The Role of Vasculature Engineering in Dental Pulp Regeneration

2017 ◽  
Vol 43 (9) ◽  
pp. S102-S106 ◽  
Author(s):  
Waruna Lakmal Dissanayaka ◽  
Chengfei Zhang
2012 ◽  
Vol 1 (2) ◽  
pp. 74
Author(s):  
SunitKumar Jurel ◽  
Shruti Sial ◽  
RaghuwarD Singh ◽  
Mayank Singh ◽  
DurgaS Gupta

2013 ◽  
Vol 44 (6) ◽  
pp. 715-721 ◽  
Author(s):  
Han-Wool Choung ◽  
Ji-Hyun Lee ◽  
Dong-Seol Lee ◽  
Pill-Hoon Choung ◽  
Joo-Cheol Park

2015 ◽  
Vol 41 (6) ◽  
pp. 797-803 ◽  
Author(s):  
Mohammad Ali Saghiri ◽  
Armen Asatourian ◽  
Christine M. Sorenson ◽  
Nader Sheibani

2017 ◽  
Vol 50 (5) ◽  
pp. e12361 ◽  
Author(s):  
Xuexin Zhang ◽  
Hui Li ◽  
Jingjing Sun ◽  
Xiangyou Luo ◽  
Hefeng Yang ◽  
...  

2021 ◽  
Vol 22 (9) ◽  
pp. 4357
Author(s):  
Sahng G. Kim

Despite the recent explosion of investigations on dental pulp regeneration using various tissue engineering strategies, the translation of the findings from such studies into therapeutic applications has not been properly achieved. The purpose of this scoping review was to systematically review the efficacy of mesenchymal stem cell transplantation for dental pulp regeneration. A literature search was conducted using five electronic databases from their inception to January 2021 and supplemented by hand searches. A total of 17 studies, including two clinical trials and 15 animal studies using orthotopic pulp regeneration models, were included for the review. The risk of bias for the individual studies was assessed. This scoping review demonstrated that the regeneration of vascularized pulp-like tissue was achieved using the stem cell transplantation strategy in animal models. Autologous cell transplantation in two clinical studies also successfully regenerated vascularized vital tissue. Dental pulp stem cell subpopulations, such as mobilized dental pulp stem cells, injectable scaffolds such as atelocollagen, and a granulocyte-colony forming factor, were the most commonly used for pulp regeneration. The overall risk of bias was unclear for animal studies and was moderate or judged to raise some concerns for clinical studies. More high-quality clinical studies are needed to further determine the safety and efficacy of the stem cell transplantation strategy for dental pulp regeneration.


2021 ◽  
Vol 02 (03) ◽  
Author(s):  
Saberian E ◽  
Jalili Sadrabad M ◽  
Petrasova A ◽  
Izadi A

2015 ◽  
Vol 21 (3-4) ◽  
pp. 550-563 ◽  
Author(s):  
Waruna Lakmal Dissanayaka ◽  
Kenneth M. Hargreaves ◽  
Lijian Jin ◽  
Lakshman P. Samaranayake ◽  
Chengfei Zhang

2012 ◽  
Vol 54 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Koichiro Muromachi ◽  
Naoto Kamio ◽  
Takashi Matsumoto ◽  
Kiyoshi Matsushima

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5808 ◽  
Author(s):  
Yanjing Ou ◽  
Yi Zhou ◽  
Shanshan Liang ◽  
Yining Wang

Background Senescence-related impairment of proliferation and differentiation limits the use of dental pulp cells for tissue regeneration. Deletion of sclerostin improves the dentinogenesis regeneration, while its role in dental pulp senescence is unclear. We investigated the role of sclerostin in subculture-induced senescence of human dental pulp cells (HDPCs) and in the senescence-related decline of proliferation and odontoblastic differentiation. Methods Immunohistochemical staining and qRT-PCR analyses were performed to examine the expression pattern of sclerostin in young (20–30-year-old) and senescent (45–80-year-old) dental pulps. HDPCs were serially subcultured until senescence, and the expression of sclerostin was examined by qRT-PCR analysis. HDPCs with sclerostin overexpression and knockdown were constructed to investigate the role of sclerostin in HDPCs senescence and senescence-related impairment of odontoblastic differentiation potential. Results By immunohistochemistry and qRT-PCR, we found a significantly increased expression level of sclerostin in senescent human dental pulp compared with that of young human dental pulp. Additionally, elevated sclerostin expression was found in subculture-induced senescent HDPCs in vitro. By sclerostin overexpression and knockdown, we found that sclerostin promoted HDPCs senescence-related decline of proliferation and odontoblastic differentiation potential with increased expression of p16, p53 and p21 and downregulation of the Wnt signaling pathway. Discussion The increased expression of sclerostin is responsible for the decline of proliferation and odontoblastic differentiation potential of HDPCs during cellular senescence. Anti-sclerostin treatment may be beneficial for the maintenance of the proliferation and odontoblastic differentiation potentials of HDPCs.


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