减少饮食负荷可降低前牙反合修复体诱导的小鼠颞下颌关节退变。
Reducing dietary loading decreases mouse temporomandibular joint degradation induced by anterior crossbite prosthesis.
作者信息
Liu Y-D, Liao L-F, Zhang H-Y, Lu L, Jiao K, Zhang M, Zhang J, He J-J, Wu Y-P, Chen D, Wang M-Q
机构信息
Department of Oral Anatomy and Physiology and TMD, School of Stomatology, Fourth Military Medical University, 145 Changlexi Road, Xi'an 710032, China.
Department of Orthopaedics, Xijing Hospital, Fourth Military Medical University, 15 Changlexi Road, Xi'an 710032, China.
出版信息
Osteoarthritis Cartilage. 2014 Feb;22(2):302-12. doi: 10.1016/j.joca.2013.11.014. Epub 2013 Dec 5.
OBJECTIVE
Dietary loading has been reported to have an effect on temporomandibular joint (TMJ) remodeling via periodontal-muscular reflex. We therefore examined whether reducing dietary loading decreased TMJ degradation induced by the unilateral anterior crossbite prosthesis as we recently reported.
METHODS
Forty 6-week-old female C57BL/6J mice were randomly divided into two experimental and two control groups. One experimental and one control group received small-size diet and the other two groups received large-size diet. Unilateral anterior crossbite prosthesis was created in the two experimental groups. The TMJ samples were collected 3 weeks after experimental operation. Histological changes in condylar cartilage and subchondral bone were assessed by Hematoxylin & Eosin, toluidine blue, Safranin O and tartrate-resistant acid phosphatase staining. Real-time polymerase chain reaction (PCR) and/or immunohistochemistry were performed to evaluate the expression levels of Collagen II, Aggrecan, a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5) and RANKL/RANK/OPG in TMJ condylar cartilage and/or subchondral bone.
RESULTS
Thinner and degraded cartilage, reduced cartilage cellular density, decreased expression levels of Collagen II and Aggrecan, loss of subchondral bone and enhanced osteoclast activity were observed in TMJs of both experimental groups. However, the cartilage degradation phenotype was less severe and cartilage ADAMTS-5 mRNA was lower while OPG/RANKL ratio in cartilage and subchondral bone was higher in the small-size than large-size diet experimental group. No differences of histomorphology and the tested molecules were found between the two control groups.
CONCLUSIONS
The current findings suggest that a lower level of functional loading by providing small-size diet could reduce TMJ degradation induced by the biomechanical stimulation from abnormal occlusion.
目的
据报道，饮食负荷可通过牙周 - 肌肉反射对颞下颌关节（TMJ）重塑产生影响。因此，我们研究了减少饮食负荷是否能降低我们最近报道的单侧前牙反合修复体诱导的TMJ退变。
方法
将40只6周龄雌性C57BL / 6J小鼠随机分为两个实验组和两个对照组。一个实验组和一个对照组给予小颗粒饮食，另外两组给予大颗粒饮食。在两个实验组中制作单侧前牙反合修复体。实验操作3周后收集TMJ样本。通过苏木精和伊红染色、甲苯胺蓝染色、番红O染色和抗酒石酸酸性磷酸酶染色评估髁突软骨和软骨下骨的组织学变化。进行实时聚合酶链反应（PCR）和/或免疫组织化学以评估TMJ髁突软骨和/或软骨下骨中胶原蛋白II、聚集蛋白聚糖、含血小板反应蛋白基序的解聚素和金属蛋白酶5（ADAMTS - 5）以及RANKL/RANK/OPG的表达水平。
结果
两个实验组的TMJ均观察到软骨变薄和退变、软骨细胞密度降低、胶原蛋白II和聚集蛋白聚糖表达水平下降、软骨下骨丢失以及破骨细胞活性增强。然而，与大颗粒饮食实验组相比，小颗粒饮食实验组的软骨退变表型较轻且软骨ADAMTS - 5 mRNA较低，而软骨和软骨下骨中的OPG/RANKL比值较高。两个对照组之间在组织形态学和检测分子方面未发现差异。
结论
目前的研究结果表明，通过提供小颗粒饮食降低功能负荷水平可减少异常咬合生物力学刺激诱导的TMJ退变。
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