naloxone and Maxillary-Diseases

The anti-inflammatory effects of exogenous opioid compounds have been demonstrated in several conditions. Nevertheless, the function of endogenous opioid peptides released by the host during inflammatory processes deserves further characterization. The aim of this study was to verify whether endogenous opioids are involved in the progression of the inflammatory alveolar bone loss induced by ligature in rats.. The experimental model of periodontal disease (PD) induced by ligature in rats was used throughout the study. A silk ligature was placed around the 2nd upper molar of male Holtzman rats, for 7 days. Rats received different doses of either the non-selective opioid antagonist naloxone or vehicle, locally into the afflicted gingival tissue, from the 3rd to the 5th day after ligature placement. In the 7th experimental day, rats were euthanized and their maxillae were collected for evaluation of alveolar bone and fiber attachment loss, presence of neutrophils (myeloperoxidase assay), osteoclast amount, and levels of cytokines IL-6, TNF-α, IL-8 and IL-10 in periodontal tissues.. Naloxone increased alveolar bone loss significantly, in a dose-dependent manner, in relation to vehicle-treated rats. In contrast, the opioid antagonist did not affect the loss of fiber attachment. The treatment with naloxone also induced a significant increase in myeloperoxidase levels, osteoclast number and cytokines in periodontal tissues of rats with ligature-induced PD.. Endogenous opioids protect the host from the progression of inflammatory alveolar bone loss that occurs in chronic periodontitis.

Topics: Alveolar Bone Loss; Animals; Cytokines; Gingiva; Male; Maxillary Diseases; Naloxone; Narcotic Antagonists; Opioid Peptides; Osteoclasts; Periodontal Diseases; Rats; Rats, Sprague-Dawley

A 21-year-old man with mitochondrial encephalomyopathy underwent surgery for removal of a maxillary cyst. During the induction of anesthesia, the patient fell into the state of apnea after intravenous administration of fentanyl 100 microgram. Trachea was successfully intubated followed by propofol 50 mg without any muscle relaxants. Anesthesia was maintained uneventfully under sevoflurane (1-2%), nitrous oxide (30%), and oxygen (70%). The respiratory depression lasted for about 120 minutes after administration of fentanyl, and was antagonized by naloxone 40 microgram. This case suggests that careful administration of fentanyl is mandatory in a patient with mitochondrial encephalomyopathy.

Topics: Adult; Anesthesia, General; Anesthetics, Intravenous; Cysts; Fentanyl; Humans; Infusions, Intravenous; Male; Maxillary Diseases; Mitochondrial Encephalomyopathies; Naloxone; Respiratory Insufficiency