Naito Y, Gibbons R J
Forsyth Dental Center, Boston, Massachusetts 02115.
J Dent Res. 1988 Aug;67(8):1075-80. doi: 10.1177/00220345880670080301.
The ability of Bacteroides gingivalis 381 to attach to hydroxyapatite (HA) beads, treated with either human type I or type IV collagen, or to particles of bovine bone collagen was studied. All preparations were blocked with human albumin prior to being incubated with 3H-thymidine-labeled B. gingivalis 381 cells. The presence of collagen on HA surfaces (C-HA) significantly promoted attachment of the organism. HA treated with Type IV collagen bound B. gingivalis cells more effectively than did HA treated with type I collagen. Attachment of two additional strains of B. gingivalis to HA was also promoted by collagen. Binding to type I or type IV C-HA occurred rapidly, and equilibrium was attained within 45 min. B. gingivalis 381 cells also bound to particles of bovine bone collagen, and this appeared to be biphasic. Heating the bacteria abolished their ability to bind to C-HA. Attachment of B. gingivalis 381 cells to HA treated with type I collagen was strongly inhibited by the presence of soluble type I or type IV collagen, or gelatin, but not by the presence of human albumin, salivary proline-rich protein 1, or saliva. Human serum, fibronectin, fibrinogen, certain protease inhibitors, and some peptides were also inhibitory. 3H-fibronectin bound to bovine bone collagen particles and blocked the attachment of 14C-B. gingivalis cells. Mild trypsin treatment of the fibronectin-collagen complex restored its ability to promote 14C-B. gingivalis attachment concomitant with the loss of 3H-fibronectin. We suggest that elevated levels of proteases in the gingival sulcus, such as are associated with poor oral hygiene and gingivitis, might remove fibronectin and expose collagen molecules in the basement membrane, thereby promoting the attachment of B. gingivalis cells and facilitating their invasion into gingival tissues.
研究了牙龈卟啉单胞菌381附着于经人I型或IV型胶原蛋白处理的羟基磷灰石（HA）珠或牛骨胶原蛋白颗粒的能力。所有制剂在与3H-胸腺嘧啶核苷标记的牙龈卟啉单胞菌381细胞孵育之前，均用人白蛋白封闭。HA表面存在胶原蛋白（C-HA）可显著促进该菌的附着。经IV型胶原蛋白处理的HA比经I型胶原蛋白处理的HA更有效地结合牙龈卟啉单胞菌细胞。另外两种牙龈卟啉单胞菌菌株附着于HA也受到胶原蛋白的促进。与I型或IV型C-HA的结合迅速，45分钟内达到平衡。牙龈卟啉单胞菌381细胞也与牛骨胶原蛋白颗粒结合，且这似乎是双相的。加热细菌消除了它们与C-HA结合的能力。可溶性I型或IV型胶原蛋白、明胶的存在强烈抑制牙龈卟啉单胞菌381细胞附着于经I型胶原蛋白处理的HA，但人白蛋白、富含脯氨酸的唾液蛋白1或唾液的存在则无此作用。人血清、纤连蛋白、纤维蛋白原、某些蛋白酶抑制剂和一些肽也具有抑制作用。3H-纤连蛋白与牛骨胶原蛋白颗粒结合并阻断14C-牙龈卟啉单胞菌细胞的附着。对纤连蛋白-胶原蛋白复合物进行轻度胰蛋白酶处理可恢复其促进14C-牙龈卟啉单胞菌附着的能力，同时3H-纤连蛋白丧失。我们认为，牙龈沟中蛋白酶水平升高，如与口腔卫生不良和牙龈炎相关的情况，可能会去除纤连蛋白并暴露基底膜中的胶原蛋白分子，从而促进牙龈卟啉单胞菌细胞的附着并便于其侵入牙龈组织。
