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氯化锂刺激大鼠拔牙窝修复中的骨形成。

Lithium chloride stimulates bone formation in extraction socket repair in rats.

机构信息

Department of Periodontology, Dental Research Division, Guarulhos University, São Paulo, Brazil.

Department of Periodontology, College of Dentistry, University of Florida, 1600 SW Archer Rd., Room D10-6, Gainesville, FL, 32610, USA.

出版信息

Oral Maxillofac Surg. 2024 Mar;28(1):169-177. doi: 10.1007/s10006-022-01124-4. Epub 2022 Oct 15.

DOI:10.1007/s10006-022-01124-4
PMID:36242702
Abstract

PURPOSE

Previous evidence shows that lithium chloride (LiCl), a suppressor of glycogen synthase kinase-3β (GSK-3β), may enhance bone formation in several medical and dental conditions. Thus, the purpose of the current study was to assess the effects of LiCl on extraction socket repair in rats.

METHODS

Thirty rats were randomly assigned into a control group (administration of water; n = 15) or a LiCl group (administration of 150 mg/kg of LiCl; n = 15). LiCl and water were given every other day, starting at 7 days before the extraction of upper first molars until the end of each experiment period. Histological sections from five rats per group were obtained at 10, 20, and 30 days post-extractions. Histometrical analysis of newly formed bone (NB) and the levels of tartrate-resistant acid phosphatase (TRAP)-stained cells were evaluated at 10, 20, and 30 days post-extractions. Immunohistochemical staining for receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), bone sialoprotein (BSP), osteocalcin (OCN), and osteopontin (OPN) was assessed at 10 days post-extractions.

RESULTS

The LiCl group had a greater proportion of NB than the control group at 20 days (P < 0.05). At 30 days, the rate of TRAP-stained cells was lower in the LiCl group than in the control group (P < 0.05). At 10 days, the LiCl group presented stronger staining for OPG, BSP, OPN, and OCN, when compared to the control group (P < 0.05).

CONCLUSION

Systemic LiCl enhanced extraction socket repair, stimulated an overall increase in bone formation markers, and restricted the levels of TRAP in rats.

摘要

目的

先前的证据表明,氯化锂(LiCl)作为糖原合酶激酶-3β(GSK-3β)的抑制剂,可能在多种医学和牙科疾病中增强骨形成。因此,本研究的目的是评估 LiCl 对大鼠拔牙窝修复的影响。

方法

30 只大鼠随机分为对照组(给予水;n=15)或 LiCl 组(给予 150mg/kg LiCl;n=15)。从拔除上颌第一磨牙前 7 天开始,每隔一天给予 LiCl 和水,直到每个实验期结束。每组取 5 只大鼠的组织学切片,分别在拔牙后 10、20 和 30 天获得。在拔牙后 10、20 和 30 天评估新形成骨(NB)和抗酒石酸酸性磷酸酶(TRAP)染色细胞水平的组织学分析。在拔牙后 10 天评估核因子κB 受体激活剂配体(RANKL)、骨保护素(OPG)、骨涎蛋白(BSP)、骨钙素(OCN)和骨桥蛋白(OPN)的免疫组织化学染色。

结果

LiCl 组在第 20 天的 NB 比例高于对照组(P<0.05)。在第 30 天,LiCl 组的 TRAP 染色细胞率低于对照组(P<0.05)。在第 10 天,LiCl 组的 OPG、BSP、OPN 和 OCN 染色强度强于对照组(P<0.05)。

结论

全身给予 LiCl 增强了拔牙窝修复,刺激了骨形成标志物的整体增加,并限制了大鼠 TRAP 的水平。

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Bioact Mater. 2021 Mar 9;6(10):3074-3084. doi: 10.1016/j.bioactmat.2021.02.015. eCollection 2021 Oct.
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