Production of cytokines around loosened cemented acetabular components. Analysis with immunohistochemical techniques and in situ hybridization.

Jiranek, William A.; Machado, Michelle; Jasty, Murali; Jevsevar, David S.; Wolfe, Hubert J.; Goldring, S.R.; Goldberg, Michael J.; Harris, William H.

doi:10.2106/00004623-199306000-00007

Cited by 426 publications

(234 citation statements)

References 51 publications

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“…12,[29][30][31] It is well recognized that activated macrophages, in response to titanium wear particles, produce pro-inflammatory cytokines, such as TNF-a, IL-6, and IL-1a/b. [32][33][34] TNF-a acts directly on osteoclast precursors, whereas IL-6 and IL-1a/b act indirectly by increasing the expression of RANK-L and M-CSF by osteoblasts. 35 In the present study, significantly increased levels of IL-1b, IL-6, and TNF-a were measured in the supernatant of OC cultured on SS discs.…”

Section: Discussionmentioning

confidence: 99%

Bio‐corrosion of stainless steel by osteoclasts—in vitro evidence

Cadosch

Chan

Gautschi

et al. 2008

Journal Orthopaedic Research

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Most metals in contact with biological systems undergo corrosion by an electrochemical process. This study investigated whether human osteoclasts (OC) are able to grow on stainless steel (SS) and directly corrode the metal alloy leading to the formation of corresponding metal ions, which may cause inflammatory reactions and activate the immune system. Scanning electron microscopy analysis demonstrated long-term viable OC cultures and evident resorption features on the surface of SS discs on which OC were cultured for 21 days. The findings were confirmed by atomic emission spectrometry investigations showing significantly increased levels of chromium, nickel, and manganese in the supernatant of OC cultures. Furthermore, significant levels of pro-inflammatory cytokines IL-1b, IL-6, and TNF-a, which are considered to be major mediators of osteolysis, were revealed in the same cultures by cytometric bead array analysis. Within the present study, it was shown that human osteoclast precursors are able to grow and differentiate towards mature OC on SS. The mature cells are able to directly corrode the metal surface and release corresponding metal ions, which induce the secretion of pro-inflammatory cytokines that are known to enhance osteoclast differentiation, activation, and survival. Enhanced corrosion and the subsequently released metal ions may therefore result in enhanced osteolytic lesions in the peri-prosthetic bone, contributing to the aseptic loosening of the implant. Keywords: osteoclast; bio-corrosion; stainless steel; osteolysis; TNF-a Over the last decades, significant developments have been taking place to provide suitable metal alloys for implants with optimal mechanical characteristics and good biocompatibility with minimal adverse host tissue reactions. 1 However, their permanent tendency to corrode when exposed to a physiological environment remains a serious concern. 2-4 Elevated concentrations of metal ions have been measured in clinically retrieved peri-prosthetic tissues, distal organs, and body fluids in total hip arthroplasty patients. [5][6][7] The biology behind corrosion inside the human body and the distribution of the metal ions throughout the organism is not fully understood. It has been suggested that extracellular body fluids have corrosive proprieties and contain metal binding proteins. 2,3 Furthermore, it has been debated whether osteoclasts (OC) are able to corrode pure metal when entering into contact with metal surfaces. However, direct evidence of metal corrosion by OC has been missing to date.Osteoclasts are highly specialized multinucleated cells, which are capable of bone resorption. They are formed by the fusion of marrow-derived mononuclear precursors, which circulate in the peripheral blood. Osteoclastic differentiation from hematopoietic and circulating monocytes occurs in the presence of macrophage-colony stimulating factor (M-CSF) and the receptor activator of NF-kB ligand (RANK-L) which are expressed on osteoblastic cells. 8 Mature OC display distinct morpholog...

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Section: Discussionmentioning

confidence: 99%

Bio‐corrosion of stainless steel by osteoclasts—in vitro evidence

Cadosch

Chan

Gautschi

et al. 2008

Journal Orthopaedic Research

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“…The pathophysiological mechanisms have yet to be defined although increasing evidence indicates that cyclic mechanical loading, production of prosthetic wear particles 1,2 and the ensuing adverse tissue response [3][4][5] are important contributors to local osteolysis and bone resorption at the bone-prosthesis interface. An interface membrane develops around the loosened prosthesis with a pseudosynovial layer adjacent to it.…”

Section: From the Royal Postgraduate Medical School London Englandmentioning

confidence: 99%

“…2 The resultant cortical bone loss is considered to be caused by activation and release of a cascade of cell mediators by the pseudosynovial macrophages and other cells capable of phagocytosis of the prosthetic particulate debris. [3][4][5] Previous studies have established the expression in interface membranes of interleukin-1 (IL-1), tumour necrosis factor-␣ (TNF-␣) and the arachidonic-acid metabolite prostaglandin E 2 (PGE 2 ) which are strongly implicated in the induction and maintenance of bone resorption. [5][6][7][8][9] Cellculture experiments have confirmed the ability of isolated macrophages and pseudomembrane-derived cells to secrete IL-1, TNF-␣ and PGE 2 and to stimulate bone resorption, as a result of stimulation by wear particles.…”

