<![CDATA[Background: Diabetes mellitus (DM) impairs fracture healing by promoting advanced glycation end products, oxidative stress, and an imbalance in the RANKL/osteoprotegerin (OPG) system, thereby increasing bone resorption and inhibiting osteoblast activity. Objective: To evaluate the effects of DM on fracture healing as reflected by RANKL and OPG levels. Methods: This systematic review followed PRISMA and Synthesis without Meta-analysis (SWiM) guidance. PubMed, Scopus, and Google Scholar were searched for English-language studies published from January 2021 through May 2026. Eligible in vivo studies compared diabetic and non-diabetic rat fracture models and reported RANKL and/or OPG outcomes. Study selection, data extraction, and risk-of-bias assessment were conducted independently using the SYRCLE tool for animal studies. Results: Three studies met the inclusion criteria. Diabetic groups consistently showed higher RANKL and lower OPG than non-diabetic controls, indicating a higher RANKL/OPG ratio and a shift toward osteoclast-mediated bone resorption. These changes were accompanied by impaired bone formation and delayed healing-related outcomes. Conclusion: DM is associated with a consistent pro-resorptive imbalance in the RANKL/OPG system during fracture healing. The concordance across animal studies supports this pathway as a potential therapeutic target, while standardized studies and clinical validation remain necessary.]]>
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