Correlations between endotoxin and clinical symptoms or radiolucent areas in infected root canals

Horiba, Naoki; Maekawa, Yoichi; Abe, Yoshie; Ito, Masato; Matsumoto, Toru; Nakamura, Hiroshi

doi:10.1016/0030-4220(91)90438-i

Cited by 64 publications

(80 citation statements)

References 14 publications

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“…The higher frequency of odontogenic pain indicated the occurrence of symptomatic pulpitis and apical periodontitis of infectious origin. These common symptomatic diseases are caused by microorganisms, as previously described (15)(16)(17)(18)(19)(20). Khabbaz et al (18) determined the presence or absence of endotoxins in the superficial and deep layers of carious lesions of symptomatic and asymptomatic teeth with vital pulps, measured the amount of endotoxin, and associated the presence of endotoxins with the acute pulpal pain caused by irreversible pulpitis.…”

Section: Discussionmentioning

confidence: 99%

“…The evaluation of pain perception by qualitative and quantitative methods has been carefully discussed (2,8). Whilst some studies have investigated the incidence of pain and its correlation with clinical factors during and after root canal treatment (13,14), others have determined the association of periapical and pulpal symptoms with bacteria, enzymes and toxins (15)(16)(17)(18). Few epidemiological studies have focused on urgencies that occur before the beginning of endodontic treatment (7).…”

Section: Introductionmentioning

confidence: 99%

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Diagnostic and clinical factors associated with pulpal and periapical pain

et al. 2011

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A retrospective survey was designed to identify diagnostic subgroups and clinical factors associated with odontogenic pain and discomfort in dental urgency patients. A consecutive sample of 1,765 patients seeking treatment for dental pain at the Urgency Service of the Dental School of the Federal University of Goiás, Brazil, was selected. Inclusion criteria were pulpal or periapical pain that occurred before dental treatment (minimum 6 months after the last dental appointment), and the exclusion criteria were teeth with odontogenic developmental anomalies and missing information or incomplete records. Clinical and radiographic examinations were performed to assess clinical presentation of pain complaints including origin, duration, frequency and location of pain, palpation, percussion and vitality tests, radiographic features, endodontic diagnosis and characteristics of teeth. Chi-square test and multiple logistic regression were used to analyze association between pulpal and periapical pain and independent variables. The most frequent endodontic diagnosis of pulpal pain were symptomatic pulpitis (28.3%) and hyperreactive pulpalgia (14.4%), and the most frequent periapical pain was symptomatic apical periodontitis of infectious origin (26.4%). Regression analysis revealed that closed pulp chamber and caries were highly associated with pulpal pain and, conversely, open pulp chamber was associated with periapical pain (p<0.001). Endodontic diagnosis and local factors associated with pulpal and periapical pain suggest that the important clinical factor of pulpal pain was closed pulp chamber and caries, and of periapical pain was open pulp chamber.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Diagnostic and clinical factors associated with pulpal and periapical pain

et al. 2011

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“…Endotoxin content in infected root canals was higher among symptomatic teeth, teeth with radiolucent areas and with exudation than in those without these alterations 8,21 . Dahlén, Bergenholtz 6 (1980) observed that the endotoxic activity of the root canal samples was correlated with the presence and the number of Gram-negative bacteria in the root canal.…”

mentioning

confidence: 92%

“…Endotoxin is also able to penetrate through obturation materials 25 and can reach the periapical region faster (23 days) than bacteria (62 days) 1 . Horiba et al 8 (1991) studied the endotoxin content in serial dentin samples of infected root canals. These authors observed that this content was significantly higher in samples from the pulpal surface to 300 µm in depth than in those taken farther toward the cementum side.…”

