Actualización sobre el síndrome de Eagle y sus complicaciones neurocardiológicas: casos clínicos / An update on Eagle´s syndrome and its neuro-cardiological complications: clinical cases

El síndrome de Eagle o síndrome estilohioideo o sín-drome de la arteria carótida es un trastorno que se origina por la mineralización y elongación del pro-ceso estiloides. Factores traumáticos agudos y cró-nicos, así como otras teorías, han sido propuestos para explicar la etiología y patogenia de esta altera-ción. El conjunto de síntomas puede incluir: dolor fa-ríngeo, odinofagia, disfagia, cefalea, con irradiación a oreja y zona cervical. Si bien existen varias clasifi-caciones, de manera universal se acepta que existen principalmente dos formas de presentación de esta patología: el tipo I o clásico, generalmente asociado a un trauma faríngeo y acompañado de dolor en la zona faríngea y cervical, y el tipo II o carotídeo, que sue-le presentar molestia cervical, cefalea y alteración de la presión arterial, con riesgo de daño de la ac-tividad cardíaca. La identificación de este síndrome suele ser confusa dada la similitud de los síntomas con otras afecciones. El diagnóstico debe realizarse en base a los síntomas y a los estudios por imágenes específicos. El tratamiento puede ser conservador y actuar simplemente sobre los síntomas, o bien, qui-rúrgico. El objetivo del presente trabajo es realizar una revisión actualizada de la literatura sobre el sín-drome de Eagle y presentar tres casos clínicos con distintas manifestaciones (AU)

Eagle's syndrome or styloid syndrome or stylo-carotid artery syndrome is a disease caused by mineralization and elongation of the styloid process. Acute and chronic traumatic factors, along with other hypothesis, have been proposed to explain the aetiology and pathogenesis of this condition. Symptoms can include: pharynx pain, odynophagia, dysphagia, headache, with radiating pain to the ear and neck. Despite there are several classifications, it is universally accepted that this pathology can present in two forms: the type I or classic, generally associated to tonsillar trauma and characterized by pharyngeal and neck pain, and the type II or carotid artery type, which frequently presents with neck pain, headache, blood pressure variation, with risk of damage to cardiac function. Identifying of Eagle's syndrome is often confusing because some symptoms are shared with other pathologies. Diagnosis must be made on the basis of symptoms and imaging studies. Treatment can be conservative, acting only on symptoms, or surgical. The aim of this paper is to provide an updated review of the literature on Eagle syndrome and to present three clinical cases with different manifestations (AU)

Molusco contagioso: actualización y casos clínicos / Molluscum contagiosum: an update and clinical cases

El molusco contagioso es una patología viral benigna muy frecuente, exclusiva del ser humano, y causada por un virus no clasificado del grupo de los Poxvirus. Las manifestaciones clínicas de la enfermedad inclu-yen lesiones en la piel, que pueden variar desde una pequeña pápula a un nódulo de mayor tamaño, pre-sentándose en forma solitaria o múltiple, dependien-do del estado inmunitario del paciente y del tiempo de evolución del proceso morboso. El estudio histo-patológico es importante para el diagnóstico, aunque en numerosas ocasiones éste se define clínicamen-te. Además del patrón histológico tradicional, y más frecuente, que exhibe hiperplasia e hipertrofia de la epidermis, se han descripto variantes poco usuales, cuyas características dependen, entre otros factores, de la sobreinfección y de la respuesta inmunitaria del paciente. En este trabajo se describen los rasgos ge-nerales del molusco contagioso y luego se presentan varios casos clínicos, uno de los cuales exhibe ma-nifestación inusual en la semimucosa del labio. Por último, se realizan comentarios referentes a la im-portancia que tiene para el odontólogo conocer esta patología y estar capacitado para detectarla, de modo de evitar sus complicaciones y su diseminación (AU)

