CRITERIA ADOPTED BY DENTISTS TO INDICATE THE EXTRACTION OF PERIODONTALLY INVOLVED TEETH

When dealing with patients with periodontal disease of variable severities, dentists must often choose between treating and restoring the involved tooth or indicating its extraction. Different criteria have been adopted in this decision-making process. The purpose of this study was to evaluate the criteria adopted by dentists to indicate the extraction of teeth with periodontitis. Dentists were interviewed at their private practices in three cities of the state of Rio Grande do Sul, Brazil. The evaluated criteria included severity of attachment loss, tooth mobility, furcation involvement, prosthetic planning, periodontal-endodontic lesion, possible systemic involvement due to the presence of periodontitis, referral to a periodontist for evaluation, radiographic bone loss greater than 50%, presence of extensive caries, socio-economic and cultural status of the patient, among others. The most often adopted criteria to indicate the extraction of periodontally affected teeth were the presence of mobility (37.5%), severity of attachment loss (24.3%) and radiographic bone loss greater than 50% (21.2%). The results of the present study demonstrated the difficulties faced by dentists to indicate the extraction of teeth with severe attachment loss, in addition to the establishment of an adequate prognosis. Aspects associated with the past disease were still the most often reported to indicate the extraction of teeth for periodontal reasons.     

Sequential Role of Hippocampus and Amygdala, Entorhinal Cortex and Parietal Cortex in Formation and Retrieval of Memory for Inhibitory Avoidance in Rats

The hippocampus and amygdala, the entorhinal cortex and the parietal cortex participate, in that sequence, both in the formation and in the expression of memory for a step-down inhibitory avoidance task in rats. Bilateral infusion of AP5 or muscimol caused retrograde amnesia when given O min after training into both hippocampus and amygdala, when given or 180 min after training into the entorhinal cortex, or when given 180 min after training into the parietal cortex. Therefore, memory formation requires the sequential and integrated activity of all these areas mediated by glutamate NMDA receptors in each case. Pre-test administration of CNQX 1 day after training into hippocampus and amygdala, 1 or 31 days after training in entorhinal cortex, or 1, 31 or 60 days after training in the parietal cortex temporarily blocked retention test performance. Therefore, 1 day after training, all these brain structures are necessary for retrieval; 1 month later, the hippocampus and amygdala are no longer necessary for retrieval but the entorhinal and parietal cortex still are; and 60 days after training only the parietal cortex is needed. In all cases the mechanisms of retrieval require intact glutamate AMPA receptors.     

Impairment of brain redox homeostasis caused by the major metabolites accumulating in hyperornithinemia–hyperammonemia–homocitrullinuria syndrome in vivo

Ornithine, ammonia and homocitrulline are the major metabolites accumulating in hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, a genetic disorder characterized by neurological regression whose pathogenesis is still not understood. The present work investigated the in vivo effects of intracerebroventricular administration of ornithine and homocitrulline in the presence or absence of hyperammonemia induced by intraperitoneal urease treatment on a large spectrum of oxidative stress parameters in cerebral cortex from young rats in order to better understand the role of these metabolites on brain damage. Ornithine increased thiobarbituric acid-reactive substances (TBA-RS) levels and carbonyl formation and decreased total antioxidant status (TAS) levels. We also observed that the combination of hyperammonemia with ornithine resulted in significant decreases of sulfhydryl levels, reduced glutathione (GSH) concentrations and the activities of catalase (CAT) and glutathione peroxidase (GPx), highlighting a synergistic effect of ornithine and ammonia. Furthermore, homocitrulline caused increases of TBA-RS values and carbonyl formation, as well as decreases of GSH concentrations and GPx activity. Hcit with hyperammonemia (urease treatment) decreased TAS and CAT activity. We also showed that urease treatment per se was able to enhance TBA-RS levels. Finally, nitric oxide production was not altered by Orn and Hcit alone or in combination with hyperammonemia. Our data indicate that the major metabolites accumulating in hyperornithinemia-hyperammonemia-homocitrullinuria syndrome provoke lipid and protein oxidative damage and a reduction of the antioxidant defenses in the brain. Therefore, it is presumed that oxidative stress may represent a relevant pathomechanism involved in the brain damage found in patients affected by this disease.     

