ABSTRACT
The purpose of this report is to describe a peripheral tumor on the mandibular alveolar ridge of a seven-month-old Caucasian boy, consisting of ectomesencymal odontogenic tissues, in particular osteodentin and cementum-like material, in a cellular or loose vascular connective tissue stroma. This case may be considered either a peripheral odontogenic hamartoma or a peripheral odontoma.
Subject(s)
Calcinosis/diagnosis , Connective Tissue/pathology , Dental Cementum/pathology , Dental Enamel/pathology , Hamartoma/diagnosis , Mandibular Neoplasms/diagnosis , Odontoma/diagnosis , Calcinosis/pathology , Calcinosis/surgery , Diagnosis, Differential , Hamartoma/pathology , Hamartoma/surgery , Humans , Infant , Male , Mandibular Neoplasms/pathology , Mandibular Neoplasms/surgery , Odontoma/pathology , Odontoma/surgeryABSTRACT
PURPOSE OF REVIEW: Children with autism often present a challenge to the anesthesiologist. This review summarizes the current experiences and recommendations for the perioperative management of this unique group of patients. RECENT FINDINGS: Autism is the fastest growing neurodevelopmental disorder in the world. Increased recognition and public awareness of the disease is driven largely by the advances in research. A large body of evidence exists that identifies the role of genetic, environmental, biological, and developmental factors in the origin of autism. The anesthesia literature consists mostly of case reports. Recent publications are reporting management strategies and evaluation of this patient population's perioperative experiences. SUMMARY: Patients with autism spectrum disorder are a heterogeneous group and often need general anesthesia for different procedures and studies. Familiarity with each patient's behavioral specifics and efforts to alleviate stress is of paramount importance for a smooth perioperative course with minimal adverse events.
Subject(s)
Anesthesia, General/methods , Anesthesiologists/psychology , Autism Spectrum Disorder/complications , Hypnotics and Sedatives/administration & dosage , Perioperative Care/methods , Physician-Patient Relations , Premedication/methods , Anesthesia Recovery Period , Anesthesia, General/adverse effects , Autism Spectrum Disorder/epidemiology , Autism Spectrum Disorder/etiology , Autism Spectrum Disorder/surgery , Child , Comorbidity , Diagnostic Techniques and Procedures/adverse effects , Diagnostic Techniques and Procedures/psychology , Humans , Preoperative Period , Psychological TechniquesABSTRACT
Traditionally, raisins have been thought to promote dental caries due to their suspected "stickiness" and sugar content. Current research identifies some evidence contrary to traditional thought, suggesting that raisins may not contribute to dental caries. This article reviews new findings with regards to raisins and the 3 conditions that are thought to contribute to the formation of dental caries; low oral pH, adherence of food to teeth, and biofilm (bacterial) behavior. The studies reviewed concluded that raisin: consumption alone does not drop oral pH below the threshold that contributes to enamel dissolution, do not remain on the teeth longer than other foods, and contain a variety of antioxidants that inhibit Streptococcus Mutans, bacteria that is a primary cause of dental caries. Further research in this area should be considered.
Subject(s)
Food, Preserved , Fruit , Oral Health , Vitis , Adenosine Triphosphate/antagonists & inhibitors , Adenosine Triphosphate/metabolism , Adhesiveness , Antioxidants/analysis , Antioxidants/therapeutic use , Biofilms/growth & development , Cariostatic Agents/analysis , Cariostatic Agents/therapeutic use , Dental Caries/etiology , Dental Caries/metabolism , Dental Caries/microbiology , Dental Caries/prevention & control , Dental Enamel/chemistry , Dental Enamel/microbiology , Food, Preserved/adverse effects , Food, Preserved/analysis , Fruit/adverse effects , Fruit/chemistry , Humans , Hydrogen-Ion Concentration , Streptococcus mutans/physiology , Vitis/adverse effects , Vitis/chemistryABSTRACT
Previous studies have shown that nitrous oxide (N(2)O)-induced antinociception is sensitive to antagonism by blockade of opioid receptors and also by inhibition of nitric oxide (NO) production. The present study was conducted to determine whether these occur within the same brain site. Mice were stereotaxically implanted with microinjection cannulae in the periaqueductal gray (PAG) area of the midbrain. In saline-pretreated mice, exposure to 70% N(2)O resulted in a concentration-dependent antinociceptive effect in the mouse abdominal constriction test. Pretreatment with an opioid antagonist in the PAG significantly antagonized the antinociceptive effect. Pretreatment with an inhibitor of NO production in the PAG also significantly antagonized the antinociceptive effect. These findings suggest that N(2)O acts in the PAG via an NO-dependent, opioid receptor-mediated mechanism to induce antinociception.
