scholarly journals HISTOLOGICAL ANALYSIS OF REPARATIVE DENTIN FORMATION USING BIO DENTINE AND MTA AS PULP CAPPING AGENT: AN IN VIVO STUDY

2020 ◽  
Vol 7 (07) ◽  
2021 ◽  
Vol 2 ◽  
Author(s):  
Anushree Vijaykumar ◽  
Mina Mina

Wnt/β-catenin signaling is known to play essential roles in odontoblast differentiation and reparative dentin formation. Various Wnt activators including LiCl have been increasingly studied for their effectiveness to induce repair of the dentin-pulp complex. LiCl is a simple salt thought to activate Wnt/β-catenin signaling by inhibiting GSK3β. Previous in vitro and in vivo studies showed that LiCl increased odontoblast differentiation and enhanced reparative dentin formation. However, the underlying molecular and cellular mechanisms by which LiCl regulates odontoblast and osteoblast differentiation during reparative dentinogenesis are not well-understood. Our in vitro studies show that exposure of early dental pulp progenitors to LiCl increased the survival and the pool of αSMA+ progenitors, leading to enhanced odontoblast and osteoblast differentiation. The positive effects of LiCl in the differentiation of osteoblasts and odontoblasts from αSMA+ progenitors are mediated by Wnt/β-catenin signaling. Our results also showed that continuous and late exposure of dental pulp cells to LiCl increased the expression of odontoblast markers through Wnt/β-catenin signaling, and the number of odontoblasts expressing DMP1-Cherry and DSPP-Cerulean transgenes. However, unlike the early treatment, both continuous and late treatments decreased the expression of Bsp and the expression of BSP-GFPtpz transgene. These observations suggest that prolonged treatment with LiCl in more mature cells of the dental pulp has an inhibitory effect on osteoblast differentiation. The inhibitory effects of LiCl on osteogenesis and Bsp were not mediated through Wnt/β-catenin signaling. These observations suggest that the effects of LiCl, and GSK3β antagonists on reparative dentinogenesis involve multiple pathways and are not specific to Wnt/β-catenin signaling.


2019 ◽  
Vol 12 (4) ◽  
pp. 182-186
Author(s):  
Mozammal Hossain ◽  
Mahmood Sajedeen ◽  
Yukio Nakamura

This study was performed to examine whether calcium silicate could induce reparative dentin formation without eliciting any adverse effect in direct pulp capping of premolar teeth. Twenty participants who need extraction of their 4 healthy permanent premolar teeth for orthodontic reasons were included in this study. Following the surgical procedure, the exposed pulp tissue was treated either with calcium silicate or covered with calcium hydroxide paste. On day 3, 7, 14 and 28, the experimental teeth was extracted and examined using light microscopy and histometric analysis to observe the inflammatory changes and the amount of reparative dentin formation. The results showed that in the calcium silicate treated teeth, substantial amounts of dentine-like tissue was formed on day 14 and mostly located on the exposure site. It was also observed in the calcium hydroxide treated teeth but dentin-like tissue located at a distance from the exposure site. The total amount of reparative dentine formed in the calcium silicate-treated teeth was significantly higher (p<0.005) than in the calcium hydroxide-treated specimens. In conclusion that the calcium silicate indices pulpal wound healing and reparative formation in the exposed teeth without affecting the normal function of the remaining pulp.


2016 ◽  
Vol 1 (1) ◽  
Author(s):  
A Njeh ◽  
E Uzunoğlu ◽  
H Ardila-Osorio ◽  
S Simon ◽  
A Berdal ◽  
...  

2001 ◽  
Vol 15 (1) ◽  
pp. 96-100 ◽  
Author(s):  
D. Tziafas ◽  
G. Belibasakis ◽  
A. Veis ◽  
S. Papadimitriou

The nature and specificity of the mechanisms by which the amputated dentin-pulp interface is therapeutically healed determine the properties of the barrier at this site and play a critical role in the outcome of vital pulp therapy. Healing of the dentin-pulp complex proceeds either by natural repair-which results in defensive hard-tissue formation, or therapeutically regulated dentin regeneration, which aims to reconstitute the normal tissue architecture at the pulp periphery. Progress in biomedical research opens new directions for the design of biologically effective pulp therapies. Application of biocompatible and biodegradable carrier vehicles for local delivery of signaling molecules in pulp-capping situations showed induction of fibrodentin/reparative dentin formation, but often at the expense of underlying pulp tissue. An alternative pre-clinical model aiming to reconstitute normal tissue architecture directly at the dentin-pulp interface should be designed on the basis of the direct induction of odontoblast-like cell differentiation and reparative dentin formation at the pulp-capping material interface. Experimental data clearly showed that pulpal cells can differentiate directly into odontoblast-like cells in association with specific extracellular matrices (dentinal or fibrodentinal matrix) or TGFβ1-containing artificial substrates. Dentin-induced dentinogenesis can be used as a master plan for the achievement of new therapeutic opportunities. In the present study, several short-term experimental studies on dog teeth for potential direct induction of odontoblast-like cell differentiation at the surface of rhTGFβ1-containing artificial substrates (Millipore filters, hydroxyapatite granules, calcium hydroxide, pure titanium) failed to induce any specific reparative dentinogenic effects.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yam Prasad Aryal ◽  
Chang-Yeol Yeon ◽  
Tae-Young Kim ◽  
Eui-Seon Lee ◽  
Shijin Sung ◽  
...  

Apigenin, a natural product belonging to the flavone class, affects various cell physiologies, such as cell signaling, inflammation, proliferation, migration, and protease production. In this study, apigenin was applied to mouse molar pulp after mechanically pulpal exposure to examine the detailed function of apigenin in regulating pulpal inflammation and tertiary dentin formation. In vitro cell cultivation using human dental pulp stem cells (hDPSCs) and in vivo mice model experiments were employed to examine the effect of apigenin in the pulp and dentin regeneration. In vitro cultivation of hDPSCs with apigenin treatment upregulated bone morphogenetic protein (BMP)- and osteogenesis-related signaling molecules such as BMP2, BMP4, BMP7, bone sialoprotein (BSP), runt-related transcription factor 2 (RUNX2), and osteocalcin (OCN) after 14 days. After apigenin local delivery in the mice pulpal cavity, histology and cellular physiology, such as the modulation of inflammation and differentiation, were examined using histology and immunostainings. Apigenin-treated specimens showed period-altered immunolocalization patterns of tumor necrosis factor (TNF)-α, myeloperoxidase (MPO), NESTIN, and transforming growth factor (TGF)-β1 at 3 and 5 days. Moreover, the apigenin-treated group showed a facilitated dentin-bridge formation with few irregular tubules after 42 days from pulpal cavity preparation. Micro-CT images confirmed obvious dentin-bridge structures in the apigenin-treated specimens compared with the control. Apigenin facilitated the reparative dentin formation through the modulation of inflammation and the activation of signaling regulations. Therefore, apigenin would be a potential therapeutic agent for regenerating dentin in exposed pulp caused by dental caries and traumatic injury.


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