Ultrastructural changes produced in the oral bacterium streptococcus mutans glucans by the action of endo-alpha-1,3-glucanase.
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Biomedical subjects
Publications and source records attributed to T Takehara.
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An enzyme hydrolyzing the water-insoluble glucans produced from sucrose by Streptococcus mutans was purified from the culture concentrate of Streptomyces chartreusis strain F2 by ion-exchange chromatography on diethylaminoethyl cellulose and carboxymethyl cellulose columns and gel filtration on Bio-Gel A-1.5m. The purification achieved was 6.4-fold, with an overall yield of 27.3%. Electrophoresis of the purified enzyme protein gave a single band on a sodium dodecyl sulfate-polyacrylamide gel slab. Its molecular weight was estimated to be approximately 68,000, but there is a possibility that the native enzyme exists in an aggregated form or is an oligomer of the peptide subunits, have a molecular weight larger than 300,000. The pH optimum of the enzyme was 5.5 to 6.0, and its temperature optimum was 55 degrees C. The enzyme lost activity on heating at 65 degrees C for 10 min. The enzyme activity was completely inhibited by the presence of 1 mM Mn2+, Hg2+, Cu2+, Ag2+, or Merthiolate. The Km value for the water-insoluble glucan of S. mutans OMZ176 was an amount of glucan equivalent to 1.54 mM glucose, i.e., 0.89 mM in terms of the alpha-1,3-linked glucose residue. The purified enzyme was specific for glucans containing an alpha-1,3-glucosidic linkage as the major bond. The enzyme hydrolyzed the S. mutans water-insoluble glucans endolytically, and the products were oligosaccharides. These results indicate that the enzyme elaborated by S. chartreusis strain F2 is an endo-alpha-1,3-glucanase (EC 3.2.1.59).
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PURPOSE: This study evaluates how various microbial- and salivary-related risk factors influenced the hazard for caries development in preschool children. METHODS: The study population consisted of 131 subjects (age: 0.5 to 6.0 yrs). Oral examination, including two bacterial tests and buffering capacity test, was conducted at six month intervals over 24 months. A survival analysis was used to describe caries hazard over a 24-month follow-up period. A Cox proportional hazards regression analysis was performed to test the influence of salivary mutans streptococci (MS), aciduric bacteria, buffering capacity and age on caries development. RESULTS: Of the total subjects, 60 children (46%) were found to be caries-free at baseline. Caries hazard correlated significantly with salivary MS levels at baseline (relative risk, 1.7; P = 0.003), but not with aciduric bacteria and buffering capacity. This analysis showed that all of children with high colonization of MS at baseline had dental caries 15 months later. CONCLUSION: The results suggest that salivary MS level at baseline influenced caries hazard in preschool children.
Dentocraniofacial structure with ectodermal dysplasia, showing complete anodontia of permanent teeth, was examined. Except for a slight decrease of the sweat pore count, the patient was free of signs of ectodermal dysplasia, other than odontoplasia. Furthermore, her family history had no record of hypodontia or anodontia. We attempted to clarify the role of tooth growth in the dentocraniofacial development. Cephalometric analyses revealed the extreme limitation of the maxillary and vertical growth of the lower face, and a retracted mandibular alveolus front. We concluded that the role of tooth growth was significant in the development of the maxillary and alveolar bone, but not in the development of the mandible.