We suppose

that this fact might be due to inhaled adminis

We suppose

that this fact might be due to inhaled administration of the corticosteroids having a topic anti-inflammatory effect, promoting lower systemic concentrations of the drug. Even if some adverse effects were expected by the corticosteroid administration, they are less pronounced when compared to other ways such as injections or via gastric administration.27 This is the specific reason why we used topical administration. Additionally, the specific research hypothesis was related to the possible adverse effects in the periodontium when corticosteroids are inhaled such as in asthma treatments, for example. There is an increase production of TNF-α in G2 as compared to G1. This finding was in agreement with the literature.28 This was probably due to the presence of periodontal inflammation, which reinforces that UK-371804 order periodontal disease is a systemic problem.29 and 30 No effect Alectinib molecular weight in TNF-α production was observed when G3 and G4 are analysed. This also strengthens the idea that inhaled steroids have little systemic anti-inflammatory effect.31 On the other hand, the literature has shown that budesonide has a high level of topical anti-inflammatory activity.32 Nevertheless, this topical glucocorticoid was not able to modulate the periodontal breakdown. The results of the present study can contribute for better understanding of the pathogenesis of alveolar bone loss. Data suggest that inhaled corticosteroid does not significantly

interfere in the mechanisms of bone loss. This can be interpreted that budesonide does not have a promising effect as a modulator of host response to future studies such Fenbendazole as other anti-inflammatory drugs.7, 33 and 34 Additional studies evaluating effects of budesonide in oral mucosa are encouraged. We concluded that different concentrations of inhaled budesonide do not interfere in the ligature-induced alveolar bone loss in Wistar rats. Additionally, no effect of budesonide was observed in TNF-α production. We would like to thank Lorena F. Orlandini for helping us with the animals. Funding: The present study was partially funded by PROCAD (Academic Cooperation Project)

Grant number NF2341 (08/2008). Competing interest: None declared. Ethical approval: The research protocol was approved (protocol number 2008128, Sep 24 2009) by the Ethical and Research Committee of the Federal University of Rio Grande do Sul. “
“The lateral parabrachial nucleus (LPBN), a pontine structure located dorsolaterally to the superior cerebellar peduncle (SCP), is an important hindbrain area involved in the inhibitory control of ingestive behaviour.1 and 2 The LPBN might also regulate central responses produced by systemic immune stimuli.3 and 4 It has been demonstrated that the LPBN plays a critical role in cytokine-induced Fos expression in the central nucleus of the amygdala (CeA), bed nucleus of the stria terminalis (BNST) and ventrolateral medulla (VLM) neurons.

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