Francisco Bruno Teixeira

Masticatory deficiency as a risk factor for cognitive dysfunction.

Several studies have demonstrated that chewing helps to maintain cognitive functions in brain regions including the hippocampus, a central nervous system (CNS) region vital for memory and learning. Epidemiological studies suggest that masticatory deficiency is associated with development of dementia, which is related to spatial memory deficits especially in older animals. The purpose of this paper is to review recent work on the effects of masticatory impairment on cognitive functions both in experimental animals and humans. We show that several mechanisms may be involved in the cognitive deficits associated with masticatory deficiency. The epidemiological data suggest a positive correlation between masticatory deficit and Alzheimers disease. It may be concluded that chewing has important implications for the mechanisms underlying certain cognitive abilities.

Chronic Ethanol Exposure during Adolescence in Rats Induces Motor Impairments and Cerebral Cortex Damage Associated with Oxidative Stress

Binge drinking is common among adolescents, and this type of ethanol exposure may lead to long-term nervous system damage. In the current study, we evaluated motor performance and tissue alterations in the cerebral cortex of rats subjected to intermittent intoxication with ethanol from adolescence to adulthood. Adolescent male Wistar rats (35 days old) were treated with distilled water or ethanol (6.5 g/kg/day, 22.5% w/v) during 55 days by gavage to complete 90 days of age. The open field, inclined plane and the rotarod tests were used to assess the spontaneous locomotor activity and motor coordination performance in adult animals. Following completion of behavioral tests, half of animals were submitted to immunohistochemical evaluation of NeuN (marker of neuronal bodies), GFAP (a marker of astrocytes) and Iba1 (microglia marker) in the cerebral cortex while the other half of the animals were subjected to analysis of oxidative stress markers by biochemical assays. Chronic ethanol intoxication in rats from adolescence to adulthood induced significant motor deficits including impaired spontaneous locomotion, coordination and muscle strength. These behavioral impairments were accompanied by marked changes in all cellular populations evaluated as well as increased levels of nitrite and lipid peroxidation in the cerebral cortex. These findings indicate that continuous ethanol intoxication from adolescence to adulthood is able to provide neurobehavioral and neurodegenerative damage to cerebral cortex.

Chronic ethanol exposure during adolescence through early adulthood in female rats induces emotional and memory deficits associated with morphological and molecular alterations in hippocampus

There is increasing evidence that heavy ethanol exposure in early life may produce long-lasting neurobehavioral consequences, since brain structural maturation continues until adolescence. It is well established that females are more susceptible to alcohol-induced neurotoxicity and that ethanol consumption is increasing among women, especially during adolescence. In the present study, we investigated whether chronic ethanol exposure during adolescence through early adulthood in female rats may induce hippocampal histological damage and neurobehavioral impairments. Female rats were treated with distilled water or ethanol (6.5 g/kg/day, 22.5% w/v) by gavage from the 35th–90th day of life. Ethanol-exposed animals displayed reduced exploration of the central area and increased number of fecal boluses in the open field test indicative of anxiogenic responses. Moreover, chronic high ethanol exposure during adolescence induced marked impairments on short-term memory of female rats addressed on social recognition and step-down inhibitory avoidance tasks. These neurobehavioral deficits induced by ethanol exposure during adolescence through early adulthood were accompanied by the reduction of hippocampal formation volume as well as the loss of neurons, astrocytes and microglia cells in the hippocampus. These results indicate that chronic high ethanol exposure during adolescence through early adulthood in female rats induces long-lasting emotional and memory deficits associated with morphological and molecular alterations in the hippocampus.

Evaluation of the Effects of Chronic Intoxication with Inorganic Mercury on Memory and Motor Control in Rats

The aims of this study were to evaluate whether chronic intoxication with mercury chloride (HgCl2), in a low concentration over a long time, can be deposited in the central nervous tissue and to determine if this exposure induces motor and cognitive impairments. Twenty animals were intoxicated for 45 days at a dose of 0.375 mg/kg/day. After this period, the animals underwent a battery of behavioral tests, in a sequence of open field, social recognition, elevated T maze and rotarod tests. They were then sacrificed, their brains collected and the motor cortex and hippocampus dissected for quantification of mercury deposited. This study demonstrates that long-term chronic HgCl2 intoxication in rats promotes functional damage. Exposure to HgCl2 induced anxiety-related responses, short- and long-term memory impairments and motor deficits. Additionally, HgCl2 accumulated in both the hippocampus and cortex of the brain with a higher affinity for the cortex.

Immunohistochemical changes and atrophy after chronic ethanol intoxication in rat salivary glands.

Alcoholism in humans is a chronic and progressive disease, characterized by loss of ethanol consumption control. Previous studies have reported that prolonged exposure to ethanol was responsible for alterations in glandular tissues of human and rodents. However, the interrelationship between ethanol and the glandular system is still the subject of numerous investigations, including the possible resistance of the submandibular gland (SG). In the present study, we investigated whether chronic ethanol exposure during adolescence may affect the parotid gland (PG) and SG in female rats. Female rats (n=16) were treated with distilled water or ethanol (dose of 6.5 g/kg/day, 22.5% w/v) through gavage for 55 days. Glands were collected, weighed and submitted to histological processing. Morphometric analysis was assessed by parenchymal and stromal area measurements. Smooth muscle actin (α-SMA), cytokeratin-19 (CK19) and apoptotic caspase-3 (CAS) were measured using ImageJ® software. Chronic ethanol administration did not alter the body weight of rats after treatment, although it increased glandular weight (p<0.001), reduced the parenchyma area (p<0.001) and decreased CK19 and α-SMA immunostainning in the PG. Besides, ethanol induced CK19 and CAS overexpression, and the occurrence of duct-like structures in SG. These results suggest that ethanol induces histological and morphometric changes in salivary glands of female rats intoxicated with ethanol during adolescence. Furthermore, the mechanism underlying these alterations needs to be investigated but may be not related to the inflammatory process.

