Мы используем Cookies Этот веб-сайт использует cookie-файлы, чтобы предлагать вам наиболее актуальную информацию. Просматривая этот веб-сайт, Вы принимаете cookie-файлы.
Survival of odontoblasts during infection and inflammation determines prognosis of the dentalpulp.
2
The DPSCs were collected from the dentalpulp of adult human third molars.
3
Inflammation and elevated IL17A secretion occurred in the dentalpulp during orthodontic tooth movement.
4
Results: The active fission activity of mitochondria and mitophagy in inflammatory dentalpulp was observed.
5
Pulpitis, inflammation of the dentalpulp, is a disease that often necessitates emergency dental care.
6
Introduction: Chronic inflammation disrupts dentalpulp regeneration by disintegrating the recruitment process of progenitors for repair.
7
Thus, our data suggest that stem cells derived from dentalpulp may have therapeutic benefits for PD.
8
Stable cell lines of dentalpulp stem cells are generated, maintained in culture, and used for subsequent experiments.
9
The treatment enhanced dentalpulp cell adhesion and proliferation, suggesting that this system is promising for medical applications.
10
We identified activation of autophagy and apoptosis in the odontoblasts due to inflammation of the human dentalpulp.
11
Information concerning cell proliferation and differentiation in dentalpulp may be important to understand tooth response to exogenous stimuli.
12
A spraying method for building-up polyelectrolyte films followed by the deposition of dentalpulp cells by spraying is presented.
13
In this study, we investigated the mitochondrial damage and mitophagy occurred in inflammatory human dentalpulp and lipopolysaccharide-stimulated preodontoblasts.
14
Furthermore, adult dentalpulp cells supplemented with these two growth factors re-established the inductive potential of postnatal dentalpulp tissue.
15
Immunohistochemical staining of infected human dentalpulp and tissue from experimental dental pulpitis in rats showed that Wnt5a levels were increased.
16
Up-regulation of VEGF expression in the dentalpulp may result in increased intra-pulpal pressure, and contribute to pain and irreversible tissue damage.