Eckols reduce dental pulp inflammation through the ERK1/2 pathway independent of COX-2 inhibition

Oral Diseases ◽  
2014 ◽  
pp. n/a-n/a ◽  
Author(s):  
U Paudel ◽  
Y-H Lee ◽  
T-H Kwon ◽  
N-H Park ◽  
B-S Yun ◽  
...  
Keyword(s):  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jie Chen ◽  
Huaxing Xu ◽  
Kun Xia ◽  
Shuhua Cheng ◽  
Qi Zhang

Abstract Background Unresolved inflammation and tissue destruction are considered to underlie the failure of dental pulp repair. As key mediators of the injury response, dental pulp stem cells (DPSCs) play a critical role in pulp tissue repair and regeneration. Resolvin E1 (RvE1), a major dietary omega-3 polyunsaturated fatty-acid metabolite, is effective in resolving inflammation and activating wound healing. However, whether RvE1 facilitates injured pulp-tissue repair and regeneration through timely resolution of inflammation and rapid mobilization of DPSCs is unknown. Therefore, we established a pulp injury model and investigated the effects of RvE1 on DPSC-mediated inflammation resolution and injured pulp repair. Methods A pulp injury model was established using 8-week-old Sprague-Dawley rats. Animals were sacrificed on days 1, 3, 7, 14, 21, and 28 after pulp capping with a collagen sponge immersed in PBS with RvE1 or PBS. Hematoxylin-eosin and Masson’s trichrome staining, immunohistochemistry, and immunohistofluorescence were used to evaluate the prohealing properties of RvE1. hDPSCs were incubated with lipopolysaccharide (LPS) to induce an inflammatory response, and the expression of inflammatory factors after RvE1 application was measured. Effects of RvE1 on hDPSC proliferation, chemotaxis, and odontogenic differentiation were evaluated by CCK-8 assay, transwell assay, alkaline phosphatase (ALP) staining, alizarin red staining, and quantitative PCR, and possible signaling pathways were explored using western blotting. Results In vivo, RvE1 reduced the necrosis rate of damaged pulp and preserved more vital pulps, and promoted injured pulp repair and reparative dentin formation. Further, it enhanced dentin matrix protein 1 and dentin sialoprotein expression and accelerated pulp inflammation resolution by suppressing TNF-α and IL-1β expression. RvE1 enhanced the recruitment of CD146+ and CD105+ DPSCs to the damaged molar pulp mesenchyme. Isolated primary cells exhibited the mesenchymal stem cell immunophenotype and differentiation. RvE1 promoted hDPSC proliferation and chemotaxis. RvE1 significantly attenuated pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) release and enhanced ALP activity, nodule mineralization, and especially, expression of the odontogenesis-related genes DMP1, DSPP, and BSP in LPS-stimulated DPSCs. RvE1 regulated AKT, ERK, and rS6 phosphorylation in LPS-stimulated DPSCs. Conclusions RvE1 promotes pulp inflammation resolution and dentin regeneration and positively influences the proliferation, chemotaxis, and differentiation of LPS-stimulated hDPSCs. This response is, at least partially, dependent on AKT, ERK, and rS6-associated signaling in the inflammatory microenvironment. RvE1 has promising application potential in regenerative endodontics.


2019 ◽  
Vol 25 (1) ◽  
pp. 15-21
Author(s):  
Iliescu Alexandru-Andrei ◽  
Gheorghiu Irina-Maria ◽  
Tănase Mihaela ◽  
Iliescu Andrei ◽  
Mitran Loredana ◽  
...  

Abstract The dentine-pulp complex response in deep caries is histological characterized by tertiary formation and mild chronic pulp inflammation. The quiescent primary odontoblasts are reactivated, laying down reactionary tertiary dentine. In more severe carious damage the primary odontoblasts die and reparative tertiary dentine is secreted by odontoblast-like cells, which are differentiated in adult teeth mainly from dental pulp stem cells DPSC. Though associated with reversible pulpitis DPSC still preserve in deep caries the capability of migration, proliferation and differentiation. Some common mechanisms of molecular signals involved in tertiary dentine formation might also explain the balance between inflammation and regeneration of dentine-pulp complex.


Author(s):  
Julia Guerrero-Gironés ◽  
Antonia Alcaina-Lorente ◽  
Clara Ortiz-Ruiz ◽  
Eduardo Ortiz-Ruiz ◽  
María P. Pecci-Lloret ◽  
...  

