Department of General Dentistry and Emergency, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi, China.
Braz J Med Biol Res. 2012 Oct;45(10):968-76. doi: 10.1590/s0100-879x2012007500102. Epub 2012 Jun 21.
Psychological factors can be correlated with temporomandibular disorders (TMDs), but the mechanisms are unknown. In the present study, we examined the microstructural changes and expression of proinflammatory cytokines in mandibular condylar cartilage of the temporomandibular joint (TMJ) in a psychological stress animal model. Male Sprague-Dawley rats (8 weeks old, 210 ± 10 g) were randomly divided into 3 groups: psychological stress (PS, N = 48), foot shock (FS, N = 24), and control (N = 48). After inducing psychological stress using a communication box with the FS rats for 1, 3, or 5 weeks, PS rats were sacrificed and compared to their matched control littermates, which received no stress and were killed at the same times as the PS rats. Body and adrenal gland weight were measured and corticosterone and adrenocorticotropic hormone levels were determined by radioimmunoassay. After hematoxylin-eosin staining for histological observation, the ultrastructure of the TMJ was examined by scanning electron microscopy. Transcription and protein levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were evaluated by ELISA and semi-quantitative RT-PCR. The PS group showed a significantly higher adrenal gland weight after 3 weeks of stress and higher hormone levels at weeks 1, 3, and 5. Histopathological changes and thinning cartilage were apparent at weeks 3 and 5. In the PS group, TNF-α increased at 1, 3, and 5 weeks and IL-1β increased significantly after 1 and 3 weeks of stress, and then decreased to normal levels by 5 weeks. Psychological stress increased plasma hormone levels and RT-PCR indicated increased IL-1β and TNF-α expression in the TMJ in a time-dependent manner. These results suggest that cytokine up-regulation was accompanied by stress-induced cartilage degeneration in the mandibular condyle. The proinflammatory cytokines play a potential role in initiating the cartilage destruction that eventually leads to the TMDs.
心理因素与颞下颌关节紊乱病(TMDs)有关,但机制尚不清楚。本研究通过建立心理应激动物模型,观察颞下颌关节(TMJ)髁突软骨的超微结构变化及促炎细胞因子的表达。雄性 Sprague-Dawley 大鼠(8 周龄,210±10 g)随机分为 3 组:心理应激组(PS,N=48)、足底电击组(FS,N=24)和对照组(N=48)。PS 组采用沟通箱对大鼠进行心理应激 1、3、5 周后处死,与同期未进行心理应激的同窝对照大鼠进行比较。测量体质量和肾上腺质量,放射免疫法检测皮质酮和促肾上腺皮质激素水平。苏木精-伊红染色后观察组织学变化,扫描电镜观察 TMJ 超微结构。ELISA 和半定量 RT-PCR 检测白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的转录和蛋白水平。3 周应激后 PS 组大鼠肾上腺质量显著增加,1、3、5 周时激素水平升高。3、5 周时可见组织学变化和软骨变薄。1、3、5 周时 PS 组 TNF-α升高,1、3 周时 IL-1β明显升高,5 周时恢复正常。心理应激导致血浆激素水平升高,RT-PCR 显示 TMJ 中 IL-1β和 TNF-α表达呈时间依赖性增加。这些结果表明,细胞因子上调伴随着应激诱导的髁突软骨退变。促炎细胞因子在启动最终导致 TMDs 的软骨破坏中发挥潜在作用。