Molluscum contagiosum is a very common benign viral pathologythat affects exclusively humans and is caused by an unclassified virus of the Poxvirus family. Clinical manifestations include skin lesions such as papule or nodule, which may range from a small papule to a larger nodule, presenting either solitary or multiple, depending on the immune status of the patient and the time of evolution of the morbid process. Histopathological study is important for the diagnosis, although in numerous occasions it is defined clinically. Classical and more frequent histology pattern exhibits hyperplasia and hypertrophy of the epidermis; however, distinct characteristics may occur depending on factors like superinfection and immune response of patients. This article describes general aspects of molluscum contagiosum and exposes several clinical cases, one of which exhibits an unusual manifestation in the semimucosa of the lip. Finally, comments are made regarding the importance for dentists to learn about the existence of this pathology and be able to recognize it in order to avoid its complications and spread (AU)

Differential Effect of Articaine on Sarcoendoplasmic Reticulum Calcium Adenosine Triphosphatase of Medial Pterygoid Muscle.

AIMS: To determine the effect of articaine on sarcoendoplasmic reticulum calcium adenosine triphosphatase (SERCA) isoforms of the medial pterygoid muscle. METHODS: Native SERCA from the medial pterygoid muscles of 24 rabbits was isolated by ultracentrifugation, and its isoforms were purified by chromatography and assessed by enzyme-linked immunosorbent assay (ELISA). SERCA activity and calcium transport capability were determined by using colorimetric and radioisotopic methods. The mean ± standard deviation (SD) half maximal inhibitory concentration (IC50) of articaine was determined for each isoform, and these values were compared by using analysis of variance (ANOVA) (P < .05). RESULTS: The native SERCA preparation consisted of 34% SERCA1a, 53% SERCA2a, 10% SERCA2b, and 3% combined SERCA3 and SERCA1b. Articaine caused inhibition of activity and calcium uptake in the native SERCA preparation and in each of the purified isoforms. The IC50 (mM) values for enzymatic activity were: SERCA1a 22.0 ± 2.3 > SERCA2a 16.4 ± 2.4 > SERCA2b 11.3 ± 1.9, and 15.1 ± 2.1 for native SERCA. For calcium transport, IC50 values were: SERCA1a 31.1 ± 3.3 > SERCA2a 24.8 ± 1.8 > SERCA2b 21.5 ± 1.5, and 25.2 ± 3.2 for native SERCA. IC50 values for inhibition of enzymatic activity were significantly different among the purified isoforms, but only the value obtained for SERCA1a was significantly different compared to native SERCA. For inhibition of calcium transport, IC50 values for both SERCA2a and SERCA2b differed significantly compared to SERCA1a, and the value for SERCA1a was significantly different compared to native SERCA. The most articaine-sensitive isoform was SERCA2b, and the native preparation showed sensitivity similar to SERCA2a. CONCLUSION: The differential inhibition of articaine on medial pterygoid SERCA isoforms is evident at concentrations lower than used in current dental practice (125 mM) and accounts for anesthetic myotoxicity. Muscle relaxation likely becomes impaired as a result of increased calcium levels in the myoplasm due to the decreased activity and calcium transport caused by the inhibition of SERCA.

Efectividad del abordaje interdisciplinario de trastornos temporomandibulares (ttm) en niños y adolescentes / Effectiveness of interdisciplinary treatments for temporomandibular disorders (TMD) in children and adolescents

