Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo (FMRP/USP), Ribeirão Preto, SP, Brazil.
J Endod. 2010 Feb;36(2):244-50. doi: 10.1016/j.joen.2009.09.004. Epub 2009 Oct 23.
Periapical lesions are chronic inflammatory disorders of periradicular tissues caused by etiologic agents of endodontic origin. The inflammatory chemokines are thought to be involved in the latter observed osteolysis. With a murine model of experimental periapical lesion, the objective of this study was to evaluate the role of the chemokine receptor CCR2 in the lesion progression, osteoclast differentiation and activation, and expression of inflammatory osteolysis-related mediators.
For lesion induction, right mandibular first molars were opened surgically with a 1/4 carbine bur, and 4 bacterial strains were inoculated in the exposed dental pulp; left mandibular first molars were used as controls. Animals were killed at 3, 7, 14, and 21 days after surgeries to evaluate the kinetics of lesion development.
CCR2 KO mice showed wider lesions than WT mice. CCR2 KO mice also expressed higher levels of the osteoclastogenic and osteolytic factors, receptor activator of nuclear factor kappa B ligand (RANKL) and cathepsin K, of the proinflammatory cytokine tumor necrosis factor-alpha, and of the neutrophil migration related chemokine, KC.
These results suggest that CCR2 is important in host protection to periapical osteolysis.
根尖周病变是由牙髓来源的病因引起的根尖周组织的慢性炎症性疾病。炎症趋化因子被认为参与了随后观察到的骨溶解。本研究通过实验性根尖周病变的小鼠模型，旨在评估趋化因子受体 CCR2 在病变进展、破骨细胞分化和激活以及炎症性骨溶解相关介质表达中的作用。
为了诱导病变，用 1/4 卡边车针在右侧下颌第一磨牙上进行手术开口，并将 4 种细菌菌株接种到暴露的牙髓中；左侧下颌第一磨牙作为对照。手术后 3、7、14 和 21 天处死动物，以评估病变发展的动力学。
CCR2 KO 小鼠的病变比 WT 小鼠更宽。CCR2 KO 小鼠还表达了更高水平的破骨细胞生成和溶骨因子，核因子κB 受体激活剂配体（RANKL）和组织蛋白酶 K，促炎细胞因子肿瘤坏死因子-α，以及与中性粒细胞迁移相关的趋化因子 KC。
这些结果表明 CCR2 在宿主对根尖周骨溶解的保护中很重要。
