Objectives The aim of this study was to clarify by histopathological examination the origin of oral membranous substances deposited on the palate, tongue, buccal mucosa and teeth. Background Several investigators have reported membranous substances deposited in the mouths of bedridden elderly persons requiring nursing care without oral intake. However, the precise nature and origin of the substances are poorly understood. Methods Sixty‐nine specimens were taken from the oral cavity of bedridden patients, that is, the palate, dorsum of the tongue, the cheek and teeth. Sections were stained with haematoxylin and eosin stain, alcian‐blue and periodic acid‐Schiff stain (AB‐PAS) and antibodies for pankeratin (AE1AE3) and leukocyte common antigen (LCA). Results All specimens showed a film‐like nature coloured from tan to white, accompanied by a mucous substance. Histologically, specimens of all sites had a similar feature of the combination of basophilic amorphous and eosinophilic lamellar features. The basophilic substance was positive for AB‐PAS, and PAS‐positive glycogen granules were also noted in the lamellar structure. Immunochemistry revealed various degrees of pankeratin positive substance and LCA‐positive inflammatory cell infiltration. Conclusion The oral membranous substance was composed of keratin and mucin with inflammation. These results suggest that the deposition of the oral membranous substance is a pathological condition or oral mucositis caused by dry mouth.
Background Antibiotic prophylaxis before invasive treatments, including dental extractions, is still recommended for patients at high risk of infective endocarditis. However, the risk from self-extraction of teeth in daily life of patients with intellectual disabilities is uncertain. Case presentation A 6-year-old patient with Ebstein’s anomaly developed cerebral abscess, which appeared associated with infective endocarditis of dental origin. Two weeks after self-extraction of his deciduous teeth, he began to experience pain in his ear and developed continuous fever, followed by vomiting, facial spasm, and a loss of consciousness. He was admitted into a hospital for 2 months, during which he received intravenously administered antibiotics and a drainage tube in his brain. Conclusions Deciduous teeth can be self-extracted before root resorption and natural shedding in patients with intellectual disabilities. When they are at high risk of infective endocarditis and frequently touch mobile deciduous teeth, it seems to be an option to extract the teeth early with antibiotic prophylaxis, rather than to wait natural fall.
Local anesthesia with vasoconstrictor-free mepivacaine is known to not evoke pressor responses. However, it is unknown whether baroreflex function and blood pressure (BP) fluctuations are preserved by using mepivacaine. We tested the hypothesis that mepivacaine reduces baroreflex sensitivity (BRS) without changing its operating point. Beat-by-beat BP, heart rate (HR), and muscle sympathetic nerve activity (MSNA) were measured upon injection of either saline (CNT) or 3% mepivacaine (MPV) in the apical regions of the premolars and around the mandibular foramen in 10 healthy young men [23±5 (SD) years]. Cardiac and sympathetic BRSs were assessed by bolus injections of sodium nitroprusside followed by phenylephrine HCl, and then determined from the slopes of regression lines between systolic BP and HR and between diastolic BP and MSNA, respectively. HR was significantly higher in MPV than CNT (P<0.05), while there were no significant differences in MSNA, the operating points, or BP fluctuations between MPV and CNT (all P>0.05). Moreover, neither cardiac nor sympathetic BRS in CNT were altered by MPV (−0.71±0.13 vs. −0.78±0.33 beats·min−1·mmHg−1, P=0.41; −0.98±0.35 vs. −0.92±0.16 units・beat−1・ mmHg−1, P=0.73). Cardiac and sympathetic baroreflex functions were preserved and BP fluctuation may be well maintained under local anesthesia using vasoconstrictor-free 3% mepivacaine.
Nitrous oxide inhalation was reported to suppress pressor response to pain stimulation, while an increase in heart rate (HR) remained unchanged. We evaluated whether nitrous oxide inhalation attenuates an increase in muscle sympathetic nerve activity (MSNA) during cold stress. MSNA (microneurography), arm cuff and beat‐to‐beat blood pressure (BP), and HR were measured during 5‐min baseline, 2‐min cold pressor test (CPT) in 12 young men [30±1 (SE) yrs] after they receive room air, 100% oxygen, 30%, and 40% nitrous oxide for 20 min through a mask, respectively. BP increased during CPT in all conditions, while the increase of systolic BP tended to be smaller during inhalation of 40% nitrous oxide than room air (26±5 vs 15±4 mmHg, P=0.081). HR also increased during CPT without any difference the increase between the conditions. MSNA burst frequency increased during CPT, while the increase was smaller during the inhalation of 40% nitrous oxide than room air (21±4 vs 12±3 burst/min, P=0.045). Change (Δ) in systolic BP during CPT was correlated with ΔMSNA burst frequency (r=0.40), but not ΔHR (r=0.06) in all conditions. These results suggest that suppressed pressor response to pain stimuli by inhalation of nitrous oxide is attributable to the attenuation of increase in muscle sympathetic nerve activity.Supported by JSPSKAKENHI70566661.
Background Procedural sedation with propofol is widely used to reduce stress and suppress cardiovascular responses to anxiety and fear during medical and dental treatments. A well‐known adverse event of propofol is a decrease in peripheral vascular resistance resulting in hypotension; however, the effects on intravascular pressure at the central arteries are unknown. Intravascular pressure is formed by the synthesis of reflected waves from the periphery with forward pulse waves produced during ejection, and the augmented pressure by the reflected waves is one of the determinants of the systolic blood pressure (BP) at the central arteries and is known to be related to cardiovascular events. We tested the hypotheses that propofol reduces the augmentation index (AIx) in the carotid artery and that the reduction is caused by a delay in the arrival time of the reflected wave (Tr). Methods Beat‐by‐beat finger BP and heart rate (HR) were continuously recorded in seven healthy young men (Age: 30 ± 2 years). Central BP, AIx, Tr of the carotid artery, and carotid‐to‐femoral pulse wave velocity (cfPWV) were measured using applanation tonometry during supine rest before (BL) and 20 min after the onset of continuous administration of propofol (PRO). This study was approved by the Institutional Review Board of Matsumoto Dental University. Results Systolic BP was lower in PRO than in BL (P < 0.001) in both peripheral and central arteries, while it was lower in the central artery than in the peripheral artery in PRO (80 ± 5 and 96 ± 6 mmHg, P < 0.001). HR in PRO remained unchanged from BL. AIx was decreased (−40.9 ± 10.3 vs −11.8 ± 11.3%, P < 0.001), and Tr was prolonged (199 ± 14 vs 173 ± 8 ms, P < 0.001) in PRO than in BL at the carotid artery. A negative correlation was found between AIx and Tr (r = −0.91, P < 0.001). Furthermore, Tr was negatively correlated with cfPWV (r = −0.72, P = 0.004), but not with the effective reflected length (P = 0.291). Conclusions Since propofol delayed the time when the reflected wave reached the large vessels, the interval between the peaks of the forward wave and the reflected wave widened, resulting in a decreased peak value of the augmented pressure. These results suggest that the carotid artery pressure is decreased by propofol‐induced reduction in augmentation pressure, which is dependent on the delay in the arrival time of the reflected wave to the central arteries.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.