Use of antibiotics by spanish dentists receiving postgraduate training in endodontics.

BACKGROUND: The incidence of endodontic infections is high. The contribution of Endodontics to the global problem of antibiotic resistance could be significant. The ESE, together with the World Health Organization, are promoting the World Antibiotic Awareness Week (13-19 November 2017) to promote the appropriate use of systemic antibiotics in Endodontics. The objective of this study was to determine the prescription pattern of antibiotics in the treatment of endodontic infections of Spanish dentists attending specialization programs in Endodontics. MATERIAL AND METHODS: Dentists from five Spanish endodontic postgraduate programs were requested to answer a one-page questionnaire surveying about antibiotics indications. Seventy-three dentists were required to participate in this investigation, and 67 (91.2%) fulfilled satisfactorily the survey and were included in the study. Data were analyzed using descriptive statistics and chi square test. RESULTS: The average duration of antibiotic therapy was 6.8±1.2 days. All respondents chose amoxicillin as first choice antibiotic in patients with no medical allergies, alone (40%) or associated to clavulanic acid (60%). The first drug of choice for penicillin allergic patients was clindamycin (72%). For cases of irreversible pulpitis, 22% of respondents prescribed antibiotics. For the scenario of a necrotic pulp, symptomatic apical periodontitis and no swelling, 37% prescribed antibiotics. A quarter of dentists prescribed antibiotics for necrotic pulps with asymptomatic apical periodontitis and a sinus tract. CONCLUSIONS: The results of this study show that postgraduate training in Endodontics provides greater awareness of the correct indications of antibiotics. Dentists who have received specialized training in Endodontics have a prescription pattern of antibiotics more adjusted to the guidelines recommended by international organizations and by scientific societies. Key words:Antibiotics, apical periodontitis, dental curriculum, endodontic infections, postgraduate endodontic training.

Respuesta inmune innata pulpar frente a la caries: mecanismos efectores / Pulp innate immune response to caries: effector mechanisms

La respuesta inmune innata de la pulpa frente a las bacterias de la caries se inicia cuando las células efectoras (monocito-macrófagos, células dendríticas inmaduras, células NK, células T y, en la pulpa, también los odontoblastos) reconocen, a través de los receptores toll-like (TLRs), los patrones moleculares inespecíficos presentes en las bacterias (ácido lipoteicoico, LPS, ARN bacteriano). Pero otros mecanismos efectores juegan también un papel fundamental en la respuesta inmune innata pulpar: a) la permeabilidad dentinaria y la presión del fluido dentinario; b) los odontoblastos, habiéndose demostrado que expresan genes de quimioquinas (CXCL2, CXCL8), de receptores de quimioquinas (CXCR2, CCRL1) y los receptores TLR2 y TLR4; c) los neuropéptidos pulpares (CGRP, SP, NKA, NPY, VIP) y la inflamación neurogénica; d) las células efectoras de la inmunidad inespecífica, incluyendo los monocito-macrófagos, las células dendríticas inmaduras (CDs), las células NK (asesinas naturales, natural killer) y las células T; e) las citoquinas innatas (TNF-α, IL-1α, IL-1β, INF-γ); f) las quimioquinas o factores quimiotácticos (CXCL12, CXCL13), y g) los factores humorales. Si esta respuesta innata consigue eliminar precozmente la mayoría de los antígenos que llegan a la pulpa, la inflamación puede ser reversible. Por el contrario, si la infección persiste termina activándose la respuesta inmune adaptativa específica, que incrementa la inflamación y aumenta el edema y la presión intrapulpar, lo que en una cavidad inextensible como lo es la cavidad pulpar, acaba por producir un daño irreversible a la pulpa (pulpitis irreversible, necrosis pulpar)

The pulp innate immune response to caries initiates when its effector cells (monocyte-macrophages, immature dendritic cells, NK cells, T cells and, in the pulp, also the odontoblasts) recognize, by the Toll-like receptors (TLRs) that expressed in their membranes, certain non-specific molecular patterns present in bacteria (lipoteichoic acid, LPS, bacterial RNA). But the effector mechanisms of the pulp innate immune response also include: a) dentin permeability and dentin fluid pressure; b) odontoblasts, who express chemokine genes (CXCL2, CXCL8), chemokine receptors genes (CXCR2, CCRL1), and TLR2 and TLR4 receptors. c) pulp neuropeptides (CGRP, SP, NKA, NPY, VIP); d) the effector cells of innate immunity, including monocyte-macrophages, immature dendritic cells (CDs), NK (natural killer) cells and T cells; e) innate cytokines (TNF-α, IL-1α, IL-1β, INF-γ); f) chemokines (CXCL12, CXCL13); and g) humoral factors. If this innate response eliminate early most of the antigens reaching the pulp, the inflammation may be reversible. On the contrary, if infection persists the specific adaptive immune response is estimulated, increasing inflammation, edema and intrapulp pressure, conducting to irreversible damage of the pulp (irreversible pulpitis, pulp necrosis)

Root canal disinfection of immature dog teeth with apical periodontitis: Comparison of three different protocols.

