scholarly journals Annexin A2 binds to endosomes following organelle destabilization by particulate wear debris

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Brian Scharf ◽  
Cristina C. Clement ◽  
Xiao-Xuan Wu ◽  
Kateryna Morozova ◽  
Diego Zanolini ◽  
...  
2006 ◽  
Vol 77A (1) ◽  
pp. 192-201 ◽  
Author(s):  
Elizabeth A. Fritz ◽  
Tibor T. Glant ◽  
Csaba Vermes ◽  
Joshua J. Jacobs ◽  
Kenneth A. Roebuck

2013 ◽  
Vol 19 (3) ◽  
pp. 336-350 ◽  
Author(s):  
Bryan W. Cunningham ◽  
Nadim J. Hallab ◽  
Nianbin Hu ◽  
Paul C. McAfee

Object The introduction and utilization of motion-preserving implant systems for spinal reconstruction served as the impetus for this basic scientific investigation. The effect of unintended wear particulate debris resulting from micromotion at spinal implant interconnections and bearing surfaces remains a clinical concern. Using an in vivo rabbit model, the current study quantified the neural and systemic histopathological responses following epidural application of 11 different types of medical-grade particulate wear debris produced from spinal instrumentation. Methods A total of 120 New Zealand White rabbits were equally randomized into 12 groups based on implant treatment: 1) sham (control), 2) stainless steel, 3) titanium alloy, 4) cobalt chromium alloy, 5) ultra–high molecular weight polyethylene (UHMWPe), 6) ceramic, 7) polytetrafluoroethylene, 8) polycarbonate urethane, 9) silicone, 10) polyethylene terephthalate, 11) polyester, and 12) polyetheretherketone. The surgical procedure consisted of a midline posterior approach followed by resection of the L-6 spinous process and L5–6 ligamentum flavum, permitting interlaminar exposure of the dural sac. Four milligrams of the appropriate treatment material (Groups 2–12) was then implanted onto the dura in a dry, sterile format. All particles (average size range 0.1–50 μm in diameter) were verified to be endotoxin free prior to implantation. Five animals from each treatment group were sacrificed at 3 months and 5 were sacrificed at 6 months postoperatively. Postmortem analysis included epidural cultures and histopathological assessment of local and systemic tissue samples. Immunocytochemical analysis of the spinal cord and overlying epidural fibrosis quantified the extent of proinflammatory cytokines (tumor necrosis factor–α, tumor necrosis factor–β, interleukin [IL]–1α, IL-1β, and IL-6) and activated macrophages. Results Epidural cultures were negative for nearly all cases, and there was no evidence of particulate debris or significant histopathological changes in the systemic tissues. Gross histopathological examination demonstrated increased levels of epidural fibrosis in the experimental treatment groups compared with the control group. Histopathological evaluation of the epidural fibrous tissues showed evidence of a histiocytic reaction containing phagocytized inert particles and foci of local inflammatory reactions. At 3 months, immunohistochemical examination of the spinal cord and epidural tissues demonstrated upregulation of IL-6 in the groups in which metallic and UHMWPe debris were implanted (p < 0.05), while macrophage activity levels were greatest in the stainless-steel and UHMWPe groups (p < 0.05). By 6 months, the levels of activated cytokines and macrophages in nearly all experimental cases were downregulated and not significantly different from those of the operative controls (p > 0.05). The spinal cord had no evidence of lesions or neuropathology. However, multiple treatments in the metallic groups exhibited a mild, chronic macrophage response to particulate debris, which had diffused intrathecally. Conclusions Epidural application of spinal instrumentation particulate wear debris elicits a chronic histiocytic reaction localized primarily within the epidural fibrosis. Particles have the capacity to diffuse intrathecally, eliciting a transient upregulation in macrophage/cytokine activity response within the epidural fibrosis. Overall, based on the time periods evaluated, there was no evidence of an acute neural or systemic histopathological response to the materials included in the current project.


1998 ◽  
Vol 550 ◽  
Author(s):  
Joshua J. Jacobs ◽  
Tibor T. Glant

AbstractBone loss (osteolysis) following total joint arthroplasty has been a subject of increasing concern in the orthopedic research community. Depending on the distribution and severity, bone loss can lead to aseptic loosening, periprosthetic fracture and formidable reconstructive problems at revision surgery. Bone loss is believed to be primarily a response to particulate wear and corrosion debris derived from the prosthetic materials. Phagocytosed particulates activate macrophages and osteoblasts (and perhaps fibroblasts) to produce factors which stimulate osteoclastic bone resorption and reduce osteoblastic bone formation. To investigate the responses of these cells to particulate corrosion and wear debris, in vitro studies have been performed by measuring factors at both the molecular and cellular levels that may trigger, maintain and/or regulate particulate biomaterial-induced pathologic bone resorption. The biological effect of a particulate species depends upon their size, concentration (number) and composition, in the order listed. Particulate wear debris of phagocytosable size (less that 10 micrometers) activate macrophages, fibroblasts and osteoblasts more effectively that those of larger sizes. As a response to phagocytosed particulates, i) macrophages produce a number of cytokines (interleukins such as II-1, II-6, TNF-alpha) and prostaglandins, which may act either in an autocrine fashion or further stimulate cells present in the periprosthetic tissue; ii) fibroblasts secrete active forms of metalloproteinases; and iii) osteoblasts have diminished collagen type I synthesis. Taken together, particulate corrosion and wear debris provoke a series of biological responses which generate an active microenvironment around prosthetic components. Strategies to modify the host response to particulate degradation products have emerged from these in vitro studies. These strategies may provide pharmacotherapeutic solutions to this important clinical problem.


1995 ◽  
Vol 3 (3) ◽  
pp. 14-18
Author(s):  
Shilest Jani ◽  
Gary Williams ◽  
Silvio P. Marchese-Ragona ◽  
Briggs Christie

Total replacement of a diseased or traumatized hip joint is fast becoming one of the most common surgical procedures. The acetabular prosthetic shell is gaining widespread acceptance as a socket replacement for this procedure. Bio-materials research is providing a wealth of information regarding the life span, wear characteristics, and performance of these replacements, with a major clinical finding being the destruction of bone (osteolysis) at interfaces with the implants. Osteolysis is widely thought to be associated with the particulate wear debris released from articulation of the ball and socket. Formation and release of these particulates will depend not only on the relative motion occurring but also on the surface roughness of the replacement materials.


2001 ◽  
Vol 83 (2) ◽  
pp. 201-211 ◽  
Author(s):  
Csaba Vermes ◽  
Raman Chandrasekaran ◽  
Joshua J. Jacobs ◽  
Jorge O. Galante ◽  
Kenneth A. Roebuck ◽  
...  

Author(s):  
Arun S. Shanbhag ◽  
William Macaulay ◽  
Maja Stefanovic-Racic ◽  
Harry E. Rubash

2005 ◽  
Vol 23 (6) ◽  
pp. 1249-1257 ◽  
Author(s):  
Elizabeth A. Fritz ◽  
Joshua J. Jacobs ◽  
Tibor T. Glant ◽  
Kenneth A. Roebuck
Keyword(s):  

2003 ◽  
Vol 3 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Bryan W Cunningham ◽  
Carlos M Orbegoso ◽  
Anton E Dmitriev ◽  
Nadim J Hallab ◽  
John C Sefter ◽  
...  

2004 ◽  
Vol 19 (4) ◽  
pp. 481-487 ◽  
Author(s):  
Ulrik Hansson ◽  
Gordon Blunn ◽  
Leif Ryd
Keyword(s):  

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