Propósito: evaluar la efectividad de tratamientos odontológicos, fonoaudiológicos, kinesiológicos y psicológicos aplicados en forma consçjunta o individual en pacientes pediátricos con TTM. De los registros de las historias clínicas se cuantificaron los resultados terapéuticos obtenidos en 97 pacientes de 12,6 años DS 2,6 con TTM con compromiso muscular. Las variables en consideración fueron dolor, limitación de movimientos mandibulares, ruido y traba. Se registró remisión, disminución, persistencia y recurrencia de signos y síntomas, utilizando un cuestionario estructurado, palpación muscular y articular y examen funcional. Las terapéuticas implementadas en forma conjunta o individual fueron: terapia sintomática de apoyo, intermediarios oclusales, reeducación fonoaudiológica y kenesiológica y orientación psicológica. Los resultados fueorn analizados mediante porcentajes con 95 por ciento de intervalo de confianza y análisis multifactorial. El tiempo promedio de los tratamientos fue de 6,8 meses DS 5,3. Se obtuvo remisión mayor al 60 por ciento para dolor, limitación, ruido y traba. El análisis multifactorial mostró asociación significativa entre tratamientos oclusal, kinesiológico y psicológico y remisión de traba (p=0.05) y entre terapia miofuncional y remisión de limitación (p=0.01). En esta muestra de pacientes pediátricos, el abordaje interdisciplinario resultó una alterantiva efectiva para mejorar los signos y síntomas de TTM con compromiso muscular.

Nitric oxide at the crossroad of immunoneuroendocrine interactions.

Nitric oxide (NO) was initially described as a mediator of endothelial relaxation, and now its participation is recognized in numerous physiological and pathological processes. It was demonstrated that lipopolysaccharide-stimulated corticotropin-releasing factor release involves NO production. Furthermore, it has been shown that interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, IL-6, and IL-2 can stimulate adrenocorticotropic hormone release from anterior pituitary via NO. Also, we found that NO released from hypothalamic NOergic neurons in response to norepinephrine diffuses to luteinizing hormone-releasing hormone (LHRH) neurons that activate cyclooxygenase and guanylate cyclase. This activation results in an increase in prostaglandin E2 and cyclic guanosine monophosphate, respectively, which leads to the exocytosis of LHRH granules. During pathological conditions, such as manganese intoxication, NO production is increased, leading to an increase in LHRH secretion that can advance puberty. In another study we demonstrated that NO reduces oxytocin as well as vasopressin secretion from the posterior pituitary, suggesting it has a modulatory role during dehydration. An increase in NO synthase (NOS) activity and protein in the hippocampus and cerebellum was found in offspring of rats that were subjected to prenatal stress, and this was correlated with behavioral changes in adults. Also NO participates in signal transduction pathways in peripheral tissue in physiological processes, such as in corticosterone release from the adrenal gland. Pathological conditions, such as tumors of the head and neck, that are treated with radiation are followed by xerostomy. In a rat model, radiation diminished NOS activity in the submandibulary gland, and this was followed by inhibition in salivary secretion. In summary, this review describes the wide participation of NO in the cross-talk between neuroendocrine and neuroimmune systems in physiological and pathological processes.

Acute effect of manganese on hypothalamic luteinizing hormone releasing hormone secretion in adult male rats: involvement of specific neurotransmitter systems.

Manganese chloride (MnCl2) is capable of stimulating luteinizing hormone releasing hormone (LHRH) secretion in adult male Sprague-Dawley rats through the activation of the hypothalamic nitric oxide/cyclic guanosine monophosphate (cGMP)/protein kinase G pathway. The present study aimed to determine the involvement of specific neurotransmitters involved in this action. Our results indicate that dopamine, but not glutamic acid and prostaglandins, mediates the MnCl2 stimulated secretion of LHRH from medial basal hypothalami in vitro, as well as increases the activity of nitric oxide synthase. Furthermore, a biphasic response was observed in that gamma aminobutyric acid (GABA) release was also increased, which acts to attenuate the MnCl2 action to stimulate LHRH secretion. Although it is clear that manganese (Mn+2) can acutely induce LHRH secretion in adult males, we suggest that the additional action of MnCl2 to release GABA, a LHRH inhibitor, may ultimately contribute to suppressed reproductive function observed in adult animals following exposure to high chromic levels of Mn+2.

IL-1 beta and PGE2 levels are increased in the saliva of children with Langerhans cell histiocytosis.

