| Co-Investigator(Kenkyū-buntansha) |
TAKAGI Michiaki Yamagata University School of Medicine, Orthopaedic Surgery, Asoociate Professor, 医学部・付属病院, 助教授 (40241707)
SANTAVIRTA Seppo University of Helsinki, Orthopaedic Surgery and Traumatology, Professor
IDA Hideo Yamagata University School of Medicine, Orthopaedic Surgery, Associate Professor (40184600)
KONTTINEN Yrjo University of Helsinki, Internal Medicine, Professor
|
|---|
| Research Abstract |
Aseptic loosening and periprosthetic osteolysis are major problems in artificial hip joint surgery, for which a solution has yet to be found. Biological host response to wear debris combined with cyclic mechanical loading onto the bone bed around hip prosthetic implants has been considered as mechanism responsible for implant-mediated periprosthetic osteolysis. Any type of artificial joint gliding surface continuously produces wear debris, which are derived from implant materials, i.e., ultra-high molecular weight polyethylene, ceramics and metals. Fragmented bone cement between the bone and implants is also a source of debris. Currently, generation of debris is still inevitable, although modern technology provides better biocompatible implants to lessen the debris. Debris induces foreign body reaction in periprosthetic connective tissues. The main loci are synovial regenerating capsular tissues and interface tissues between the bone and implants, where macrophages play an important ro
… More
le. Various cellular mediators, bone resorbing cytokines, matrix metalloproteinases (MMP), and tissue inhibitors of metalloproteinase (TIMP) are produced in the process. Over-expression of MMP-1, -9, -13, -14, -15, -16, -17, and TIMP -1, -2, -3 were peculiar findings in ribonucleic acid level analysis of interface tissues between bone and implants. The reaction affects periprosthetic bone remodeling and can provoke imbalanced bone metabolism around implants. It weakens the bone and causes periprosthetic osteolysis. In addition, the joint fluid, which is released from the inflamed connective tissues, has osteolytic potential. Pumping effect on gait and poor integration of bone-implant interface allow penetration of the fluid into intact interface, thus enhancing osteolytic reactions around implants. Osteolytic change finally seems to be induced by both osteoclast and non-osteoclast pathway. In osteoclastic pathway, high level of macrophage colony stimulating factor and osteoclast-inducing factor were deeply related to this process. In non-osteolytic pathway, CD-68, cathepsin K and tartrate resistant acid phosphatase positive-macrophage may be able to digest weakened calcified matrix under acidic circumstance of lower pH in bone implant interface. Further studies on interface biology and implant-related osteolysis with modern technique should lead to a better solution to provide longer survivorship of the artificial hip joint. Less
|
