Li Qiang, Huang Fei, Liu Jia, Zhao Yin Hua, Zhang Min, Chen Yong Jin
Chin J Dent Res. 2017;20(3):125-135. doi: 10.3290/j.cjdr.a38767.
To explore the effect of long-term stress on the temporomandibular joint (TMJ) condyle and its possible underlying mechanism.
A 12-week, chronic unpredictable mild stress (CUMS) model was used to induce long-term psychological stress in rats. Rats were randomly divided into control group (CONT), chronic unpredictable mild stress group (CUMS) and chronic unpredictable mild stress with fluoxetine treatment group (CUMS + DT) (n = 30 per group). A 5 mg/kg dose of fluoxetine was intraperitoneally injected daily 0.5 h before stress. A sucrose preference test, plasma corticosterone test and open-field test were performed to verify the feasibility of the CUMS model. Histopathology was used to observe the pathological changes of condyle. The expression levels of inflammatory cytokines, matrix metalloproteases (MMPs) and extracellular matrix (ECM) were measured by real-time polymerase chain reaction, western blotting and immunohistochemistry.
At 8 and 12 weeks after exposure to CUMS, the rats showed higher plasma corticosterone than the control rats. Additionally, for the open-field test, the rats exposed to CUMS spent more time in the centre zone and moved a shorter distance than the control and drug treatment rats. In addition, pathological changes in the condylar cartilage occurred in the 8-week CUMS subgroup and were more obvious in the 12-week CUMS subgroup. The CUMS caused an increase in the secretion of inflammatory cytokines, imbalanced expression of MMPs and tissue inhibitor of metalloproteinase-1 and accelerated degradation of ECM in condylar cartilage in a time-dependent manner.
Osteoarthritis-like lesions can be caused by long-term CUMS in the mandibular condyles, which suggests that the imbalance in chondrocyte-secreted regulatory factors within the cartilage of the TMJ may play an important role in cartilage injury induced by psychological stress.
探讨长期应激对颞下颌关节（TMJ）髁突的影响及其可能的潜在机制。
采用为期12周的慢性不可预测轻度应激（CUMS）模型诱导大鼠长期心理应激。大鼠随机分为对照组（CONT）、慢性不可预测轻度应激组（CUMS）和慢性不可预测轻度应激加氟西汀治疗组（CUMS + DT）（每组n = 30）。在应激前0.5小时每天腹腔注射5 mg/kg剂量的氟西汀。进行蔗糖偏好试验、血浆皮质酮试验和旷场试验以验证CUMS模型的可行性。采用组织病理学观察髁突的病理变化。通过实时聚合酶链反应、蛋白质免疫印迹法和免疫组织化学法检测炎性细胞因子、基质金属蛋白酶（MMPs）和细胞外基质（ECM）的表达水平。
暴露于CUMS后8周和12周，大鼠血浆皮质酮水平高于对照大鼠。此外，在旷场试验中，暴露于CUMS的大鼠在中央区域停留的时间比对照和药物治疗组大鼠更长，移动距离更短。另外，8周CUMS亚组的髁突软骨出现病理变化，并在12周CUMS亚组中更明显。CUMS导致炎性细胞因子分泌增加、MMPs和金属蛋白酶组织抑制剂-1表达失衡，并以时间依赖性方式加速髁突软骨中ECM的降解。
长期CUMS可导致下颌髁突出现骨关节炎样病变，这表明颞下颌关节软骨内软骨细胞分泌的调节因子失衡可能在心理应激诱导的软骨损伤中起重要作用。
