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Margaret R Byers - One of the best experts on this subject based on the ideXlab platform.
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Dexamethasone effects on Na_v1.6 in Tooth pulp, dental nerves, and alveolar osteoclasts of adult rats
Cell and Tissue Research, 2009Co-Authors: Margaret R Byers, Matthew M. Rafie, Ruth E WestenbroekAbstract:Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Na_v1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Na_v1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Na_v1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Na_v1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after Tooth Injury, pulpal vasodilation and increased Na_v1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Na_v1.6-IR in normal teeth, but different mechanisms occur after Tooth Injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Na_v1.6-IR and osteoclast number, but not with any changes in Na_v1.6-IR for nodes of Ranvier in myelinated dental axons.
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dexamethasone effects on nav1 6 in Tooth pulp dental nerves and alveolar osteoclasts of adult rats
Cell and Tissue Research, 2009Co-Authors: Margaret R Byers, Matthew M. Rafie, Ruth E WestenbroekAbstract:Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Nav1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Nav1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Nav1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Nav1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after Tooth Injury, pulpal vasodilation and increased Nav1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Nav1.6-IR in normal teeth, but different mechanisms occur after Tooth Injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Nav1.6-IR and osteoclast number, but not with any changes in Nav1.6-IR for nodes of Ranvier in myelinated dental axons.
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Behavioural responses following Tooth Injury in rats.
Archives of oral biology, 2005Co-Authors: Eric H. Chudler, Margaret R ByersAbstract:Summary Early changes in spontaneous behaviour (exploration, grooming, freezing, rearing, jaw motion, yawning) and body weight were measured at two and three days after pulp exposure Injury and implantation of Fluorogold (FG) into molar teeth of rats. Rats with FG and injuries to three teeth gained weight less rapidly, explored less frequently and froze more often than sham-operated rats. Yawning was not observed in any rats prior to surgery and it was seen more frequently in Tooth-injured rats than in sham-operated rats. These results suggest that careful observation of spontaneous behaviour after Tooth injuries can be used to assess dental pain in rats and may provide behavioural markers to correlate with anatomical changes after Injury. The dental nerve cell bodies that had accumulated transported FG were medium to large, and they only co-localized calcitonin gene-related peptide (CGRP) in a subset of the medium neurons. Chromatolytic or moribund FG-labelled neurons were also found.
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altered localization of cav1 2 l type calcium channels in nerve fibers schwann cells odontoblasts and fibroblasts of Tooth pulp after Tooth Injury
Journal of Neuroscience Research, 2004Co-Authors: Ruth E Westenbroek, N L Anderson, Margaret R ByersAbstract:We have determined the localization of Ca v 1.2 (L-Type) Ca 2 + channels in the cells and nerve fibers in molars of normal or injured rats. We observed high levels of immunostaining of L-type Ca 2 + channels in odontoblastcell bodies and their processes, in fibroblast cell bodies and in Schwann cells. Many Ca v 1.2-containing unmyelinated and myelinated axons were also present in root nerves and proximal branches in coronal pulp, but were usually missing from nerve fibers in dentin. Labeling in the larger fibers was present along the axonal membrane, localized in axonal vesicles, and in nodal regions. After focal Tooth Injury, there is a marked loss of Ca v 1.2 channels in injured teeth. Immunostaining of Ca v 1.2 channels was lost selectively in nerve fibers and local cells of the Tooth pulp within 10 min of the lesion, without loss of other Ca v channel or pulpal labels. By 60 min, Ca v 1.2 channels in odontoblasts were detected again but at levels below controls, whereas fibroblasts were labeled well above control levels, similar to upregulation of Ca v 1.2 channels in astrocytes after Injury. By 3 days after the Injury, Ca v 1.2 channels were again detected in nerve fibers and immunostaining of fibroblasts and odontoblasts had returned to control levels. These findings provide new insight into the localization of Ca v 1.2 channels in dental pulp and sensory fibers, and demonstrate unexpected plasticity of channel distribution in response to nerve Injury.
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Chronic Tooth pulp inflammation causes transient and persistent expression of Fos in dynorphin-rich regions of rat brainstem.