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confidence: 99%

Diffusion ability of endotoxin through dentinal tubules

et al. 2005

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ABSTRACT:The aim of this study was to evaluate the ability of endotoxin to diffuse through dentinal tubules towards the cement and to observe the period of time needed for it to reach the external root surface. Thirty singlerooted human teeth had their crowns and apices removed in order to standardize the root length to 15 mm. Teeth were instrumented until #30 K-file and made externally impermeable with epoxy adhesive, leaving 10 mm of the exposed root (middle third). The specimens were placed in plastic vials and irradiated (60Co gamma-rays). Then, they were divided into 2 groups (n = 15): G1) Escherichia coli endotoxin was inoculated into the root canal of the specimens and 1 ml of pyrogen-free water was put in the tubes; G2) (control): pyrogen-free water was inoculated into the root canals and 1 ml of pyrogen-free water was put in each tube. After 30 min, 2 h, 6 h, 12 h, 24 h, 48 h, 72 h and 7 days, the water of the tubes was removed and replaced. The removed aliquot was tested for the presence of endotoxin. Considering that the endotoxin is a B-lymphocyte polyclonal activator, at each experimental period, B-lymphocyte culture was stimulated with a sample of water removed from each tube and antibody (IgM) production was detected by ELISA technique. The results of IgM production were higher in groups of 24 h, 48 h, 72 h and 7 days in relation to the other studied groups, with statistically significant differences (ANOVA and Tukey's test p < 0.05). Endotoxin was able to diffuse through the dentinal tubules towards the cement, reaching the external root surface after the period of 24 h. DESCRIPTORS: Endotoxins; Tooth permeability; Dentin; Root canal. RESUMO:O objetivo desta pesquisa foi avaliar in vitro a capacidade e o tempo necessário para a endotoxina se difundir pelos túbulos dentinários em direção ao cemento. Foram utilizados 30 dentes humanos unirradiculados, que tiveram suas coroas e seus ápices seccionados, padronizando-se o tamanho em 15 mm. Os dentes foram instrumentados até a lima K30 e impermeabilizados externamente com adesivo epóxi, deixando-se 10 mm de raiz exposta (terço médio). Os espécimes foram acondicionados em tubos plásticos e submetidos à radiação gama cobalto 60. Após a radiação, foram divididos em 2 grupos (n = 15): G1) foi inoculada uma solução de endotoxina de Escherichia coli no canal radicular dos espécimes e 1 mL de água apirogênica foi colocado no interior dos tubos; G2 (controle): foi inoculada água apirogênica nos canais radiculares e 1 mL de água apirogência foi colocado em cada tubo. Após 30 min, 2 h, 6 h, 12 h, 24 h, 48 h, 72 h e 7 dias, a água do interior dos tubos foi removida e substituída por outra. A alíquota removida foi testada para se detectar presença de endotoxina através da produção de anticorpos (IgM) em cultura de linfócitos B, pois a endotoxina é um ativador policlonal dessas células. Os resultados foram submetidos à análise estatística ANOVA (5%) e teste de Tukey, em que foi verificado que a água removida dos tubos após 24 h, 48 h, 72 h e 7 dias induziu maior pr...

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“…Studies have revealed that the content of endotoxin or LPS in infected root canals is higher in teeth with symptomatic apical periodontitis, teeth with periradicular bone destruction, or teeth with persistent exudation than in those without them (32)(33)(34)(35)(36). Murakami et al (37) detected Porphyromonas endodontalis LPS in samples from infected root canals or in the pus samples of acute abscesses of about 90% of the patients tested.…”

Section: Lipopolysaccharide (Lps)mentioning

confidence: 99%

Bacterial pathogenesis and mediators in apical periodontitis

2007

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Apical periodontitis is a group of inflammatory diseases caused by microorganisms (mainly bacteria) infecting the necrotic root canal system. The pathogenesis of different types of apical periodontitis and even the same type in different individuals is unlikely to follow a stereotyped fashion with regard to the involved bacterial mediators. Disease pathogenesis is rather complex and involves a multitude of bacteria-and host-related factors. This review article discusses the bacterial pathogenesis of acute and chronic apical periodontitis, with the main focus on the bacterial mediators conceivably involved in the different stages of the infectious process, including secreted products (enzymes, exotoxins, N-formyl-methionyl-leucyl-phenylalanine peptides, heat-shock proteins and metabolic end-products) and structural components (lipopolysaccharide, peptidoglycan, lipoteichoic acid, lipoproteins, fimbriae, flagella, outer membrane proteins and vesicles, DNA, and exopolysaccharides). Knowledge of the bacterial factors involved in the pathogenesis of apical periodontitis is important to the understanding of the disease process and to help establishing proper therapeutic measures to inactivate this bacterial "artillery".

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Correlations between endotoxin and clinical symptoms or radiolucent areas in infected root canals

Cited by 64 publications

References 14 publications

Diagnostic and clinical factors associated with pulpal and periapical pain

Diagnostic and clinical factors associated with pulpal and periapical pain

Diffusion ability of endotoxin through dentinal tubules

Bacterial pathogenesis and mediators in apical periodontitis

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