start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=5 article-no= start-page=345 end-page=349 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201010 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Intraoral Vertical Ramus Osteotomy Improved the Stomatognathic Function in an Elderly Patient with Mandibular Protrusion:A Case Report en-subtitle= kn-subtitle= en-abstract= kn-abstract=This article reports the successful surgical-orthodontic treatment of an elderly patient with dentofacial deformity and signs and symptoms of temporomandibular disorder (TMD). The patient was a 63-year-old woman with a concave profile due to mandibular protrusion. To correct skeletal deformities, the mandible was posteriorly repositioned by employing intraoral vertical ramus osteotomy (IVRO) following presurgical orthodontic treatment. After active treatment for 31 months, the facial profile was significantly improved and satisfactory occlusion was achieved. In addition, TMD symptoms of clicking sounds on the left side and difficulty in mouth opening were resolved. Regarding the findings of magnetic resonance imaging, anterior disc displacement in the opening phase was improved in the temporomandibular joint on the left side. Furthermore, stomatognathic functions were also improved without any aggravation of age-related problems. In conclusion, surgical repositioning of the mandible using IVRO leads to both morphological and functional improvements even in elderly patients. en-copyright= kn-copyright= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KurodaShingo en-aut-sei=Kuroda en-aut-mei=Shingo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KawanabeNoriaki en-aut-sei=Kawanabe en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Takano-YamamotoTeruko en-aut-sei=Takano-Yamamoto en-aut-mei=Teruko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamashiroTakashi en-aut-sei=Yamashiro en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Orthodontics and Dentofacial Orthopedics, The University of Tokushima Graduate School of Oral Sciences affil-num=3 en-affil= kn-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Division of Orthodontics and Dentofacial Orthopedics, Tohoku University Graduate School of Dentistry affil-num=5 en-affil= kn-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=elderly patient kn-keyword=elderly patient en-keyword=orthodontics kn-keyword=orthodontics en-keyword=temporomandibular disorder kn-keyword=temporomandibular disorder en-keyword=intraoral vertical ramus osteotomy kn-keyword=intraoral vertical ramus osteotomy END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=5 article-no= start-page=437 end-page=443 dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=201710 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Modification of Dentofacial Growth Associated with Goldenhar Syndrome en-subtitle= kn-subtitle= en-abstract= kn-abstract= The rare developmental defect, Goldenhar syndrome is characterized by complex craniofacial and dentofacial anomalies. Here we describe the successful orthodontic treatment of a 5-year-old Japanese Goldenhar syndrome patient with mild facial asymmetry, right microtia, right-side hearing loss, and tongue-thrusting by a modification of dentofacial growth using a non-surgical orthopedic treatment approach. Improvement of the vertical discrepancies on the affected side and canted occlusal plane as well as mandibular deviation were achieved with a functional orthopaedic approach. Stable and acceptable occlusion were obtained over the 32-month post-retention period. A non-surgical orthodontic treatment approach offers satisfactory facial aesthetic outcomes in Goldenhar syndrome. en-copyright= kn-copyright= en-aut-name=Ei Ei Hsu Hlaing en-aut-sei=Ei Ei Hsu Hlaing en-aut-mei= kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HaraChikako en-aut-sei=Hara en-aut-mei=Chikako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=4 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Goldenhar syndrome kn-keyword=Goldenhar syndrome en-keyword=orthodontic treatment kn-keyword=orthodontic treatment en-keyword=functional appliance kn-keyword=functional appliance END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=ニワトリ胚頭蓋骨中骨細胞におけるConnexin 43を介した蛍光色素の細胞間移動はホルモンやpH、カルシウムイオンによって調節を受ける kn-title=Hormonal, pH, and Calcium Regulation of Connexin 43-Mediated Dye Transfer in Osteocytes in Chick Calvaria. en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name=石原嘉人 kn-aut-sei=石原 kn-aut-mei=嘉人 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol=13 cd-vols= no-issue=2 article-no= start-page=108 end-page=117 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080921 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Primary cultures of chick osteocytes retain functional gap junctions between osteocytes and between osteocytes and osteoblasts en-subtitle= kn-subtitle= en-abstract= kn-abstract=

The inaccessibility of osteocytes due to their embedment in the calcified bone matrix in vivo has precluded direct demonstration that osteocytes use gap junctions as a means of intercellular communication. In this article, we report successfully isolating primary cultures of osteocytes from chick calvaria, and, using anti-connexin 43 immunocytochemistry, demonstrate gap junction distribution to be comparable to that found in vivo. Next, we demonstrate the functionality of the gap junctions by (1) dye coupling studies that showed the spread of microinjected Lucifer Yellow from osteoblast to osteocyte and between adjacent osteocytes and (2) analysis of fluorescence replacement after photobleaching (FRAP), in which photobleaching of cells loaded with a membrane-permeable dye resulted in rapid recovery of fluorescence into the photobleached osteocyte, within 5 min postbleaching. This FRAP effect did not occur when cells were treated with a gap junction blocker (18 alpha-glycyrrhetinic acid), but replacement of fluorescence into the photobleached cell resumed when it was removed. These studies demonstrate that gap junctions are responsible for intercellular communication between adjacent osteocytes and between osteoblasts and osteocytes. This role is consistent with the ability of osteocytes to respond to and transmit signals over long distances while embedded in a calcified matrix.

