Macrophages are critical contributors to bone regeneration via intramembranous ossification. In some tissue repair models recruited monocyte-derived macrophages are required to clear pathogens, and remove damaged tissues and cells to permit regeneration. The etymology of macrophages that contribute to bone regeneration via intramembranous ossification is not well characterized. C-C chemokine receptor type 2 (CCR2) is commonly used as a marker of monocyte-derived macrophages. Bone marrow macrophages, like several other tissue-resident macrophage populations, can repopulate independent of CCR2. Here, we demonstrated that CCR2-dependent monocyte recruitment was not critical for intramembranous-mediated bone repair. A tibial bone injury that heals primarily through intramembranous officiation was generated on Ccr2^-/- mice. There was no difference in F4/80⁺ macrophage number, distribution or morphology, or the amount of regenerating bone in the injury site between the Ccr2^-/- mice and wild type controls, when assessed in the anabolic phase. This is in contrast to a requirement for CCR2-dependent macrophage recruitment to the injury site in other bone repair models. However, these observations are not necessarily incompatible as dependence on monocyte-derived macrophages may be relative to the degree of tissue injury and the tibial injury model utilized is relatively contained. Thus, our findings suggest that the macrophages supporting intramembranous bone formation are either locally proliferating resident macrophages or arise from recruited monocytes that migrate via an alternate pathway.