Periodontal disease is an inflammatory and destructive disease of periodontal support tissue caused by microorganisms in dental plaque. During the development of periodontal disease, host immune regulation plays an im...Periodontal disease is an inflammatory and destructive disease of periodontal support tissue caused by microorganisms in dental plaque. During the development of periodontal disease, host immune regulation plays an important role, and unnecessary excessive immune regulation often exacerbates the course of chronic periodontal disease. Mesenchymal stem cells (MSCs) are adult stem cells with self replication ability and multi-directional differentiation potential. Many studies have found that MSCs have strong immunosuppressive effects on both adaptive and innate immunity. In recent years, literature has reported that MSCs are involved in the immune regulatory effect of chronic periodontal disease, inhibiting its inflammatory response and alveolar bone resorption, but the specific regulatory mechanism has not been elucidated. This article reviews the current research status of the immune regulatory effects of MSCs on chronic periodontitis.展开更多
背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed...背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed、Web of Science、中国生物医学文献数据库和中国知网数据库进行文献检索,设置检索时限为2010-2023年,总结了2010年以来正畸与自噬相关研究进展,最终纳入76篇文献进行分析讨论。结果与结论:(1)正畸力可通过牙周机械感受器和其造成的无菌性炎症引发一系列生物化学信号的转变,进而引起牙周组织自噬。(2)自噬通过级联放大的信号通路如磷脂酰肌醇-3-激酶/蛋白激酶B通路、河马通路及丝裂原活化蛋白激酶通路等,产生相应反馈从而促进牙周组织改建,最终实现牙齿的移动与稳定。正畸力诱导的自噬可差异性调节牙齿压力侧骨吸收和张力侧骨形成,相关靶点在正畸临床治疗的应用中具有良好前景。(3)然而,正畸力与自噬的机制较为复杂,现有研究仅停留在探究自噬对正畸牙齿移动的作用,自噬与正畸牙齿移动过程中的相互调节作用、涉及相关通路上游机械受体及信号通路间的交互作用均需要进一步的探究。展开更多
Regulator of G-protein Signaling 10 （Rgsl0） plays an important function in osteoclast differentiation. However, the role of Rgsl0 in immune cells and inflammatory responses, which activate osteoclasts in inflam- mat...Regulator of G-protein Signaling 10 （Rgsl0） plays an important function in osteoclast differentiation. However, the role of Rgsl0 in immune cells and inflammatory responses, which activate osteoclasts in inflam- matory lesions, such as bacteria-induced periodontal disease lesions, remains largely unknown. In this study, we used an adeno-associated virus （AAV-） mediated RNAi （AAV-shRNA-Rgs10） knockdown approach to study Rgsl0＇s function in immune cells and osteoclasts in bacteria-induced inflammatory lesions in a mouse model of periodontal disease. We found that AAV-shRNA-Rgs10 mediated Rgs10 knockdown impaired osteoclastogenesis and osteoclast-mediated bone resorption, in vitro and in vivo. Interestingly, local injection of AAV-shRNA-Rgs10 into the periodontal tissues in the bacteria-induced inflammatory lesion greatly decreased the number of dendritic cells, T-cells and osteoclasts, and protected the periodontal tissues from local inflammatory damage and bone destruction. Importantly, AAV-mediated Rgs10 knockdown also reduced local expression of osteoclast markers and pro-inflammatory cytokines. Our results demonstrate that AAV- shRNA-Rgs10 knockdown in periodontal disease tissues can prevent bone resorption and inflammation simultaneously. Our data indicate that Rgsl0 may regulate dendritic cell proliferation and maturation, as well as the subsequent stimulation of T-cell proliferation and maturation, and osteoclast differentiation and acti- vation. Our study suggests that AAV-shRNA-Rgs10 can be useful as a therapeutic treatment of periodontal disease.展开更多
文摘Periodontal disease is an inflammatory and destructive disease of periodontal support tissue caused by microorganisms in dental plaque. During the development of periodontal disease, host immune regulation plays an important role, and unnecessary excessive immune regulation often exacerbates the course of chronic periodontal disease. Mesenchymal stem cells (MSCs) are adult stem cells with self replication ability and multi-directional differentiation potential. Many studies have found that MSCs have strong immunosuppressive effects on both adaptive and innate immunity. In recent years, literature has reported that MSCs are involved in the immune regulatory effect of chronic periodontal disease, inhibiting its inflammatory response and alveolar bone resorption, but the specific regulatory mechanism has not been elucidated. This article reviews the current research status of the immune regulatory effects of MSCs on chronic periodontitis.
文摘背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed、Web of Science、中国生物医学文献数据库和中国知网数据库进行文献检索,设置检索时限为2010-2023年,总结了2010年以来正畸与自噬相关研究进展,最终纳入76篇文献进行分析讨论。结果与结论:(1)正畸力可通过牙周机械感受器和其造成的无菌性炎症引发一系列生物化学信号的转变,进而引起牙周组织自噬。(2)自噬通过级联放大的信号通路如磷脂酰肌醇-3-激酶/蛋白激酶B通路、河马通路及丝裂原活化蛋白激酶通路等,产生相应反馈从而促进牙周组织改建,最终实现牙齿的移动与稳定。正畸力诱导的自噬可差异性调节牙齿压力侧骨吸收和张力侧骨形成,相关靶点在正畸临床治疗的应用中具有良好前景。(3)然而,正畸力与自噬的机制较为复杂,现有研究仅停留在探究自噬对正畸牙齿移动的作用,自噬与正畸牙齿移动过程中的相互调节作用、涉及相关通路上游机械受体及信号通路间的交互作用均需要进一步的探究。
基金supported by NIH grants RC1DE-020533 (Y.P.L.) and AR-055307 (Y.P.L.)
文摘Regulator of G-protein Signaling 10 （Rgsl0） plays an important function in osteoclast differentiation. However, the role of Rgsl0 in immune cells and inflammatory responses, which activate osteoclasts in inflam- matory lesions, such as bacteria-induced periodontal disease lesions, remains largely unknown. In this study, we used an adeno-associated virus （AAV-） mediated RNAi （AAV-shRNA-Rgs10） knockdown approach to study Rgsl0＇s function in immune cells and osteoclasts in bacteria-induced inflammatory lesions in a mouse model of periodontal disease. We found that AAV-shRNA-Rgs10 mediated Rgs10 knockdown impaired osteoclastogenesis and osteoclast-mediated bone resorption, in vitro and in vivo. Interestingly, local injection of AAV-shRNA-Rgs10 into the periodontal tissues in the bacteria-induced inflammatory lesion greatly decreased the number of dendritic cells, T-cells and osteoclasts, and protected the periodontal tissues from local inflammatory damage and bone destruction. Importantly, AAV-mediated Rgs10 knockdown also reduced local expression of osteoclast markers and pro-inflammatory cytokines. Our results demonstrate that AAV- shRNA-Rgs10 knockdown in periodontal disease tissues can prevent bone resorption and inflammation simultaneously. Our data indicate that Rgsl0 may regulate dendritic cell proliferation and maturation, as well as the subsequent stimulation of T-cell proliferation and maturation, and osteoclast differentiation and acti- vation. Our study suggests that AAV-shRNA-Rgs10 can be useful as a therapeutic treatment of periodontal disease.
