RESUMEN
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)
Asunto(s)
Humanos , Caries Dental/complicaciones , Pulpitis/fisiopatología , Periodontitis Periapical/fisiopatología , Tratamiento del Conducto Radicular/métodos , Vías Eferentes , Infecciones/fisiopatología , Mediadores de Inflamación/análisis , Inflamación/fisiopatología , Permeabilidad de la DentinaRESUMEN
OBJECTIVE: To analyse the influence of root canal instrumentation and obturation techniques on intra-operative pain experienced by patients during endodontic therapy. METHOD AND MATERIALS: A descriptive cross-sectional study was carried out in Ponferrada and Sevilla, Spain, including 80 patients (46 men and 34 women), with ages ranged from 10 to 74 years, randomly recruited. Patient gender and age, affected tooth, pulpal diagnosis, periapical status, previous NSAID or antibiotic (AB) treatment, and root canal instrumentation and obturation techniques were recorded. After root canal treatment (RCT), patients completed a 10-cm visual analogue scale (VAS) that ranked the level of pain. Results were analysed statistically using the Chi-square and ANOVA tests and logistic regression analysis. RESULTS: The mean pain level during root canal treatment was 2.9±3.0 (median=2) in a VAS between 0 and 10. Forty percent of patients experienced no pain. Gender, age, arch, previous NSAIDs or AB treatment and anaesthetic type did not influence significantly the pain level (p>0.05). Pain during root canal treatment was significantly greater in molar teeth (OR=10.1; 95% C.I.=1.6-63.5; p=0.013). Root canal instrumentation and obturation techniques did not affect significantly patients' pain during root canal treatment (p>0.05). CONCLUSION: Patients feel more pain when RCT is carried out on molar teeth. The root canal instrumentation and obturation techniques do not affect significantly the patients' pain during RCT.