Asymptomatic prospective and retrospective cohorts with metal‐on‐metal hip arthroplasty indicate acquired lymphocyte reactivity varies with metal ion levels on a group basis

Hallab, Nadim J.; Caicedo, Marco S.; McAllister, Kyron; Skipor, Anastasia K.; Amstutz, Harlan C.; Jacobs, Joshua J.

doi:10.1002/jor.22214

Cited by 39 publications

(32 citation statements)

References 37 publications

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“…The adverse local tissue reaction and lymphocyte response to metals debris can develop prior to clinical symptoms 37 . Therefore, metal ion levels have been used as a surrogate marker of corrosion wear at the articulating surface or modular junction 38 , which may continue to increase for years after surgery 39 .…”

Section: Discussionmentioning

confidence: 99%

Early Corrosion-Related Failure of the Rejuvenate Modular Total Hip Replacement

Meftah

Haleem

Burn

et al. 2014

Journal of Bone and Joint Surgery

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Section: Discussionmentioning

confidence: 99%

Early Corrosion-Related Failure of the Rejuvenate Modular Total Hip Replacement

Meftah

Haleem

Burn

et al. 2014

Journal of Bone and Joint Surgery

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“…Lymphocytes have been shown that they can play a central role in the failure of some kinds of orthopedic implants (33–36). The subtypes of T-cells that dominate implant debris-associated responses are T-helper (TH) cells (33–36).…”

Section: Adaptive Immune Responsesmentioning

confidence: 99%

Chemokines Associated with Pathologic Responses to Orthopedic Implant Debris

Hallab

Jacobs

2017

Front. Endocrinol.

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Despite the success in returning people to health saving mobility and high quality of life, the over 1 million total joint replacements implanted in the US each year are expected to eventually fail after approximately 15–25 years of use, due to slow progressive subtle inflammation to implant debris compromising the bone implant interface. This local inflammatory pseudo disease state is primarily caused by implant debris interaction with innate immune cells, i.e., macrophages. This implant debris can also activate an adaptive immune reaction giving rise to the concept of implant-related metal sensitivity. However, a consensus of studies agree the dominant form of this response is due to innate reactivity by macrophages to implant debris danger signaling (danger-associated molecular pattern) eliciting cytokine-based and chemokine inflammatory responses. This review covers implant debris-induced release of the cytokines and chemokines due to activation of the innate (and the adaptive) immune system and how this leads to subsequent implant failure through loosening and osteolysis, i.e., what is known of central chemokines (e.g., IL-8, monocyte chemotactic protein-1, MIP-1, CCL9, CCL10, CCL17, and CCL22) associated with implant debris reactivity as related to the innate immune system activation/cytokine expression, e.g., danger signaling (e.g., IL-1β, IL-18, IL-33, etc.), toll-like receptor activation (e.g., IL-6, tumor necrosis factor α, etc.), bone catabolism (e.g., TRAP5b), and hypoxia responses (HIF-1α). More study is needed, however, to fully understand these interactions to effectively counter cytokine- and chemokine-based orthopedic implant-related inflammation.

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“…NOTE: For the purpose of statistical analysis, mass spectroscopy values of half the detection limit was assigned to ions concentrations levels below that limit 29 .…”

Section: Protocolmentioning

confidence: 99%

Removal of Trace Elements by Cupric Oxide Nanoparticles from Uranium <em>In Situ</em> Recovery Bleed Water and Its Effect on Cell Viability

Schilz¹,

Reddy²,

Nair³

et al. 2015

JoVE

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In situ recovery (ISR) is the predominant method of uranium extraction in the United States. During ISR, uranium is leached from an ore body and extracted through ion exchange. The resultant production bleed water (PBW) contains contaminants such as arsenic and other heavy metals. Samples of PBW from an active ISR uranium facility were treated with cupric oxide nanoparticles (CuO-NPs). CuO-NP treatment of PBW reduced priority contaminants, including arsenic, selenium, uranium, and vanadium. Untreated and CuO-NP treated PBW was used as the liquid component of the cell growth media and changes in viability were determined by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay in human embryonic kidney (HEK 293) and human hepatocellular carcinoma (Hep G2) cells. CuO-NP treatment was associated with improved HEK and HEP cell viability. Limitations of this method include dilution of the PBW by growth media components and during osmolality adjustment as well as necessary pH adjustment. This method is limited in its wider context due to dilution effects and changes in the pH of the PBW which is traditionally slightly acidic however; this method could have a broader use assessing CuO-NP treatment in more neutral waters.

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Asymptomatic prospective and retrospective cohorts with metal‐on‐metal hip arthroplasty indicate acquired lymphocyte reactivity varies with metal ion levels on a group basis

Cited by 39 publications

References 37 publications

Early Corrosion-Related Failure of the Rejuvenate Modular Total Hip Replacement

Early Corrosion-Related Failure of the Rejuvenate Modular Total Hip Replacement

Chemokines Associated with Pathologic Responses to Orthopedic Implant Debris

Removal of Trace Elements by Cupric Oxide Nanoparticles from Uranium <em>In Situ</em> Recovery Bleed Water and Its Effect on Cell Viability

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