The effect of opioids on biomechanical parameters of bone

Bone is a dynamic and living tissue that continuously undergoes change throughout life. Current literature indicates that prolonged opioid exposure disrupts bone remodeling by inhibiting osteoblast activity and predisposing individuals to increased bone failure resistance. Our study builds upon proof-of-principle data from a pre-clinical rabbit-opioid model system to investigate 1) the biomechanical impact of opioid exposure on bone failure resistance, 2) the relationship between cross-sectional geometric values and fracture patterns, and 3) how microstructural parameters inform bone failure resistance. We hypothesize that bone specimens from opioid animals will demonstrate increased bone failure resistance, increased medullary area and cortical porosity, decreased cortical area and a diminished cellular network (e,g., lacunar parameters). Twenty-one male, skeletally mature New Zealand White rabbits were divided into three groups of seven animals each: morphine sulphate, fentanyl, and controls for eight weeks of experimental drug treatment. A multi-modal approach was used to collect data including high- resolution imaging (SRμCT) and biomechanical 3-point bend tests. Analyses revealed significantly greater cortical porosity in the morphine group compared to fentanyl and control animals. When examining the graphs visually, opioid groups demonstrated greater cortical and medullary areas and diminished markers of structural competence compared to controls. Analyses revealed that increased lacunar parameters are associated with reduced structural competence. Increased cortical area and medullary area are positively correlated with structural competence. Ultimately, evidence suggests that opioid exposure stimulated cellular dysregulation of the remodeling process and increased bone failure resistance in the opioid experimental groups.