Particle disease. A comprehensive theory of periprosthetic osteolysis: a review.

Gallo, Jiří; Kamínek, Petr; Tichá,; Riháková, P; Ditmar, R

doi:10.5507/bp.2002.004

Cited by 91 publications

(100 citation statements)

References 62 publications

(61 reference statements)

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“…Although animal models have shown T cells are dispensable in the development of osteolysis [25,39,72], a recent in vitro study showed depletion of T cells or the addition of RANK-Fc to human peripheral blood cell cultures equally reduced osteoclast formation in response to RANKL [65]. Additionally, the current findings and those of others [28,61] support the potential involvement of T cells in human osteolytic responses after recruitment by chemotactic factors released from activated macrophages [5,19,63,68]. In agreement with other reports, we observed distinct regional and patient differences in the immune cell responses [8,28,36,40] and notably a corresponding heterogeneity in UHMWPE particle number.…”

Section: Discussionsupporting

confidence: 69%

Do Tissues From THA Revision of Highly Crosslinked UHMWPE Liners Contain Wear Debris and Associated Inflammation?

Baxter

Freeman

Kurtz

et al. 2011

Clinical Orthopaedics &Amp; Related Research

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Background Polyethylene wear debris is a major contributor to inflammation and the development of implant loosening, a leading cause of THA revisions. To reduce wear debris, highly crosslinked ultrahigh-molecular-weight polyethylene (UHMWPE) was introduced to improve wear properties of bearing surfaces. As highly crosslinked UHMWPE revision tissues are only now becoming available, it is possible to examine the presence and association of wear debris with inflammation in early implant loosening. Questions/purposes We asked: (1) Does the presence of UHMWPE wear debris in THA revision tissues correlate with innate and/or adaptive immune cell numbers? (2) Does the immune cell response differ between conventional and highly crosslinked UHMWPE cohorts?Methods We collected tissue samples from revision surgery of nine conventional and nine highly crosslinked UHMWPE liners. Polarized light microscopy was used to determine 0.5-to 2-lm UHMWPE particle number/mm 2 , and immunohistochemistry was performed to determine macrophage, T cell, and neutrophil number/mm 2 . Results For the conventional cohort, correlations were observed between wear debris and the magnitude of individual patient macrophage (q = 0.70) and T cell responses (q = 0.71) and between numbers of macrophages and T cells (q = 0.77) in periprosthetic tissues. In comparison, the highly crosslinked UHMWPE cohort showed a correlation between wear debris and the magnitude of macrophage responses (q = 0.57) and between macrophage and T cell numbers (q = 0.68). Although macrophages and T cells were present in both cohorts, the highly crosslinked UHMWPE cohort had lower numbers, which may be associated with shorter implantation times. Conclusions The presence of wear debris and inflammation in highly crosslinked UHMWPE revision tissues may contribute to early implant loosening.

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Section: Discussionsupporting

confidence: 69%

Do Tissues From THA Revision of Highly Crosslinked UHMWPE Liners Contain Wear Debris and Associated Inflammation?

Baxter

Freeman

Kurtz

et al. 2011

Clinical Orthopaedics &Amp; Related Research

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“…1,2 AL due to wear debrisinduced osteolysis is the most common cause of implant failure. 3 Wear debris-induced persistent inflammation and osteoclastogenesis are two critical factors in the etiology of AL. 15 There is currently no cure for AL except surgical revision.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 Recent studies have demonstrated that the RANKL expression is increased in tissues adjacent to loose prostheses in patients. 3,6,8,11 Using a mouse inflammation model, 12 we have demonstrated that ultrahigh molecular-weight polyethylene (UHMWPE) debris provokes tissue inflammation associated with a significant increase of RANKL gene expression. 4 In fact, blocking RANKL activity using either an antagonist RANK:Fc IgG 13 or an adeno-associated virus (AAV)-mediated OPG gene therapy 14 inhibit wear debris-stimulated osteoclast formation and bone resorption.…”

Section: Introductionmentioning

confidence: 99%

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Erythromycin inhibits wear debris‐induced inflammatory osteolysis in a murine model

