Semaglutide Investigated for Phenotype-Specific Inflammatory Modulation in Diabetic Spinal Implant Infection Models

Diabetes mellitus is a rapidly expanding global health crisis, significantly elevating the risk of complications following orthopedic and spine surgery. Patients with diabetes face higher incidences of surgical site infection, delayed wound healing, and hardware failure compared to non-diabetic individuals, particularly in spine surgery where infection can lead to severe morbidity and revision procedures. Current clinical studies often group all forms of diabetes, primarily using hemoglobin A1c (HbA1c) as a severity metric, which overlooks the fundamental pathophysiological differences between Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM). T1DM involves autoimmune beta-cell destruction and absolute insulin deficiency, leading to a catabolic state, while T2DM is characterized by peripheral insulin resistance and relative insulin deficiency, often linked to obesity and chronic low-grade inflammation. These distinctions are crucial as they influence immune competence and inflammatory responses, which are critical for understanding and treating implant-associated infections.