Section: From the Royal Postgraduate Medical School London Englandmentioning

confidence: 99%

“…[3][4][5] Previous studies have established the expression in interface membranes of interleukin-1 (IL-1), tumour necrosis factor-␣ (TNF-␣) and the arachidonic-acid metabolite prostaglandin E 2 (PGE 2 ) which are strongly implicated in the induction and maintenance of bone resorption. [5][6][7][8][9] Cellculture experiments have confirmed the ability of isolated macrophages and pseudomembrane-derived cells to secrete IL-1, TNF-␣ and PGE 2 and to stimulate bone resorption, as a result of stimulation by wear particles. 3,10,11 Nitric oxide (NO) has now been shown to be one of the principal mediators of the actions of many cytokines and is known to induce PGE 2 production.…”

Section: From the Royal Postgraduate Medical School London Englandmentioning

confidence: 99%

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Aseptic Loosening Of Total Hip Replacement: Macrophage Expression Of Inducible Nitric Oxide Synthase And Cyclo-oxygenase-2, Together With Peroxynitrite Formation, As A Possible Mechanism For Early Prosthesis Failure

Hukkanen¹,

Corbett²,

Batten³

et al. 1997

The Journal of Bone and Joint Surgery

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Aseptic loosening is a major cause of failure of total hip arthroplasty. The adverse tissue response to prosthetic wear particles, with activation of cytokine and prostanoid production, contributes to bone loss around the implants. We have investigated the possibility that inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) are expressed in macrophages in the pseudomembrane at the bone-implant interface, thereby contributing to the periprosthetic bone resorption.We also assessed whether peroxynitrite, a nitric oxide (NO)-derived oxidant associated with cellular injury, is generated in the membrane. Enzymatic activity of iNOS was measured using the arginine-citrulline assay technique and prostaglandin E 2 (PGE 2 ), as an indicator of COX-2 activity, was measured using an enzyme immunoassay.Cellular immunoreactivity for iNOS, nitrotyrosine (a marker of peroxynitrite-induced cellular injury) and COX-2 was assessed by quantitative peroxidase immunocytochemistry while immunofluorescence methods were used for subsequent co-localisation studies with CD68 + macrophages.

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“…In this model, macrophages in the periprosthetic environment express proinflammatory cytokines and enzymes in response to implant-derived wear particles. Both in vitro and in vivo evidence shows that wear debris-stimulated macrophages release interleukin-1 (IL-1) family and IL-6 cytokines, and these cytokines are found at high levels in osteolytic tissues (2)(3)(4)(5)(6), synovial fluid (7), and regional lymph nodes retrieved from failed THAs, while they are not found in stable implants (8). These cytokines are known to mediate bone resorption, both in vivo and in vitro.…”

mentioning

confidence: 99%

Polymorphisms in the interleukin‐1 receptor antagonist and interleukin‐6 genes affect risk of osteolysis in patients with total hip arthroplasty

Gordon¹,

Kiss-Tóth²,

Stockley³

et al. 2008

Arthritis & Rheumatism

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Objective. To determine whether osteolysis after total hip arthroplasty (THA) is associated with common polymorphisms within the genes encoding the interleukin-1 (IL-1) family and IL-6, and to determine whether polymorphisms that are associated with osteolysis affect in vitro messenger RNA (mRNA) expression in human peripheral blood mononuclear cells (PBMCs) in response to wear particles.Methods. Unrelated white subjects of North European descent (n ‫؍‬ 612) were recruited a mean of 11 years after cemented THA for primary osteoarthritis. Of these subjects, 272 had previous osteolysis and 340 had no radiographic evidence of osteolysis (control group). Genomic DNA was genotyped for the following singlenucleotide polymorphisms (SNPs): IL1A ؉4845, IL1B ؉3954, IL1B -3737, IL1B -511, IL1RA ؉2018, IL6 -174, IL6 -572, and IL6 -597. In a subset of 60 subjects, PBMCs were extracted and stimulated with titanium particles and/or endotoxin, and cytokine mRNA expression was measured using quantitative real-time reverse transcriptase-polymerase chain reaction.Results. The odds ratio (OR) for osteolysis associated with carriage of the IL1RA ؉2018C allele was 0.66 (95% confidence interval [95% CI] 0.48-0.91) (P ‫؍‬ 0.012). The remaining SNPs were not individually associated with osteolysis. The uncommon IL6 haplotype ؊174G/؊572G/؊597A (osteolysis group frequency 2.4%, control group frequency 0.8%) was associated with osteolysis (P ‫؍‬ 0.02, calculated using Haploview software). The IL1RA ؉2018CC genotype was associated with increased mRNA expression compared with the ؉2018TT genotype in both unstimulated and stimulated PBMCs (P ‫؍‬ 0.01 by analysis of variance, after Bonferroni correction).Conclusion. The IL1RA ؉2018C allele is associated with a decreased risk of osteolysis after THA and with increased IL-1 receptor antagonist mRNA expression in vitro. An uncommon haplotype within the promoter region of the gene for IL-6 is positively associated with osteolysis.

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Production of cytokines around loosened cemented acetabular components. Analysis with immunohistochemical techniques and in situ hybridization.

Cited by 426 publications

References 51 publications

Bio‐corrosion of stainless steel by osteoclasts—in vitro evidence

Bio‐corrosion of stainless steel by osteoclasts—in vitro evidence

Aseptic Loosening Of Total Hip Replacement: Macrophage Expression Of Inducible Nitric Oxide Synthase And Cyclo-oxygenase-2, Together With Peroxynitrite Formation, As A Possible Mechanism For Early Prosthesis Failure

Polymorphisms in the interleukin‐1 receptor antagonist and interleukin‐6 genes affect risk of osteolysis in patients with total hip arthroplasty

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