Cortical activity evoked by inoculation needle prick in infants up to one-year old

Inoculation is one of the first and most common experiences of procedural pain in infancy. However, little is known about how needle puncture pain is processed by the central nervous system in children. In this study, we describe for the first time the event-related activity in the infant brain during routine inoculation using electroencephalography. Fifteen healthy term-born infants aged 1 to 2 months (n = 12) or 12 months (n = 5) were studied in an outpatient clinic. Pain behavior was scored using the Modified Behavioral Pain Scale. A distinct inoculation event-related vertex potential, consisting of 2 late negative-positive complexes, was observable in single trials after needle contact with the skin. The amplitude of both negative-positive components was significantly greater in the 12-month group. Both inoculation event-related potential amplitude and behavioral pain scores increased with age but the 2 measures were not correlated with each other. These components are the first recordings of brain activity in response to real-life needle pain in infants up to a year old. They provide new evidence of postnatal nociceptive processing and, combined with more traditional behavioral pain scores, offer a potentially more sensitive measure for testing the efficacy of analgesic protocols in this age group

Degeneration and regeneration of peripheral nerves: role of thrombin and its receptor PAR-1

The peripheral nervous system has a striking regeneration potential and after damage extensive changes in the differentiation state both of the injured neurons and of the Schwann cells are observed. Schwann cells, in particular, undergo a large scale change in gene expression becoming able to support axonal regeneration. Nerve injury is generally associated to inflammation and activation of the coagulation cascade. Thrombin acts as a polyfunctional signalling molecule exerting its physiological function through soluble target proteins and G-protein-coupled receptors, the protease-activated receptors (PARs) [1]. Recently, we have demonstrated that the activation of the main thrombin receptor, PAR-1, in Schwann cells favours their regenerative potential determining the release of factors which promote axonal regrowth [2]. The pro-regenerative potential of thrombin seems to be exerted in a narrow range of concentrations (pM-nM range). In fact, our preliminary data indicate that high levels of thrombin in the micromolar range slow down Schwann cell proliferation and induce cell death. On the contrary, PAR-1 activating peptides mimic the pro-survival but not the pro-apoptotic effects of thrombin. Controlling thrombin concentration may preserve neuronal health during nerve injury and represent a novel target for pharmacologic therapies

Papel etiológico de los virus en la enfermedad periodontal

El objetivo de esta revisión es presentar la evidencia disponible que relaciona la infección por virus con el desarrollo de periodontitis. Esta relación se ha visto con los virus de la familia herpes, sobretodo el citomegalovirus humano (CMV) y el virus Epstein-Barr (VEB), así como con el virus de la inmunodeficiencia humana (HIV). Las infecciones por herpesvirus generalmente sucede en dos fases, durante la primoinfección la clínica suele ser leve o asintomática y a esta le sigue una fase asintomática en la que el virus se encuentra en estado de latencia. Dicho estado se verá interrumpido esporádicamente por periodos de activación en los que se produce una replicación viral y posiblemente se dé una manifestación de la enfermedad que explicaría, en parte, el progreso en episodios de la enfermedad periodontal. De hecho, algunas de las causas que llevan a la reactivación del virus también se consideran factores de riesgo de la enfermedad periodontal y podrían relacionar a ambas patologías. The purpose of this review is to evaluate the evidence supporting the hypothesis that viral infection plays a role in the development of periodontitis. This relationship has been found mainly with the herpesvirus family, especially with human cytomegalovirus (CMV) and with Epstein-Barr virus (EBV), but also with human immunodeficiency virus (HIV). The herpesvirus infection generally involves a mild or asymptomatic primary phase followed by an asymptomatic latent phase interrupted sporadically by periods of activation, where viral replication and possibly clinical disease become manifest and which will in part, explain the episodic progressive nature of human periodontitis. In fact, herpesvirus reactivation is triggered by a number of immunosuppressing factors, some of which have also been shown to be risk indicators of periodontal disease and which could relate both patologies

Impairment of the autophagic flux in astrocytes intoxicated by trimethyltin

Autophagy is a lysosomal catabolic route for protein aggregates and damaged organelles which in different stress conditions, such as starvation, generally improves cell survival. An impairment of this degradation pathway has been reported to occur in many neurodegenerative processes. Trimethyltin (TMT) is a potent neurotoxin present as an environmental contaminant causing tremors, seizures and learning impairment in intoxicated subjects. The present data show that in rat primary astrocytes autophagic vesicles (AVs) appeared after few hours of TMT treatment. The analysis of the autophagic flux in TMT-treated astrocytes was consistent with a block of the late stages of autophagy and was accompanied by a progressive accumulation of the microtubule associated protein light chain 3 (LC3) and of p62/SQSTM1. Interestingly, an increased immunoreactivity for p62/SQSTM1 was also observed in hippocampal astrocytes detected in brain slices of TMT-intoxicated rats. The time-lapse recordings of AVs in EGFP-mCherry-LC3B transfected astrocytes demonstrated a reduced mobility of autophagosomes after TMT exposure respect to control cells. The observed block of the autophagic flux cannot be overcome by known autophagy inducers such as rapamycin or 0.5mM lithium. Although ineffective when used at 0.5mM, lithium at higher concentrations (2mM) was able to protect astrocyte cultures from TMT toxicity. This effect correlated well with its ability to determine the phosphorylation/inactivation of glycogen kinase synthase-3β (GSK-3β)

