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It was the purpose of this investigation to study the suitability of a controlled release delivery system fro endodontic medicaments, making it possible to maintain a constant concentration of a medicament in the root canal for an extended period of time. The delivery system compressed an inner core matrix containing the medicament surrounded by a polymeric membrane allowing a controlled release of the active ingredient. Controlled release preparations containing formocresol, camphorated, paramonochlorphenol, Cresatin, and a quaternary ammonium compound (dodecyl-dimethyl-benzylammonum chloride) were manufactured and applied to root canals of dogs' teeth. In control experiments the same medicaments, were applied to root canals by means of cotton pellets. After 1,3,7 and 45 days the picces of polymeric materials and the cotton pellets were removed from the root canals and tested for antibacterial cotton pellets had an effect. Of the controlled release preparations, the quaternary ammonium compound had a fairly constant effect on bacterial growth for the duration of the experiment (45d). The results suggested that the idea of improving the effect of endodontic medicaments by means of controlled release delivery systems is valid, and may gain clinical importance in the future. [ABSTRACT FROM AUTHOR]

The effect of a weak direct current and silver ions on microorganisms commonly found in the root canal was studied. Pour plates with the various microorganisms were prepared in petri dishes and 2 identical silver wire electrodes were submerged in the agar. The plates were incubated at 37°C for 24 hours with the electrodes attached to the positive and negative poles of constant current generators set to deliver currents of 0.2, 0.4, 0.8, 1.5 and 10.0 µamp. Zones of inhibition were evident at the positive electrode in all experiments. The widest, zones were found at 1.5 µamp followed by 0.8 and 10.0 µamp. Statistically, the responses at these current levels could not be differentiated, but they were different From the results obtained at 0.2 and 0.4 µamp. [ABSTRACT FROM AUTHOR]

The article presents a report which discusses the antigens and surface components related to the virulence of Actinomyces viscosus. The attention focused upon A. viscosus due to implications of the association between the microorganism and the onset of periodontal disease is mentioned. A cell surface antigen associated with A. viscosus which contains the sugar 6-deoxytalose (6-DOT) is described as a correlate of virulence, noting that the antigen may be related to the presence of an extrachromosomal piece of DNA which possesses many of the qualities of a bacterial plasmid.

Fourteen strains of Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) have been examined by transmission electron microscopy. The cells, which grow as cocco-bacillary forms on agar medium, have a cell periphery ultrastructurally compatible with that of other Gram-negative species. However, the cell membrane and peptidoglycan layer are not readily visualized following standard processing. Of particular interest was the finding of numerous extracellular membranous vesicles in A. actinomyceteincomitans strains known to have leukotoxic activity, while non-leukotoxic strains demonstrated few or no extracellular vesicles. Similar findings were noted whether cells were grown on blood agar plates or in thioglycollate broth. Antisera were obtained in rabbits against whole cells of leukotoxic strain Y4. The resulting antisera successfully labeled vesicles associated with 4 separate leukotoxic strains. The label was completely retained on the vesicles after absorption of the antisera with non-leukotoxic strain ATCC 29523. Non-leukotoxic strains showed some patchy surface labeling with non-absorbed antiserum to Y4 and no labeling after absorption with ATCC strain 29523. These observations suggest that extracellular membranous vesicles are associated with leukotoxic activity and may serve as a useful source of leukotoxic factor. These conclusions are strengthened by the observation of a strong correlation between the concentration of extracellular vesicles in strains grown on agar and their relative leukotoxicity as reported by other investigators.

This article discusses research into the role of capsular or mucoid polysaccharides in the proliferation of lactobacilli in the mouth. Encapsulation of bacteria is presented as a survival mechanism for resisting shortages of nutrients and phage-induced lysis. The chemical characteristics of these mucoids are also explored.

This article discusses the results of a research study conducted to determine the toxicity of Lactobacillus casei (L. casei) and its role in the production of local and systemic lesions. The toxicity of viable cells, non-viable cells, and subcellular fractions was tested in a group of male albino rabbits.

Leukotriene B4 (LTB4) is an inflammatory lipid produced in response to pathogens that is critical for initiating the inflammatory cascade needed to control infection. However, during plague, Yersinia pestis inhibits the timely synthesis of LTB4 and subsequent inflammation. Using bacterial mutants, we previously determined that Y. pestis inhibits LTB4 synthesis via the action of the Yop effector proteins that are directly secreted into host cells through a type 3 secretion system (T3SS). Here, we show that the T3SS is the primary pathogen associated molecular pattern (PAMP) required for production of LTB4 in response to both Yersinia and Salmonella. However, we also unexpectantly discovered that T3SS-mediated LTB4 synthesis by neutrophils and macrophages require the activation of two distinctly different host signaling pathways. We identified that phagocytosis and the NLRP3/CASP1 inflammasome significantly impact LTB4 synthesis by macrophages but not neutrophils. Instead, the SKAP2/PLC signaling pathway is required for T3SS-mediated LTB4 production by neutrophils. Finally, while recognition of the T3SS is required for LTB4 production, we also discovered that a second unrelated PAMP-mediated signal activates the MAP kinase pathway needed for synthesis. Together, these data demonstrate significant differences in the host factors and signaling pathways required by macrophages and neutrophils to quickly produce LTB4 in response to bacteria. Moreover, while macrophages and neutrophils might rely on different signaling pathways for T3SS-dependent LTB4 synthesis, Y. pestis has evolved virulence mechanisms to counteract this response by either leukocyte to inhibit LTB4 synthesis and colonize the host., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Brady et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Leukotriene B4 (LTB 4 ) is critical for initiating the inflammatory cascade in response to infection. However, Yersinia pestis colonizes the host by inhibiting the timely synthesis of LTB 4 and inflammation. Here, we show that the bacterial type 3 secretion system (T3SS) is the primary pathogen associated molecular pattern (PAMP) responsible for LTB 4 production by leukocytes in response to Yersinia and Salmonella , but synthesis is inhibited by the Yop effectors during Yersinia interactions. Moreover, we unexpectedly discovered that T3SS-mediated LTB 4 synthesis by neutrophils and macrophages require two distinct host signaling pathways. We show that the SKAP2/PLC signaling pathway is essential for LTB 4 production by neutrophils but not macrophages. Instead, phagocytosis and the NLRP3/CASP1 inflammasome are needed for LTB 4 synthesis by macrophages. Finally, while recognition of the T3SS is required for LTB 4 production, we also discovered a second unrelated PAMP-mediated signal independently activates the MAP kinase pathway needed for LTB 4 synthesis. Together, these data demonstrate significant differences in the signaling pathways required by macrophages and neutrophils to quickly respond to bacterial infections.

This study investigated the effect of in vivo low-dose acetylsalicylic acid (ASA, aspirin) on human platelet aggregation induced in vitro by Porphyromonas gingivalis cells. Blood was collected from volunteers (n = 20), half of whom ingested 81 mg of aspirin 24 hours before donating blood. Low-dose aspirin inhibited P. gingivalis cell-induced platelet aggregation and produced an inverse correlation of inhibition to number of cells. At the higher concentration of cells used in this in vitro assay, aspirin inhibition was significant (P = 0.001); however, partial platelet activation was observed. The significance of partial platelet activation is discussed in this article, as is the relevance of platelet aggregation to the putative link between inflammatory periodontal disease and cardiovascular disease.