Brain Research, 2000Co-Authors: Margaret R Byers, Eric H. Chudler, Michael J IadarolaAbstract:Abstract We have analyzed central Fos immunoreactivity (Fos-IR) brainstems of adult rats after three clinically relevant dental injuries: filled dentin (DF) cavities that cause mild pulp Injury and heal within 1–2 weeks; open pulp exposures (PX) that cause gradual pulp loss and subsequent periodontal lesions; and filled pulp exposures (PXF). By 1 week after DF cavities, no Fos-IR remained except for sites such as lateral–ventral periolivary nucleus (LVPO) that had Fos-IR in all rats including controls. PX Injury induced (1) a delayed transient expression of Fos at 1–2 weeks at three loci (ipsilateral neurons in dorsomedial nucleus oralis, paratrigeminal nucleus, and trigeminal tract), (2) persistent ipsilateral Fos for at least 4 weeks after Injury in dynorphin (Dyn)-rich regions (rostral lateral solitary nucleus, periobex dorsal nucleus caudalis), and (3) late Fos-IR at 2–4 weeks (bilateral superficial cervical dorsal horn, contralateral dorsal nucleus caudalis, contralateral rostral lateral solitary nucleus). Rats with PXF Injury were examined at 2 weeks, and they had greater numbers and more extensive rostro-caudal distribution of Fos neurons than the PX group. One week after PX Injury, Fos-IR neurons were found in regions with strong Dyn-IR central fibers. Co-expression of Dyn and Fos was found in some unusually large neurons of the ipsilateral rostral lateral solitary nucleus, trigeminal tract, and dorsal nucleus caudalis. Immunocytochemistry for the p75 low affinity neurotrophin receptor (p75NTR) or for calcitonin gene-related peptide (CGRP) showed no consistent change in trigeminal central endings in any Fos-reactive brainstem areas, despite the extensive structural and cytochemical reorganization of the peripheral endings of the dental neurons. The Fos responses of central neurons to Tooth Injury have some unusual temporal and spatial patterns in adult rats compared to other trigeminal Injury models.
Ruth E Westenbroek - One of the best experts on this subject based on the ideXlab platform.
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Dexamethasone effects on Na_v1.6 in Tooth pulp, dental nerves, and alveolar osteoclasts of adult rats
Cell and Tissue Research, 2009Co-Authors: Margaret R Byers, Matthew M. Rafie, Ruth E WestenbroekAbstract:Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Na_v1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Na_v1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Na_v1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Na_v1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after Tooth Injury, pulpal vasodilation and increased Na_v1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Na_v1.6-IR in normal teeth, but different mechanisms occur after Tooth Injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Na_v1.6-IR and osteoclast number, but not with any changes in Na_v1.6-IR for nodes of Ranvier in myelinated dental axons.
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dexamethasone effects on nav1 6 in Tooth pulp dental nerves and alveolar osteoclasts of adult rats
Cell and Tissue Research, 2009Co-Authors: Margaret R Byers, Matthew M. Rafie, Ruth E WestenbroekAbstract:Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Nav1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Nav1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Nav1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Nav1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after Tooth Injury, pulpal vasodilation and increased Nav1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Nav1.6-IR in normal teeth, but different mechanisms occur after Tooth Injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Nav1.6-IR and osteoclast number, but not with any changes in Nav1.6-IR for nodes of Ranvier in myelinated dental axons.
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altered localization of cav1 2 l type calcium channels in nerve fibers schwann cells odontoblasts and fibroblasts of Tooth pulp after Tooth Injury
Journal of Neuroscience Research, 2004Co-Authors: Ruth E Westenbroek, N L Anderson, Margaret R ByersAbstract:We have determined the localization of Ca v 1.2 (L-Type) Ca 2 + channels in the cells and nerve fibers in molars of normal or injured rats. We observed high levels of immunostaining of L-type Ca 2 + channels in odontoblastcell bodies and their processes, in fibroblast cell bodies and in Schwann cells. Many Ca v 1.2-containing unmyelinated and myelinated axons were also present in root nerves and proximal branches in coronal pulp, but were usually missing from nerve fibers in dentin. Labeling in the larger fibers was present along the axonal membrane, localized in axonal vesicles, and in nodal regions. After focal Tooth Injury, there is a marked loss of Ca v 1.2 channels in injured teeth. Immunostaining of Ca v 1.2 channels was lost selectively in nerve fibers and local cells of the Tooth pulp within 10 min of the lesion, without loss of other Ca v channel or pulpal labels. By 60 min, Ca v 1.2 channels in odontoblasts were detected again but at levels below controls, whereas fibroblasts were labeled well above control levels, similar to upregulation of Ca v 1.2 channels in astrocytes after Injury. By 3 days after the Injury, Ca v 1.2 channels were again detected in nerve fibers and immunostaining of fibroblasts and odontoblasts had returned to control levels. These findings provide new insight into the localization of Ca v 1.2 channels in dental pulp and sensory fibers, and demonstrate unexpected plasticity of channel distribution in response to nerve Injury.
