The Role of Pericyte Migration and Osteogenesis in Periodontitis.

Journal of dental research Pub Date : 2024-07-01 Epub Date: 2024-05-31 DOI:10.1177/00220345241244687
Y Cao, Q Ni, C Bao, C Cai, T Wang, X Ruan, Y Li, H Wang, R Wang, W Sun
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Abstract

A ligature-induced periodontitis model was established in wild-type and CD146CreERT2; RosatdTomato mice to explore the function of pericytes in alveolar bone formation. We found that during periodontitis progression and periodontal wound healing, CD146+/NG2+ pericytes were enriched in the periodontal tissue areas, which could migrate to the alveolar bone surface and colocalize with ALP+/OCN+ osteoblasts. Chemokine C-X-C motif receptor 4 (CXCR4) inhibition using AMD3100 blocked CD146-Cre+ pericyte migration and osteogenesis, as well as further exacerbated periodontitis-associated bone loss. Next, primary pericytes were sorted out by magnetic-activated cell sorting and demonstrated that C-X-C motif chemokine ligand 12 (CXCL12) promotes pericyte migration and osteogenesis via CXCL12-CXCR4-Rac1 signaling. Finally, the local administration of an adeno-associated virus for Rac1 overexpression in NG2+ pericytes promotes osteoblast differentiation of pericytes and increases alveolar bone volume in periodontitis. Thus, our results provided the evidence that pericytes may migrate and osteogenesis via the CXCL12-CXCR4-Rac1 axis during the pathological process of periodontitis.

牙周膜迁移和骨生成在牙周炎中的作用。
为了探索周细胞在牙槽骨形成中的功能,我们在野生型小鼠和CD146CreERT2; RosatdTomato小鼠中建立了结扎诱导的牙周炎模型。我们发现,在牙周炎进展和牙周伤口愈合过程中,CD146+/NG2+周细胞在牙周组织区域富集,它们可以迁移到牙槽骨表面并与ALP+/OCN+成骨细胞共定位。使用AMD3100抑制趋化因子C-X-C受体4(CXCR4)可阻断CD146-Cre+周细胞的迁移和成骨,并进一步加剧牙周炎相关骨质流失。接着,用磁激活细胞分选法分选出原发性周细胞,并证明 C-X-C motif趋化因子配体 12(CXCL12)通过 CXCL12-CXCR4-Rac1 信号传导促进周细胞迁移和成骨。最后,在局部注射腺相关病毒使 Rac1 在 NG2+周细胞中过度表达,可促进周细胞的成骨细胞分化,并增加牙周炎患者的牙槽骨体积。因此,我们的研究结果为牙周炎病理过程中周细胞可能通过CXCL12-CXCR4-Rac1轴迁移和成骨提供了证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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