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Christensen T.,NIOM Nordic Institute of Dental Materials | Christensen T.,Norwegian Radiation Protection Authority | Bruzell E.M.,NIOM Nordic Institute of Dental Materials
Photochemical and Photobiological Sciences | Year: 2010

Induction of cell death by optical radiation in the wavelength range 350-500 nm was significantly increased by commonly used methacrylate monomers, not mediated by absorption of radiation by the methacrylate monomers, but through a mechanism involving rapid reduction in the level of glutathione (GSH). © 2010 The Royal Society of Chemistry and Owner Societies. Source

Huumonen S.,University of Turku | Huumonen S.,NIOM Nordic Institute of Dental Materials | Orstavik D.,NIOM Nordic Institute of Dental Materials | Orstavik D.,University of Oslo
Clinical Oral Investigations | Year: 2013

Objectives: The aim was to assess objectively the rate of changes in periapical status after endodontic treatment in relation to preoperative radiographic status (Periapical Index Score, PAI) and to tooth type. Material and methods: Radiographic data from a total of 1,410 teeth in seven prospective clinical studies was pooled. The periapical status was evaluated blindly using the PAI scoring system. The longest follow-up period was 4 years; intervals between controls varied from 3 months to 1 year. Results: Teeth with preoperative PAI score 1 maintained excellent periapical health throughout. Teeth with preoperative PAI score 2 showed some impairment in health over the first 6 months, but improved to approach 95 % healthy teeth at 2 years of observation. Teeth with PAI 3-5 at the start showed significant improvement at 3 months; 27 % were considered healthy (PAI 1 or 2) increasing to 41 % after 1 year. Improvement of periapical status was slower in PAI groups 4 and 5 compared with PAI 3 during the first year. After 2 years, improvement continued similarly in all preoperative PAI 3-5 groups of teeth. Upper lateral incisors showed the poorest healing rate. Conclusions: Healing of pre-existing periapical lesions is most pronounced from 3 months to 2 years. Teeth with initially healthy periapical structures predictably maintain good periapical health. Maxillary teeth, especially lateral incisors, showed poorer healing rates than mandibular teeth. Clinical relevance: Radiographic healing rates may vary among tooth groups within the dentition. Periapically healthy teeth that are root filled may not need postoperative controls. © 2013 Springer-Verlag Berlin Heidelberg. Source

Rakkestad K.E.,Norwegian Institute of Public Health | Skaar I.,National Veterinary Institute | Ansteinsson V.E.,University of Bergen | Ansteinsson V.E.,NIOM Nordic Institute of Dental Materials | And 7 more authors.
Toxicological Sciences | Year: 2010

We have characterized cell death in THP-1 cells after exposure to heat-treated spores from satratoxin G-producing Stachybotrys chartarum isolate IBT 9631, atranone-producing S. chartarum isolate IBT 9634, and sterigmatocystin-producing Aspergillus versicolor isolate IBT 3781, as well as the trichothecenes T-2 and satratoxin G. Spores induced cell death within 3-6 h, with Stachybotrys appearing most potent. IBT 9631 induced both apoptosis and necrosis, while IBT 9634 and IBT 3781 induced mostly necrosis. T-2 toxin and satratoxin G caused mainly apoptosis. Comet assay ± formamidopyrimidine DNA glycosylase showed that only the spore exposures induced early (3h) oxidative DNA damage. Likewise, only the spores increased the formation of reactive oxygen species (ROS), suggesting that spores as particles may induce ROS formation and oxidative DNA damage. Increased Ataxia Telangiectasia Mutated (ATM) phosphorylation, indicating DNA damage, was observed after all exposures. The DNA damage response induced by IBT 9631 as well as satratoxin G was characterized by rapid (15 min) activation of p38 and H2AX. The p38 inhibitor SB 202190 reduced IBT 9631-induced H2AX activation. Both IBT 9631 and T-2 induced activation of Chk2 and H2AX after 3 h. The ATM inhibitor KU 55933, as well as transfection of cells with ATM siRNA, reduced this activation, suggesting a partial role for ATM as upstream activator for Chk2 and H2AX. In conclusion, activation of Chk2 and H2AX correlated with spore- and toxin-induced apoptosis. For IBT 9631 and satratoxin G, additional factors may be involved in triggering apoptosis, most notably p38 activation. © The Author 2010. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. Source

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