## Abstract The ability of prosthetic wear debris to induce proβinflammatory responses in macrophages is widely appreciated, but little is known about the molecular mechanisms involved in particle recognition. Specifically, the nature of the cell surface receptors that interact with wear debris is
Nitric oxide release by macrophages in response to particulate wear debris
β Scribed by Shanbhag, Arun S. ;Macaulay, William ;Stefanovic-Racic, Maja ;Rubash, Harry E.
- Book ID
- 101257695
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 201 KB
- Volume
- 41
- Category
- Article
- ISSN
- 0021-9304
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β¦ Synopsis
At the interface between a prosthetic implant and bone, macrophage interaction with particulate wear debris is a key event in the initiation of localized bone resorption, leading to aseptic loosening of the prostheses. Numerous investigators have reported that macrophages release a variety of cytokines and mediators including tumor necrosis factor, interleukin-1, prostaglandin E 2 , and interleukin-6 when they are stimulated with particulate wear debris. In this study, we have demonstrated that macrophages stimulated with particulate debris are also capable of releasing in copious amounts a key inflammatory chemical, nitric oxide. This release of nitric oxide was dependent upon the period of culture and the type and dosage of the challenging particles. Titanium-alloy particles were the most stimulatory, followed by commercially pure titanium and polymethylmethacrylate. While the role of nitric oxide in osteolysis is not clearly understood, the literature suggests that it may be a key mediator in inhibiting DNA synthesis, in cell proliferation, and in stimulating PGE 2 release. This finding enhances our understanding of the sequence of events occurring at the bone-implant interface during wear debrismediated osteolysis, and exposes potential avenues to interrupt this sequence.
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