A review of the biologic effects of spine implant debris: Fact from fiction

Abstract

Background

Biologic-reactivity to implant-debris is the primary determinant of long-term clinical performance. The following reviews: 1) the physical aspects of spinal-implant debris and 2) the local and systemic biologic responses to implant debris.

Methods

Methods included are: 1) gravimetric wear analysis; 2) SEM and LALLS; 3) metal-ion analysis; 4) ELISA, toxicity testing, patch testing; and 5) metal-lymphocyte transformation testing (metal-LTT).

Results

Wear and corrosion of spine-implants produce particles and ions. Particles (0.01–1000 μm) are generally submicron (<1 μm). Wear rates of metal-on-polymer and metal-on-metal disc arthroplasties are approximately 2–20 and 1 mm³/yr, respectively. Metal-on-metal total disc replacement components have significant increases in circulating metal (less than 10-fold that of controls at 4 ppb-Co and 3 ppb-Cr or ng/mL). Debris reactivity is local and systemic. Local inflammation is caused primarily by ingestion of debris by local macrophages, which produce pro-inflammatory cytokines TNFα, IL-1β, IL-6, and PGE2. Systemic responses associated with implant-debris have been limited to hypersensitivity reactions. Elevated amounts of in the liver, spleen, etc of patients with failed TJA have not been associated with remote toxicological or carcinogenic pathology to date. Implant debris are differentially bioreactive. Greater numbers are pro-inflammatory; the smaller-sized debris are more bioreactive by virtue of their greater numbers (dose) for a given amount of implant mass loss (one 100-μm-diameter particle is equivalent in mass to 1 million 1-μm-diameter particles). Elongated particles are pro-inflammatory (ie, aspect ratio of greater than 3). Metal particles are more proinflammatory than polymers, ceteris paribus.

Conclusion

Spinal arthroplasty designs have been in use for more than 20 years internationally; therefore, concerns about neuropathology, toxicity, and carcinogenicity are mitigated. Debris-induced inflammation still depends on the individual and the type of debris. The consequence of debris-induced inflammation is continued; vigilance by physicians is recommended monitoring of spinal implants using physical exams and testing of metal content and bioreactivity, as is planning for the likelihood of revision in younger individuals.