PDGF-BB与IGF-I联合应用对大鼠正畸牙移动的影响

目的:观察血小板衍生生长因子-BB(PDGF-BB)与胰岛素样生长因子-I(IGF-I)联合应用对大鼠正畸牙移动的影响,为正畸临床治疗加快正畸牙移动.缩短正畸治疗时间进行探索.方法:在32只SD雄性大鼠上颌安装施加50 g力正畸装置牵引上颌第一磨牙近中移动,隔日在正畸牙颊侧牙龈黏膜下分别或联合注射200 ng rIfl...     

功能矫形前伸大鼠下颌后翼外肌胰岛素含量变化的定量研究

目的：了解功能矫形前伸大鼠下颌后胰岛素对翼外肌适用性改建的作用。方法：采用放射免疫分析技术分别检测实验组和对照组大鼠翼外肌内胰岛素的含量。结果;功能矫形前伸下颌后,生长期大鼠外肌内胰岛素含量增加。结论：胰岛素在功能矫形前伸大鼠下颌后翼外肌的适应性改建中有重要作用。     

脑溢安对大鼠舌下神经压榨伤后神经元型一氧化氮合酶nNOS表达的影响

目的：观察大鼠舌下神经压榨伤后,舌下神经核内nNOS的表达变化及中药脑溢安对其表达的影响。方法：建立大鼠舌下神经压榨伤模型,脑溢安治疗组用脑溢安药液灌胃,正常对照组和实验对照组用灭菌生理盐水灌胃。采用NADPH-d组化＋中性红复染组织化学方法,分别于第1、4、7、14天检测舌下神经核内nNOS表达变化。结果：正常对照组大鼠两侧舌下神经核内均未检测到nNOS免疫阳性细胞;与生理盐水对照组相比,脑溢安治疗组损伤后第4、7、14天损伤侧舌下神经核内阳性细胞数少,细胞成活率高,有统计学差异（P〈0.05）。结论：脑溢安降低大鼠舌下神经压榨伤后神经元胞体nNOS的表达。     

氨基胍干预对创伤性面瘫大鼠外周面神经及周围组织一氧化氮合酶表达的影响

目的　研究诱导型一氧化氮合酶抑制剂氨基胍对创伤性面瘫大鼠外周面神经及周围组织一氧化氮合酶表达的影响。方法　通过大鼠面瘫前后腹膜内小剂量给予氨基胍,在伤后各个时间点切取损伤面神经和软组织, 采用兔抗大鼠一氧化氮合酶(NOS)抗血清免疫组织化学ABC法对面神经和肌肉软组织内NOS表达的变化进行研究。结果　氨基胍组面神经和肌肉软组织伤后诱导型一氧化氮合酶免疫反应性明显降低。结论　氨基胍慢性干预明显抑制面神经和肌肉软组织内诱导型一氧化氮合酶的表达,为面神经再生与组织创伤修复创造了有利条件。     

辛伐他汀4种给药方法影响大鼠骨缺损愈合的实验研究

目的探讨辛伐他汀的4种给药方式对骨缺损愈合的影响。方法在40只SD大鼠胫骨上建立3mm的骨缺损模型，械侧缺损部位不作处理设为空白对照组、右侧分别给予单纯骨粉修复（A组）、单纯骨粉修复加局部注射辛伐他汀（B组）、局部骨粉复合2.5％辛伐池汀（C组）和骨粉复合15.0％辛伐他汀（D组）修复。术后第4周、8周分别处死各组大鼠，观察骨缺损区成骨情况，结果C组局部愈合正常，无破溃及组织反应，缺损处骨量和骨密度增加明显（比A组高32％．P〈0.05），镜下成骨细胞多，纤维组织最少，整体愈合效果最佳；而B组和D组局部都有破溃及类排斥反应性奶酪状分泌物，缺损局部骨量及骨密度与A组相比没有明显增加（P〉0.05）．炎性细胞及纤维组织较多．个别大鼠局部发生骨折。A组骨密度较空白组高，未见局部有破溃和组织反应，缺损侧胫骨未见完全骨折。而空白组缺损未完全骨性愈合．局部皮肤无破溃及类排除反应．部分大鼠局部发生骨折，结论骨粉复合一定浓度的辛代他汀对正常大鼠的胫骨缺损愈合有促进作用。     