Esther F. Wheeler - One of the best experts on this subject based on the ideXlab platform.
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A model experimental system for monitoring changes in sensory neuron phenotype evoked by Tooth Injury.
Journal of neuroscience methods, 2003Co-Authors: Yan Pan, Esther F. Wheeler, Hong Yang, Jayne M Bernanke, John P NaftelAbstract:The dental pulp is a favorable model for studies of interactions between nociceptive sensory neurons and their peripheral target tissues. In the present study, we retrogradely labeled pulpal afferent neurons with an improved method that permits monitoring of changes in neuronal phenotype in response to controlled Tooth injuries. The capacity of retrograde neuronal tracers to diffuse through dentinal tubules was exploited, thereby avoiding the severe Injury to the pulp associated with previous tracer application methods. The strategy was to apply the durable fluorescent tracer, Fluoro-gold (FG), to exposed dentin in the floor of shallow cavities in molars, in order to pre-label pulpal neurons in trigeminal ganglia of young adult Sprague-Dawley rats. A high percentage of pupal afferent neurons were retrogradely labeled by application of FG to exposed dentin and the FG fluorescent signal persisted in most labeled neurons for at least 8 weeks. Following tracer application to dentin, the pulp tissue appeared normal histologically, with the exception that a layer of reactive dentin was deposited at the pulp-dentin border beneath the shallow cavities. Assessment of expression of calcitonin gene-related peptide (CGRP) and brain derived neurotrophic factor (BDNF) indicated that pulpal neurons remained in a quiescent, baseline condition cytochemically following application of tracer to cavities in dentin and upregulation of these markers could be detected in neurons that projected to teeth that received a test Injury subsequent to tracer application. Thus, labeling of trigeminal neurons via dentinal tubules provides the basis for a useful model for precisely assessing properties of pulpal afferents in both quiescent and activated states.
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Time Course of the Increase in trk A Expression in Trigeminal Neurons After Tooth Injury
Journal of endodontics, 2000Co-Authors: J. Scott Sullins, David L. Carnes, Roy N. Kaldestad, Esther F. WheelerAbstract:Injury to Tooth pulp often results in extensive sprouting of sensory nerve fibers at the site of wound repair due to local increases in nerve growth factor (NGF) concentration. NGF interacts with high-affinity binding sites, termed trk A receptors, located on the cell membranes of responsive neurons. If NGF induces wound repair and/or nociceptive responses in Tooth pulp, then changes in expression of NGF receptors (trk A receptors) in response to dentin Injury would be expected. To characterize the role of trk A receptors in mediating NGF-induced signals to sensory neurons, trigeminal ganglia from adult male rats were examined for changes in expression of trk A as a function of time after Injury to maxillary molar dentin. In situ hybridization was performed with 35S-labeled riboprobes encoding the sense or antisense trk A sequences, and grain densities quantified over maxillary neurons. As early as 12 h after Tooth Injury, grain density counts increased by 71% above control level, indicating an increase in trk A receptor mRNA expression. Grain densities obtained from ganglia harvested at all time points through 168 h after Injury remained elevated. At 336 h (14 days) after Injury, trk A receptor expression had decreased such that grain density counts were not different from preInjury levels. Thus our results suggest that NGF may be mediating repair and pain responses by the sustained upregulation of its cell surface receptor, trk A, in neurons of the trigeminal ganglia.