OBJECTIVES: The present in vivo study was designed to assess the efficacy of 3 root canal disinfection protocols in immature dog teeth with apical periodontitis (AP). MATERIAL AND METHODS: Forty immature premolars with pulp necrosis and AP of five Beagle dogs were used. Three experimental disinfection protocols were established. After irrigation with 40 ml 5.25% sodium hypochlorite using the Endovac system, in Group 1 canals were flushed with QMix solution; in Group 2, canals were flushed with QMix solution and 2% chlorhexidine gel dressing was placed for two weeks; and in Group 3, triantibiotic paste dressing was placed for two weeks. Canals were sampled after periapical lesions were radiographically visible (S1), after the first disinfection session (S2) and, in groups 2 and 3, after dressing (S3). RESULTS: After the first session of the disinfection protocol (S2), there was significant (p < 0.05) bacterial reduction in the three experimental groups. Microorganisms were absent in 100% of S2 samples in groups 1 and 2, and in 75% of group 3 (p > 0.05). After dressing, 87.5% of the S3 samples showed increased bacterial count: in group 2, CFU counts (median = 891) were significantly higher than in group 3 (median = 18) (p = 0.03). CONCLUSIONS: In immature dog teeth with AP, root canal irrigation using QMix solution, with or without chlorhexidine gel dressing, or a triantibiotic paste dressing, provides the same level of disinfection than irrigation with 5.25% sodium hypochlorite alone in only one session. Key words:Apical periodontitis, chlorhexidine, Endovac, immature teeth, QMix solution, root canal disinfection, triantibiotic paste.

Respuesta inmune pulpar frente a la caries: mecanismos de reconocimiento inespecífico de antígenos bacterianos / Pulpal immune response to caries: inespecific mechanisms of bacterial antigens recognition

La respuesta inflamatoria pulpar frente a la caries se produce antes de que las bacterias alcancen físicamente la pulpa, cuando los antígenos y subproductos bacterianos difunden a través de los túbulos dentinarios y desencadenan, por un mecanismo inmunopatológico, la pulpitis. Inicialmente se activa la inmunidad innata o inespecífica y, solo si ésta es incapaz de eliminar la agresión, se estimulará la respuesta inmune adaptativa específica celular y humoral. La respuesta inmune natural se inicia cuando sus células efectoras (monocito-macrófagos, células dendríticas inmaduras, células NK, células T y, en la pulpa, también los odontoblastos) reconocen, mediante los receptores tipo Toll (Toll-like receptor o TLRs) que expresan en sus membranas, determinados patrones moleculares inespecíficos presentes en las bacterias (ácido lipoteicoico / TLR2; LPS / TLR4; ARN bacteriano / TLR3). La interacción del TLR con el patrón molecular bacteriano activa el factor NF-B, que a su vez activa la transcripción de genes implicados en la respuesta inflamatoria, induciendo la producción de IL-1, IL-6, IL-8, TNF-α, e IL-12, conectándose las respuestas inmunes innata y adaptativa. Sin embargo, la localización de las bacterias en el interior de los túbulos dentinarios impide su completa eliminación por las células fagocíticas, por lo que si la lesión cariosa no se trata y la infección persiste, termina activándose la respuesta inmune específica. La inflamación se incrementa y aumenta el edema y la presión intrapulpar, produciéndose un daño irreversible a la pulpa (pulpitis irreversible, necrosis pulpar) (AU)

The inflammatory pulp response to caries occurs before the bacteria physically reach the pulp, when antigens and bacteria by-products spread through the dentin tubules and trigger, by an immunopathological mechanism, the pulpitis. Initially, innate or nonspecific immune response turns on, and only if this is unable to eliminate aggression, adaptive and specific immune response is developed. The natural immune response is initiated when its effector cells (monocyte-macrophages, immature dendritic cells, NK cells, T cells and, in the pulp, also the odontoblasts) recognize, by the Toll-like receptors (TLRs) that expressed in their membranes, certain non-specific molecular patterns present in bacteria (lipoteichoic acid / TLR2; LPS / TLR4; bacterial RNA / TLR3). The interaction TLR-bacterial molecular pattern activates factor NF-κB, which in turn activates the transcription of genes involved in the inflammatory response, inducing the production of IL-1, IL-6, IL-8, TNF-α, and IL-12, connecting the immune innate and adaptive responses. However, the location of the bacteria inside the dentin tubules prevents their complete elimination by phagocytic cells and the infection persists (AU)

Endodontic treatment failure consecutive to unsystematic radiographic examination.

This case report describes the endodontic therapy on a three-rooted mandibular first molar. The initial endodontic treatment was carried out after misreading preoperative periapical radiograph. Moreover, the working length was determined only with the apex locator. So, the additional disto-lingual root left unidentified and remained untreated, failing the treatment. A thorough radiographic examination in the initial therapy would have allowed the identification of the supernumerary root and its canal. Although the apex locators determine accurately the working length, it does not inform about the root canal morphology. It can be concluded and remarked that a systematic radiographic examination, including preoperative radiographs, is essential for success in endodontic therapy.