Department of Periodontics and Oral Biology, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Nanjing North Street No. 117, Shenyang, 110002, Liaoning Province, China.
Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Nanjing North Street No. 117, Shenyang, 110002, Liaoning Province, China.
Arch Oral Biol. 2020 Apr;112:104652. doi: 10.1016/j.archoralbio.2020.104652. Epub 2020 Feb 20.
To ascertain the role of inducible nitric oxide synthase (iNOS) in the periodontitis response during diabetes.
Twenty-four male SD rats were randomly divided into four groups: control group (Control), diabetes mellitus group (D), diabetes mellitus plus periodontitis group (DP), and periodontitis group (P). Periodontitis and diabetes were established separately. Then the gingival tissue and alveolar bone were collected. A stereomicroscope was used to evaluate bone loss. The expression of iNOS, TNF-α, and NF-κB in the gingiva was detected by immunohistochemical staining, real-time PCR, and western blot analysis.
Significant bone loss was observed in the DP and P groups and more extensive bone resorption was discovered in the DP group than in the P group (P < 0.05). The immunohistochemical staining analysis revealed enhanced expression of iNOS located in the gingiva of the three disease groups compared with the control group (P < 0.05). In particular, the level of iNOS was significantly higher in the DP group than in the P group (P < 0.05). This elevated trend of iNOS was further demonstrated by quantitative PCR and western blot analysis. Similarly, the mRNA and protein expression levels of NF-κB in the D, DP, and P groups were significantly higher than those of the control group, as was the level of TNF-α protein (P < 0.05).
Our results proved diabetes exacerbated alveolar bone resorption in a periodontitis rat model. iNOS may be the inflammatory mediator in the course of periodontal injury promoted by diabetes.
确定诱导型一氧化氮合酶（iNOS）在糖尿病牙周炎反应中的作用。
将 24 只雄性 SD 大鼠随机分为四组：对照组（Control）、糖尿病组（D）、糖尿病伴牙周炎组（DP）和牙周炎组（P）。分别建立牙周炎和糖尿病模型。然后收集牙龈组织和牙槽骨。立体显微镜用于评估骨丢失。通过免疫组织化学染色、实时 PCR 和 Western blot 分析检测牙龈中 iNOS、TNF-α 和 NF-κB 的表达。
DP 和 P 组均出现明显的骨丢失，且 DP 组的骨吸收较 P 组更为广泛（P<0.05）。免疫组织化学染色分析显示，与对照组相比，三组疾病组的 iNOS 在牙龈中的表达增强（P<0.05）。特别是 DP 组的 iNOS 水平明显高于 P 组（P<0.05）。定量 PCR 和 Western blot 分析进一步证实了这一升高趋势。同样，D、DP 和 P 组的 NF-κB mRNA 和蛋白表达水平以及 TNF-α 蛋白水平均明显高于对照组（P<0.05）。
我们的结果证明糖尿病在牙周炎大鼠模型中加重了牙槽骨吸收。iNOS 可能是糖尿病促进牙周损伤过程中的炎症介质。
