■骨质疏松症是老年人使用牙科植入物治疗牙齿缺陷的重要障碍。脂肪来源的干细胞(ADSC)已显示出广泛的组织修复和再生潜力。本研究旨在探讨工程化表达高水平骨保护素(OPG)的ADSCs在治疗因雌激素缺乏引起的种植牙科骨丢失中的有效性。
■通过双卵巢切除术建立骨质疏松大鼠模型,并对大鼠进行基因修饰细胞Adv-OPG-ADSCs处理。使用HE染色和micro-CT评估治疗对上颌骨组织变化的影响。此外,ALP和TRAP染色用于评估成骨细胞和破骨细胞的改变。最后,用RT-qPCR检测成骨细胞和破骨细胞相关指标的变化,蛋白质印迹,和ELISA。
■成功生成的高OPG表达ADSC导致细胞活力增加,扩散,和成骨细胞分化。Adv-OPG-ADSCs治疗显著改善上颌骨形态,小梁体积减少,雌激素缺乏的上颌骨种植牙科模型中的骨密度下降。此外,治疗有利于促进成骨细胞的生成和抑制破骨细胞的生成。Adv-OPG-ADSC增加OPG,ALP,OCN,和Runx-2在上颌骨中的表达,同时抑制RANKL表达,也增加了COLI和PINP的浓度,以及降低CTX-1的浓度。
■Adv-OPG-ADSCs促进成骨细胞的形成,抑制破骨细胞的生成,从而抑制骨骼吸收,促进骨形成,在存在骨质疏松相关并发症的情况下促进上颌骨的修复,尤其是在雌激素缺乏的情况下,为Adv-OPG-ADSCs在种植体相关性骨质疏松治疗中的应用提供科学依据。
UNASSIGNED: Osteoporosis is a significant barrier to the use of dental implants in the elderly for the treatment of tooth defects. Adipose derived stem cells (ADSCs) have demonstrated extensive potential for tissue repair and regeneration. The present study aimed to investigate the effectiveness of ADSCs engineered to express high levels of osteoprotegerin (OPG) for the treatment of bone loss in implant dentistry caused by estrogen deficiency.
UNASSIGNED: A rat model of osteoporosis was established through double oophorectomy, and the rats were treated by gene modified cells Adv-OPG-ADSCs. The effects of the treatment on maxilla tissue changes were evaluated using HE staining and micro-CT. Additionally, ALP and TRAP staining were used to assess osteoblast and osteoclast alterations. Finally, the changes in related osteoblast and osteoclast indicators were measured by RT-qPCR, Western blot, and ELISA.
UNASSIGNED: The successfully generated high-OPG-expressing ADSCs led to increase of cell viability, proliferation, and osteoblast differentiation. Treatment with Adv-OPG-ADSCs significantly ameliorated maxillary morphology, trabecular volume reduction, and bone mineral density decline in the model of estrogen-deficient maxillary implant dentistry. Furthermore, the treatment was beneficial to promoting the generation of osteoblasts and inhibiting the generation of osteoclast. Adv-OPG-ADSCs increased OPG, ALP, OCN, and Runx-2 expressions in the maxilla while suppressing RANKL expression, and also increased the concentration of COL I and PINP, as well as decreased the concentration of CTX-1.
UNASSIGNED: Adv-OPG-ADSCs promote the formation of osteoblasts and inhibit the generation of osteoclasts, thereby inhibiting bone absorption, facilitating bone formation, and promoting the repair of maxillary bone after dental implantation in the presence of osteoporosis-related complications, especially in the setting of estrogen deficiency, providing scientific basis for the application of Adv-OPG-ADSCs in the treatment of implant related osteoporosis.