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Root Canal Infections (root + canal_infections)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

How does the periapical inflammatory process compromise general health?

ENDODONTIC TOPICS, Issue 1 2004
Idikó.
Several lines of evidence support the causative role of oral inflammatory lesions and certain systemic diseases, such as atherosclerosis and cardiovascular diseases, adverse pregnancy outcome and lung diseases. Properly executed epidemiologic studies identified increased odds ratios. Local or metastatic spread of oral microorganisms, local production of microbial or host-derived soluble regulatory molecules, that may initiate or sustain inflammatory events in remote tissues and organs and the presence of (a) common , extrinsic- or intrinsic-pathological mechanism(s) may result in or contribute to both local and systemic inflammation. A number of cross-sectional studies addressing a possible association between oral health and systemic diseases have also investigated the presence or the absence of periapical lesions. However, these studies cannot either confirm or refute a role of the periapical inflammatory lesion in the observed associations, since other variables of oral health might have exerted an inestimable influence on general health of the assessed population. The literature, dealing with patients with root canal infections and apical periodontitis as sole oral inflammatory lesions is extremely sparse. Our group has demonstrated that young adults with apical periodontitis exhibit certain biochemical changes, such as elevated levels of C-reactive protein and an increased whole blood chemiluminescence, which have been shown to elevate the risk for cardiovascular diseases. Future research will be required to determine whether and to what extent may endodontic diseases affect general health. [source]

Development of an ex vivo model for the study of microbial infection in human teeth

INTERNATIONAL ENDODONTIC JOURNAL, Issue 5 2007
B. Patel
Aims, (1) To infect human teeth artificially to mimic root canal and dentine infection, using the Constant Depth Film Fermenter (CDFF); (2) To verify the similarity of the infections to those found, in vivo, using culture and microscopy (SEM, LM and TEM). Methodology, Human teeth [n = 38 and n = 28, for phases I (preliminary) and II (definitive), respectively] were infected within the CDFF for a period of 28 days and at pre-selected time points were removed, externally decontaminated using validated protocols and subjected to either culture-dependent or microscopy protocols. The condition of the teeth was varied in phase I to establish the feasibility of the approach and identify optimal conditions. This informed the selection of optimal conditions for definitive test in phase II. For culture-dependent analysis in this phase, a dentine filing sample was obtained from the apical 5 mm of the root canal and cultured anaerobically to allow isolation of individual strains. Bacterial DNA was extracted from purified isolates, the 16S rRNA genes amplified by PCR and the amplicons sequenced for identity using sequence databases. Teeth assigned for microscopy were post-fixed in 3% gluteraldehyde after removal from the CDFF and then subjected to appropriate protocols prior to microscopic evaluation of the infection. Results, All three microscopy techniques and culture-dependent analysis confirmed infection of the human teeth using the CDFF, with root canal infections visually resembling closely those seen in vivo. Furthermore, partial 16S rRNA gene sequencing of DNA from cultured isolates confirmed a selective number of 7,9 genera/species in the apical portion of two teeth each at 7 and 28 days; these taxa are also commonly recovered from teeth with apical periodontitis, in vivo. There were no objective measures other than speciation and topographical evaluation to compare the artificial and real (in vivo) infections. Conclusions, The proposed ex vivo model has the potential for development into an investigative tool for studying the dynamics of bacterial ecology in infected root canals, both before and after treatment. Its advantage is the ability to control both the abiotic and biotic factors. There is a need for the development of objective measures to compare artificial and real bacterial biofilms. [source]

Oral treponemes in primary root canal infections as detected by nested PCR

INTERNATIONAL ENDODONTIC JOURNAL, Issue 1 2003
I. N. Rôças
No abstract is available for this article. [source]

Virulence, phenotype and genotype characteristics of endodontic Enterococcus spp.

MOLECULAR ORAL MICROBIOLOGY, Issue 1 2005
C. M. Sedgley
Background/aims:, Enterococci have been implicated in persistent root canal infections but their role in the infection process remains unclear. This study investigated the virulence, phenotype and genotype of 33 endodontic enterococcal isolates. Methods:, Phenotypic tests were conducted for antibiotic resistance, clumping response to pheromone, and production of gelatinase, hemolysin and bacteriocin. Genotype analysis involved polymerase chain reaction amplification of virulence determinants encoding aggregation substances asa and asa373, cytolysin activator cylA, gelatinase gelE, gelatinase-negative phenotype ef1841/fsrC, adherence factors esp and ace, and endocarditis antigen efaA. Physical DNA characterization involved pulsed-field gel electrophoresis of genomic DNA, and plasmid analysis. Results:, Potential virulence traits expressed included production of gelatinase by Enterococcus faecalis (n = 23), and response to pheromones in E. faecalis culture filtrate (n = 16). Fourteen strains produced bacteriocin. Five strains were resistant to tetracycline and one to gentamicin, whereas all were susceptible to ampicillin, benzylpenicillin, chloramphenicol, erythromycin, fusidic acid, kanamycin, rifampin, streptomycin and vancomycin. Polymerase chain reaction products encoding efaA, ace, and asa were detected in all isolates; esp was detected in 20 isolates, cylA in six isolates, but asa373 was never detected. The gelatinase gene (gelE) was detected in all isolates of E. faecalis (n = 31) but not in Enterococcus faecium (n = 2); a 23.9 kb deletion sequence corresponding to the gelatinase-negative phenotype was detected in six of the eight E. faecalis isolates that did not produce gelatinase. Pulsed-field gel electrophoresis and plasmid analyses revealed genetic polymorphism with clonal types evident. Plasmid DNA was detected in 25 strains, with up to four plasmids per strain and a similar (5.1 kb) plasmid occurring in 16 isolates. Conclusions:, Phenotypic and genotypic evidence of potential virulence factors were identified in endodontic Enterococcus spp., specifically production of gelatinase and response to pheromones. [source]

Detection of Treponema denticola in endodontic infections by 16S rRNA gene-directed polymerase chain reaction

MOLECULAR ORAL MICROBIOLOGY, Issue 5 2000
J. F. Siqueira Jr.
A 16S rDNA-based polymerase chain reaction (PCR) method was used to detect the occurrence of Treponema denticola in root canal infections. Samples were collected from 21 single-root teeth having carious lesions, necrotic pulps and radiographic evidences of periradicular bone loss. DNA extracted from the samples was amplified using the PCR assay, which yielded specific fragment of T. denticola 16S rDNA. T. denticola was detected in 11 of 21 cases (52.4%), regardless of the presence or absence of symptoms. Since this spirochete was found in a relatively high percentage of the endodontic infections examined and because it is a pathogenic microorganism involved in periodontal diseases, there are reasons to believe that T. denticola can also participate in the pathogenesis of periradicular lesions of endodontic origin. [source]