Ren

Peng

et al. 2005

Journal Orthopaedic Research

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Up to 20% of patients with total joint arthroplasty will develop radiographic evidence of aseptic loosening (AL), which most likely results from an inflammatory response to billions of wear debris shed from the implant. Our previous work has demonstrated that erythromycin (EM), a macrolide antibiotic, inhibits wear debris-induced inflammatory osteoclastogenesis through the reduction of cytokine production and osteoclast differentiation, both of which involve the NF-kB pathway. The aim of the current study was to determine whether EM inhibits wear debris-induced inflammatory osteolysis in a murine osteolysis model. Ultrahigh molecular-weight polyethylene (UHMWPE) debris was introduced into established air pouches on BALB/c mice, followed by implantation of calvaria bone from syngeneic littermates. EM (2 mg/kg/day) was given to mice intraperitoneally 2 days before UHMWPE introduction and maintained until the sacrifice of the mice. Mice with and without EM treatment, as well as control mice injected with saline alone were included in this study. Pouch tissues were collected 14 days after UHMWPE inoculation for molecular and histology analysis. Our findings indicate that: (1) EM reduced UHMWPE-induced tissue inflammation, including the diminished pouch membrane thickness, reduced inflammatory cellular infiltration, and lowered IL-1b and TNF-a expression (mRNA and protein); (2) EM inhibited UHMWPE-induced osteoclastogenesis, with reduced gene activation of RANK, RANKL, and CPK, and diminished RANKL expression in UHMWPE stimulated pouches, and (3) EM markedly reduced the number of TRAP þ cells in pouch tissues, and protected against bone collagen depletion. In conclusion, this study provides the evidence that EM inhibits the UHMWPE particles-induced inflammatory osteolysis in a murine model, and represents a promising therapeutic candidate for the prevention and treatment of AL. ß

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“…These data are interesting because one favored hypothesis concerning the pathogenesis of AL is that wear particles generated from the prosthesis stimulate phagocytosis by macrophages with the subsequent release of proinflammatory cytokines. [14][15][16] Ultra high molecular weight polyethylene (UHMWPE) has been widely used in total joint prosthesis, and UHMWPE components removed at revision surgery usually show evidence of wear. 17,18 Using our established mouse osteolysis model, we have demonstrated that UHMWPE particles provoke significant inflammation, osteoclastogenesis, and bone resorption.…”

Section: Introductionmentioning

confidence: 99%

Implant wear induces inflammation, but not osteoclastic bone resorption, in RANK^–/– mice

Ren

Peng

et al. 2006

Journal Orthopaedic Research

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Signaling of RANK (receptor activator of nuclear factor kappa B) through its ligand RANKL appears critical in osteolysis associated with aseptic loosening (AL). The purpose of this study was to investigate the role of RANK in a murine osteolysis model developed in RANK knockout (RANK À/À ) mice. Ultra high molecular weight polyethylene (UHMWPE) debris was introduced into established air pouches on RANK À/À mice, followed by implantation of calvaria bone from syngeneic littermates. Wild type C57BL/6 (RANK þ/þ ) mice injected with either UHMWPE or saline alone were included in this study. Pouch tissues were collected 14 days after UHMWPE inoculation for molecular and histology analysis. Results showed that UHMWPE stimulation induced strong pouch tissue inflammation in RANK À/À mice, as manifested by inflammatory cellular infiltration, pouch tissue proliferation, and increased gene expression of IL-1b, TNFa, and RANKL. However, the UHMWPE-induced inflammation in RANK À/À mice was not associated with the osteoclastic bone resorption observed in RANK þ/þ mice. In RANK þ/þ mice subjected to UHMWPE stimulation, a large number of TRAP þ cells were found on the implanted bone surface, where active osteoclastic bone resorption was observed. No TRAP þ cells were found in UHMWPE-containing pouch tissues of RANK À/À mice. Consistent with the lack of osteoclastic activity shown by TRAP staining, no significant UHMWPE particle-induced bone resorption was found in RANK À/À mice. A well preserved bone collagen content (Van Gieson staining) and normal plateau surface contour [microcomputed tomography (mCT)] of implanted bone was observed in RANK À/À mice subjected to UHMWPE stimulation. In conclusion, this study provides the evidence that UHMWPE particles induce strong inflammatory responses, but not associated with osteoclastic bone resorption in RANK À/À mice. This indicates that RANK signaling is essential for UHMWPE particle-induced osteoclastic bone resorption, but does not participate in UHMWPE particle-induced inflammatory response. ß

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Particle disease. A comprehensive theory of periprosthetic osteolysis: a review.

Cited by 91 publications

References 62 publications

Do Tissues From THA Revision of Highly Crosslinked UHMWPE Liners Contain Wear Debris and Associated Inflammation?

Do Tissues From THA Revision of Highly Crosslinked UHMWPE Liners Contain Wear Debris and Associated Inflammation?

Erythromycin inhibits wear debris‐induced inflammatory osteolysis in a murine model

Implant wear induces inflammation, but not osteoclastic bone resorption, in RANK^–/– mice

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Particle disease. A comprehensive theory of periprosthetic osteolysis: a review.

Cited by 91 publications

References 62 publications

Do Tissues From THA Revision of Highly Crosslinked UHMWPE Liners Contain Wear Debris and Associated Inflammation?

Do Tissues From THA Revision of Highly Crosslinked UHMWPE Liners Contain Wear Debris and Associated Inflammation?

Erythromycin inhibits wear debris‐induced inflammatory osteolysis in a murine model

Implant wear induces inflammation, but not osteoclastic bone resorption, in RANK–/– mice

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Implant wear induces inflammation, but not osteoclastic bone resorption, in RANK^–/– mice