Melatonin plays an essential role in the regulation of bone growth. The actions that melatonin exerts on odontoblasts may be similar to its action on osteoblasts. This research aimed to evaluate the pulp response to melatonin used for direct pulp capping to evaluate the antioxidant effect of melatonin administered orally and its influence on dental pulp. Direct pulp capping was performed on the upper molars of Sprague Dawley rats using melatonin or Mineral Trioxide Aggregate (MTA). The study groups were: MTA; Melatonin; MTA + Melatonin administered orally; and Melatonin + Melatonin administered orally. In the latter two groups, the animals drank water dosed with melatonin ad libitum (10 mg/100 mL). After 30 days, the animals were sacrificed, and 5 ml of blood, the kidneys, and the liver were extracted in order to evaluate oxidative stress using thiobarbituric acid reactive substances testing (TBARS). Fragments of the maxilla containing the study molars were prepared for histological evaluation. The degree of pulp inflammation and pulp necrosis, the presence of reparative dentin and dentin bridging the pulp chamber, the presence and regularity of the odontoblastic layer, and the presence of pulp fibrosis were evaluated. No significant differences were found between the four study groups for any of the studied histological variables. The oral administration of melatonin did not modify the local effects of MTA or melatonin on dental pulp, or reduce basal-level oxidative stress. The effect of melatonin on pulp is similar to that of MTA and may be used as an agent for direct pulp capping.


Author(s):  
Daniele Paraguassú FAGUNDES-DE-SOUZA ◽  
Marcelo Henrique NAPIMOGA ◽  
Andresa Borges SOARES ◽  
Vera Cavalcanti ARAÚJO ◽  
Cecilia Pedroso TURSSI

ABSTRACT Objective: This study investigated the presence of inflammatory response in the dental pulp of rats showing hypersensitive dentin, induced by erosive episodes. Methods: Sixteen Wistar rats were fed with commercial sucrose-free pellet diet for 12 hours; whereas the food was removed during the remainder of the day, and the animals received mineral water or a lemon-based sucrose-free soft drink, according to the group to which they belonged. Eight animals consumed the soft drink to induce hypersensitivity, while the other 8 animals received mineral water (control). After six weeks, the animals were euthanized, the mandible was removed and subjected to a median incision in the sagittal plane, to obtain right and left hemimandibles. The slides stained with hematoxylin-eosin were analyzed using light microscopy. Results: Histological evaluation of the control and experimental groups revealed no inflammatory process in the pulp tissue, and the presence of inflammatory cells, such as lymphocytes, plasma cells, eosinophils and macrophages, was not observed. In addition, there was no edema or dilated and congested blood vessels. The Mann-Whitney test showed no significant difference (p = 1.000) between the experimental and the control groups. Conclusion: In the animal model used, dentin hypersensitivity does not trigger dental pulp inflammatory response.


2004 ◽  
Vol 15 (2) ◽  
pp. 104-108 ◽  
Author(s):  
Italo Medeiros Faraco Junior ◽  
Roberto Holland

This study was conducted to observe the response of dogs' dental pulp to white mineral trioxide aggregate (MTA) when used as pulp capping material. The pulp of 15 dogs' teeth was experimentally exposed and capped with white MTA. The animals were sacrificed two months later and the specimens were prepared for histomorphological study. The pulp capped with white MTA showed a healing process with complete dentin bridge formation in all samples. In some cases, there was not a tubular dentin shape, but only a structure with an interesting morphological aspect sealing the exposure site. Only 2 specimens exhibited pulp inflammation. In conclusion, the data obtained in this study showed that white MTA has the necessary properties of a pulp capping material.


2018 ◽  
Vol 85 ◽  
pp. 16-22 ◽  
Author(s):  
Tianqian Hui ◽  
Peng A. ◽  
Yuan Zhao ◽  
Jing Yang ◽  
Ling Ye ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Riffat Mehboob ◽  
Sana Hassan ◽  
Syed Amir Gilani ◽  
Amber Hassan ◽  
Imrana Tanvir ◽  
...  

Substance P (SP) is a peptide involved in many biological processes, including nociception and inflammation. SP has a high affinity for its receptor neurokinin-1 (NK-1R). SP/NK-1R complex plays a major role in the interactions going on during the onset of dental pain and inflammation. Objective. To identify the expression of NK-1R in healthy and inflamed human dental pulp, as well as to identify any association with severity of dental pain. Methods. This case-control study included ten irreversibly inflamed samples of dental pulp, which were extirpated from patients presenting with chief complaint of dental pain due to caries. Ten healthy pulps, extirpated from those teeth which were indicated for extraction due to orthodontic reasons, were used as the control group. Visual analog scale (VAS) and modified McGill Pain Questionnaire were used to assess the characteristic and severity of pain. Immunohistochemical study was performed using monoclonal antibodies against NK-1R. Results. The results showed that the NK-1R was expressed intensely in patients with higher pain score. The mean pain score in cases was 7.0 ± 2.0 . The healthy dental pulps had negative or mild NK-1R staining of +1 intensity. The NK-1R score in cases was 2.4 ± 0.516 and 0.2 ± 0.4216 in controls. There was significant difference in NK-1R score between both groups ( p value <0.05). There was a strong positive correlation between the pain score and NK-1R expression score. As the pain increased, the NK-1R expression score was also increased (0.95 ∗ ∗ , p value 0.000). Conclusions. NK-1R is overexpressed in inflamed dental pulp. SP/NK-1R modulation may provide a novel approach for the treatment of pulpal inflammation and pain.


Oral Diseases ◽  
2016 ◽  
Vol 23 (1) ◽  
pp. 22-28 ◽  
Author(s):  
T Hui ◽  
C Wang ◽  
D Chen ◽  
L Zheng ◽  
D Huang ◽  
...  

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