Van Hoogmoed C G, Geertsema-Doornbusch G I, Teughels W, Quirynen M, Busscher H J, Van der Mei H C
Department of Biomedical Engineering, University Medical Center Groningen, and University of Groningen, Groningen, The Netherlands.
Oral Microbiol Immunol. 2008 Feb;23(1):43-8. doi: 10.1111/j.1399-302X.2007.00388.x.
Periodontitis results from a shift in the subgingival microflora into a more pathogenic direction with Porphyromonas gingivalis, Prevotella intermedia, and Actinobacillus actinomycetemcomitans considered as periodontopathogens. In many cases, treatment procures only a temporary shift towards a less pathogenic microflora. An alternative treatment could be the deliberate colonization of pockets with antagonistic microorganisms to control the adhesion of periodontopathogens. The aim of this study was to identify bacterial strains that reduce adhesion of periodontopathogens to surfaces.
Streptococcus sanguinis, Streptococcus crista, Streptococcus salivarius, Streptococcus mitis, Actinomyces naeslundii, and Haemophilus parainfluenzae were evaluated as potential antagonists against P. gingivalis ATCC 33277, P. intermedia ATCC 49046, and A. actinomycetemcomitans ATCC 43718 as periodontopathogens. Adhesion of periodontopathogens to the bottom plate of a parallel plate flow chamber was studied in the absence (control) and the presence of pre-adhering antagonistic strains up to a surface coverage of 5%.
The largest reduction caused by antagonistic strains was observed for P. gingivalis. All antagonistic strains except S. crista ATCC 49999 inhibited the adhesion of P. gingivalis by at least 1.6 cells per adhering antagonist, with the largest significant reduction observed for A. naeslundii ATCC 51655 (3.8 cells per adhering antagonist). Adhering antagonists had a minimal effect on the adhesion of A. actinomycetemcomitans ATCC 43718. Intermediate but significant reductions were perceived for P. intermedia, most notably caused by S. mitis BMS.
The adhesion of P. gingivalis was inhibited best by antagonistic strains, while S. mitis BMS appeared to be the most successful antagonist.
牙周炎是由龈下微生物群向更具致病性的方向转变引起的,牙龈卟啉单胞菌、中间普氏菌和伴放线放线杆菌被视为牙周病原体。在许多情况下,治疗仅能使微生物群暂时向致病性较低的方向转变。另一种治疗方法可能是有意让拮抗微生物在牙周袋中定殖,以控制牙周病原体的黏附。本研究的目的是鉴定能减少牙周病原体与表面黏附的细菌菌株。
评估血链球菌、嵴链球菌、唾液链球菌、缓症链球菌、内氏放线菌和副流感嗜血杆菌作为针对牙龈卟啉单胞菌ATCC 33277、中间普氏菌ATCC 49046和伴放线放线杆菌ATCC 43718这几种牙周病原体的潜在拮抗剂。在不存在(对照)和存在预先黏附的拮抗菌株的情况下,研究牙周病原体在平行平板流动腔底板上的黏附情况,拮抗菌株的表面覆盖率最高达5%。
观察到拮抗菌株对牙龈卟啉单胞菌的黏附抑制作用最大。除嵴链球菌ATCC 49999外,所有拮抗菌株均能使牙龈卟啉单胞菌的黏附减少至少每黏附一个拮抗剂1.6个细胞,内氏放线菌ATCC 51655的黏附减少最为显著(每黏附一个拮抗剂3.8个细胞)。黏附的拮抗剂对伴放线放线杆菌ATCC 43718的黏附影响最小。观察到中间普氏菌的黏附减少程度中等但显著,最明显的是由缓症链球菌BMS引起的。
拮抗菌株对牙龈卟啉单胞菌的黏附抑制效果最佳,而缓症链球菌BMS似乎是最有效的拮抗剂。