Langerhans cell histiocytosis (LCH) is a rare disorder mainly of children, whose pathogenesis is still unknown. Some studies have demonstrated that LCH lesions produce different cytokines abnormally that may be relevant to the pathogenesis of the disease. The purpose of this study was to investigate interleukin-1 beta (IL-1 beta) and prostaglandin E2 (PGE(2)) levels in saliva from children with different clinical subtypes of LCH. We studied 29 children with LCH: seven unifocal (Group I), seven multifocal (Group II), 15 multisystemic (Group III) and 12 healthy volunteers (Group IV). Salivary IL-1 beta and PGE(2) levels were significantly higher in LCH than in normal children. A multi-comparison test showed significantly (P < 0.001) higher levels of both IL-1 beta and PGE(2) in saliva from Group III compared with Groups II and I. A significant correlation (r = 0.05) between IL-1 beta and PGE(2) concentrations in saliva from each group was determined. Our findings demonstrated an association between high concentrations of salivary IL-1 beta and PGE(2) and advanced stages of the disease. This allows us to suggest that the abnormal amount of these factors in saliva may serve as a risk marker for disease progression.

Hipertrofia muscular: caso clínico / Musclular hypertrophy: a clinical case

Introducción. En este trabajo, presentamos el tratamiento interdisciplinario y seguimiento de una paciente adolescente de 15 años con hipertrofia del músculo maseterino del lado izquierdo, con limitación de la apertura bucal y dolor, de etiología parafuncional. Objetivos: realizar terapia de apoyo y el tratamiento fonoaudiológico y kinesiológica para eliminar la sintomatología dolorosa, disminuir la asimetría facial y recuperar la funcionalidad. Evaluar los valores de movilidad mandibular, durante todo el tratamiento como indicadores funcionales. Materiales y métodos: en una primera etapa, se indicó terapia de apoyo por medio de la aplicación de calor húmedo local con fomentos y buches calientes y analgésicos cada 8 hs. El tratamiento fonoaudiológico realizado incluye ejercicios de tonificación, linguales de masticación, posturales y de movimiento mandibular y además, masajes maseterinos como terapia kinesiológica. En ejes de coordenadas en milímetros en función del tiempo, se graficaron los valores obtenidos de apertura máxima confortable, apertura máxima forzada, protrusión y lateralidades.

Hipertrofia muscular: caso clínico / Musclular hypertrophy: a clinical case

Introducción. En este trabajo, presentamos el tratamiento interdisciplinario y seguimiento de una paciente adolescente de 15 años con hipertrofia del músculo maseterino del lado izquierdo, con limitación de la apertura bucal y dolor, de etiología parafuncional. Objetivos: realizar terapia de apoyo y el tratamiento fonoaudiológico y kinesiológica para eliminar la sintomatología dolorosa, disminuir la asimetría facial y recuperar la funcionalidad. Evaluar los valores de movilidad mandibular, durante todo el tratamiento como indicadores funcionales. Materiales y métodos: en una primera etapa, se indicó terapia de apoyo por medio de la aplicación de calor húmedo local con fomentos y buches calientes y analgésicos cada 8 hs. El tratamiento fonoaudiológico realizado incluye ejercicios de tonificación, linguales de masticación, posturales y de movimiento mandibular y además, masajes maseterinos como terapia kinesiológica. En ejes de coordenadas en milímetros en función del tiempo, se graficaron los valores obtenidos de apertura máxima confortable, apertura máxima forzada, protrusión y lateralidades.(AU)

Inhibition of salivary secretion by activation of cannabinoid receptors.