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neurotrophin receptor expression is induced in a subpopulation of trigeminal neurons that label by retrograde transport of ngf or fluoro gold following Tooth Injury
Molecular Brain Research, 1998Co-Authors: Esther F. Wheeler, John P Naftel, Min Pan, Christopher S Von Bartheld, Margaret R ByersAbstract:Abstract Tissue responses to Injury are regulated by neurotrophins and neurotrophin receptor levels and can involve both retrograde and paracrine/autocrine trophic signaling. To determine how neurotrophins may contribute to the Injury response, the timing and the extent of the up-regulation of neurotrophins and their receptors was examined in a model system which is particularly well suited for the analysis of trophic signaling pathways in response to Injury. Injury to the occlusal surfaces of rat molar cusps induces a localized increase in nerve growth factor (NGF) expression in the dental pulp within 4–6 h. Radiolabeled NGF was transported in a receptor-mediated fashion from the teeth to a subset of neurons in the trigeminal ganglion within 15 h, indicating that these neurons possess NGF receptors (trk A and/or p75 NTR ). To test for NGF responses in the Tooth sensory afferent neurons, levels of expression of neurotrophins and their receptors were examined by in situ hybridization in the trigeminal ganglion at 0, 4, 12, 20, 28 and 52 h post-Injury. Within the maxillary division of the trigeminal ganglion, trk A expression was elevated at 4 h post-Injury, with a maximum increase (2-fold) after 52 h. p75 NTR was increased by 28 h post-Injury and was increased 1.35-fold by 52 h. BDNF mRNA was increased 12 h after Injury (1.8-fold), and 2.5–3-fold at 52 h post-Injury. The trk B expression was increased only late after Injury (28 and 52 h). To determine the receptor/neurotrophin phenotype of trigeminal neurons with projections to the molar teeth, these neurons were double-labeled with the retrograde tracer fluoro-gold and probes for either BDNF or trk B. The results show that Tooth-innervating trigeminal neurons express BDNF, but not trk B. The timing of mRNA expression after Injury and the phenotype of identified trigeminal neurons suggests a complex signaling cascade in which NGF at the Injury site regulates NGF receptor expression at the levels of the cell body as well as increases in BDNF expression. Upregulated BDNF may act in a paracrine fashion on neighboring trigeminal cells expressing trk B. This signaling cascade may be a common feature of the response to mild peripheral inflammatory injuries within nociceptive pathways.
Hayato Ohshima - One of the best experts on this subject based on the ideXlab platform.
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Dentin Matrix Protein 1 Compensates for Lack of Osteopontin in Regulating Odontoblastlike Cell Differentiation after Tooth Injury in Mice.
Journal of endodontics, 2019Co-Authors: Kotaro Saito, Mitsushiro Nakatomi, Hayato OhshimaAbstract:Abstract Introduction Although dentin matrix protein 1 (DMP1) and osteopontin (OPN) act as substrates and signaling molecules for odontoblastlike cell differentiation after Tooth Injury, the mutual interaction between these proteins in the mechanism of odontoblastlike cell differentiation remains to be clarified. This study aimed to elucidate the role of DMP1 and OPN in regulating odontoblastlike cell differentiation after Tooth Injury. Methods A groove-shaped cavity was prepared on the mesial surface of the upper first molars in wild-type and Opn knockout (KO) mice. The demineralized paraffin sections were processed for immunohistochemistry for nestin and DMP1 and in situ hybridization for Dmp1. For the in vitro assay, the experiments of organ culture for evaluating dentin-pulp complex regeneration using small interfering RNA treatment were performed. Results Once preexisting odontoblasts died, nestin-positive newly differentiated odontoblastlike cells were arranged along the pulp-dentin border and began to express DMP1/Dmp1. In Opn KO mice, the expression of DMP1/Dmp1 was up-regulated compared with that of wild-type mice. The in vitro assay showed that the gene suppression of Dmp1 by small interfering RNA showed a tendency to decrease the differentiation rate of odontoblastlike cells from 70.1% to 52.2% in wild-type teeth. In addition, the suppression of Dmp1 in Opn KO teeth tended to lead to the inhibition of odontoblastlike cell differentiation. Conclusions These results suggest that the expression of Dmp1 is up-regulated in Opn KO mice both in vivo and in vitro, and DMP1 compensates for the lack of OPN in regulating odontoblastlike cell differentiation after Tooth Injury.
