| Title | In vitro effects of protein kinases and MAP Kinases inhibitors on IL-6, prostaglandin E2, matrix metalloproteinases and their tissue inhibitor-1 production by interface tissue from loose arthtroplasty endoprostheses | |
| Authors | Anna Niarakis¹, Polyxeni Katsinopoulou¹, Panagiotis Gouvousis¹, Elias Panagiotopoulos², Eleftheria Giannopoulou³ and Alexis J. Aletras¹
1. Laboratory of Biochemistry, Department of Chemistry, and Departments of 2. Orthopaedic and 3. Pharmacology, Medical School, University of Patras, Patra, Greece |
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| Citation | Niarakis, A., Katsinopoulou, P., Gouvousis, P., Panagiotopoulos, E., Giannopoulou, E. et al: In vitro effects of protein kinases and MAP Kinases inhibitors on IL-6, prostaglandin E2, matrix metalloproteinases and their tissue inhibitor-1 production by interface tissue from loose arthtroplasty endoprostheses, Epitheorese Klin. Farmakol. Farmakokinet. 20(2): 261-262 (2006) | |
| Publication Date | Accepted for publication: 19-20 May 2006 | |
| Full Text Language | English | |
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| Keywords | Arthroplasty endoprostheses loosening, protein kinases, MAP kinases, prostaglandin E2, IL-6, MMPs, TIMP-1. | |
| Other Terms | review article | |
| Introduction | The biocompatibility of total knee or hip arthroplasty endoprostheses has been a subject of debate for 3 decades. It appears that loosening of well inserted prostheses, is usually produced by a cascade of mechanical and biological events. This sequence of events consists of fragmentation and wear of the implanted materials and subsequently the release of wear particles into the periprosthetic tissues, evoking a foreign-body granulomatous reaction and activation of cells to produce a variety of cytokines and growth factors, such as IL-1β, IL-6, TNF-α and PDGF, prostaglandins, such as PGE2 and proteolytic enzymes, such as metalloproteinases, elastase, cathepsins and plasminogen activators. Through complex mechanisms, these cell products cause periprosthetic osteolysis that exceeds the reparative capacity of the fibrous and osseous tissues, resulting in loosening of the components from the skeleton (1-4). […] | |
| References | 1. Archibeck M.J., et al.: The basic science of periprosthetic osteolysis. J. Bone Joint. Surg. 82-A: 1478-1489 (2000)
2. Jiranek W.A., et al.: Production of cytokines around loosened cemented acetabular components. J. Bone Joint. Surg. 75-A: 863-879 (1993) 3. Mohanty M.: Cellular basis for failure of joint prosthesis. Biomed. Mater. Eng. 6: 165-172 (1996) 4. Takagi M.: Neutral proteinases and their inhibitors in the loosening of total hip arthroplasty. Acta Orthop. Scand. 67 (Suppl. 271): (1996) 5. Johnson G.L., Lapadat R.: Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 289: 1911-1912 (2002) |
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| Relative Papers |
Online ISSN 1011-6575
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Articles published in this Journal are Indexed or Abstracted in: • Chemical Abstracts • Elsevier’s Bibliographic Databases: Scopus, EMBASE, EMBiology, Elsevier BIOBASE SCImago Journal and Country Rank Factor
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