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牙龈卟啉单胞菌对体外骨代谢的直接及免疫细胞介导作用

Direct and immune-cell-mediated effects of Bacteroides gingivalis on bone metabolism in vitro.

作者信息

Bom-van Noorloos A A, van Steenbergen T J, Burger E H

机构信息

Department of Oral Cell Biology, Vrije Universiteit, Amsterdam, The Netherlands.

出版信息

J Clin Periodontol. 1989 Aug;16(7):412-8. doi: 10.1111/j.1600-051x.1989.tb01669.x.

Abstract

We investigated direct and immune-cell-mediated effects of Bacteroides gingivalis on bone metabolism in vitro. Fetal mouse long-bone rudiments were cultured under aerobic conditions in the presence of (a) intact bacteria, (b) low molecular weight (MW less than 1000) metabolic products of the bacteria, or (c) conditioned media of mouse spleen cells activated by whole bacteria. A suspension of intact bacteria, added directly to the bone culture, had no effect on bone resorption or bone formation. Low molecular weight (MW less than 1000) excretion products of the bacteria inhibited bone resorption and transiently reduced mineralization of the diaphysis, while the growth in length of the bones was not affected. However, conditioned media of bacteria-activated spleen cells strongly enhanced bone resorption and increased osteoclast numbers in the bone culture, while inhibiting mineral formation in the diaphysis. This led to a strongly negative mineral balance. These data do not support a direct effect of either bacteria or bacterial products on bone tissue as a likely explanation for bone loss in periodontal disease. Rather, they favour the concept that the loss of bone in this disease is an indirect effect of the host response, resulting from the contact of immune cells with the bacteria. This implies that bacterial invasion of the connective tissue of the gingiva may not be a prerequisite for alveolar bone loss.

摘要

我们在体外研究了牙龈卟啉单胞菌对骨代谢的直接作用和免疫细胞介导的作用。将胎鼠长骨原基在有氧条件下培养,培养体系中分别加入:(a) 完整细菌;(b) 细菌的低分子量(分子量小于1000)代谢产物;或 (c) 由完整细菌激活的小鼠脾细胞的条件培养基。直接添加到骨培养物中的完整细菌悬液对骨吸收或骨形成没有影响。细菌的低分子量(分子量小于1000)排泄产物抑制骨吸收,并暂时降低骨干的矿化程度,而骨的长度生长不受影响。然而,细菌激活的脾细胞的条件培养基强烈增强骨吸收,并增加骨培养物中的破骨细胞数量,同时抑制骨干中的矿物质形成。这导致了严重的负矿物质平衡。这些数据不支持细菌或细菌产物对骨组织有直接作用这一观点,而这一观点本可能是牙周病中骨质流失的解释。相反,它们支持这样一种概念,即该疾病中的骨质流失是宿主反应的间接作用,是免疫细胞与细菌接触的结果。这意味着牙龈结缔组织的细菌入侵可能不是牙槽骨丧失的先决条件。

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