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The Role of Dendritic Cells during Physiological and Pathological Dentinogenesis

期刊

JOURNAL OF CLINICAL MEDICINE
卷 10, 期 15, 页码 -

出版社

MDPI
DOI: 10.3390/jcm10153348

关键词

cell differentiation; dental pulp; dendritic cells; dentin; extracellular matrix proteins; histocompatibility antigens class II; macrophages; odontoblasts; stem cells; tooth injuries

资金

  1. Japan Society for the Promotion of Science (JSPS) [P20412]
  2. [20K21672]

向作者/读者索取更多资源

The dental pulp is a vital connective tissue responsible for maintaining tooth vitality after injuries. This literature review focuses on the role of dendritic cells in dentinogenesis and proposes the concept of dentin-pulp immunology for understanding the interactions among different cell types in the pulp tissue.
The dental pulp is a soft connective tissue of ectomesenchymal origin that harbors distinct cell populations, capable of interacting with each other to maintain the vitality of the tooth. After tooth injuries, a sequence of complex biological events takes place in the pulpal tissue to restore its homeostasis. The pulpal response begins with establishing an inflammatory reaction that leads to the formation of a matrix of reactionary or reparative dentin, according to the nature of the exogenous stimuli. Using several in vivo designs, antigen-presenting cells, including macrophages and dendritic cells (DCs), are identified in the pulpal tissue before tertiary dentin deposition under the afflicted area. However, the precise nature of this phenomenon and its relationship to inherent pulp cells are not yet clarified. This literature review aims to discuss the role of pulpal DCs and their relationship to progenitor/stem cells, odontoblasts or odontoblast-like cells, and other immunocompetent cells during physiological and pathological dentinogenesis. The concept of dentin-pulp immunology is proposed for understanding the crosstalk among these cell types after tooth injuries, and the possibility of immune-based therapies is introduced to accelerate pulpal healing after exogenous stimuli.

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