Effects of Melatonin on Oxidative Stress Index and Alveolar Bone Loss in Diabetic Rats With Periodontitis

Background: The aim of this study is to evaluate the effects of systemic melatonin treatment on serum oxidative stress index (OSI) and alveolar bone loss (ABL) in rats with diabetes mellitus (DM) and periodontitis. Methods: Seventy Sprague Dawley rats were divided into control, experimentally induced periodontitis (EP), DM, EP‐DM, EP and melatonin treatment (EP‐MEL), DM and melatonin treatment (DMMEL), and EP‐DM‐MEL groups. DM was induced by alloxan, after which periodontitis was induced by ligature for 4 weeks. After removal of the ligature, the rats in the melatonin groups (EP‐MEL, DM‐MEL, and EP‐DM‐MEL) were treated with a single dose of melatonin (10 mg/body weight) every day for 14 consecutive days. At the end of the study, all of the rats were euthanized, and intracardiac blood samples and mandible tissues were obtained for biochemical and histologic analyses. Serum levels of total oxidant status/total antioxidant status and OSI were measured. In addition, neutrophil and osteoclast densities and myeloperoxidase activities were determined in gingival tissue homogenates, and ABL was evaluated with histometric measurements. Results: Melatonin treatment significantly reduced fasting plasma glucose levels in the rats with DM. In addition, reduced OSI and ABL levels were detected in the EP‐MEL and DM‐MEL groups; the reductions in the EP‐DM‐MEL group were found to be more prominent. Melatonin also significantly decreased the increased myeloperoxidase activities and osteoclast and neutrophil densities in the EP, DM, and EP‐DM groups. Conclusion: It is revealed in this experimental study that melatonin significantly inhibited hyperglycemia‐induced oxidative stress and ABL through antiDM and antioxidant effects in rats with DM and periodontitis.     

Therapeutic Effects of Melatonin on Alveolar Bone Resorption After Experimental Periodontitis in Rats: A Biochemical and Immunohistochemical Study

Background: The present study aims to investigate the effects of systemic melatonin administration on alveolar bone resorption in experimental periodontitis in rats. Methods: Twenty‐four male Sprague‐Dawley rats were divided into three groups (control, experimental periodontitis [Ped], and experimental periodontitis treated with melatonin [Mel‐Ped]). For periodontitis induction, first molars were ligatured submarginally for 4 weeks. After ligature removal, rats in the Mel‐Ped group were treated with a daily single dose of 10 mg/kg body weight melatonin for 15 consecutive days. At the end of the study, intracardiac blood samples and mandible tissues were obtained for histologic, biochemical, and radiographic analysis. Serum markers related to bone turnover, calcium, phosphorus, bone alkaline phosphatase (b‐ALP), and terminal C telopeptide of collagen Type I (CTX) were analyzed. Myeloperoxidase levels were determined in gingival tissue homogenates, and receptor activator of nuclear factor‐kappa B ligand (RANKL) activation was analyzed in the mandible samples stereologically. Alveolar bone loss was also evaluated radiographically in the mandible samples of each group. Results: Melatonin treatment decreased serum CTX levels and increased b‐ALP levels. Serum calcium and phosphorus levels were not statistically different among groups (P >0.05). Alveolar bone resorption and myeloperoxidase activity were statistically higher in the Ped group compared to the Mel‐Ped group (P <0.05). Immunohistochemical staining of RANKL and osteoclast activity were significantly lower in the Mel‐Ped group compared to the Ped group (P <0.05). Conclusion: This study reveals that melatonin treatment significantly inhibits regional alveolar bone resorption and contributes to periodontal healing in an experimental periodontitis rat model.     

