Fístula cutánea de origen Dental / Cutaneous fistula of dental origin

Muchas veces las fístulas cutáneas orofaciales son diagnosticadas como lesiones dermatológicas sin tener en cuenta su relación con una patología dental, prescribiéndose tratamientos erróneos e innecesarios para el paciente, que no ve resuelto su problema, y retrasando el tratamiento endodóntico que eliminará la infección dental con el consiguiente cierre y cicatrización de la fístula extraoral. Es por tanto necesario, siempre que aparezca este tipo de lesiones, buscar una causa dental y hacer un diagnóstico temprano por parte de los especialistas que están tratando al paciente para remitirlo al odontoestomatólogo y que éste realice el tratamiento de conductos radiculares (AU)

Orofacial cutaneous fistulas are often misdiagnosed as dermatological lesions without taking into account their relationship with dental disease. This leads to mistaken and unnecessary treatment for the patient., whose problem remains unresolved, and delays the endodontic therapy which will eliminate the dental infection and subsequent closure and scarring of the extraoral fistula. Accordingly, whenever this type of fistula occurs the physician should look for a dental cause and thus make an early diagnosis and refer the patient to his/her dentist so that treatment of the pulp canals can be performed (AU)

Protective effect of new nitrosothiols on the early inflammatory response to kidney ischemia/reperfusion and transplantation in rats.

Renal ischemia/reperfusion (I/R) is characterized by severe inflammatory damage. We assessed the effect of administrating recently developed nitrosothiol compounds acting as nitric oxide (NO) donors on the production of cytokines and other markers of acute inflammatory reaction in an experimental model of warm (I/R), and in a model of cold ischemia and transplant in rats. Warm ischemia was achieved by ligation of left renal pedicle for 60 min, followed by contralateral nephrectomy. NO-donors LA-803, LA-807, LA-810 were administered i.v. (1.8 micromol/kg) during 30 min before reperfusion. Cold ischemia was achieved by preservating the kidney for 24 h in Euro Collins and grafting it in consanguineous Fisher 344/Ico rats. LA-803 was administered in the preservation fluid and in the recipient rat. Reperfusion time was 4 h in warm ischemia and 3 h in cold ischemia + transplantation. Administration of LA-803, LA-807 and, in a lower proportion, LA-810 prevented from the enhanced production of tumor necrosis factor (TNF), interferon-gamma (IFN-gamma), and interleukin-1beta (IL-1beta), the decrease in interleukin-6 (IL-6) and interleukin-10 (IL-10), the increase in tissue level of superoxide anion (SOA) and superoxide dismutase (SOD), and the increase in neutrophil infiltration induced by warm I/R. Treatment with LA-803 in animals with renal transplantation after cold ischemia was also associated with reduced plasma levels of TNF, IFN-gamma, and IL-1beta, increased plasma levels of IL-6 and IL-10, reduced renal levels of SOA and SOD, and reduced neutrophil infiltration. These data demonstrate that systemic administration of new NO-donors with nitrosothiol structure diminished inflammatory responses in a kidney subjected to warm I/R or cold ischemia and transplantation.

Aetiology, classification and pathogenesis of pulp and periapical disease.

At present, the majority of the treatments that are performed in the clinic are due to disease entities involving the dental pulp and periapex. Dental pulp is a richly vascularized and innervated tissue, enclosed by surrounding tissues that are incapable of expanding, such as dentin. It has terminal blood flow and small-gauge circulatory access the periapex. All of these characteristics severely constrain the defensive capacity of the pulp tissue when faced with the different aggressions it may be subjected to. Pulp tissue can also be affected by a retrograde infection, arising from the secondary canaliculi, from the periodontal ligament or from the apex during the course of periodontitis. Due to the fact that periapical disease is almost inevitably preceded by pulp disease, we shall begin by describing the causes of pulp disease and will then proceed to a discussion of the causes of periapical disease. The course of illness and classification of these pathological entities will depend on the aetiology involved. We will analyse pulp necrosis and pulp degeneration that are capable of triggering reversible apical periodontitis or irreversible apical periodontitis.

Etiología, clasificación y patogenia de la patología pulpar y periapical / Aetiology, classification and pathogenesis of pulp and periapical disease

En la actualidad, gran parte de los tratamientos que se realizan en la clínica son debidos a patologías que afectan a la pulpa y al periápice. La pulpa es un tejido ricamente vascularizado e inervado, delimitado por un entorno inextensible como es la dentina, con una circulación sanguínea terminal y con una zona de acceso circulatorio –periápice– de pequeño calibre. Todo ello, hace que la capacidad defensiva del tejido pulpar sea muy limitada ante las diversas agresiones que pueda sufrir. El tejido pulpar también puede ser afectado por una infección retrógrada (1), a partir de los canalículos secundarios, desde el ligamento periodontal o desde el ápice durante un proceso de periodontitis. Debido a que la patología periapical va casi siempre precedida de una afectación de la pulpa, describiremos en primer lugar las causas (2) de enfermedad pulpar y a continuación las causas de la patología periapical. De dicha etiología dependerá la evolución y la clasificación de estas patologías. Analizaremos la necrosis pulpar y la degeneración pulpar que pueden desencadenar una periodontitis apical reversible o una periodontitis apical irreversible (AU)

At present, the majority of the treatments that are performed in the clinic are due to disease entities involving the dental pulp and periapex. Dental pulp is a richly vascularized and innervated tissue, enclosed by surrounding tissues that are incapable of expanding, such as dentin. It has terminal blood flow and small-gauge circulatory access – the periapex. All of these characteristics severely constrain the defensive capacity of the pulp tissue when faced with the different aggressions it may be subjected to. Pulp tissue can also be affected by a retrograde infection (1), arising from the secondary canaliculi, from the periodontal ligament or from the apex during the course of periodontitis. Due to the fact that periapical disease is almost inevitably preceded by pulp disease, we shall begin by describing the causes (2) of pulp disease and will then proceed to a discussion of the causes of periapical disease. The course of illness and classification of these pathological entities will depend on the aetiology involved. We will analyse pulp necrosis and pulp degeneration that are capable of triggering reversible apical periodontitis or irreversible apical periodontitis (AU)