All metals in contact with biological systems undergo corrosion. This electrochemical process leads to the formation of metal ions, which may activate the immune system by forming complexes with endogenous proteins.
Implant degradation products have been shown to be associated with dermatitis, urticaria, and vasculitis. If cutaneous signs of an allergic response appear after implantation of a metal device, metal sensitivity should be considered. Currently, there is no generally accepted test for the clinical determination of metal hypersensitivity to implanted devices.
The prevalence of dermal sensitivity in patients with a joint replacement device, particularly those with a failed implant, is substantially higher than that in the general population.
Until the roles of delayed hypersensitivity and humoral immune responses to metallic orthopaedic implants are more clearly defined, the risk to patients may be considered minimal.
It is currently unclear whether metal sensitivity is a contributing factor to implant failure.
Implant-related metal sensitivity has been well documented in case and group studies; however, overall it remains a relatively unpredictable and poorly understood phenomenon in the context of orthopaedic implant materials1-3. Dermal hypersensitivity to metal is common, affecting about 10% to 15% of the population1,2,4,5. Dermal contact with and ingestion of metals have been reported to cause immune reactions, which most typically manifest as hives, eczema, redness, and itching1,6,7. Historically, the ability of implant materials to demonstrate appropriate host and material responses has resulted in the elimination of candidate materials based on observation of adverse host responses. However, some adverse responses are difficult to characterize in preclinical and clinical settings because of their infrequent or subtle nature. In vivo metal hypersensitivity or hypersensitivity-like reactivity to metallic biomaterials is one such response. Although little is known …
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