Therapeutic Effects of Systemic Vitamin K2 and Vitamin D3 on Gingival Inflammation and Alveolar Bone in Rats With Experimentally Induced Periodontitis

Background: The synergistic effects of vitamin D3 and vitamin K2 on bone loss prevention have been reported. This study evaluates the effects of vitamin D3 and vitamin K2 supplementation in conjunction with conventional periodontal therapy (scaling and root planing [SRP]) on gingival interleukin (IL)‐1β and IL‐10, serum bone alkaline phosphatase (B‐ALP) and tartrate‐resistant acid phosphatase 5b (TRAP‐5b), and calcium and alveolar bone levels in rats with experimentally induced periodontitis. Methods: Seventy‐two rats were divided into the following groups: 1) healthy; 2) periodontitis; 3) SRP; 4) SRP + vitamin D3; 5) SRP + vitamin K2; and 6) SRP + vitamins K2 and D3. Periodontitis was induced by ligature placement for 7 days, and vitamin K2 (30 mg/kg) and/or vitamin D3 (2 μg/kg) were administered for 10 days in the SRP + vitamin D3, SRP + vitamin K2, and SRP + vitamins K2 and D3 groups by oral gavage. On day 18, the animals were sacrificed, serum B‐ALP, TRAP‐5b, and calcium levels were measured, gingiva specimens were extracted for IL‐1β and IL‐10 analysis, and distances between the cemento‐enamel junction and alveolar bone crest were evaluated. Results: Alveolar bone levels in the periodontitis group were significantly greater than those in the other five groups. No significant differences were found in gingival IL‐1β and IL‐10, serum B‐ALP and TRAP‐5b, and calcium and alveolar bone levels between the groups receiving SRP and vitamins and the group receiving SRP alone. Conclusion: Within the limitations of this study, vitamin D3 and K2 alone or in combination did not affect gingival IL‐1β and IL‐10, serum B‐ALP and TRAP‐5b levels, or alveolar bone compared with conventional periodontal therapy alone.     

Therapeutic Effects of Alpha Lipoic Acid and Vitamin C on Alveolar Bone Resorption After Experimental Periodontitis in Rats: A Biochemical,Histochemical, and Stereologic Study

Background: Alpha lipoic acid (ALA) and vitamin C (Vit‐C) are very important and powerful antioxidants that have been used for the treatment of many diseases. The present study aims to investigate the role of ALA and Vit‐C substances in the treatment of alveolar bone resorption in periodontal diseases. Methods: Thirty‐six male Wistar albino rats were randomly divided into four groups as follows: 1) control rats; 2) rats with experimental periodontitis (PED); 3) rats with PED treated with ALA (ALA); and 4) rats with PED treated with ALA+Vit‐C (ALA+Vit‐C). PED was simulated by placing ligatures around the neck of teeth for 5 weeks. After ligature removal, the PED group was given a single intragastric dose of 1 mL saline, and the ALA and ALA+Vit‐C groups were treated with an intragastric dose of 50 mg/kg ALA and ALA+Vit‐C for 15 days, respectively. Levels of serum bone alkaline phosphatase (B‐ALP) and myeloperoxidase (MPO) activity in gingival tissues were analyzed. To evaluate the osteoclast activation, expression of activated receptor activator nuclear factor‐kappa B ligand (RANKL) and bone density index (BDI) were determined stereologically in the bone sections obtained from the mandibles of the rats. Results: The results showed statistically significant differences between the PED group and groups treated with antioxidant according to B‐ALP, MPO, RANKL, and BDI values (P <0.05). ALA and ALA+Vit‐C treatments showed beneficial effects on the mesial/distal periodontal bone support at the ligature‐induced periodontitis tooth areas. Conclusion: This study shows that ALA and Vit‐C treatment provides therapeutic effects on inhibition of alveolar bone resorption and periodontal tissue destruction.