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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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T Cell Types and Functions01:24

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Jun 11, 2025

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
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Roles of Toll-like Receptor Signaling in Inflammatory Bone Resorption.

Tsukasa Tominari1, Chiho Matsumoto1, Yuki Tanaka2

  • 1Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi, Tokyo 184-8588, Japan.

Biology
|September 28, 2024
PubMed
Summary
This summary is machine-generated.

Toll-like receptors (TLRs) trigger inflammatory bone loss in periodontal disease by promoting osteoclast differentiation. Inhibiting prostaglandin E2 (PGE2) synthesis blocks this bone resorption, highlighting a key pathway in inflammatory bone diseases.

Keywords:
Toll-like receptorsbone resorptioninnate immunityosteoblastsosteoclastsperiodontal diseaseprostaglandin E2

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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
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Area of Science:

  • Immunology
  • Oral Biology
  • Pathology

Background:

  • Toll-like receptors (TLRs) recognize microbial patterns, initiating immune responses.
  • Periodontal disease involves inflammation and alveolar bone resorption, driven by factors like prostaglandin E2 (PGE2).
  • Previous studies linked mPGES-1 deficiency to reduced LPS-induced bone resorption.

Purpose of the Study:

  • To review the role of TLRs in osteoclast differentiation and bone resorption in inflammatory conditions.
  • To summarize findings on TLR ligand-induced osteoclastogenesis and its mediators.
  • To highlight the connection between TLR signaling and periodontal bone loss.

Main Methods:

  • Review of existing literature on TLRs, osteoclast differentiation, and bone resorption.
  • Analysis of studies involving TLR ligand stimulation in co-culture and in vivo models.
  • Examination of the roles of PGE2 and RANKL in TLR-mediated bone resorption.

Main Results:

  • Various TLR ligands (TLR2/1, TLR2/6, TLR3, TLR4, TLR5) induce osteoclast differentiation.
  • TLR-induced osteoclastogenesis is associated with increased PGE2 and RANKL production.
  • In vivo administration of TLR ligands leads to significant alveolar bone resorption.
  • mPGES-1 deficiency impairs LPS-induced bone resorption.

Conclusions:

  • TLRs are critical mediators of osteoclast differentiation and bone resorption in inflammatory diseases like periodontitis.
  • PGE2 and RANKL are key downstream effectors in TLR-driven bone loss.
  • Targeting TLR pathways may offer therapeutic strategies for inflammatory bone diseases.