The accurately establishment of the eruptive pathway is of vital importance. The mechanisms governing tooth eruption pathway remain little known. This study is to elucidate the roles of Semaphorin 3A (Sema 3A) in mouse tooth eruptive pathway. C57BL/6 mice (11–13 and 15–17 days after birth) were chosen to observe eruptive pathway of mouse lower first molar. Expressions of Sema 3A and its receptor neuropilin 1 and plexin A1 were detected. Osteoclasts were identified by TRAP staining. Co-localization of Sema 3A and osteoclast maker CD68 was detected by double immunofluorescence staining. Picrosirius red staining was applied to observe collagen fibers during mucosal penetration phase. In vitro, Bone marrow-derived macrophages (BMMs) were prepared from 4 week C57BL/6 mice to observe the effect of Sema 3A on the differentiation of BMMs into osteoclasts by TRAP staining. Expressions of Sema 3A was observed by immunofluorescence and western blotting. At osseous eruption phase, many TRAP-positive multi-nucleated cells were distributed around occlusal alveolar bone. The positive expressions of Sema 3A were observed in the multi-nucleated cells. Fluorescence double staining showed that Sema 3A and CD68 were co-expressed in osteoclasts. Its receptor neuropilin 1 and plexin A1 were also found in osteoclasts. In vitro, Sema3A negatively regulated osteoclast differentiation. At mucosal penetration, occlusal alveolar bone had been completely resorbed and collagen fires were gradually degraded for eruptive pathway. Similar positive expressions of Sema 3A and its receptor neuropilin 1 and plexin A1 were also found in the mucosal penetration pathway. Sema 3A gets involved in the establishment of mouse tooth eruptive pathway by modulating osteoclast activity. Sema3A should be considered as a novel nervous agent or a potential biomarker for mouse tooth eruptive pathway.

中文翻译：

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Semaphorin 3A参与了小鼠牙齿萌发途径的建立。

准确建立喷发途径至关重要。控制牙齿萌发途径的机制仍然鲜为人知。这项研究旨在阐明Semaphorin 3A（Sema 3A）在小鼠牙齿萌发途径中的作用。选择C57BL / 6小鼠（出生后11-13天和15-17天）观察小鼠下颌第一磨牙的爆发途径。检测Sema 3A及其受体neuropilin 1和plexin A1的表达。通过TRAP染色鉴定破骨细胞。通过双重免疫荧光染色检测Sema 3A和破骨细胞制造商CD68的共定位。应用Picrosirius红染色观察粘膜渗透阶段的胶原纤维。体外，从4周的C57BL / 6小鼠制备骨髓来源的巨噬细胞（BMM），以观察Sema 3A通过TRAP染色对BMMs分化为破骨细胞的作用。通过免疫荧光和蛋白质印迹观察到Sema 3A的表达。在骨萌发期，许多TRAP阳性的多核细胞分布在牙槽骨周围。在多核细胞中观察到Sema 3A的阳性表达。荧光双染色显示Sema 3A和CD68在破骨细胞中共表达。在破骨细胞中也发现了其受体Neuropilin 1和plexin A1。在体外，Sema3A负调节破骨细胞分化。在粘膜穿透时，咬合牙槽骨已被完全吸收，胶原蛋白火逐渐降解，形成爆发途径。在黏膜渗透途径中也发现了Sema 3A及其受体Neuropilin 1和plexin A1的相似阳性表达。Sema 3A通过调节破骨细胞活性参与了小鼠牙齿萌发途径的建立。Sema3A应该被认为是一种新颖的神经毒剂或小鼠牙齿爆发途径的潜在生物标记。