Bone fractures may result in delayed union (DU) or non‐union (NU) in some patients. Evidence suggests that the skewing of the immune system toward the proinflammatory type is a contributing factor. Because B cells were previously found to infiltrate the fracture healing site at abundant levels, we examined the regulatory B cells (Bregs) in DU/NU patients. In bone fracture patients with normal healing, the frequency of interleukin (IL)‐10‐expressing B cells was significantly upregulated in the early healing process (6 weeks post‐surgery) and was downregulated later on (18 weeks post‐surgery), whereas in DU/NU patients, the early upregulation of IL‐10‐expressing B cells was missing. The majority of IL‐10‐expressing B cells were concentrated in the IgM+CD27+ fraction in both controls and patients. IgM+CD27+ B cells effectively suppressed interferon gamma (IFN‐γ), tumor necrosis factor alpha (TNF‐α), and IL‐2 expression from CD4+ T cells, as well as IFN‐γ and TNF‐α expression from CD8+ T cells. The IgM+CD27+ B cell‐mediated suppression was restricted to the sample from the early healing time point in controls, as the IgM+CD27+ B cells from normal healing patients later on or from DU/NU patients did not present significant regulatory function. In addition, culturing of CD4+CD25+ Tregs with IgM+CD27+ B cells from controls at early healing time point resulted in higher Foxp3 expression, a function absent in controls at later time point, or in DU/NU patients. In conclusion, our results support a role of B cell‐mediated regulation early during the bone healing process.