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Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
Published on: March 18, 2019
DC-STAMP Is an Osteoclast Fusogen Engaged in Periodontal Bone Resorption.
W Wisitrasameewong1,2,3, M Kajiya4, A Movila2
11 Department of Periodontology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
Dendritic cell-specific transmembrane protein (DC-STAMP) promotes osteoclast fusion and periodontal bone loss. Targeting DC-STAMP with an antibody suppressed bone loss and osteoclast formation in a mouse model.
Area of Science:
- Immunology
- Cell Biology
- Periodontology
Background:
- Dendritic cell-specific transmembrane protein (DC-STAMP) is crucial for osteoclast (OC) fusion and immune regulation.
- DC-STAMP expression is elevated in periodontitis, but its role in the disease is unclear.
Purpose of the Study:
- To investigate the role of DC-STAMP in ligature-induced periodontitis.
- To evaluate the therapeutic potential of anti-DC-STAMP monoclonal antibody (mAb) in preventing periodontal bone loss.
Main Methods:
- A mouse model of ligature-induced periodontitis was used.
- Anti-DC-STAMP-mAb was administered systemically and locally.
- Osteoclastogenesis, cell fusion, and periodontal bone loss were assessed.
- Immune responses to Pasteurella pneumotropica were evaluated.
Main Results:
- DC-STAMP is expressed on osteoclasts and involved in late-stage cell fusion.
- Anti-DC-STAMP-mAb inhibited osteoclast fusion and bone resorption in vitro.
- Ligature-induced periodontitis led to increased DC-STAMP expression, osteoclastogenesis, and alveolar bone loss.
- Both systemic and local administration of anti-DC-STAMP-mAb significantly reduced bone loss and osteoclast numbers.
- Anti-DC-STAMP-mAb did not affect anti-bacterial immune responses.
Conclusions:
- DC-STAMP plays a significant role in promoting osteoclast fusion and periodontal bone loss.
- Targeting DC-STAMP represents a potential therapeutic strategy for periodontitis.
- DC-STAMP inhibition offers a localized approach to managing periodontal bone destruction without impacting systemic immunity.
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