en-copyright= kn-copyright= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=RisHans en-aut-sei=Ris en-aut-mei=Hans kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MurshidSakhr A. en-aut-sei=Murshid en-aut-mei=Sakhr A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SugawaraYasuyo en-aut-sei=Sugawara en-aut-mei=Yasuyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamamotoTeruko Takano en-aut-sei=Yamamoto en-aut-mei=Teruko Takano kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=LimSoo-Siang en-aut-sei=Lim en-aut-mei=Soo-Siang kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Orthodontics and Dentofacial Orthopedics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Orthodontics and Dentofacial Orthopedics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Zoology and Integrated Microscopy Resource, University of Wisconsin affil-num=4 en-affil= kn-affil=Department of Orthodontics and Dentofacial Orthopedics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Orthodontics and Dentofacial Orthopedics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Orthodontics and Dentofacial Orthopedics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=National Science Foundation en-keyword=osteocytes kn-keyword=osteocytes en-keyword=osteoblasts kn-keyword=osteoblasts en-keyword=gap junctions kn-keyword=gap junctions en-keyword=intercellular communication kn-keyword=intercellular communication en-keyword=dye coupling kn-keyword=dye coupling en-keyword=FRAP kn-keyword=FRAP END start-ver=1.4 cd-journal=joma no-vol=33 cd-vols= no-issue=9 article-no= start-page=10409 end-page=10424 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=201909 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Role of intracellular Ca2+?based mechanotransduction of human periodontal ligament fibroblasts en-subtitle= kn-subtitle= en-abstract= kn-abstract=Human periodontal ligament (hPDL) fibroblasts are thought to receive mechanical stress (MS) produced by orthodontic tooth movement, thereby regulating alveolar bone remodeling. However, the role of intracellular calcium ([Ca2+]i)‐based mechanotransduction is not fully understood. We explored the MS‐induced [Ca2+]i responses both in isolated hPDL fibroblasts and in intact hPDL tissue and investigated its possible role in alveolar bone remodeling. hPDL fibroblasts were obtained from healthy donors' premolars that had been extracted for orthodontic reasons. The oscillatory [Ca2+]i activity induced by static compressive force was measured by a live‐cell Ca2+ imaging system and evaluated by several feature extraction method. The spatial pattern of cell‐cell communication was investigated by Moran's I , an index of spatial autocorrelation and the gap junction (GJ) inhibitor. The Ca2+‐transporting ionophore A23187 was used to further investigate the role of [Ca2+]i up‐regulation in hPDL cell behavior. hPDL fibroblasts displayed autonomous [Ca2+]i responses. Compressive MS activated this autonomous responsive behavior with an increased percentage of responsive cells both in vitro and ex vivo . The integration, variance, maximum amplitude, waveform length, and index J in the [Ca2+]i responses were also significantly increased, whereas the mean power frequency was attenuated in response to MS. The increased Moran's I after MS indicated that MS might affect the pattern of cell‐cell communication via GJs. Similar to the findings of MS‐mediated regulation, the A23187‐mediated [Ca2+]i uptake resulted in the up‐regulation of receptor activator of NF‐κB ligand (Rankl) and Sost along with increased sclerostin immunoreactivity, suggesting that [Ca2+]i signaling networks may be involved in bone remodeling. In addition, A23187‐treated hPDL fibroblasts also showed the suppression of osteogenic differentiation and mineralization. Our findings suggest that augmented MS‐mediated [Ca2+]i oscillations in