared aetiology as in population in general [26].
Transglutaminase 2 as a therapeutic target for neurological conditions
Published in Expert Opinion on Therapeutic Targets, 2021
Jeffrey W. Keillor, Gail V.W. Johnson
Early studies demonstrated that TG2 expression was significantly elevated in TBI [12], SCI [11] and stroke [13,110]. Interestingly, in a middle cerebral artery occlusion (MCAO) model of stroke, overexpression of TG2 in neurons resulted in significantly smaller stroke volumes [20]. However, complete deletion of TG2 also resulted in smaller stroke volumes in the same model [21]. Closer examination revealed that this was due to the fact that deletion of TG2 from astrocytes makes them more resistant to ischemic-induced cell death and significantly increases their ability to protect neurons from ischemic-induced cell death [21,22,111]. Deletion of TG2 from astrocytes resulted in a significant upregulation of genes associated with axonal outgrowth and ECM matrix remodeling, and in a mouse model where TG2 is selectively deleted from astrocytes, there was significantly less astrogliosis following a contusive SCI [22]. Interestingly, transduction of TG2 into ectomesenchymal stem cells (EMSCs) that were then transplanted into the site of a SCI resulted in significantly improved outcomes compared to control EMSCs [112]. Although depletion of TG2 from astrocytes results in a significant decrease in ischemic-induced cell death, depletion of TG2 from neurons significantly compromises cell viability [1,113]. Treatment of wild-type astrocytes with the irreversible TG2 inhibitor VA4 [114], which also locks TG2 in an open conformation [44], phenocopies the effects of TG2 deletion in the ischemic model [111]. Treatment of neurons with the same inhibitor had no effect on viability [114] even though depletion resulted in an increase in cell death [113]. This suggests that neurons require the presence of TG2 to remain viable, but it does not need to be catalytically active. Further, a recent study in mice demonstrated that selective deletion of TG2 from astrocytes or treatment with the TG2 inhibitor VA4 resulted in a significant improvement in motor function recovery following a contusive SCI [115].
Dental stem cells in tooth regeneration and repair in the future
Published in Expert Opinion on Biological Therapy, 2018
Christian Morsczeck, Torsten E. Reichert
For the initiation of the tooth root development the Hertwig’s epithelial root sheath is formed as an extension of the enamel organ. This thin cell-sheath separates a second dental mesenchymal tooth-germ tissue from the dental mesenchymal pulp/dentin complex. This tooth germ tissue is known as the dental sac or the dent follicle and surrounds the tooth germ. The dental follicle is crucial both for tooth eruption and for the development of the tooth root [79,80]. It contains dental mesenchymal progenitor cells for the periodontium, which consists of the alveolar bone, the PDL, and the cementum. Moreover, this tissue contains also epithelial cells, which are derived from the epithelial cells of the Hertwig’s epithelial root sheath, which disappears during tooth root development [79]. The dental follicle is similar to the dental apical pad-like tissue and can be isolated from impacted human wisdom teeth. It contains multipotent ectomesenchymal stem cells that are known as dental follicle precursor cells, dental follicle stem cells, or dental follicle cells (DFCs). Human DFCs were initially isolated as plastic-adherent and clonogenic cells [81]. They have a DPSC-like morphology and also express typical markers of progenitor/stem cells such as NESTIN, NOTCH-1, CD44, CD105, and STRO-1 [81,82]. DFCs can be cultivated under serum-free cell culture conditions for an extended period of time and then behave like neural progenitor cells [83]. DFCs are multipotent stem cells, and especially the genuine precursor cells of periodontal tissue cells [81–85]. Even under in vitro condition, DFCs formed a robust connective tissue-like structure with many mineralized clusters after long-term cultures in osteogenic differentiation medium. Interestingly, this periodontium-like tissue occasionally had blood-vessel-like structures [81]. We suppose that DFCs should be considered for the treatment of periodontitis and/or for the reconstruction of a tooth attachment apparatus [86,87]. Tian and colleagues, for example, showed that rat DFCs formed a tooth root when seeded on scaffolds of a treated dentin matrix (TDM) and transplanted into alveolar fossa microenvironment [88]. Interestingly, this particular environment is necessary for the production of a tooth root, since DFCs do not form a tooth root after transplantation in skull and omental pockets [88]. Unfortunately, autologous TDM is rare as scaffolds and the use of xenogenic scaffolds, for example, porcine TDM, in combination with allogeneic DFCs is problematic, since this combination induces bone resorption [89]. DFCs are also considered for bone regeneration, because they support bone regeneration in critical size defect models of the calvaria of immunocompromised rats [86]. Here, compared to untreated animals, stem cells improved the process of bone regeneration. Therefore, DFCs as the genuine progenitors of alveolar osteoblasts are an attractive source for bone tissue engineering. We expect DFCs to be taken into account for dental stem cell-based therapies in the future.