Subject(s)
Analgesics, Non-Narcotic/pharmacology , Mesencephalon/metabolism , Nitric Oxide/physiology , Nitrous Oxide/pharmacology , Periaqueductal Gray/metabolism , Receptors, Opioid/drug effects , Animals , Dose-Response Relationship, Drug , Male , Mesencephalon/drug effects , Mice , Microinjections , Naltrexone/analogs & derivatives , Naltrexone/pharmacology , Pain Measurement/drug effects , Periaqueductal Gray/drug effectsABSTRACT
Nitrous oxide (N(2)O) has been used for well over 150 years in clinical dentistry for its analgesic and anxiolytic properties. This small and simple inorganic chemical molecule has indisputable effects of analgesia, anxiolysis, and anesthesia that are of great clinical interest. Recent studies have helped to clarify the analgesic mechanisms of N(2)O, but the mechanisms involved in its anxiolytic and anesthetic actions remain less clear. Findings to date indicate that the analgesic effect of N(2)O is opioid in nature, and, like morphine, may involve a myriad of neuromodulators in the spinal cord. The anxiolytic effect of N(2)O, on the other hand, resembles that of benzodiazepines and may be initiated at selected subunits of the gamma-aminobutyric acid type A (GABA(A)) receptor. Similarly, the anesthetic effect of N(2)O may involve actions at GABA(A) receptors and possibly at N-methyl-D-aspartate receptors as well. This article reviews the latest information on the proposed modes of action for these clinical effects of N(2)O.
Subject(s)
Analgesics/pharmacology , Anesthetics, Local/pharmacology , Anti-Anxiety Agents/pharmacology , Nitrous Oxide/pharmacology , GABA Modulators/pharmacology , Humans , Neurotransmitter Agents/pharmacology , Receptors, GABA-A/drug effects , Receptors, N-Methyl-D-Aspartate/drug effectsABSTRACT
RATIONALE: In earlier studies, we have shown that nitrous oxide (N2O)-induced behavioral effects in rats and mice are mediated by benzodiazepine receptors. OBJECTIVES: This two-part study was conducted in order to investigate the possible role of serotonin (5-HT) in the behavioral effects of N2O by clarifying its effects on regional brain concentrations of 5-HT and assessing the influence of 5-HT antagonist and reuptake inhibiting drugs on the anxiolytic-like behavioral effect of N2O. METHODS: In experiment A, male, 150-200 g Sprague-Dawley rats were killed following a 15-min exposure to room air or 70% N2O. The frontal cortex, hippocampus, corpus striatum and hypothalamus were dissected out and analyzed by HPLC with electrochemical detection for content of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA); dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) were also measured. In experiment B, male 18-22 g NIH Swiss mice were pretreated with the 5-HT2 antagonist cinanserin, the 5-HT3 antagonist LY-278,584, the 5-HT reuptake inhibitor fluoxetine or saline and tested in the light/dark exploration test under 70% N2O 30 min after pretreatment. RESULTS: In experiment A, N2O produced differential effects on 5-HT neurons in distinct brain areas. There was increased 5-HT turnover in the hypothalamus, decreased turnover in the frontal cortex but no changes in either hippocampus or corpus striatum. By comparison, dopamine turnover in these brain regions was unaltered by N2O exposure. In experiment B, pretreatment with neither cinanserin, LY-278,584 nor fluoxetine had any appreciable effect on the N2O-induced increase in time spent in the light compartment. Only cinanserin significantly reduced the N2O-induced increase in transitions. CONCLUSIONS: While neurochemical results suggest an effect of N2O on brain 5-HT function, there was no effect of 5-HT2 or 5-HT3 antagonists or 5-HT reuptake inhibitor on N2O-induced anxiolytic-like behavior.
