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Dr. Hallab’s research involves the study of implant degradation and biologic reactivity to soluble and particulate implant debris with four areas of focus: 1) Immune reactivity to implant debris, from both an adaptive (T-cell) and innate (macrophage) perspective, 2) Implant connections (modular junctions) and implant fretting corrosion, metal release and metal-protein complex formation, 3) Peri-implant cell toxicity responses to implant degradation products such as metals, 4) Study of how material surfaces can be used to control immune and cell function such as bone deposition. Over the years his group has found different types of implant debris (ions vs particles) bind to different specific serum proteins in people with total joint replacements, these differences translate into quantifiable person- and material-specific immune responses that can be used as diagnostic measures of performance. His research has dealt with the engineering aspects of implant degradation (wear and corrosion) and innate/adaptive immune responses to implant debris. He has discovered how metal implant debris induces inflammasome danger signaling and how DTH responses to implants metal depend on both the innate and adaptive immune system. His group has been at the for front of discovery in this field of improving implant performance over the past 20 years and reported that implant metals induce person-dependent monocyte-macrophage activation, where metals such as Cobalt ions and Co-Cr-Mo alloy particles were found to consistently induced inflammasome dependent co-stimulatory molecule increases, lysosome destabilization, hypoxia type responses, and increased DTH immune responses in prospective THA cohorts. Additnionally, he has developed methods for diagnosing metal sensitivity that are being used clinically to help people with or receiving orthopedic implants. They have quantified toxicity responses of many implant metals (e.g. Al, Co, Cr, Cu, Fe, Mo Nb, Ni and Zr) to peri-implant cells. These areas are focused on the continuing mission of his lab to improve implant performance through increased knowledge of person-dependent immune-implant debris interactions.
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Biotribology (2023): 100259-100259
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