| Autor: |
Kohilas, K., Lyons, M., Lofthouse, R., Frondoza, C. G., Jinnah, R., Hungerford, D. S. |
| Zdroj: |
Journal of Biomedical Materials Research; October 1999, Vol. 47 Issue: 1 p95-103, 9p |
| Abstrakt: |
Wear debris generated by joint implant components has been reported to activate inflammatory and immune cells. Particulate debris derived from prosthetic material induces monocytesmacrophages, lymphocytes, synoviocytes, and fibroblasts to secrete cellular products, such as cytokines, which mediate inflammation. It has been speculated that degradation products impair the ability of inflammatory and immune cells to mount a protective response against noxious agents and infectious organisms by interfering with cell activation. Recent in vitrostudies suggest that soluble metal ions inhibit T and B cell activation, but it is not known whether insoluble metal particles generated by prosthetic wear in tissue have the same effect. The purpose of the present study was to determine whether titanium wear debris retrieved from periprosthetic tissues surrounding a failed knee prosthesis suppresses activation of human monocytic and lymphoid cells. Peripheral blood monocytes and lymphocytes were incubated with the nonspecific activator pokeweed mitogen PWM in the presence or absence of titanium particles. Cell proliferative capacity and production of interleukins IL1β and IL2 were determined as measures of activation. Titanium wear debris induced monocyte secretion of IL1β at levels comparable to those induced by PWM alone. In combination with PWM, titanium wear debris stimulated monocytes to secrete higher concentrations of IL1β than is stimulated by titanium itself or by PWM alone. Titanium wear debris did not activate lymphocytes, as indicated by marginal changes in DNA synthesis and IL2 secretion, nor did it suppress the PWMinduced stimulation of DNA synthesis and IL2 secretion. Our study suggests that nonspecific mitogen activators in spite of exposure to titanium wear debris can stimulate monocytic and lymphoid cells. © 1999 John Wiley & Sons, Inc. J Biomed Mater Res, 47, 95–103, 1999. |
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