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An Improved Mechanical Testing Method to Assess Bone-implant Anchorage
Published on: February 10, 2014
Peri-implant crestal bone loss: a putative mechanism
Yuko Ujiie1, Reynaldo Todescan, John E Davies
1Institute of Biomaterials Biomedical Engineering and Faculty of Dentistry, University of Toronto, 164 College Street, Room 407, Toronto, ON, Canada M5S 3G9.
International Journal of Dentistry
|October 24, 2012
Summary
Bacterial products near dental implants trigger immune responses, leading to bone loss. Cytokines produced by peri-implant cells stimulate osteoclast formation, causing resorption of bone around implants.
Area of Science:
- Immunology
- Oral Biology
- Biomaterials Science
Background:
- Peri-implant crestal bone loss is a significant clinical concern.
- The immunological mechanisms driving this bone loss remain poorly understood.
Purpose of the Study:
- To investigate the role of bacterial products in peri-implant bone loss.
- To test the hypothesis that microgap bacteria upregulate cytokines, leading to osteoclastogenesis and bone resorption.
Main Methods:
- RT-PCR and ELISA were used to analyze cytokine mediators.
- Experiments involved rat and human macrophages, bone marrow stromal cells, and gingival fibroblasts.
- Lipopolysaccharide (LPS) was used to stimulate cells, and osteoclast formation was assessed.
Main Results:
- Interleukin-1 alpha (IL-1α), IL-1β, and IL-6 were expressed by all cell types.
- Tumor necrosis factor-alpha (TNF-α) was upregulated in human gingival fibroblasts.
- LPS stimulated IL-1α and IL-1β secretion in macrophages and IL-6 secretion in stromal cells and fibroblasts.
- Both LPS and RANKL induced osteoclast-like cells capable of bone resorption.
Conclusions:
- Bacterial endotoxins upregulate osteoclastogenesis mediators in peri-implant cells.
- Synergistic cytokine action leads to the formation of resorptively active osteoclasts.
- This supports the hypothesis that bacterial products drive peri-implant crestal bone loss.
