Molecular-neurovascular mechanisms of metal implant hypersensitivity as a cause of osteosynthesis failure and delayed bone union: a clinical case study

Metal hypersensitivity is a rare but clinically significant cause of aseptic inflammation and delayed bone union after osteosynthesis. The release of nickel, cobalt, and chromium ions from metal implants induces a T-lymphocyte–mediated delayed-type immune response, which leads to chronic inflammation, endothelial dysfunction, and suppression of osteogenesis. Differentiation of metal-induced hypersensitivity from infectious complications or mechanical instability remains a challenging diagnostic task in orthopedic practice. The aim of the study was to analyze a clinical case of chronic hypersensitivity to a metal implant after tibial osteosynthesis and to identify clinical and diagnostic features linking immune-mediated inflammation with delayed bone union. A retrospective analysis of a clinical case of a patient after tibial osteosynthesis using metal plates was performed. The clinical course, laboratory inflammatory markers, and serial radiographic examinations were evaluated to exclude infection and mechanical fixation failure. The postoperative course was characterized by persistent edema, hyperemia, recurrent seropurulent exudation, and chronic pain in the absence of laboratory signs of bacterial infection. Radiography revealed a lack of progression in bone callus formation despite stable implant fixation. Eight months after surgery, removal of the metal construct led to rapid regression of inflammation, reduction of pain syndrome, and restoration of radiological signs of bone union. Chronic hypersensitivity to metal implants is an underestimated cause of aseptic inflammation and delayed fracture healing. Persistent local inflammatory manifestations without signs of infection, combined with the absence of radiological progression of bone union, should prompt evaluation of a metal-induced immune reaction. Timely implant removal contributes to the restoration of osteogenic balance and bone consolidation.