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The putative role of insulin-like growth factor (IGF)-binding protein 5 independent of IGF in the maintenance of pulpal homeostasis in mice.
Regenerative therapy, 2019Co-Authors: Kotaro Saito, Hayato OhshimaAbstract:Although insulin-like growth factor binding protein 5 (IGFBP5) may play a crucial role in activating the functions of periodontal and bone marrow stem cells, the factors responsible for regulating the maintenance of dental pulp stem cells (DPSCs) remain to be clarified. This study aimed to elucidate the role of IGFBP5 in maintaining pulpal homeostasis during Tooth development and pulpal healing after Tooth Injury in doxycycline-inducible TetOP-histone 2B (H2B)-green fluorescent protein (GFP) transgenic mice (GFP expression was induced at E14.5 or E15.5) by using TUNEL assay, RT-PCR, in situ hybridization for Igfbp5, and immunohistochemistry for IGFBP5, Nestin, and GFP. To observe the pulpal response to exogenous stimuli, the roots of the maxillary first molars were resected, and the coronal portion was autografted into the sublingual region. Intense IGFBP5/Igfbp5 expression was observed in cells from the center of the pulp tissue and the subodontoblastic layer in developing teeth during postnatal Week 4. Intense H2B-GFP-expressing label-retaining cells (LRCs) were localized in the subodontoblastic layer in addition to the center of the pulp tissue, suggesting that slowly dividing cell populations reside in these areas. During postoperative days 3-7, the LRCs were maintained in the dental pulp, showed an IGFBP5-positve reaction in their nuclei, and lacked a TUNEL-positive reaction. In situ hybridization and RT-PCR analyses confirmed the expression of Igfbp5 in the dental pulp. These findings suggest that IGFBP5 play a pivotal role in regulating the survival and apoptosis of DPSCs during both Tooth development and pulpal healing following Tooth Injury.
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Differentiation capacity and maintenance of dental pulp stem/progenitor cells in the process of pulpal healing following Tooth injuries
Journal of Oral Biosciences, 2017Co-Authors: Kotaro Saito, Hayato OhshimaAbstract:Abstract Background Recently, we demonstrated that a pulse of 5-bromo-2’-deoxyuridine (BrdU) given to prenatal animals discloses the existence of slow-cycling long-term label-retaining cells (LRCs), or putative adult stem/progenitor cells, which reside in the dental pulp. Using several Tooth Injury models such as cavity preparation, Tooth replantation, Tooth or Tooth crown transplantation, and Tooth germ transplantation, we have clarified the dynamics and differentiation capacity of LRCs postoperatively. Our recent studies have demonstrated that allogenic Tooth transplantation may influence the maintenance of dental pulp stem/progenitor cells. Highlight Dense LRCs are competent to proliferate and differentiate into odontoblast-like cells after Tooth injuries. In the case of Tooth replantation and autogenic Tooth transplantation, dense LRCs remain in the perivascular environment in the center of the dental pulp for a long period. In contrast, allograft LRCs disappear from this niche during postoperative weeks 2–4. The loss of LRCs, even in cases without immunological rejection, is attributed to the extensive apoptosis taking place in these cells, with the exception of newly differentiated odontoblast-like cells. Conclusion Host and recipient interactions that occur with allografts disturb the maintenance of putative stem/progenitor cells, resulting in the disappearance of these cell types.
