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Developing the Coupling or De-Coupling of Osteoclastogenesis vs. Osteogenesis at the Osteoimmune Interface

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 15 July 2026 | Viewed by 888

Special Issue Editor


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Guest Editor
1. Center for Osteoimmunology and Biotechnology Research (COBR), School of Dentistry, College of Dental Medicine, Kaohsiung Medical University (KMU) & KMU-Hospital, Kaohsiung 80708, Taiwan
2. Laboratory of Molecular Microbial Immunity, Division of Periodontology, The Eastman Institute for Oral Health (EIOH), School of Medicine & Dentistry, University of Rochester, Rochester, NY 14620, USA
3. For the Elder & Young’s Center of Oral Medicine Investigation (FEYLOMI), Kaohsiung, Taiwan
Interests: periodontology; oral microbiology and immunology

Special Issue Information

Dear Colleagues,

There have been great advancements in recent years in the osteoimmunology field, whose dawn began a quarter of a century ago. Several innovative breakthroughs linking the underpinning complex interactions and crosstalk at the osteoimmune or mucosae–mesenchymal interface have hinged, bridged, and transcended the early ontogenetic and/or subsequent cascades involving the coupling vs. de-coupling of osteoclastogenesis and osteogenesis towards bone resorption, the formation or repairs/regeneration, etc., consequentially leading to the pathophysiological conditions for homeostasis vs. pathogenesis associated with health or diseases. This Special Issue welcomes the submission of reviews, original research, and short communications, based on the Information for Authors instruction on the IJMS’s webpage (https://www.mdpi.com/authors). With this Special Issue, we aim to provide a platform for new trends, as outlined and showcased, but not limited to, below:

Main topics of interest:

  1. Cellular or molecular crosstalk associated with coupling or de-coupling of osteoclastogenesis vs. osteogenesis at the osteoimmune interface;
  2. Specific microenvironment at the osteoimmune interface favoring (or disfavoring) the overall progression of osteoclastogenic pathways;
  3. Mesenchymal stromal vs. stem cells and hematopoietic progenitors during osteoclastogenesis in bone homeostasis and/or related pathologies;
  4. Biomaterials or bio-mimics favoring (or disfavoring) the pathways leading to the (de)coupling of osteoclastogenesis and/or osteogenesis;
  5. Development of ontogenetic lineages (i.e., progenitors vs. precursors associated with hematopoietic or myeloid lineages of monocytes, macrophages, dendritic cells, neutrophils, erythro-megakaryocytes, etc.), consequently leading to osteoclastogenesis and/or osteogenesis.

Dr. Andy Yen-Tung Teng
Guest Editor

Manuscript Submission Information

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Keywords

  • bone and immune cells
  • osteoclasts vs. osteoblasts
  • interactions between osteoclasts and osteoblasts
  • osteoimmune interactions in health and/or disease
  • developmental lineages or pathways of osteoclastogenesis
  • coupling and/or de-coupling (or crosstalk) for osteoclastogenesis and/or osteogenesis
  • biomaterials and/or bio-mimics for bone genesis and/or loss

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Published Papers (1 paper)

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Review

15 pages, 1502 KB  
Review
Developmental Pathways of Immature CD11c+ Myeloid Dendritic Cells (mDCs) for Bona Fide Osteoclastogenesis Revisited: A Narrative Review
by Yen Chun G. Liu, Chen-Yi Liang and Andy Yen-Tung Teng
Int. J. Mol. Sci. 2026, 27(1), 480; https://doi.org/10.3390/ijms27010480 - 2 Jan 2026
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Abstract
Recent studies support that hematopoietic stem cell (HSC)-derived myeloid dendritic cells, monocytes/macrophages (Mo/Mϕ), and osteoclast precursors (OCps) share common progenitor(s) during development. This occurs mainly through receptor activator of NF-κB ligand (RANKL) signaling via its cytoplasmic adaptor protein complex (TRAF6) to subsequent osteoclastogenesis [...] Read more.
Recent studies support that hematopoietic stem cell (HSC)-derived myeloid dendritic cells, monocytes/macrophages (Mo/Mϕ), and osteoclast precursors (OCps) share common progenitor(s) during development. This occurs mainly through receptor activator of NF-κB ligand (RANKL) signaling via its cytoplasmic adaptor protein complex (TRAF6) to subsequent osteoclastogenesis for bone loss and/or remodeling. Presently, mounting new evidence suggests that erythro-myeloid progenitor (EMP)-derived macrophages (Mϕ) and HSC-derived monocytes (Mo) produce embryonic, fetal, and postnatal OCp pools (i.e., primitive OCp), pinpointing a complex network of multiple OCp developmental origins. However, their ontogenic developments, lineage interactions, and contributions to the alternative osteoclastogenesis—in contrast to overall bone remodeling or loss—remain elusive. Interestingly, studies have also elucidated the contributions of immature CD11c+ myeloid DC-like OCps to osteoclastogenesis, with or without the classical so-called Mo/Mϕ-derived OCp subsets, and described that CD11c+ myeloid DCs (mDCs) develop into functionally active OCs; meanwhile, the cytokine TGF-β mediates a stepwise regulation of de novo immature mDCs/OCps through distinct crosstalk(s) with IL-17, an unrecognized interaction featuring TRAF6(−/−)CD11c+ mDDOCps that coexist and proficiently colocalize in the local environment to drive a bona fide route for alternative osteoclastogenesis in vivo. Collectively, new findings—critically hinged on progenitor osteoclastogenic pathways (primitive OCps, mDCs/OCps, osteomorphs, etc.) and involving classical and/or alternative routes to inflammation-induced bone loss—are discussed via the illustrated schemes. This review highlights plausible ontogenic vs. principal or alternative developmental paths and their consequential downstream effects. Full article
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