The effects of hydroxychloroquine-induced oxidative stress on fracture healing in an experimental rat model

This is the authors' abstract. We don't add key points for this paper.

OBJECTIVES: The purpose of this study was to investigate whether hydroxychloroquine (HCQ) sulfate causes oxidative stress (OS) and its effect on fracture healing in an experimental rat model. MATERIALS AND METHODS: day. After sacrifice, malondialdehyde levels induced by OS were calculated for each rat, and fracture healing was evaluated radiographically, histomorphometrically, histopathologically, and immunohistochemically. RESULTS: Malondialdehyde levels were higher in the HCQ groups than in the control groups (p<0.05). Hydroxychloroquine caused OS in rats. The ratio of total callus diameter to femur bone diameter was lower in HCQ groups compared to control groups (p<0.05). No differences were observed when comparing radiological and histological healing results between the control and HCQ groups. Alkaline phosphatase levels were lower in the HCQ-4 group than the C-4 group at week four (p<0.05), although osteocalcin and osteopontin levels did not differ between groups (p>0.05). Oxidative stress had no adverse effects on histologic healing outcomes and osteoblast functions. Cathepsin K and tartrate-resistant acid phosphatase-5b levels were higher in the HCQ-4 group than in the C-4 group (p<0.05). While the number and function of osteoclasts increased due to OS in callus tissue, a decrease in the number of chondrocytes was observed. CONCLUSION: Hydroxychloroquine-induced OS increases the number and function of osteoclasts and decreases the number of hypertrophic chondrocytes and endochondral ossification but has no significant effect on mid-late osteoblast products and histological fracture healing scores.