Objectives: Bone resorption associated to chronic diseases, such as arthritis and periodontitis, results from exacerbated immuno-inflammatory host response that leads to tissue breakdown. The significance of opioid pathways as endogenous modulators of inflammatory events has already been described. Thus, the aim of this work is to determine whether some of the main three opioid receptors are endogenously activated to prevent bone loss during experimentally-induced alveolar bone resorption.
View Article and Find Full Text PDFAlthough, the excellent level of success of titanium surfaces is based on the literature, there are some biological challenges such as unfavorable metabolic conditions or regions of poor bone quality where greater surface bioactivity is desired. Seeking better performance, we hypothesized that silica-based coating via sol-gel route with immersion in potassium hydroxide basic solution induces acceleration of bone mineralization. This in vitro experimental study coated titanium surfaces with bioactive glass synthesized by route sol-gel via hydrolysis and condensation of chemical alkoxide precursor, tetraethylorthosilicate (TEOS) and/or deposition of chemical compound potassium hydroxide (KOH) to accelerate bone apposition.
View Article and Find Full Text PDFAngiotensin II (Ang II) may be produced directly from angiotensinogen by tonin. Studies have demonstrated that Ang II and its metabolite Ang-(1-7) produce antinociception in pain animal models. The aim of the present study was to determine whether the transgenic mice that express rat tonin (TGM(rTon)) show altered nociceptive behavior and investigate the possible involvement of angiotensin metabolites.
View Article and Find Full Text PDFObjectives: The aim of this study was to determine whether Ca(2+)-activated Cl(-) channels (CaCCs) are involved in central antinociception induced by the activation of µ-, δ- and κ-opioid receptors.
Methods: The nociceptive threshold for thermal stimulation was measured using the tail-flick test in Swiss mice. The drugs were administered via the intracerebroventricular route.
Studies have demonstrated that the L-arginine/NO/cGMP pathway and the potassium and calcium channels are involved in the mechanisms underlying opioid receptor activation. As additional pathways may participate in the observed antinociceptive effects following opioid exposure, the aim of our study was to determine whether Ca(2+)-activated Cl(-) channels (CaCCs) are involved in peripheral antinociception induced by μ-, δ- and κ-opioid receptor activation. Hyperalgesia was induced by intraplantar injection of prostaglandin E(2) (PGE(2), 2 μg).
View Article and Find Full Text PDFObjective: The beneficial effects of kappa opioid agonist U-50,488 in preventing periodontal disease (PD) progression in rats have already been described, but its mechanism of action is unknown. The present study evaluated the expression of TNF-α, IL-6, IL-8 and IL-10 in the gingival tissues of rats with ligature-induced PD, treated with U-50,488. It also correlated the effects of this agonist with myeloperoxidase (MPO) activity and the presence of osteoclasts.
View Article and Find Full Text PDFAim: The aim of this study was to evaluate early detection of temporomandibular joint (TMJ) inflammatory changes based on 1-thio-beta-d-glucose radiolabeled with technetium-99m.
Method: The method applied a TMJ inflammation model in rats followed by radiopharmaceutical synthesis, intravenous administration of (99m)Tc-1-TG and kinetic scintigraphy imaging.
Results: Results show a significant difference of (99m)Tc-1-TG uptake between inflamed TMJ and the control joint.
The study aimed to evaluate the suitability of myeloperoxidase (MPO) content as a local indicator of chronic inflammation, using the periodontal disease model. Anesthetized adult male Holtzman rats had their second left maxilar molar tied by a thread for 11 days and were then killed. Blood samples and photographic images from histopathological inflamed and noninflamed (contralateral) neighboring gingivomucosal specimens were collected for cell counts and MPO level analysis.
View Article and Find Full Text PDFBackground And Purpose: It has been demonstrated that cannabinoids evoke the release of endogenous opioids to produce antinociception; however, no information exists regarding the participation of cannabinoids in the antinociceptive mechanisms of opioids. The aim of the present study was to determine whether endocannabinoids are involved in central antinociception induced by activation of mu-, delta- and kappa-opioid receptors.
Experimental Approach: Nociceptive threshold to thermal stimulation was measured according to the tail-flick test in Swiss mice.