Variability of the fimA gene in Porphyromonas gingivalis isolated from periodontitis and non-periodontitis patients

Objective: The goal of this study was to determine the genetic variability of the fimA gene in Porphyromonas gingivalis isolates from Spanish patients. Study Design: Pooled subgingival samples were taken, processed and cultured in non-selective blood agar medium. Pure cultures of one to six isolates per patient were obtained and PCR and PCR-RFLP were used for fimbrillin gene (fimA) type determination of the extracted genomic (DNA). Results: Two hundred and twenty four Porphyromonas gingivalis isolates from 65 patients were analyzed consisting of 15 non-periodontitis patients (66 isolates) and 50 with periodontitis (158 isolates). Genotype II was the most prevalent (50.9%), while the other types of fimbriae did not exceed fifteen percent of prevalence. Isolates with types II and IV of fimbriae were significantly more prevalent in periodontitis patients than isolates with genotype I. Co-infection was observed in 17.65% of the patients analyzed. Conclusion: The results suggest that in this population Porphyromonas gingivalis with type II of fimbriae are significantly more predominant in periodontitis patients than genotype I

Tratamiento quirúrgico vs terapia periodontal básica: estudios longitudinales en periodoncia clínica

Las enfermedades periodontales son unas graves infecciones bacterianas que destruyen las fibras de inserción y el hueso de soporte que mantienen los dientes en la boca. Sin tratar, esta enfermedad puede llevar a la pérdida dental (Medical Dictionary). Los estudios longitudinales han centrado su atención hacia la periodontitis crónica. Se ha documentado el decisivo papel de la placa bacteriana en la iniciación y en el mantenimiento de la gingivitis, y que, los efectos dañinos sobre los tejidos y la gravedad de estos efectos están regulados por una compleja interacción entre el parásito y huésped. El tratamiento de la lesión periodontal cumple, para el tratamiento periodontal básico, con el propósito de eliminar y prevenir la recurrencia de los depósitos bacterianos localizados en las superficies dentarias supragingivales y subgingivales y, para el tratamiento quirúrgico con el objetivo de crear acceso para el desbridamiento profesional correcto de las superficies radiculares infectadas y establecer una morfología gingival adecuada que facilite el autocontrol de la placa por parte del paciente. Diferentes técnicas se han utilizado para alcanzar el objetivo de mejorar el pronóstico de los dientes a largo plazo. Desafortunadamente no son muchos los estudios que consiguen demostrar la efectividad de las técnicas utilizadas, con una evolución a lo largo del tiempo dejando entonces algunas incertidumbres. Periodontal diseases are bacterial infections that destroy the attachment fibres and supporting bone that hold the teeth in the mouth. Left untreated, these diseases can lead to tooth loss (Medical Dictionary). Longitudinal studies centred their attention on chronic periodontitis. It has been documented the decisive role played by microbiological plaque in the initiation of gingivitis and that, the harmful effect on the tissues and its severity, are controlled by the complex host-parasite interaction. Treatment of periodontal lesion can be carried out either by non-surgical treatment, to eliminate and prevent the recurrence of bacterial deposits, or by surgical treatment, to create access for professional debridment of infected root surface and establish adequate gingival morphology to facilitate self plaque control. Different techniques are used to achieve the objective to improve teeth long term prognosis. Unfortunately no many studies have been able to demonstrate the effectiveness of the used technique in a long term intervals leaving unclear some questions

Encoding of mechanical nociception differs in the adult and infant brain

Newborn human infants display robust pain behaviour and specific cortical activity following noxious skin stimulation, but it is not known whether brain processing of nociceptive information differs in infants and adults. Imaging studies have emphasised the overlap between infant and adult brain connectome architecture, but electrophysiological analysis of infant brain nociceptive networks can provide further understanding of the functional postnatal development of pain perception. Here we hypothesise that the human infant brain encodes noxious information with different neuronal patterns compared to adults. To test this we compared EEG responses to the same time-locked noxious skin lance in infants aged 0-19 days (n = 18, clinically required) and adults aged 23-48 years (n = 21). Time-frequency analysis revealed that while some features of adult nociceptive network activity are present in infants at longer latencies, including beta-gamma oscillations, infants display a distinct, long latency, noxious evoked 18-fold energy increase in the fast delta band (2-4 Hz) that is absent in adults. The differences in activity between infants and adults have a widespread topographic distribution across the brain. These data support our hypothesis and indicate important postnatal changes in the encoding of mechanical pain in the human brain

Electrophysiological Measurements and Analysis of Nociception in Human Infants

Pain is an unpleasant sensory and emotional experience. Since infants cannot verbally report their experiences, current methods of pain assessment are based on behavioural and physiological body reactions, such as crying, body movements or changes in facial expression. While these measures demonstrate that infants mount a response following noxious stimulation, they are limited: they are based on activation of subcortical somatic and autonomic motor pathways that may not be reliably linked to central sensory processing in the brain. Knowledge of how the central nervous system responds to noxious events could provide an insight to how nociceptive information and pain is processed in newborns

Thrombin in the peripheral nervous system as regulator of Schwann cell neurotrophic potentials

Coagulation and inflammation are tightly and reciprocally regulated. Inflammation initiates clotting, decreases the activity of natural anticoagulant mechanisms and impairs the fibrinolytic system. Thrombin is the main effector protease in hemostasis and it also plays a role in various non-hemostatic biological and pathophysiologic processes, predominantly mediated through activation of protease-activated receptors (PARs)