De Rossi Andiara, Fukada Sandra Yasuyo, De Rossi Moara, da Silva Raquel Assed Bezerra, Queiroz Alexandra Mussolino, Nelson-Filho Paulo, da Silva Léa Assed Bezerra
Department of Pediatric Dentistry, School of Dentistry of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Department of Physics and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
J Endod. 2016 Aug;42(8):1251-7. doi: 10.1016/j.joen.2016.05.009. Epub 2016 Jun 21.
Although studies have recently shown that osteocytes embedded in mineralized bone matrix play an important role in bone diseases, the participation of cementocytes in apical periodontitis has not been evaluated. The aim of the present study was to evaluate the possible involvement of cementocytes in the development of apical periodontitis.
Apical periodontitis was experimentally induced in the lower first molars of wild-type mice by pulp exposure to the oral environment. At 0, 7, 21, and 42 days after pulp infection, the animals were euthanized, and the jaws were prepared for analysis under conventional and fluorescence microscopy (morphologic and morphometric analysis), immunohistochemistry and immunofluorescence (receptor activator of nuclear factor kappa-B [RANK], receptor activator of the nuclear factor kappa-B ligand [RANKL], and osteoprotegerin [OPG]), enzyme histochemistry (osteoclasts and cementoclasts), and real-time polymerase chain reaction (RANK, RANKL, OPG, and cathepsin K).
At 7, 21, and 42 days after pulp exposure, there was a progressive increase in periodontal ligament, cementum and bone resorption areas, osteoclasts, and cementoclast counts as well as higher messenger RNA levels of RANK, RANKL, OPG, and cathepsin K. In intact teeth, cementocytes and osteocytes did not express RANKL. After infection, RANKL was strongly expressed in cementocytes, but not in osteocytes, and its expression increased with lesion progression.
Our findings show that cementocytes express RANKL in response to endodontic infection and may be involved in the pathogenesis of apical periodontitis.
尽管最近的研究表明，嵌入矿化骨基质中的骨细胞在骨疾病中起重要作用，但尚未评估牙骨质细胞在根尖周炎中的参与情况。本研究的目的是评估牙骨质细胞在根尖周炎发展过程中可能的参与情况。
通过将牙髓暴露于口腔环境，在野生型小鼠的下颌第一磨牙中实验性诱导根尖周炎。在牙髓感染后0、7、21和42天，对动物实施安乐死，并准备下颌骨用于常规显微镜和荧光显微镜分析（形态学和形态计量学分析）、免疫组织化学和免疫荧光分析（核因子κB受体激活剂[RANK]、核因子κB配体受体激活剂[RANKL]和骨保护素[OPG]）、酶组织化学分析（破骨细胞和成牙骨质细胞）以及实时聚合酶链反应（RANK、RANKL、OPG和组织蛋白酶K）。
在牙髓暴露后7、21和42天，牙周膜、牙骨质和骨吸收面积、破骨细胞和成牙骨质细胞计数逐渐增加，RANK、RANKL、OPG和组织蛋白酶K的信使核糖核酸水平也更高。在完整牙齿中，牙骨质细胞和骨细胞不表达RANKL。感染后，RANKL在牙骨质细胞中强烈表达，但在骨细胞中不表达，并且其表达随病变进展而增加。
我们的研究结果表明，牙骨质细胞在牙髓感染时表达RANKL，可能参与根尖周炎的发病机制。
