RESUMO
RESUMEN La retención y sobrevivencia de microorganismos orales (MO) en la bombilla para tomar infusiones representa una posible fuente de contaminación de la boca, principalmente en personas con enfermedades periodontales. El objetivo del trabajo fue identificar la presencia de bacterias en bombillas para infusiones y en cavidad oral de pacientes con salud periodontal y antecedentes de enfermedad periodontal. Este fue un estudio observacional, descriptivo de corte transversal con componente analítico. Los participantes del estudio se agruparon en G1 (pacientes con salud periodontal, bombillas estériles para infusiones, con oxido etileno para su uso por 30 días) y G2 (pacientes con antecedente de enfermedad periodontal, bombillas estériles para infusión, con oxido etileno para su uso por 30 días). Participaron del estudio 50 pacientes. En los pacientes sanos (Grupo1) el promedio de Unidades Formadoras de Colonias (UFC) fue de 676± 226, mientras que en los pacientes con enfermedad periodontal (Grupo 2) el promedio de UFC fue de 817± 345. En los pacientes sanos (Grupo1) el promedio de MO fue de 668± 165, mientras que en los pacientes con enfermedad periodontal (Grupo 2) el promedio de MO fue de 774± 156. Se evidencia la presencia de microorganismos en bombillas para infusiones y en cavidad oral de pacientes con salud periodontal y antecedentes de enfermedad periodontal. El recuento de UFC presentes en la cavidad oral de los pacientes con salud periodontal y antecedentes de enfermedad periodontal fue similar.
ABSTRACT The retention and survival of oral microorganisms (OM) in the bombillas to take infusions represents a possible source of contamination of the mouth, mainly in people with periodontal diseases. The objective was to identify the presence of bacteria in infusion bombillas and in the oral cavity of patients with periodontal health and a history of periodontal disease. This was an observational, descriptive, cross-sectional study with analytical component. Study participants were grouped into G1 (patients with periodontal health, sterile infusion bulbs, with ethylene oxide for use for 30 days) and G2 (patients with a history of periodontal disease, sterile infusion bulbs, with ethylene oxide for use for 30 days). Fifty patients participated in the study. In healthy patients (Group1) the mean CFU was 676 ± 226, while in patients with periodontal disease (Group 2) the mean of Colony Forming Units (CFU) was 817 ± 345. In healthy patients (Group1) the mean OM It was 668 ± 165, while in patients with periodontal disease (Group 2) the mean OM was 774 ± 156. The presence of microorganisms is evidenced in bombillas for infusions and in the oral cavity of patients with periodontal health and a history of periodontal disease. The count of CFU present in the oral cavity of patients with periodontal health and a history of periodontal disease was similar.
RESUMO
RESULTS: The lysophosphatidic acid receptors LPA1, LPA2, and LPA3 were individually expressed in C9 cells and their signaling and regulation were studied. Agonist-activation increases intracellular calcium concentration in a concentration-dependent fashion. Phorbol myristate acetate markedly inhibited LPA1- and LPA3-mediated effect, whereas that mediated by LPA2 was only partially diminished; the actions of the phorbol ester were inhibited by bisindolylmaleimide I and by overnight incubation with the protein kinase C activator, which leads to down regulation of this protein kinase. Homologous desensitization was also observed for the three LPA receptors studied, with that of LPA2 receptors being consistently of lesser magnitude; neither inhibition nor down-regulation of protein kinase C exerted any effect on homologous desensitization. Activation of LPA1-3 receptors induced ERK 1/2 phosphorylation; this effect was markedly attenuated by inhibition of epidermal growth factor receptor tyrosine kinase activity, suggesting growth factor receptor transactivation in this effect. Lysophosphatidic acid and phorbol myristate acetate were able to induce LPA1-3 phosphorylation, in time- and concentration-dependent fashions. It was also clearly observed that agonists and protein kinase C activation induced internalization of these receptors. Phosphorylation of the LPA2 subtype required larger concentrations of these agents and its internalization was less intense than that of the other subtypes. CONCLUSION: Our data show that these three LPA receptors are phosphoproteins whose phosphorylation state is modulated by agonist-stimulation and protein kinase C-activation and that differences in regulation and cellular localization exist, among the subtypes.