hPDL fibroblasts enhance the production and release of bone regulatory signals via Rankl/Osteoprotegerin and the canonical Wnt/β‐catenin pathway as an early process in tooth movement?initiated alveolar bone remodeling.?Ei Hsu Hlaing, E., Ishihara, Y., Wang, Z., Odagaki, N., Kamioka, H. Role of intracellular Ca2+‐based mechanotransduction of human periodontal ligament fibroblasts. FASEB J. 33, 10409?10424 (2019). en-copyright= kn-copyright= en-aut-name=HlaingEi Ei Hsu en-aut-sei=Hlaing en-aut-mei=Ei Ei Hsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=WangZiyi en-aut-sei=Wang en-aut-mei=Ziyi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OdagakiNaoya en-aut-sei=Odagaki en-aut-mei=Naoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=5 en-affil=Department of Orthodontics and Dentofacial Orthopedics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= en-keyword=hPDL kn-keyword=hPDL en-keyword=intracellular calcium kn-keyword=intracellular calcium en-keyword=SOST/sclerostin kn-keyword=SOST/sclerostin en-keyword=Rankl/Opg kn-keyword=Rankl/Opg en-keyword=bone remodeling kn-keyword=bone remodeling END start-ver=1.4 cd-journal=joma no-vol=16 cd-vols= no-issue=1 article-no= start-page=12 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200602 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Occlusal reconstruction of a patient with ameloblastoma ablation using alveolar distraction osteogenesis: a case report en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background Ameloblastoma is one of the most common benign odontogenic neoplasms. Its surgical excision has the potential to lead to postoperative malocclusion. In this case report, we describe the successful interdisciplinary orthodontic treatment of a patient with ameloblastoma who underwent marginal mandibulectomy. Case presentation A woman of 20-year-old was diagnosed with ameloblastoma, and underwent marginal mandibulectomy when she was 8 years of age. She had an excessive overjet (11.5 mm) and a mild open bite (- 1.5 mm) with a severely resorbed atrophic edentulous ridge in the area around the mandibular left lateral incisor, canine and first premolar. An alveolar bone defect associated with tumor resection was regenerated by vertical distraction osteogenesis (DO). Subsequently, 3 dental implants were placed into the reconstructed mandible. Orthodontic treatment using implant-anchored mechanics provided a proper facial profile with significantly improved occlusal function. The occlusion appeared stable for a 7-year retention period. Conclusions These results suggest that surgically assisted and implant anchored-orthodontic approaches might be effective for the correction of such malocclusions. en-copyright= kn-copyright= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ArakawaHikaru en-aut-sei=Arakawa en-aut-mei=Hikaru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NishiyamaAkiyoshi en-aut-sei=Nishiyama en-aut-mei=Akiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Ameloblastoma kn-keyword=Ameloblastoma en-keyword=Alveolar distraction osteogenesis kn-keyword=Alveolar distraction osteogenesis en-keyword=Implant anchorage kn-keyword=Implant anchorage en-keyword=Postoperative malocclusion kn-keyword=Postoperative malocclusion END start-ver=1.4 cd-journal=joma no-vol=39 cd-vols= no-issue= article-no= start-page=148 end-page=159 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200825 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Changes in the intra- and peri-cellular sclerostin distribution in lacuno-canalicular system induced by mechanical unloading en-subtitle= kn-subtitle= en-abstract= kn-abstract=Introduction
Mechanical stimuli regulate Sclerostin (Scl), a negative regulator of bone formation, expression in osteocytes. However, the detailed Scl distribution in osteocytes in response to mechanical unloading remains unclear.
