1.Mediating role of psychological resilience between family intimacy and adaptability and experiential avoidance among undergraduate nursing students
Jiahui ZHOU ; Kangjiao XIAO ; Rui WANG ; Zhihe DENG ; Meifen DAI
China Occupational Medicine 2023;50(1):63-68
2.Histopathological study on the healing of orthodontic implant-bone interface adjacent to extraction.
Yangming ZHOU ; Yun HU ; Leilei ZHENG ; Zhihe ZHAO ; Tian TANG ; Feng DENG ; Guangxi WEI ; Jinfeng HUO ; Xiaoge ZHANG
West China Journal of Stomatology 2013;31(5):509-513
OBJECTIVEOsseointegration of orthodontic microscrew implant is influenced by tooth extraction. This study aims to evaluate the safety margin of the osseointegration of orthodontic implants by investigating the healing process of the implant-bone interface through histopathological studies and quantitative determination.
METHODSTwelve male beagles were selected and randomly divided into four groups. An orthodontic microscrew was implanted beside the tooth extraction area. Animals were killed in 1, 3, 8, and, 12 weeks to investigate tissue response. Histomorphological observation and bone implant contact ratio (BIC) tests were performed at different healing time after implantation.
RESULTSA new bone was formed on the implant-bone interface of the control group. Bone resorptions were also detected in the experimental group 3 weeks after implantation. The BIC level of the control groups increased during the first 8 weeks; no change was observed anymore after the 8th week. On the other hand, the BIC value in the experimental group decreased in the first 3 weeks. It then increased rapidly and reached its peak of 80.08% in the 8th week. No significant difference wa s found between the experimental and control groups in the first 3 weeks. After the 3rd week, the BIC value of the experimental group (44.35%) was lower than that of the control group (55.46%) (P < 0.01).
CONCLUSIONThe healing process after implantation was influenced by tooth extraction. Bone resorption was detected at an early stage. However, vigorous bone remodeling was observed subsequently.
Animals ; Bone Remodeling ; Bone and Bones ; Dental Implantation, Endosseous ; Dental Implants ; Dogs ; Male ; Mandible ; Osseointegration ; Prostheses and Implants ; Tooth Extraction ; Wound Healing
3.Atp6i deficient mouse model uncovers transforming growth factor-β1 /Smad2/3 as a key signaling pathway regulating odontoblast differentiation and tooth root formation.
Jue WANG ; Abigail MCVICAR ; Yilin CHEN ; Hong-Wen DENG ; Zhihe ZHAO ; Wei CHEN ; Yi-Ping LI
International Journal of Oral Science 2023;15(1):35-35
The biomolecular mechanisms that regulate tooth root development and odontoblast differentiation are poorly understood. We found that Atp6i deficient mice (Atp6i-/-) arrested tooth root formation, indicated by truncated Hertwig's epithelial root sheath (HERS) progression. Furthermore, Atp6i deficiency significantly reduced the proliferation and differentiation of radicular odontogenic cells responsible for root formation. Atp6i-/- mice had largely decreased expression of odontoblast differentiation marker gene expression profiles (Col1a1, Nfic, Dspp, and Osx) in the alveolar bone. Atp6i-/- mice sample RNA-seq analysis results showed decreased expression levels of odontoblast markers. Additionally, there was a significant reduction in Smad2/3 activation, inhibiting transforming growth factor-β (TGF-β) signaling in Atp6i-/- odontoblasts. Through treating pulp precursor cells with Atp6i-/- or wild-type OC bone resorption-conditioned medium, we found the latter medium to promote odontoblast differentiation, as shown by increased odontoblast differentiation marker genes expression (Nfic, Dspp, Osx, and Runx2). This increased expression was significantly blocked by anti-TGF-β1 antibody neutralization, whereas odontoblast differentiation and Smad2/3 activation were significantly attenuated by Atp6i-/- OC conditioned medium. Importantly, ectopic TGF-β1 partially rescued root development and root dentin deposition of Atp6i-/- mice tooth germs were transplanted under mouse kidney capsules. Collectively, our novel data shows that the prevention of TGF-β1 release from the alveolar bone matrix due to OC dysfunction may lead to osteopetrosis-associated root formation via impaired radicular odontoblast differentiation. As such, this study uncovers TGF-β1 /Smad2/3 as a key signaling pathway regulating odontoblast differentiation and tooth root formation and may contribute to future therapeutic approaches to tooth root regeneration.
Female
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Animals
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Mice
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Transforming Growth Factor beta1
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Odontoblasts
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Culture Media, Conditioned
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Cell Differentiation
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Signal Transduction
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Disease Models, Animal
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Tooth Root