Curl Linda, Tan Chien Wei, Dreyer Craig W, Sampson Wayne
Orthodontic Unit, The University of Adelaide, South Australia, Australia.
Aust Orthod J. 2014 Nov;30(2):143-51.
Previous studies have found ankylosis occurs as a part of the inflammatory process of aseptic root resorption initiated in a rat model. The physiologic mechanisms behind the development of dentoalveolar ankylosis and healing response are still unclear. While receptor activator of nuclear factor-κβ ligand (RANKL), receptor activator of nuclear factor-κβ (RANK) and osteoprotegerin (OPG) have gained momentum in the understanding of resorption, no study to date has investigated their role in dentoalveolar ankylosis.
The aims of this study were to investigate if, and when, ankylosis occurred in the rat PDL, whether the resolution of ankylosis occurred with time and, finally, to observe the expression of RANKL, RANK and OPG during the ankylotic process.
Dry ice was applied for 20 minutes to the upper right first molar crown of 15 eight-week-old, male Sprague-Dawley rats. An additional three rats served as untreated external controls. Groups of three rats were sacrificed after the thermal insult on day 0, 4, 7, 14 and 28 respectively. Each maxilla was dissected out and processed for histological examination and RANKL, OPG and RANK immunohistochemistry.
By the use of light microscopy and H&E staining, no ankylosis was detected in the external control group and the experimental groups at days 0 and 4. On day 7, disruption within the periodontal ligament was observed in the interradicular region and the initial signs of ankylosis were seen in the form of finger-like projections extending from the alveolar bone towards the cementum. Fourteen days after the thermal insult, all animals exhibited extensive ankylosis that spanned the entire interradicular periodontal space. At 28 days, the development of ankylosis appeared to have ceased and repair was observed, together with an intact periodontal ligament in all but one rat. Positive staining results were obtained with RANKL, RANK and OPG antibodies. The expressions of RANKL, RANK and OPG were similar in the external control group, 0-, 4-, and 28-day experimental groups. In the 7- and 14-day experimental groups, RANKL, RANK and OPG were expressed in the blood vessels within the ankylotic regions.
During the development of ankylosis and its resolution, it was concluded from their simultaneous presence that there is a complex interaction between RANKL, RANK and OPG that requires further investigation.
先前的研究发现，在大鼠模型中，强直作为无菌性牙根吸收炎症过程的一部分而发生。牙槽骨强直发展及愈合反应背后的生理机制仍不清楚。虽然核因子κβ配体受体（RANKL）、核因子κβ受体（RANK）和骨保护素（OPG）在理解吸收过程中受到了更多关注，但迄今为止尚无研究调查它们在牙槽骨强直中的作用。
本研究的目的是调查大鼠牙周膜中是否以及何时发生强直，强直是否会随时间消退，最后观察强直过程中RANKL、RANK和OPG的表达情况。
对15只8周龄雄性Sprague-Dawley大鼠的右上第一磨牙牙冠施加干冰20分钟。另外3只大鼠作为未处理的外部对照。分别在热损伤后第0、4、7、14和28天处死每组3只大鼠。取出每个上颌骨并进行组织学检查以及RANKL、OPG和RANK免疫组织化学检测。
通过光学显微镜和苏木精-伊红染色，在第0天和第4天，外部对照组和实验组均未检测到强直。在第7天，在根间区域观察到牙周膜破坏，并且出现了强直的初始迹象，表现为从牙槽骨向牙骨质延伸的指状突起。热损伤后14天，所有动物均表现出广泛的强直，跨越整个根间牙周间隙。在第28天，强直的发展似乎已经停止并观察到修复，除一只大鼠外，所有大鼠的牙周膜均完整。使用RANKL、RANK和OPG抗体获得了阳性染色结果。RANKL、RANK和OPG在外部对照组、第0、4和28天实验组中的表达相似。在第7天和第14天实验组中，RANKL、RANK和OPG在强直区域内的血管中表达。
在强直的发展及其消退过程中，由于它们同时存在，得出结论认为RANKL、RANK和OPG之间存在复杂的相互作用，需要进一步研究。
