Inhibition of Porphyromonas gingivalis adhesion to Streptococcus gordonii by human submandibular-sublingual saliva

Coaggregations between bacterial species have been widely studied in vitro but not in the mouth. A new in vivo assay was used to measure the rate and composition of indigenous plaque formation onto bovine enamel chips covered with a continuous layer of bacteria. Chips were covered with Streptococcus oralis ATCC 10557, which coaggregated with many oral species, or Streptococcus gordonii S7, which did not coaggregate with these oral species, and placed in the mouth for 4 and 24 h. There were no differences in the number of most indigenous bacterial species isolated from the two streptococcal surfaces. However, the number of Actinomyces viscosus as a proportion of total Actinomyces spp. was significantly different on the two surfaces at 24 h. With the exception of Actinomyces naeslundii and A. viscosus removed from the S7 surface, all indigenous species increased significantly in number from 4 to 24 h, irrespective of the streptococcal surface. This study demonstrated that interbacterial coaggregation had only a limited effect on in vivo plaque development. Thus suggesting that environmental factors, growth or other adherence phenomena are dominant in in vivo plaque formation.

Section: I'orph Vroiuonas Gingivalis Atcc 33277 Atcc 25260supporting

confidence: 77%

Dental plaque development on defined streptococcal surfaces

Skopek

Liljemark

Bloomquist

et al. 1993

“…Fibrinogenolysis by P. gingivalis W12 generated two main cleavage products (Mr 97 kDa and 50 kDa) (8), whereas P. gingivalis 381 could degrade fibrinogen to lower-molecularweight components. Stinson et al (19) showed that the adhesion of P. gingivalis W50 to S. gordonii G9B was inhibited by a 43 kDa protein purified from submandibular-sublingual saliva. The binding of the intact salivary component to P. gingivalis did not occur unless the bacterial surface proteases were inactivated by phenylmethylsulfonyl fluoride and sodium iodoacetate.…”

Section: Discussionmentioning

confidence: 99%

“…The binding of fibrinogen to P. gingivalis 381 may be an important process in the inhibition of the coaggregation by fibrinogen. Several investigators suggested that the cell-associated proteases of P. gingi valis contribute to its coadhesion with gram-positive bacteria such as A. viscosus (11) and S. gordonii (19). Thus, the proteases of P. gingivalis that can bind fibrinogen might interact with the surface of S. oralis.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of binding of fibrinogen to each bacterium on coaggregation between Porphymmonas gingivalis and Streptococcus oralis

Nagata

Amano

Ojima

et al. 1994

Fibrinogen inhibits the coaggregation between Porphyromonas gingivalis and Streptococcus oralis. In this study, we determined which bacterium interacts with fibrinogen in this inhibitory process. Although preincubation of each bacterium with fibrinogen did not inhibit coaggregation, its activity was completely eliminated by the addition of protease inhibitors such as N-ethylmaleimide (NEM), p-chloromercuriphenyl sulfonate and N alpha-p-tosyl-L-lysine chloromethyl ketone to the preincubation mixture with fibrinogen and P. gingivalis. However, the inhibition of coaggregation was not found after preincubation of S. oralis with fibrinogen in the presence or absence of the protease inhibitors. Labelled materials were recovered from the extract of P. gingivalis cells incubated with radioiodinated fibrinogen in the presence of NEM but not in the absence of NEM. In the binding experiment, P. gingivalis showed a much higher binding activity to fibrinogen than S. oralis. These findings suggest that fibrinogen and its fragment(s) may mask directly or indirectly the aggregation site with S. oralis on the P. gingivalis cells in its inhibitory process of coaggregation.

“…27). Studies to date have demonstrated both an enhancement and inhibition of interbacterial adherence by saliva or salivary components, depending on the bacterial pair studied (13,21,23,26). Thus it is conceivable that the adsorption of saliva to different bacteria in the mouth will form different bacterial salivary pellicles, which could influence interbacterial adherence and thus subsequent plaque colonization.…”

mentioning

confidence: 99%

The influence of saliva on interbacterial adherence

Skopek

Liljemark

1994

The mechanism of bacterial adherence to the mat of bacteria in preformed dental plaque is not well defined. This study measured the influence of saliva on the adherence of bacteria in suspension to a continuous bacterial surface in vitro. Twenty different pairs of bacteria were tested, consisting of Streptococcus spp., Haemophilus spp. and Actinomyces spp. The species were chosen based on the parameters of coaggregation, and salivary agglutination. The results were expressed as bacteria that adhered per mm2 of bacterial surface. When both the surface bacteria and the bacteria in suspension agglutinated in saliva, interbacterial adherence was increased 2.5-fold when a salivary coating was placed on the surface. When one or both of the bacteria did not agglutinate in saliva, interbacterial adherence was increased only slightly when the surface was saliva-coated. The results suggested that salivary-mediated adherence is significant to plaque formation once the tooth surface becomes covered with bacteria. Thus bacteria that are capable of agglutinating in saliva may have a distinct advantage in colonization of the plaque surface.