Materials and methods
Twelve-week-old male rats were used. The sciatic and femoral nerves on the right side were excised as mechanical unloading treatment. A sham operation was performed on the left side. One week after neurotrauma, the bone density of the femora was evaluated by peripheral quantitative computed tomography, and immunofluorescence was performed in coronal sections of the femoral diaphysis. The mean fluorescence intensity and fluorescent profile of Scl from the marrow to the periosteal side were analyzed to estimate the Scl expression and determine to which side (marrow or periosteal) the Scl prefers to distribute in response to mechanical unloading. The most sensitive region indicated by the immunofluorescence results was further investigated by transmission electron microscopy (TEM) with immunogold staining to show the Scl expression changes in different subcellular structures.
Results
In femur distal metaphysis, neurotrauma-induced mechanical unloading significantly decreased the bone density, made the distribution of Scl closer to the marrow on the anterior and medial side, and increased the Scl expression only on the lateral side. TEM findings showed that only the expression of Scl in canaliculi was increased by mechanical unloading.
Conclusions
Our results showed that even short-term mechanical unloading is enough to decrease bone density, and mechanical unloading not only regulated the Scl expression but also changed the Scl distribution in both the osteocyte network and subcellular structures. en-copyright= kn-copyright= en-aut-name=OsumiRyuta en-aut-sei=Osumi en-aut-mei=Ryuta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=WangZiyi en-aut-sei=Wang en-aut-mei=Ziyi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OdagakiNaoya en-aut-sei=Odagaki en-aut-mei=Naoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IimuraTadahiro en-aut-sei=Iimura en-aut-mei=Tadahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=2 en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=4 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=5 en-affil=Department of Pharmacology, Graduate School of Dental Medicine, Hokkaido University kn-affil= affil-num=6 en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=Sclerostin distribution kn-keyword=Sclerostin distribution en-keyword=Lacuno-canalicular system kn-keyword=Lacuno-canalicular system en-keyword=Mechanical unloading kn-keyword=Mechanical unloading END start-ver=1.4 cd-journal=joma no-vol=8 cd-vols= no-issue= article-no= start-page=e10244 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20201109 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Loading history changes the morphology and compressive force-induced expression of receptor activator of nuclear factor kappa B ligand/osteoprotegerin in MLO-Y4 osteocytes en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background
In this study, we investigated the effect of the mechanical loading history on the expression of receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) in MLO-Y4 osteocyte-like cells.
Methods
Three hours after MLO-Y4 osteocytes were seeded, a continuous compressive force (CCF) of 31 dynes/cm2 with or without additional CCF (32 dynes/cm2) was loaded onto the osteocytes. After 36 h, the additional CCF (loading history) was removed for a recovery period of 10 h. The expression of RANKL, OPG, RANKL/OPG ratio, cell numbers, viability and morphology were time-dependently examined at 0, 3, 6 and 10 h. Then, the same additional CCF was applied again for 1 h to all osteocytes with or without the gap junction inhibitor to examine the expression of RANKL, OPG, the RANKL/OPG ratio and other genes that essential to characterize the phenotype of MLO-Y4 cells. Fluorescence recovery after photobleaching technique was also applied to test the differences of gap-junctional intercellular communications (GJIC) among MLO-Y4 cells.
Results
The expression of RANKL and OPG by MLO-Y4 osteocytes without a loading history was dramatically decreased and increased, respectively, in response to the 1-h loading of additional weight. However, the expression of RANKL, OPG and the RANKL/OPG ratio were maintained at the same level as in the control group in the MLO-Y4 osteocytes with a loading history but without gap junction inhibitor treatment. Treatment of loading history significantly changed the capacity of GJIC and protein expression of connexin 43 (Cx43) but not the mRNA expression of Cx43. No significant difference was observed in the cell number or viability between the MLO-Y4 osteocyte-like cells with and without a loading history or among different time checkpoints during the recovery period. The cell morphology showed significant changes and was correlated with the expression of OPG, Gja1 and Dmp1 during the recovery period.
