Preventive Effect of Intraoral Treatment by Antibody Against Purified Surface Antigen from S. Mutans on Experimental Dental Caries

从S. mutans中纯化表面蛋白抗原（SAI/II）并分离为低分子量蛋白。纯化后的抗原主要由100KDa-和50KDa-蛋白组成，并含有少量的低分子蛋白。这些低分子蛋白也与抗sai /II抗体发生反应。抗sai /II抗体与变形链球菌（血清型a、c-h）、血链球菌、唾液链球菌和轻微链球菌的抗原反应。粗抗体、SAI/II抗体、SA 100KDa抗体分别抑制抗羟基磷灰石（HA）抗体IgG片段对变形链球菌细胞的吸附，抑制率分别为87%、73%、70%和95%。纯化抗体和SAI/II抗体预处理HA的抑制率分别为21%和11%。变异链球菌PA-14 (c)感染大鼠，饲粮中添加6%抗sai /II抗体，其龋齿发生率显著低于同一菌株饲粮中添加6%正常血清的大鼠（p<0.05）。平均龋病评分降低47.7%。将牙釉质板固定的牙内龋齿试验器具置于志愿者口腔内。携带试验搪瓷板的器具切片每天经口外浸泡3次，浸泡在一个含有蔗糖溶液的容器中，然后浸泡在一个含有抗sai /II抗体溶液的容器中，另一个含有正常血清溶液的容器中。通过测定实验开始和结束时（2周后）牙釉质显微硬度的变化来评估牙釉质脱矿。对照组平均（<正负> SE）脱矿值为200 ([>SY.+-。[) 3.9，实验组242 <正负> 4.9。这些值之间的差异在0.05的水平上是显著的

Surface protein antigen (SAI/II) from S. mutans was purified and resolved to a lower-molecular-weight protein. The purified antigen was mainly composed of 100KDa- and 50KDa- proteins, and a trace amount of some lower-molecular proteins. These lower-molecular proteins also reacted With anti-SAI/II antibody. Anti-SAI/II antibody reacted with antigens from S. mutans (serotype a, c-h), S. sanguis, S. salivarius and S. mitior.Adsorption of S. mutans cells which treated IgG fraction of antibody to hydroxyapatite (HA) was inhibited by 87, 73, 70 and 95% by treatment of cells with crude, SAI/II, SA 100KDa antibodies, respectively. Pretreatment of HA with purified and SAI/II antibodies was inhibited by 21 and 11%, respectively.The incidence of caries in rats infected with S. mutans PA-14 (c) and fed diet containing 6% of anti-SAI/II antibody was significantly lower (p<0.05) than in rats infected with the same strain and receiving diet containing 6% of normal serum. The mean caries score was reduced by 47.7%.The Intraoral Cariogenicity Test (ICT) appliances mounted with enamel slabs were placed in the human mouth of volunteers. The sections of the appliance carrying the test enamel-slab were immersed extraorally 3 times daily, in a vessel containing sucrose solution followed by in a two-compartment vesssel containing anti-SAI/II antibody solution in one compartment and normal serum solution in the other. Enamel demineralization was assessed by measuring the change of enamel microhardness at the beginning and at the end (2 weeks later) of the experiment. The mean (<plus-minus> SE) demineralization value of the control group was 200 ([>SY.+-.[) 3.9 and that of experimental group was 242 <plus-minus> 4.9. The difference between these values was significant at the 0.05 le