Role of Particulate Debris in Periprosthetic Osteolysis

Wang, Jeng-Tzung; Harada, Yoshitada; Doppalapudi, Vivek A.; Goldring, Steven R.

doi:10.1097/00013611-199300840-00005

Cited by 4 publications

(5 citation statements)

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“…Cell apoptosis in periprosthetic membrane are directly affected by physical stimuli represented by wear debris produced by different materials composing prosthesis, different characteristics of debris are able to determine different cellular response. 5,8,15,38 Cell death and biological stimuli, as represented by cell secreting cytokines, are events that widely occur in periprosthetic environment. 6,8,37 In the present study the most common debris detected in periprosthetic membrane are polyethylene and metallic debris, while cement PMMA particles were detected in cemented ones as a consequence of structural composition of implant.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…The arthroplasty clinical failure will be taken after the loss of bone that occurs through the activity of resorption stimulated by inflammatory cells in response to the presence of debris. [4][5][6][7] Primary fixation of the prosthetic components can be achieved by polymethylmetacrylate (PMMA, cement, covering the metal stem of the implant) or mechanical interference (press-fit). Cemented prostheses generate particulate wear debris that activate mononuclear phagocytic cells, inducing the release of inflammatory factors, leading to osteoclastic bone resorption, 4,[6][7][8] whilst cementless prostheses have been seen to release ion debris that have a cytotoxic effect and induce inflammatory processes.…”

Section: Introductionmentioning

confidence: 99%

“…The presence of a pseudosynovial, radiographically detectable, and fibrous membrane at the interface of the host bone and implant is a granulomatous tissue developed by foreign‐body inflammatory response to particulate debris released by materials forming prosthesis;1–3 it is a characteristic finding in patients with orthopedic implant loosening. The arthroplasty clinical failure will be taken after the loss of bone that occurs through the activity of resorption stimulated by inflammatory cells in response to the presence of debris 4–7…”

Section: Introductionmentioning

confidence: 99%

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Expression of Concern: Different apoptosis modalities in periprosthetic membranes

Sabbatini

Piffanelli

Boccafoschi

et al. 2009

J Biomedical Materials Res

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This study reports on an investigation into apoptotic and proliferation signals in leukocyte and membrane fibroblasts in periprosthetic membranes collected during revision surgery for loosened total hip joint arthroplasty. Cementless and cemented prosthesis were studied under both aseptic and septic conditions. Fluorescence colocalization immunohistochemistry and colorimetric immunohistochemistry were used to investigate cell death signals. In aseptic cementless prosthesis macrophages and membrane fibroblasts show high bax signal, implying the occurrence of toxic/oxidative cell death caused by the debris of titanium alloy metal implant. Instead in aseptic cemented prosthesis only a moderate number of apoptotic leukocytes were observed, whilst the fibroblasts were affected by a diffuse apoptotic-like cell death, the Co-Cr ions debris released from cemented stem, may be at basis of apoptotic cell death induction. Furthermore cement debris is recognized to induce macrophages to produce cytokine, that may be responsible for the cell death observed and implant failure. The septic environment seems to protect leukocytes cell death. Septic cementless prosthesis showed only a few apoptotic leukocytes, instead fibroblasts remain affected by cell death signals. Similarly in septic cemented prosthesis, scanty apoptotic leukocytes were detected, whereas membrane fibroblasts showed an increase in proliferation index (Ki-67) along with caspase-3 activation. These findings indicate some kind of caspase-3 involvement in tissue proliferation, rather than in cell death pathway. Apoptotic periprosthetic sites have been interpreted as signs of inflammation resolution and normal tissue turnover. Nevertheless apoptosis may also be a sign of cell renewal associated to tissue proliferation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Expression of Concern: Different apoptosis modalities in periprosthetic membranes

Sabbatini

Piffanelli

Boccafoschi

et al. 2009

J Biomedical Materials Res

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“…The condition is characterized by an area of osteolysis found at the bone-prosthesis interface and can be identified radiographically as the presence of radiolucent zones at the bone-implant interface (3)(4)(5)(6). Previously, aseptic loosening was thought to be a purely mechanical event resulting from the instability of the prosthesis (7)(8)(9).…”

mentioning

confidence: 99%

Effects of titanium particle size on osteoblast functions in vitro and in vivo

Choi

Koh

Kluess

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

104

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The formation of titanium (Ti)-wear particles during the lifetime of an implant is believed to be a major component of loosening due to debris-induced changes in bone cell function. Radiographic evidence indicates a loss of fixation at the implant-bone interface, and we believe that the accumulation of Ti particles may act on the bone-remodeling process and impact both long-and short-term implant-fixation strengths. To determine the effects of various sizes of the Ti particles on osteoblast function in vivo, we measured the loss of integration strength around Ti-pin implants inserted into a rat tibia in conjunction with Ti particles from one of four size-groups. Implant integration is mediated primarily by osteoblast adhesion͞focal contact pattern, viability, proliferation and differentiation, and osteoclast recruitment at the implant site in vivo. This study demonstrates the significant attenuation of osteoblast function concurrent with increased expression of receptor activator of nuclear factor B ligand (RANKL), a dominant signal for osteoclast recruitment, which is regulated differentially, depending on the size of the Ti particle. Zymography studies have also demonstrated increased activities of matrix metalloproteinases (MMP) 2 and 9 in cells exposed to larger Ti particles. In summary, all particles have adverse effects on osteoblast function, resulting in decreased bone formation and integration, but different mechanisms are elicited by particles of different sizes.implant stability ͉ focal contact ͉ integration strength ͉ receptor activator of nuclear factor B ligand ͉ matrix metalloproteinase A septic loosening is emerging as the most common cause of failure for total joint replacements (1, 2). The condition is characterized by an area of osteolysis found at the bone-prosthesis interface and can be identified radiographically as the presence of radiolucent zones at the bone-implant interface (3-6). Previously, aseptic loosening was thought to be a purely mechanical event resulting from the instability of the prosthesis (7-9). However, a biological mechanism of aseptic loosening has recently been proposed that focuses on the bone-prosthesis interface (10, 11). To gain insight into the mechanisms by which particular wear debris induces osteolysis, a number of investigators have studied tissue from revision-surgery patients who have developed aseptic loosening (12-14). Willert and coworkers (15) have reported that the release of wear debris into the bone-implant bed leads to the development of a foreign-body reaction. This reaction is often made worse by repetitive exposure to the foreign substance.In conjunction with the recent literature (16) describing the evidence of abrasion and burnishing in failed cementless implants, the particles generated from micromotion between bone and implant in the femoral bone bed at the bone-implant interface are believed to be the major cause of numerous osteoblast functional changes that eventually result in improper participation of bone-bed formation and remodeling (16...

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