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PubMed · 13785728

Eusol.

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W R WILSON. 1961. Eusol.. https://pubmed.ncbi.nlm.nih.gov/13785728/

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Oral microbial biofilms and plaque-related diseases: microbial communities and their role in the shift from oral health to disease.

Many oral pathologies, such as dental caries, periodontal disease and peri-implantitis are plaque-related. Dental plaque is a microbial biofilm formed by organisms tightly bound to a solid substrate and each other by means of an exopolymer matrix. Bacteria exhibit different properties when contained within a biofilm. Knowing the mechanisms controlling the formation and development of biofilms can help to understand the emergence and progression of such pathologies and to plan effective treatment. Most periodontal pathogens are common saprophytes of the oral cavity, expressing their virulence only in a susceptible host or when some changes come about in the oral environment. Physical, metabolic and physiological interactions may cause positive or negative effects among the various microbiota present. Such mechanisms of antagonism/synergy select the bacterial population and alterations of its composition affect the balance with the host and may lead to pathology. The effectiveness of antimicrobial agents, as measured through in vitro tests, is dramatically reduced in vivo due to the properties of the microbial community: mature, intact biofilms are less sensitive to such agents, as the exopolymer matrix, bacterial enzymes and slow growth rate hinder the action of chemotherapeutic agents. The present literature review aims to examine the most representative studies, focusing on the characteristics of bacterial communities and the crucial shift from oral health to plaque-related diseases.

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Inhibition of Streptococcus mutans biofilm accumulation and polysaccharide production by apigenin and tt-farnesol.

OBJECTIVES: Apigenin is a potent inhibitor of glucosyltransferases and tt-farnesol affects the membrane integrity of Streptococcus mutans. We investigated the influence of apigenin and tt-farnesol, alone and in combination, on the accumulation, polysaccharide composition and viability of S. mutans UA159 biofilms. METHODS: Initially, biofilms were grown for 54 h; then, the early-formed biofilms were treated for 1 min twice daily with one of the following: (i). 1.33 mM tt-farnesol; (ii). 1.33 mM apigenin; (iii). apigenin + tt-farnesol (1.33 mM each); (iv). vehicle control (20% ethanol with 0.75% dimethyl sulphoxide); (v). 0.12% chlorhexidine (1.33 mM); or (vi). physiological saline (145 mM NaCl). The procedure was repeated at biofilm ages of 78 and 102 h, and biofilms were harvested at 126 h. The dry weight, protein concentration, number of cfu, and polysaccharide composition per biofilm were determined. RESULTS: The dry weights of the biofilms treated with the test agents were significantly less (30-50%) than those treated with vehicle control (P < 0.05). Biofilms treated with the test agents also resulted in lower amounts of extracellular alkali-soluble glucans, intracellular iodophilic polysaccharides and, to a lesser extent, fructans. The fructosyltransferase activity was affected only by apigenin and apigenin + tt-farnesol. The recoverable viable counts of S. mutans were slightly lower (0.5 to 1 log10 decrease in cfu/biofilm) after apigenin and tt-farnesol treatments compared with the vehicle control. Chlorhexidine displayed potent bactericidal activity, and virtually halted the further accumulation of early-formed (54 h old) biofilms. CONCLUSIONS: Apigenin and tt-farnesol affected the accumulation and polysaccharide content of S. mutans biofilms without major impact on the bacterial viability.

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Evaluation of an oral preventive protocol in children with acute lymphoblastic leukemia.

This study was designed to assess the effectiveness of a preventive oral protocol in children receiving antineoplastic treatment for acute lymphoblastic leukemia (ALL) before initiating a larger intervention study. During a seven month period, fourteen children from two to ten years old with a diagnosis of ALL were evaluated. Patients with ALL who received a 0.12% chlorhexidine mouth rinse (seven children) were compared to a control group of patients who were not given the same preventive treatment (seven children) as to the occurrence of oral mucosal complications. Children in both groups received daily oral hygiene care, and were examined daily by the pediatric dentistry team until discharge. A significant decrease in the incidence of oral mucositis and ulceration was observed in the children who received a 0.12% chlorhexidine mouth rinse (p < 0.05 by Fisher's exact test). The findings obtained in the present trial are encouraging, and suggest that the systematic application of a preventive protocol reduces the incidence of oral complications in children with ALL receiving chemotherapy.

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