Analysis of periodontal ligament cells derived from permanent teeth and primary teeth on tooth root resorption.

虽然乳牙的牙根吸收发生在恒牙萌出的生理时期，但当根管中的细菌感染引起根尖周围的炎症时，经常发生异常牙根吸收。此外，乳牙的牙根吸收有时会在后续恒牙缺失时自发发生。因此，牙周膜细胞可能通过调节破骨细胞的生成而在牙根吸收中发挥作用。在与颅骨成骨细胞和纯化的骨髓细胞共培养中，釉原蛋白抑制破骨细胞的生成。氟替卡松、釉原蛋白抑制成骨细胞核因子κ B受体激活因子配体（RANKL）、巨噬细胞集落刺激因子（M-CSF）和纤连蛋白的表达，而RANKL的表达被纤连蛋白诱导，被纤连蛋白小干扰RNA抑制。这些结果表明，釉原蛋白抑制破骨细胞的生成，导致成骨细胞RANKL、M-CSF和FN的表达下调，因此，含有Malassez上皮剩余物的PDL细胞可能抑制牙根吸收。

Although root resorption of deciduous teeth occurs physiologically in periods of permanent tooth eruption, abnormal root resorption frequently occurs when bacterial infection in the root canal caused inflammation around the root apex. Moreover, root resorption of a deciduous tooth sometimes occurs spontaneously when the succeeding permanent tooth is lacking. Therefore, it is possible that periodontal ligament (PDL) cells can play a role in root resorption by regulating osteoclastogenesis.This study investigated the effect of amelogenin on osteoclastogenesis. In co-cultures with calvaria osteoblasts and purified bone marrow cells, amelogenin inhibited osteoclastogenesis. Futhermore, amelogenin inhibited the expression of receptor activator of nuclear factor kappaB ligand (RANKL) ,macrophage-colony stimulating factor (M-CSF) and fibronectin in osteoblasts, while RANKL expression was induced by fibronectin and inhibited by treatment with fibronectin small interfering RNA. These results suggest that the inhibitory effect of amelogenin on osteoclastogenesis lead to downregulation of RANKL, M-CSF and fibronectin production in osteoblasts.Therefore, these data suggest that PDL cells which contain the epithelial rests of Malassez may inhibit root resorption.