Department of Diagnosis and Surgery, Araraquara School of Dentistry, University of São Paulo State, UNESP, Araraquara, SP, Brazil.
Department of Stomatology, Federal University of Paraná, UFPR, Curitiba, PR, Brazil.
J Periodontol. 2018 Apr;89(4):466-475. doi: 10.1002/JPER.17-0457.
Testosterone is known to affect bone in physiological and pathological conditions. The purpose of this study is to evaluate the role of testosterone in experimental periodontal disease in rats.
In this study we used a ligature model of periodontal disease in rats submitted to orchiectomy (OCX, testosterone depletion) with and without testosterone replacement therapy (TR). Control animals were sham-operated and retained physiological testosterone levels. Sixty-two days after orchiectomy and sham operations, ligatures were placed around the lower first molars for 2 weeks to induce experimental periodontal disease. Negative control animals received no ligatures. The outcomes assessed in the periodontal tissues were: inflammatory cytokine expression by enzyme-linked immunosorbent assay (ELISA), stereometric analysis of the inflammatory process and quantitation of inflammatory bone resorption by microcomputed tomography (μ-CT).
The OCX+TR group showed the greatest increase in fibroblastic cells and blood vessels with reduced inflammatory cell numbers in the gingival tissue with induction of periodontal disease. There were no significant differences between OCX and Sham-operated groups in all the stereometric parameters assessed. Ligature placement induced inflammatory bone resorption, which was significantly attenuated in OCX animals. Experimental periodontitis induced a significant increase in interleukin (IL)-1β, but the lowest levels were observed in the periodontitis/OCX group. IL-6 levels were not affected by OCX, but were significantly reduced in OCX+TR animals.
The findings of the present study suggest that testosterone depletion attenuates inflammatory bone resorption in ligature-induced periodontitis, which may be partly mediated via decreased production of IL-1β.
睾酮在生理和病理条件下已知会影响骨骼。本研究旨在评估睾酮在大鼠实验性牙周病中的作用。
在这项研究中，我们使用了大鼠牙周病结扎模型，进行了睾丸切除术（OCX，睾酮耗竭），并进行了睾酮替代治疗（TR）。对照动物接受了假手术，并保留了生理水平的睾酮。在睾丸切除术和假手术后的 62 天，在下第一磨牙周围放置结扎线 2 周，以诱导实验性牙周病。阴性对照动物未接受结扎。在牙周组织中评估的结果包括：酶联免疫吸附测定（ELISA）测定炎症细胞因子的表达、炎症过程的体视学分析以及微计算机断层扫描（μ-CT）定量炎症性骨吸收。
OCX+TR 组在诱导牙周病时，牙龈组织中纤维母细胞和血管增加最多，炎症细胞数量减少。在所有评估的体视学参数方面，OCX 组与 Sham 组之间没有显著差异。结扎放置诱导了炎症性骨吸收，OCX 动物的骨吸收明显减弱。实验性牙周炎诱导白细胞介素（IL）-1β显著增加，但在牙周炎/OCX 组中观察到的水平最低。OCX 不影响 IL-6 水平，但在 OCX+TR 动物中显著降低。
本研究的结果表明，睾酮耗竭可减轻结扎诱导的牙周炎中的炎症性骨吸收，这可能部分通过减少 IL-1β的产生来介导。
