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The craniofacial skeleton is the foundation of most stomatological treatments, including prosthodontics and maxillofacial surgery. Although histologically similar to the appendicular skeleton, the craniofacial skeleton manifests many unique properties in response to external stimuli and signals. However, the mandibular or maxillary bone marrow mesenchyme, which is the intrinsic foundation of the functions of craniofacial skeleton, has not been well studied, and its homeostasis mechanism remains elusive. Osteoporosis is a systemic disease that affects all skeletons and is characterized by bone mass loss. Osteoporotic bone marrow mesenchymal stem cells (BMMSCs) exhibit disturbed homeostasis and distorted lineage commitment. Many reports have shown that microRNAs (miRNAs) play important roles in regulating MSCs homeostasis. Here, to obtain a better understanding of mandibular bone marrow MSCs homeostasis, we isolated and cultured mandible marrow MSCs from mouse mandibles. Using miR-705 mimics and an inhibitor, we demonstrated that miR-705 played a vital role in shifting the mandibular MSCs lineage commitment  in vitro . Utilizing an osteoporosis mouse model, we demonstrated that MSCs from ovariectomized (OVX) mouse mandibular bone marrow exhibited impaired osteogenic and excessive adipogenic differentiation. miR-705 was found overexpressed in OVX mandibular MSCs. The knock down of miR-705  in vitro  partially attenuated the differentiation disorder of the OVX mandibular MSCs by upregulating the expression of osteogenic marker genes but suppressing adipogenic genes. Taken together, our findings provide a better understanding of the homeostasis mechanism of mandibular BMMSCs and a novel potential therapeutic target for treating mandibular osteoporosis.

MicroRNA-705 regulates the differentiation of mouse mandible bone marrow mesenchymal stem cells