Document Detail


Effects of root canal sealers on immunocompetent cells in vitro and in vivo.
MedLine Citation:
PMID:  10321164     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Over the years of testing biocompatibility of endodontic filling materials, little attention has been paid to the potential adverse influences on the function of the immune system. Therefore, the purpose of this study was to investigate the extent to which extractable components of some commonly used root canal sealing materials (ERCS) may interfere with immunocompetent cells in vitro. The potential of these materials to cause delayed-type hypersensitivity (DTH) was also addressed in a rat model system. Extractable components were drawn in cell culture medium from freshly mixed or set material of AH 26. Grossman's sealer, Endomethasone, and Apexit. In-vitro assays included either spleen cells or rat pulp tissue cells that were released following enzymatic digestion with collagenase. Purified T cells for the pulpal cell assay were obtained from rat mesenteric lymph nodes. The effect of ERCS on the proliferation of concanavalin A (con A) stimulated spleen cell was measured by 3H-thymidine incorporation. Pulpal accessory cell function was monitored by the capacity of pulpal cells, pretreated with components of ERCS, to provide signals to con A stimulated T cells. DTH was tested after subcutaneous implantation of root canal sealers (RCS) in rats and challenge by ear injection. Pretreatment of pulpal cells with low dilutions of eluates from extracted AH 26 and Endomethasone resulted in a strong reduction of the T cell proliferation rate. The effect was considerably reduced (P < 0.01) when extracts of the solid material were employed. Extracts of Grossmans' sealer and Apexit affected T cell proliferation only to a limited extent in the pulpal cell assay. In general, assays on spleen cells showed a similar profile, although increased cell division was induced by Grossman's sealer at high eluate dilutions and a concentration-dependent decrease of cell division at lower concentrations of this material. ERCS evoked both immunosuppression and, in some instances, immunostimulation, but they did not release DTH.
Authors:
J Bratel; M Jontell; U Dahlgren; G Bergenholtz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International endodontic journal     Volume:  31     ISSN:  0143-2885     ISO Abbreviation:  Int Endod J     Publication Date:  1998 May 
Date Detail:
Created Date:  1999-05-18     Completed Date:  1999-05-18     Revised Date:  2010-07-05    
Medline Journal Info:
Nlm Unique ID:  8004996     Medline TA:  Int Endod J     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  178-88     Citation Subset:  D    
Affiliation:
Department of Endodontology/Oral Diagnosis, Faculty of Odontology, University Göteborg, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Administration, Topical*
Animals
Anti-Inflammatory Agents / toxicity
Bismuth / toxicity
Calcium Hydroxide / toxicity
Cells, Cultured
Dental Pulp / cytology,  drug effects*
Dexamethasone / toxicity
Drug Combinations
Epoxy Resins*
Female
Formaldehyde / toxicity
Hydrocortisone*
Hypersensitivity, Delayed / chemically induced
Immunity, Cellular / drug effects*
Male
Methenamine / toxicity
Rats
Rats, Inbred Lew
Rats, Wistar
Root Canal Filling Materials / toxicity*
Silver / toxicity
Spleen / cytology,  drug effects
T-Lymphocytes / drug effects*
Thymol / analogs & derivatives,  toxicity
Titanium / toxicity
Zinc Oxide-Eugenol Cement / toxicity
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Apexit; 0/Drug Combinations; 0/Epoxy Resins; 0/Root Canal Filling Materials; 0/Zinc Oxide-Eugenol Cement; 0/corticosteroid methanetriol mixture; 100-97-0/Methenamine; 100092-04-4/Grossman's sealer; 1305-62-0/Calcium Hydroxide; 50-00-0/Formaldehyde; 50-02-2/Dexamethasone; 50-23-7/Hydrocortisone; 55599-25-2/epoxy resin AH-26; 7440-22-4/Silver; 7440-32-6/Titanium; 7440-69-9/Bismuth; 89-83-8/Thymol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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