It is known that marijuana use decreases saliva secretion. Therefore, we hypothesized that cannabinoid receptors (CBs) are located in salivary glands to mediate that effect. In these experiments, we used the submandibular gland (SMG) of male rats, which is one of the major salivary glands. Mammalian tissues contain at least two types of CBs, CB1 and CB2, mainly located in the nervous system and peripheral tissues, respectively. Both receptors are coupled to Gi protein and respond by inhibiting the activity of adenylyl cyclase. We demonstrated that both CB1 and CB2 are present in the SMG, each showing specific localizations. The best-known endocannabinoid is anandamide (AEA), which binds with high affinity to CB1 and CB2. We showed that AEA markedly reduced forskolin-induced increase of cAMP content in vitro. This effect was blocked by AM251 and AM630 (CB1 and CB2 antagonists, respectively), indicating that both receptors are implicated in SMG physiology. In addition, we showed that AEA injected intraglandularly to anesthetized rats inhibited norepinephrine (NE)- and methacholine (MC)-stimulated saliva secretion in vivo and that both AM251 or AM630 prevented the inhibitory action of AEA. Also, the intraglandular injection of AM251 increased saliva secretion induced by lower doses of NE or MC. This increase was synergized after coinjection with AM630. Therefore, we concluded that AEA decreases saliva secretion in the SMG acting through CB1 and CB2 receptors.

Decrease in salivary secretion by radiation mediated by nitric oxide and prostaglandins.

OBJECTIVE: In the present work, we evaluated the effect of exposing the submandibular glands (SMG) to radiation, studying different functional parameters such as salivary secretion, nitric oxide (NO) production, reactive oxygen species formation, prostaglandin (PGE) content and apoptosis. METHODS: We irradiated rats in the head and neck region with a single dose of gamma-ray radiation of 15 Gy. Two hours after radiation, we measured norepinephrine-induced salivary secretion. After that, the SMG were dissected, and in this tissue, we measured the activity of NO synthase (NOS), the PGE content, the amount of reactive oxygen species, apoptotic cells and mitochondrial inducible NOS (iNOS) expression. RESULTS: We found that radiation decreased salivary secretion when 10 and 30 microg/kg of norepinephrine was administered via the right femoral vein. We observed that iNOS activity was reduced and PGE content increased after radiation in SMG, indicating that NO and PGEs may participate in salivary secretion. The expression of mitochondrial NOS was increased after radiation leading to the formation of large amounts of NO that acts as a proapoptotic signal. In fact, we observed an augmentation in apoptotic cells. In this study, we also observed an increase in lipid peroxidation induced by radiation that may contribute to tissue damage. CONCLUSIONS: Our results indicate that radiation induced a decrease in salivary secretion and SMG iNOS activity, meanwhile the PGE content, the lipid peroxidation and apoptosis increased in the tissue. These modifications decrease salivary secretion.

The rapid release of corticosterone from the adrenal induced by ACTH is mediated by nitric oxide acting by prostaglandin E2.

The adrenal cortex is a major stress organ in mammals that reacts rapidly to a multitude of external and internal stressors. Adrenocorticotropin (ACTH) is the main stimulator of the adrenal cortex, activating corticosteroid synthesis and secretion. We evaluated the mechanism of action of ACTH on adrenals of male rats, preserving the architecture of the gland in vitro. We demonstrated that both sodium nitroprusside (NP), a nitric oxide (NO) donor, and ACTH stimulate corticosterone release. NO mediated the acute response to ACTH because Nomega-nitro-l-arginine methyl ester, a NO synthase inhibitor, and hemoglobin, a NO scavenger, blocked the stimulation of corticosterone release induced by ACTH. NP stimulated prostaglandin E release, which in turn stimulated corticosterone release from the adrenal. Additionally, indomethacin, which inhibits cyclooxygenase, and thereby, prostaglandin release, prevented corticosterone release from the adrenal induced by both NP and ACTH, demonstrating that prostaglandins mediate acute corticosterone release. Corticosterone content in adrenals after incubation with ACTH or NP was lower than in control glands, indicating that any de novo synthesis of corticosterone during this period was not sufficient to keep up with the release of the stored hormone. The release induced by ACTH or NP depleted the corticosterone content in the adrenal by approximately 40% compared with the content of glands incubated in buffer. The mechanism of rapid release is as follows: NO produced by NO synthase activation by ACTH activates cyclooxygenase, which generates PGE(2), which in turn releases corticosterone stored in microvesicles and other organelles.