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Implant Material Bio-compatibility, Sensitivity, and Allergic Reactions

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Handbook of Spine Technology

Abstract

Generally biocompatibility to implant-debris governs long-term clinical performance. The following chapter covers: the kinds of implant-debris and the biologic responses to implant-debris. Implants produce debris from wear and corrosion that take the form of particles and ions. Particulate debris generally ranges from 0.01 to 100 s um. Wear rates of articulating bearing such as total hip arthroplasties generally range from 0.1 to 50mm3/yr. Metal-on-metal total joint replacement components are well known to produce increases in circulating metal in people (>ten-fold that of people without implant, i.e., 2-5parts per billion-Cobalt and 1-3 ppb-Chromiun). Debris bioreactivity is both local and systemic. Local inflammation is primarily mediated by local immune cells called macrophages, which produce pro-inflammatory mediators/cytokines TNFα, IL-1β, IL-6, and PGE2. Although there are many concerns associated with systemic reactivity to implant-debris, to date well-established systemic reactivity has been limited to developed hypersensitivity/allergy reactions. Elevated amounts of in the remote organs such as the liver, spleen of patients with TJA and high levels of circulating metal have not (yet) been associated with remote toxicological or carcinogenic pathologies. Not all implant debris is similarly biocompatible/nonbiocompatible. Additionally, the amount of debris-induced-inflammation depends on both the person and amount/kind/size of implant debris. The inflammation and bone loss associated with debris necessitates continued surveillance by physicians to monitor patients/implants over time using traditional physical exams, x-rays, and when appropriate new biological assays such as the testing of metal content and individual biological response such as hypersensitivity metal-LTT assays.

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Abbreviations

Al:

Aluminum

ALVAL:

Aseptic lymphocyte vasculitis associated lesion

Co:

Cobalt

Cr:

Chromium

Cr(PO4)4H2O:

Chromium orthophosphate

DAMP:

Danger associated molecular patterns

DTH:

Delayed type hypersensitivity adaptive (lymphocyte mediated) immune response that occurs over days to weeks to years (vs. that of an immediate response).

Hypersensitivity:

Adaptive immune responses typically local inflammation mediated by T-cells or B-cells where antigen presenting cells such as macrophages act as gate keepers.

IL-1b:

Interleukin 1 almost exclusively produced by inflammasome reaction, such as occurs in a macrophage response to implant debris particles

IL-6:

Interleukin 6

IL-18:

Interleukin 18

IL-33:

Interleukin 33

Inflammasome:

Key molecular components of a pro-inflammatory pathway that reacts to danger signals (not pathogens) that are produced when cells are damaged, typically composed of multiprotein oligomers consisting of caspase 1, PYCARD, NALP, and sometimes caspase 5 (also known as caspase 11 or ICH-3).

LALLS:

Low angle laser light scattering

metal-LTT:

Metal-lymphocyte transformation test (proliferation assay) used as a human diagnostic test for delayed type hypersensitivity responses to implant metals

NALP3/ASC:

Inflammasome complex of proteins

PAMP:

Pathogen associated molecular pattern

PGE2:

Prostaglandin E2

PMMA:

Polymethylmethacrylate

ppb:

Parts per billion (ng/mL or ug/L)

PTFE:

Teflon (polytetraflouroethylene)

RANKL:

Receptor activator of nuclear factor Kappa Beta ligand

ROS:

Reactive oxygen species

SEM:

Scanning electron microscopy

TEM:

Transmission electron microscopy

THA:

Total hip arthroplasty

Ti:

Titanium

TJA:

Total joint arthroplasty

TJR:

Total joint replacement

TNF-a:

Tumor necrosis factor – alpha

UHMWPE:

Ultra high molecular weight polyethylene

V:

Vanadium

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Hallab, N.J., Samelko, L., Caicedo, M. (2019). Implant Material Bio-compatibility, Sensitivity, and Allergic Reactions. In: Cheng, B. (eds) Handbook of Spine Technology. Springer, Cham. https://doi.org/10.1007/978-3-319-33037-2_29-1

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