Suomalainen K, Sorsa T, Saxén L, Vauhkonen M, Uitto V J
Department of Periodontology, University of Helsinki, Finland.
Oral Microbiol Immunol. 1991 Feb;6(1):24-9. doi: 10.1111/j.1399-302x.1991.tb00447.x.
The nature and origin of collagenases in gingival crevicular fluid of juvenile periodontitis patients was investigated. Gingival crevicular fluid collected from deep untreated periodontal pockets of juvenile periodontitis patients was found to contain only vertebrate collagenase (EC 3.4.24.7) activity that cleaved soluble type-I and -III collagens into 3/4 and 1/4 length fragments, as analyzed by SDS-polyacrylamide gel electrophoresis. Type II collagen was degraded at a markedly slower rate. This substrate specificity is indicative of collagenases produced by fibroblasts, epithelial cells and macrophages. We have previously found that collagenase in gingival crevicular fluid of adult periodontics patients appears to be mainly derived from polymorphonuclear leukocytes (PMN). The reasons for the apparent difference in collagenase source between the groups were investigated. We examined whether the pathogen characteristic for juvenile periodontitis, Actinobacillus actinomycetemcomitans, can release collagenase from normal human PMNs. All 10 A. actinomycetemcomitans strains tested, freshly isolated from the subgingival plaque of juvenile periodontitis patients, caused release of collagenase from PMNs in vitro. These results suggest that the lack of normally functioning PMNs in the periodontium of juvenile periodontitis patients may result in a colonization of bacteria that activate the resident periodontal cells to produce increased amounts of collagenase.
对青少年牙周炎患者龈沟液中胶原酶的性质和来源进行了研究。从青少年牙周炎患者未经治疗的深牙周袋中收集的龈沟液，经十二烷基硫酸钠-聚丙烯酰胺凝胶电泳分析，发现其中仅含有脊椎动物胶原酶（EC 3.4.24.7）活性，该酶可将可溶性I型和III型胶原切割成3/4和1/4长度的片段。II型胶原的降解速度明显较慢。这种底物特异性表明该胶原酶是由成纤维细胞、上皮细胞和巨噬细胞产生的。我们之前发现，成人牙周炎患者龈沟液中的胶原酶似乎主要来源于多形核白细胞（PMN）。研究了两组之间胶原酶来源明显不同的原因。我们检测了青少年牙周炎的病原体伴放线放线杆菌是否能从正常人的PMN中释放胶原酶。从青少年牙周炎患者龈下菌斑中新鲜分离的所有10株伴放线放线杆菌，在体外均可使PMN释放胶原酶。这些结果表明，青少年牙周炎患者牙周组织中缺乏正常功能的PMN，可能导致细菌定植，进而激活牙周常驻细胞产生更多的胶原酶。
