Elucidation of roles and functions of cementoblasts in the destruction and regeneration of periodontal tissue

本研究以小鼠成牙骨质细胞系OC-CM 30细胞为研究对象，观察了白细胞介素（IL）-1α或脂多糖（LPS）对成牙骨质细胞系OC-CM 30细胞增殖的影响。gingivalis和放线杆菌（A.）放线菌共生菌产生考克斯-2依赖的PGE_2，并进一步研究所产生的PGE_2是否影响IL-1α诱导的IL-6的产生。牙龈卟啉单胞菌和伴放线菌的IL-1α和LPS诱导PGE_2的产生具有时间依赖性。考克斯1/-2抑制剂消炎痛和考克斯2抑制剂NS-398可完全抑制IL-1 α和LPS诱导的PGE_2生成。17-phenyl-ω-trinor PGE_2（EP_1激动剂）和ONO-AE 1 -329（EP_4激动剂）模拟PGE_2增强IL-1α和牙龈卟啉单胞菌和伴放线放线菌LPS诱导OC-CM 30细胞产生IL-6。进一步研究PGE_2对RANKL和OPG表达的影响。PGE_2对RANKL和OPG蛋白表达无明显影响。提示牙龈卟啉单胞菌和伴放线菌的IL-1α和LPS以考克斯-2依赖的方式诱导OC-CM 30细胞产生PG_2，而考克斯-2诱导的PGE_2通过EP_1和/或EP_4受体上调IL-1α和LPS诱导IL-6的产生。成牙骨质细胞分泌PGE_2和IL-6可能参与牙周病的发病。

In the present study, we investigated whether a mouse cementoblast cell line, OC-CM 30 cells, stimulated with interleukin(IL)-1α or lipopolysaccharides (LPS) from Prophyomonas(P.) gingivalis and Actinobacillus(A.) actinomycetemcomitans produced COX-2-dependent PGE_2 and furthermore whether the produced PGE_2 affected IL-1α-induced IL-6 production. IL-1α and LPS from P.gingivalis and A.actinomycetemcomitans time-dependently induced PGE_2 production. Indomethacin (a COX-1/-2 inhibitor) and NS-398 (a COX-2 inhibitor) completely inhibited IL-1 α-and LPS-induced PGE_2 production. 17-phenyl-ω-trinor PGE_2 (an EP_1 agonist) and ONO-AE1-329 (an EP_4 agonist) mimicked PGE_2 enhancement of IL-1α-and LPS from P.gingivalis and A.actinomycetemcomitans induced IL-6 production in OC-CM 30 cells. Furthermore, we investgated the effect of PGE_2 on RANKL and OPG expression. PGE_2 did not enhance RANKL and OPG prtotein expression. From these data, we suggest that in OC-CM 30 cells IL-1α and LPS from P.gingivalis and A.actinomycetemcomitans induced PG_2 production in a COX-2-dependent manner and that the COX-2-derived PGE_2 up-regulates IL-1α-and LPS from P.gingivalis and A.actinomycetemcomitans elicited IL-6 production via EP_1 and/or EP_4 receptors. PGE_2 and IL-6 produced by cementoblasts may be involved in the pathogenesis of periodontal disease.