• TNI-'-u also stiniuialcs bone resorption thiough a mechanism \vhirh ,.., at least partially dependent upon the produetion of prostaghmdin !-..' (P(n-2) by cells in bone. Ofthe mediators studied, TNI^;-u is by far i !•,•_• most consistently released; it is released by both monocyles and macrophages in response to polymethyhnethacrylate, titanium, and polyethylene (l).
  in a study by Baldwin L. et al.. they used the techniques o! iminunoliistoeheniistry and reverse transcription polymerase chain reaction to identify the inflammatory cell types, cytokin.es and chcmokines within the interface ^fissue surrounding failed Accord Knee proslheses. Many T cells were identified within the tissue; however, the classical marker of activation, CD25 was expressed on very few cells. Molecular analysis failed"to detect the synthesis of either T-helper ! (Thl) or T-helper 2 (Th2) cytokines (68).
  These results suggest that the T cells are being actively recruited to the
  site   of inflammation   along  the  chemokine  gradients   but   are  not
  participating in a classical immune response (68).
  Ultra-high molecular weight polyethylene particle:; - isolated from human tissue stimulated osteoblast,proliferation and prostaglandin-H2 production and inhibited ceil differentiation and matrix production. These 'results indicate that particles of wear debris inhibit cell functions associated with bone formation and that osteoblasts may produce factors in response to wear debris that influence neighboring cells, such as osteoclasts and macrophages (69).
  prior studies  have demonstrated that particles of wear debris  induce eytokine secretion in,macrophages, which  initiates the _i production of promflamaiory cytokines. such as TNF-a (tumor necrosis factor-a), IL-l(intcrieukin-l), and IL-6 (interleukin-6) (70).
  More importantly, these factors directly or indirectly stimulate RANK-ligand expression in osteoblasts and stromal cells, leading to osteoclast formation and activation (71).