Binge Drinking of Ethanol during Adolescence Induces Oxidative Damage and Morphological Changes in Salivary Glands of Female Rats

This study investigates morphological and biochemistry effects of binge ethanol consumption in parotid (PG) and submandibular (SG) salivary glands of rats from adolescence to adulthood. Female Wistar rats (n = 26) received ethanol at 3 g/kg/day (20% w/v) for 3 consecutive days/week from the 35th until the 62nd day of life. Animals were treated in two periods: 1 week (G1) and 4 weeks (G2), with a control (treated with distilled water) and an ethanol group to each period. In morphological analysis, morphometric and immunohistochemistry evaluation for smooth muscle actin (αSMA), cytokeratin-18 (CK-18), and vimentin (VIM) were made. Biochemical changes were analyzed by concentration of nitrites and levels of malondialdehyde (MDA). The difference between groups in each analysis was evaluated by Mann-Whitney U test or Students t-test (p ≤ 0.05). PG showed, at one week of ethanol exposure, lower CK-18 and α-SMA expression, as well as MDA levels. After four weeks, lower CK-18 and higher MDA levels were observed in PG exposed to ethanol, in comparison to control group. SG showed lower α-SMA expression after 1 and 4 weeks of ethanol exposure as well as higher MDA levels after 1 week. Ethanol binge consumption during adolescence promotes tissue and biochemical changes with only one-week binge in acinar and myoepithelial PG cells.

Morphology of the dentin structure of sloths Bradypus tridactylus: a light and scanning electron microscopy investigation.

The aim of this study was to describe the dentine morphology of sloths (Bradypus tridactylus). The sloth teeth were removed and prepared for light microscopy (LM) and scanning electron microscopy analyses (SEM). LM revealed two patterns of tubular dentins: an outer with dentinary tubules over the all tooth length and one in the inner part with larger diameter and more spaced tubules, when compared to those present in the outer dentine. These findings were confirmed by SEM, which revealed a tubular pattern in the outer dentine like in humans. The inner dentine displayed pared grouped tubules that were characterized as vascular channels. It can be concluded that this sloth species present two types of dentins: an inner dentin (ortodentin) and an outer dentin characterized as a vascular dentin. This suggests a partial evolutive/adaptive process of this dental tissue, as compared to other mammalian species.

Periodontitis and Alzheimer’s Disease: A Possible Comorbidity between Oral Chronic Inflammatory Condition and Neuroinflammation

Periodontitis is an oral chronic infection/inflammatory condition, identified as a source of mediators of inflammation into the blood circulation, which may contribute to exacerbate several diseases. There is increasing evidence that inflammation plays a key role in the pathophysiology of Alzheimer’s disease (AD). Although inflammation is present in both diseases, the exact mechanisms and crosslinks between periodontitis and AD are poorly understood. Therefore, this article aims to review possible comorbidity between periodontitis and AD. Here, the authors discuss the inflammatory aspects of periodontitis, how this oral condition produces a systemic inflammation and, finally, the contribution of this systemic inflammation for worsening neuroinflammation in the progression of AD.

Physical, Chemical, and Immunohistochemical Investigation of the Damage to Salivary Glands in a Model of Intoxication with Aluminium Citrate

Aluminum absorption leads to deposits in several tissues. In this study, we have investigated, to our knowledge for the first time, aluminum deposition in the salivary glands in addition to the resultant cellular changes in the parotid and submandibular salivary glands in a model of chronic intoxication with aluminum citrate in rats. Aluminum deposits were observed in the parotid and submandibular glands. Immunohistochemical evaluation of cytokeratin-18 revealed a decreased expression in the parotid gland with no changes in the submandibular gland. A decreased expression of α-smooth muscle actin was observed in the myoepithelial cells of both glands. The expression of metallothionein I and II (MT-I/II), a group of metal-binding proteins, which are useful indicators for detecting physiological responses to metal exposure, was higher in both glands. In conclusion, we have shown that at a certain time and quantity of dosage, aluminum citrate promotes aluminum deposition in the parotid and submandibular glands, leads to an increased expression of MT-I/II in both the glands, damages the cytoskeleton of the myoepithelial cells in both glands, and damages the cytoskeleton of the acinar/ductal cells of the parotid glands, with the submandibular glands showing resistance to the toxicity of the latter.

Avaliação comparativa da ultraestrutura e propriedades físicas do esmalte bovino, bubalino e humano

This study aimed to compare the morphology and physical properties of the enamel structure of bovine, buffalo and human teeth. Analysis of this tissue was performed by scanning electron microscopy, mineral composition, microhardness and surface roughness of enamel in 41 buffalo incisors (Bos taurus indicus), 41 bovine incisors (Pelorovis antiques), and 30 human permanent incisors. The results showed a significant similarity between the ultrastructure of enamel in these animal species and the one found in human samples. The chemical elements which presented higher concentration in bovine and buffalo enamel were: O,Ca and P, precisely those that form hydroxyapatite crystals - Ca10 (PO4)6 (OH)2. Knoop microhardness values showed no statistically significant differences between the three species. However, the surface roughness of buffalo enamel (2.16µm ±0.23) was significantly higher when compared with human (0.36µm ±0.05) and bovine teeth (0.41µm ±0.07). It is concluded that the characteristics and properties of bovine and buffalo enamel, as obtained from our analysis and testing, showed a similar morphology to that of humans. They showed a similar ultrastructural architecture, microhardness and mineral composition equivalent to the human dental tissue, becoming reference models for research.