Kumamoto H, Ooya K
Division of Oral Pathology, Department of Oral Medicine and Surgery, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.
J Oral Pathol Med. 2006 Jul;35(6):345-51. doi: 10.1111/j.1600-0714.2006.00432.x.
To evaluate the roles of matrix-degrading proteinase regulators in progression of odontogenic tumors, expression of membrane-bound matrix metalloproteinase (MMP) MT1-MMP, MMP inhibitor RECK and MMP inducer EMMPRIN was analyzed in ameloblastic tumors as well as in tooth germs.
Tissue specimens of 11 tooth germs, 40 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against MT1-MMP, RECK, and EMMPRIN.
Immunohistochemical reactivity for MT1-MMP, RECK and EMMPRIN was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and benign and malignant ameloblastic tumors. The level of immunoreactivity for MT1-MMP was slightly higher in benign and malignant ameloblastic tumors than in tooth germs. RECK expression was lower in ameloblastomas than in tooth germs. Follicular ameloblastomas showed significantly lower expression of RECK than plexiform ameloblastomas, and immunoreactivity for RECK in acanthomatous ameloblastomas was slightly lower than that in other cellular variants.
Expression of MT1-MMP, RECK and EMMPRIN in tooth germs and ameloblastic tumors suggests that these normal and neoplastic epithelial components control MMP-dependent extracellular matrix (ECM) degradation during tooth development and tumor progression via epithelial-mesenchymal interactions.
为评估基质降解蛋白酶调节剂在牙源性肿瘤进展中的作用，分析了膜结合基质金属蛋白酶（MMP）MT1-MMP、MMP抑制剂RECK和MMP诱导剂EMMPRIN在成釉细胞瘤以及牙胚中的表达情况。
使用抗MT1-MMP、RECK和EMMPRIN的抗体，对11个牙胚、40个成釉细胞瘤和5个恶性成釉细胞瘤的组织标本进行免疫组织化学检查。
在牙胚以及良性和恶性成釉细胞瘤中，MT1-MMP、RECK和EMMPRIN的免疫组织化学反应主要在基底膜附近的牙源性上皮细胞中检测到。MT1-MMP的免疫反应性水平在良性和恶性成釉细胞瘤中略高于牙胚。RECK在成釉细胞瘤中的表达低于牙胚。滤泡状成釉细胞瘤中RECK的表达明显低于丛状成釉细胞瘤，棘皮瘤型成釉细胞瘤中RECK的免疫反应性略低于其他细胞亚型。
MT1-MMP、RECK和EMMPRIN在牙胚和成釉细胞瘤中的表达表明，这些正常和肿瘤性上皮成分在牙齿发育和肿瘤进展过程中，通过上皮-间充质相互作用控制MMP依赖的细胞外基质（ECM）降解。
