Objective To investigate the role of proteoglycan form of dentin matrix protein 1 (DMP1-PG) in mandibular bone injury. Methods We created mandibular bone defects in wild-type mice (control group) and DMP1 glycosylation point mutant (S89G-DMP1) mice (experimental group). Samples of mandibles were collected at 7, 14 and 28 days after model construction and subjected to micro-computed tomography scans, tissue sectioning, and hematoxylin eosin and toluidine blue staining to compare defect healing between the two groups. We also examined differences in the expression of osteogenesis-related proteins in the injured areas by immunofluorescence staining, and compared osteogenesis-related gene expression levels between the experimental and control groups post-surgery using real-time quantitative polymerase chain reaction. Mandibular bone marrow mesenchymal stem cells were extracted from both groups and their osteogenic differentiation abilities were compared. Results Mandibular injury healing was significantly reduced in the experimental compared with the control mice, and expression levels of osteogenesis-related proteins in the bone-injury area were decreased. In addition, the osteogenic differentiation ability of bone marrow mesenchymal stem cells from the experimental group was significantly weaker than that of cells from the control group. Conclusions DMP1-PG is involved in the repair of jaw injury, and lack of DMP1-PG can lead to delayed healing of jaw defects in mice.