Bone fracture healing is a multistage regenerative process that requires the collaboration of various cell types, with approximately 5%‐10% of fractures not healing properly. Accumulating evidence suggests that dysregulations in the immune system are associated with defective healing. In a cohort of 30 bone fracture patients between 50 and 62 years of age, 8 patients displayed delayed healing. Compared to the 22 normal healing patients, these 8 delayed healing patients presented significantly lower frequencies of CD4+CD25hiFoxp3+ canonical regulatory T cells immediately following bone fracture and early on during the healing process. The CD4+CD25+/hi T cells from delayed healing patients also presented reduced capacity to express transforming growth factor beta (TGF‐β), and presented reduced surface expression levels of inhibitory molecules, including CTLA‐4 and Lag‐3, compared to CD4+CD25+/hi T cells from normal healing patients. Moreover, CD4+CD25+/hi T cells from delayed healing patients were less potent in the suppression of CD4+CD25− autologous conventional T cell proliferation, and presented reduced expansion capacity in response to interleukin (IL)‐2 stimulation. Overall, our results demonstrated multiple reductions in regulatory T cell function in delayed healing patients that could produce long‐lasting consequences in the bone fracture healing process.