Conclusion
Our findings indicated that the compressive force-induced changes in the RANKL/OPG expression could be habituated within at least 11 h by 36-h CCF exposure. GJIC and cell morphology may play roles in response to loading history in MLO-Y4 osteocyte-like cells. en-copyright= kn-copyright= en-aut-name=WangZiyi en-aut-sei=Wang en-aut-mei=Ziyi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=WengYao en-aut-sei=Weng en-aut-mei=Yao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OdagakiNaoya en-aut-sei=Odagaki en-aut-mei=Naoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HlaingEi Ei Hsu en-aut-sei=Hlaing en-aut-mei=Ei Ei Hsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IzawaTakashi en-aut-sei=Izawa en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OkamuraHirohiko en-aut-sei=Okamura en-aut-mei=Hirohiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Oral Morphology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=5 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=Department of Oral Morphology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=Osteocytes kn-keyword=Osteocytes en-keyword=Habituation kn-keyword=Habituation en-keyword=18 alpha-Glycyrrhetinic acid kn-keyword=18 alpha-Glycyrrhetinic acid en-keyword=Fluorescence recovery after photobleaching kn-keyword=Fluorescence recovery after photobleaching en-keyword=Gap junctional intercellular communication kn-keyword=Gap junctional intercellular communication END start-ver=1.4 cd-journal=joma no-vol=13 cd-vols= no-issue=1 article-no= start-page=22028 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2023 dt-pub=20231212 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Bundling of collagen fibrils influences osteocyte network formation during bone modeling en-subtitle= kn-subtitle= en-abstract= kn-abstract=Osteocytes form a cellular network by gap junctions between their cell processes. This network is important since intercellular communication via the network is essential for bone metabolism. However, the factors that influence the formation of this osteocyte network remain unknown. As the early stage of osteocyte network formation occurs on the bone surface, we observed a newly formed trabecular bone surface by orthogonal focused ion beam-scanning electron microscopy. The embedding late osteoblast processes tended to avoid bundled collagen fibrils and elongate into sparse collagen fibrils. Then, we examined whether the inhibition of bundling of collagen fibrils using a potent lysyl oxidase inhibitor, beta-aminopropionitrile (BAPN) changed the cellular network of the chick calvaria. The osteocyte shape of the control group was spindle-shape, while that of the BAPN group was sphere-shaped. In addition, the osteocyte processes of the control group were elongated vertically to the long axis of the cell body, whereas the osteocyte processes of the BAPN group were elongated radially. Therefore, it was suggested that the bundling of collagen fibrils influences normal osteocyte network formation during bone modeling. en-copyright= kn-copyright= en-aut-name=HashimotoMana en-aut-sei=Hashimoto en-aut-mei=Mana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakahashiHaruka en-aut-sei=Takahashi en-aut-mei=Haruka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=Tabata-OkuboKaori en-aut-sei=Tabata-Okubo en-aut-mei=Kaori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NagaokaNoriyuki en-aut-sei=Nagaoka en-aut-mei=Noriyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TokunagaKazuaki en-aut-sei=Tokunaga en-aut-mei=Kazuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsumoriHaruka en-aut-sei=Matsumori en-aut-mei=Haruka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IshiharaYoshihito en-aut-sei=Ishihara en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KakuMasaru en-aut-sei=Kaku en-aut-mei=Masaru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IimuraTadahiro en-aut-sei=Iimura en-aut-mei=Tadahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=HaraToru en-aut-sei=Hara en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KamiokaHiroshi en-aut-sei=Kamioka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Orthodontics, Okayama University Hospital kn-affil= affil-num=4 en-affil=Advanced Research Center for Oral and Craniofacial Sciences, Okayama University Dental School kn-affil= affil-num=5 en-affil=Nikon Corporation kn-affil= affil-num=6 en-affil=Nikon Corporation kn-affil= affil-num=7 en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil=Division of Bio?prosthodontics, Faculty of Dentistry and Graduate School of Medical and Dental Sciences, Niigata University kn-affil= affil-num=9 en-affil=Department of Pharmacology, Faculty and Graduate School of Dental Medicine, Hokkaido University kn-affil= affil-num=10 en-affil=Research Center for Structural Materials, National Institute for Materials Science kn-affil= affil-num=11 en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= END