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Cells
Special Issues
Signaling Regulation of Bone and Tooth Development
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Signaling Regulation of Bone and Tooth Development

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 March 2025 | Viewed by 335

Special Issue Editor

Dr. Xiaofang Wang

E-Mail Website
Guest Editor
Texas A&M College of Dentistry, Dallas, TX, USA
Interests: signaling regulation of bone and tooth development

Special Issue Information

Dear Colleagues,

Bones and teeth belong to hard tissues. Both are formed by highly differentiated functional cells that secrete extracellular matrix and subsequently deposit crystallized minerals. However, their tissue origins, developmental processes, and corresponding signal regulatory mechanisms are quite different. Tooth development begins with the mutual induction between the dental epithelium and dental mesenchyme. This interaction continues throughout the development of the tooth crown and roots. The components of a tooth, including enamel, dentin-pulp complex, dental pulp, and cementum, each have their unique tissue structure and associated signal regulation mechanisms. The tissue origin of bone is more complex and involves both neural-crest-derived and mesoderm-derived mesenchymal cells. These cells either form cartilage as a template for endochondral ossification or directly initiate intramembranous ossification by forming ossification centers. The two types of bone formation exhibit distinct tissue morphologies and signal regulatory mechanisms along different developmental stages. The development and homeostasis of bone are also regulated by biomechanical forces, hematopoiesis, and the immune system through interactions with muscles, bone marrow, and the neurovascular system. This Special Issue aims to collect review and research articles which showcase recent advancements in understanding the signaling regulatory mechanisms of tooth and bone development, including, but not limited to, embryonic and postnatal development, tissue turnover and remodeling, matrix assembly and biomineralization, and interactions between bone and immune and endocrine systems, etc.

Dr. Xiaofang Wang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bone
  • tooth
  • osteogenesis
  • odontogenesis
  • enamel
  • dentin
  • cementum
  • amelogenesis
  • dentinogenesis

Published Papers (1 paper)

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Research

14 pages, 15375 KiB  
Article
Fat Phagocytosis Promotes Anti-Inflammatory Responses of Macrophages in a Mouse Model of Osteonecrosis
by Zhuo Deng, Harry K. W. Kim, Paula A. Hernandez and Yinshi Ren
Cells 2024, 13(14), 1227; https://doi.org/10.3390/cells13141227 (registering DOI) - 20 Jul 2024
Viewed by 126
Abstract
Osteonecrosis (ON) of the femoral head (ONFH) is a devastating bone disease affecting over 20 million people worldwide. ONFH is caused by a disruption of the blood supply, leading to necrotic cell death and increased inflammation. Macrophages are the key cells mediating the [...] Read more.
Osteonecrosis (ON) of the femoral head (ONFH) is a devastating bone disease affecting over 20 million people worldwide. ONFH is caused by a disruption of the blood supply, leading to necrotic cell death and increased inflammation. Macrophages are the key cells mediating the inflammatory responses in ON. It is unclear what the dynamic phenotypes of macrophages are and what mechanisms may affect macrophage polarization and, therefore, the healing process. In our preliminary study, we found that there is an invasion of macrophages into the repair tissue during ON healing. Interestingly, in both ONFH patients and a mouse ON model, fat was co-labeled within macrophages using immunofluorescence staining, indicating the phagocytosis of fat by macrophages. To study the effects of fat phagocytosis on the macrophage phenotype, we set up an in vitro macrophage and fat co-culture system. We found that fat phagocytosis significantly decreased M1 marker expression, such as IL1β and iNOS, in macrophages, whereas the expression of the M2 marker Arg1 was significantly increased with fat phagocytosis. To investigate whether the polarization change is indeed mediated by phagocytosis, we treated the cells with Latrunculin A (LA, which inhibits actin polymerization and phagocytosis). LA supplementation significantly reversed the polarization marker gene changes induced by fat phagocytosis. To provide an unbiased transcriptional gene analysis, we submitted the RNA for bulk RNA sequencing. Differential gene expression (DGE) analysis revealed that the top upregulated genes were related to anti-inflammatory responses, while proinflammatory genes were significantly downregulated. Additionally, using pathway enrichment and network analyses (Metascape), we confirmed that gene-enriched categories related to proinflammatory responses were significantly downregulated in macrophages with fat phagocytosis. Finally, we validated the similar macrophage phenotype changes in vivo. To summarize, we discovered that fat phagocytosis occurs in both ONFH patients and an ON mouse model, which inhibits proinflammatory responses with increased anabolic gene expression in macrophages. This fat-phagocytosis-induced macrophage phenotype is consistent with the in vivo changes shown in the ON mouse model. Our study reveals a novel phagocytosis-mediated macrophage polarization mechanism in ON, which fills in our knowledge gaps of macrophage functions and provides new concepts in macrophage immunomodulation as a promising treatment for ON. Full article
(This article belongs to the Special Issue Signaling Regulation of Bone and Tooth Development)
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