Glycine Intracerebroventricular Administration Disrupts Mitochondrial Energy Homeostasis in Cerebral Cortex and Striatum of Young Rats

High tissue levels of glycine (GLY) are the biochemical hallmark of nonketotic hyperglycinemia (NKH), an inherited metabolic disease clinically characterized by severe neurological symptoms and brain abnormalities. Considering that the mechanisms underlying the neuropathology of this disease are not fully established, the present work investigated the in vivo effects of intracerebroventricular administration of GLY on important parameters of energy metabolism in cerebral cortex and striatum from young rats. Our results show that GLY reduced CO₂ production using glucose as substrate and inhibited the activities of citrate synthase and isocitrate dehydrogenase in striatum, whereas no alterations of these parameters were verified in cerebral cortex 30 min after GLY injection. We also observed that GLY diminished the activities of complex IV in cerebral cortex and complex I–III in striatum at 30 min and inhibited complex I–III activity in striatum at 24 h after its injection. Furthermore, GLY reduced the activity of total and mitochondrial creatine kinase in both brain structures 30 min and 24 h after its administration. In contrast, the activity of Na⁺, K⁺-ATPase was not altered by GLY. Finally, the antioxidants N-acetylcysteine and creatine, and the NMDA receptor antagonist MK-801 attenuated or fully prevented the inhibitory effects of GLY on creatine kinase and respiratory complexes in cerebral cortex and striatum. Our data indicate that crucial pathways for energy production and intracellular energy transfer are severely compromised by GLY. It is proposed that bioenergetic impairment induced by GLY in vivo may contribute to the neurological dysfunction found in patients affected by NKH.     

Laparoscopic Heller Myotomy Can Be Used As Primary Therapy for Esophageal Achalasia Regardless of Age

Introduction

Laparoscopic Heller-Dor surgery is the current treatment of choice for patients with esophageal achalasia, but elderly patients are generally referred for less invasive treatments (pneumatic dilations or botulinum toxin injections).

Aim

To assess the effect of age on the surgical outcome of patients receiving laparoscopic Heller-Dor as primary treatment.

Methods

Demographic and clinical findings were prospectively collected on patients undergoing laparoscopic Heller-Dor from 1992 to 2012. Patients were classified in three age brackets: group A (≤45 years), group B (45–70), and group C (≥70). Treatment was defined as a failure if the postoperative symptom score was >10th percentile of the preoperative score (i.e., >8). We consecutively performed the Heller-Dor in 571 achalasia patients, 305 (53.4 %) in group A, 226 (39.6 %) in group B, and 40 (7 %) in group C.

Results

The mortality was nil; the conversion and morbidity rates were both 1.1 %. Group C patients had higher preoperative symptom scores (p?=?0.02), while the symptom duration was similar in all three groups. Mucosal tears occurred in 17 patients (3 %): 6 (2 %) in group A, 8 (3.5 %) in group B, and 3 (7.5 %) in group C (p?=?0.09). The postoperative hospital stay was slightly longer for group C (p?=?0.06).

Discussion

The treatment failure rate was quite similar: 31 failures in group A (10.1 %), 19 in group B (8.4 %), and 3 in group C (7.5 %; p?=?0.80). These failures were seen more in manometric pattern III (22.2 %, p?=?0.002). Laparoscopic Heller-Dor can be used as the first therapeutic approach to achalasia even in elderly patients with an acceptable surgical risk.     

Pristanic Acid Provokes Lipid,Protein, and DNA Oxidative Damage and Reduces the Antioxidant Defenses in Cerebellum of Young Rats

Zellweger syndrome (ZS) and some peroxisomal diseases are severe inherited disorders mainly characterized by neurological symptoms and cerebellum abnormalities, whose pathogenesis is poorly understood. Biochemically, these diseases are mainly characterized by accumulation of pristanic acid (Prist) and other fatty acids in the brain and other tissues. In this work, we evaluated the in vitro influence of Prist on redox homeostasis by measuring lipid, protein, and DNA damage, as well as the antioxidant defenses and the activities of aconitase and α-ketoglutarate dehydrogenase in cerebellum of 30-day-old rats. The effect of Prist on DNA damage was also evaluated in blood of these animals. Some parameters were also evaluated in cerebellum from neonatal rats and in cerebellum neuronal cultures. Prist significantly increased malondialdehyde (MDA) levels and carbonyl formation and reduced sulfhydryl content and glutathione (GSH) concentrations in cerebellum of young rats. It also caused DNA strand damage in cerebellum and induced a high micronuclei frequency in blood. On the other hand, this fatty acid significantly reduced α-ketoglutarate dehydrogenase and aconitase activities in rat cerebellum. We also verified that Prist-induced increase of MDA levels was totally prevented by melatonin and attenuated by α-tocopherol but not by the nitric oxide synthase inhibitor N^ω-nitro-l-arginine methyl ester, indicating the involvement of reactive oxygen species in this effect. Cerebellum from neonate rats also showed marked alterations of redox homeostasis, including an increase of MDA levels and a decrease of sulfhydryl content and GSH concentrations elicited by Prist. Finally, Prist provoked an increase of dichlorofluorescein (DCFH) oxidation in cerebellum-cultivated neurons. Our present data indicate that Prist compromises redox homeostasis in rat cerebellum and blood and inhibits critical enzymes of the citric acid cycle that are susceptible to free radical attack. The present findings may contribute to clarify the pathogenesis of the cerebellar alterations observed in patients affected by ZS and some peroxisomal disorders in which Prist is accumulated.