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lymphoid enhancer binding factor 1 expression precedes dentin sialophosphoprotein expression during rat odontoblast differentiation and regeneration
Journal of Endodontics, 2013Co-Authors: Mitsushiro Nakatomi, Hiroko Idayonemochi, Hayato OhshimaAbstract:Abstract Introduction The molecular mechanisms behind odontoblast differentiation remain obscure. Lymphoid enhancer-binding factor 1 (Lef1) is a transcription factor that mediates Wnt signaling and has been suggested to regulate dentin sialophosphoprotein ( Dspp ) expression in vitro . This study aimed to clarify their precise relationship in the process of odontoblast differentiation in vivo . Methods The detailed spatiotemporal expression patterns of Lef1 and Dspp together with other known and putative odontoblast differentiation markers such as P21 and heat-shock protein 25 ( Hsp25 ) were examined by in situ hybridization and immunohistochemistry on paraffin sections of rat incisors and developing molars at postnatal days 1–100. To observe odontoblast regeneration following Tooth Injury, a cavity was prepared on the upper first molar of 10-week-old rats and the expressions of Lef1 and Dspp were investigated. Results Following undifferentiated state expressing none of these examined markers, preodontoblasts begun to express P21 , Lef1 and Hsp25 according to their progress of differentiation, although Dspp was undetectable. Immature odontoblasts commenced transcribing Dspp simultaneously with dentin calcification. Lef1, Dspp and Hsp25 were co-expressed in mature odontoblasts. In contrast to continuously growing incisors, Lef1, Dspp and P21 were down-regulated in the resting odontoblasts in molars when primary dentin formation was completed. Remarkably, Lef1 expression also preceded Dspp expression in newly differentiated odontoblast-like cells during the pulpal healing process after Tooth Injury. Conclusions Lef1 expression precedes Dspp expression without exception in both primary and reparative dentinogeneses. Our results suggest that Lef1 might play a key role in odontoblast differentiation through regulating Dspp expression.
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Histochemical and immunocytochemical study of hard tissue formation in dental pulp during the healing process in rat molars after Tooth replantation
Cell and Tissue Research, 2006Co-Authors: Hiroko Tsukamoto-tanaka, Mika Ikegame, Ritsuo Takagi, Hidemitsu Harada, Hayato OhshimaAbstract:Dental pulp is assumed to possess the capacity to elaborate both bone and dentin matrix under the pathological conditions following Tooth Injury. This study was undertaken to clarify the mechanism inducing bone formation in the dental pulp by investigating the pulpal healing process, after Tooth replantation, by micro-computed tomography (μ-CT), immunocytochemistry for heat-shock protein (HSP)-25 and cathepsin K (CK), and histochemistry for both alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP). Under deep anesthesia, the upper right first molar of 4-week-old Wistar rats was extracted and immediately repositioned in the original socket. In control teeth at this age, the periphery of the coronal dental pulp showed intense ALP-positive and HSP-25-positive reactions, whereas there were no TRAP-positive or CK-positive cells. Tooth replantation weakened or terminated ALP-positive and HSP-25-positive reactions in the pulp tissue at the initial stages. At 3–7 days after operation, the ALP-positive region recovered from the root apex to the coronal pulp followed by HSP-25-positive reactions in successful cases showing tertiary dentin formation. In other cases, TRAP-positive and CK-positive cells appeared in the pulp tissue of the replanted Tooth at postoperative days 5–10 and remained associated with the bone tissue after 12–60 days. Immunoelectron microscopy clearly demonstrated that CK-positive osteoclast-lineage cells made contact with mesenchymal cells with prominent nucleoli and well-developed cell organelles. These data suggest that the appearance of TRAP-positive and CK-positive cells is involved in the induction of bone tissue formation in dental pulp.
Michael S. Gold - One of the best experts on this subject based on the ideXlab platform.
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Changes in TrkB-like immunoreactivity in rat trigeminal ganglion after Tooth Injury.
Journal of endodontics, 2003Co-Authors: Ali Behnia, Lei Zhang, Makepeace Charles, Michael S. GoldAbstract:The purpose of this study was to characterize the impact of Tooth Injury on the distribution of tyrosine receptor kinase B (TrkB) among trigeminal ganglion neurons and assess the time course for Tooth Injury-induced TrkB distribution changes. In addition, we sought to further characterize the subpopulation of the afferents expressing TrkB receptors. Fifteen adult male Sprague-Dawley rats were studied. Pulpal inflammation was induced and ganglia were subsequently harvested and processed at different time points. Standard immunohistochemical fluorescence techniques were used to visualize TrkB-like immunoreactivity and isolectin B4 binding. Results indicate that full-length TrkB receptors are present in 36.6% of trigeminal ganglion neurons. This percentage decreases for the first 48 h and then increases to 41% by 7 days after Tooth Injury. Finally, TrkB appears to be present in a large percentage (54%) of isolectin B4+ neurons, suggesting that it is present in nociceptive afferents. These data highlight the fact that even mild Injury results in sustained changes in nociceptive circuitry and raise the possibility that the brain-derived neurotrophic factor/TrkB system may contribute to persistent pain after Tooth repair.