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Short lingual frenulum as a risk factor for sleep-disordered breathing in school-age children.


  • 影响因子:2.78
  • DOI:10.1016/j.sleep.2019.09.019
  • 作者列表:"Villa MP","Evangelisti M","Barreto M","Cecili M","Kaditis A
  • 发表时间:2020-02-01

BACKGROUND:Recent evidence has emphasized the role of a short lingual frenulum in the pathogenesis of sleep-disordered breathing (SDB) in childhood. The oral dysfunction induced by a short frenulum may promote oral-facial dysmorphism, decreasing the size of upper airway lumen and increasing the risk of upper airway collapsibility during sleep. The aim of this study was to evaluate the presence of a short lingual frenulum as risk factor for SDB in children of school age, with and without snoring, who were recruited from the community. METHODS:Children aged 6-14 years were recruited from a school in Rome. For all participants, the previously described Sleep Clinical Record (SCR) was completed, and orthodontic evaluation and measurement of lingual frenulum were performed. Tongue strength and endurance were evaluated in all participants using the Iowa Oral Performance Instrument (IOPI). SDB was defined as positive SCR (≥6.5). RESULTS:We assessed 504 children with mean age of 9.6 ± 2.3 years, and in 114 of them (22.6%) a short frenulum was identified. Children with a short lingual frenulum were at significantly higher risk for a positive SCR compared to those with a frenulum of normal length (odds ratio = 2.980, 95% confidence interval = 1.260-6.997). Participants with positive or negative SCR did not differ in tongue strength or endurance. CONCLUSION:Short lingual frenulum is a risk factor for SDB. An early multidisciplinary approach and screening for SDB are indicated when this anatomical abnormality is recognized.


背景: 最近的证据强调了短舌系带在儿童睡眠呼吸障碍 (SDB) 发病机制中的作用。短系带引起的口腔功能障碍可能促进口腔-面部畸形,减少上气道管腔的大小,增加睡眠时上气道塌陷的风险。本研究的目的是评估从社区招募的学龄儿童 (有打鼾和无打鼾) 是否存在短舌系带作为 SDB 的危险因素。 方法: 从罗马的一所学校招募 6-14 岁的儿童。对于所有参与者,完成先前描述的睡眠临床记录 (SCR),并进行正畸评估和舌系带测量。使用 Iowa 口腔性能仪 (IOPI) 对所有参与者的舌头强度和耐力进行评价。SDB 定义为 SCR 阳性 (≥ 6.5)。 结果: 我们评估了 504 例儿童,平均年龄为 9.6 ± 2.3 岁,其中 114 例 (22.6%) 确定为短系带。与舌系带长度正常的儿童相比,舌系带短的儿童 SCR 阳性的风险显著较高 (比值比 = 2.980,95% 置信区间 = 1.260-6.997)。SCR 阳性或阴性的参与者在舌头强度或耐力方面没有差异。 结论: 舌系带短是 SDB 的危险因素。当这种解剖异常被识别时,就需要早期的多学科方法和 SDB 筛查。



作者列表:["De Cunto G","Brancaleone V","Riemma MA","Cerqua I","Vellecco V","Spaziano G","Cavarra E","Bartalesi B","D'Agostino B","Lungarella G","Cirino G","Lucattelli M","Roviezzo F"]

METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.

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作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

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作者列表:["Zaragosi LE","Deprez M","Barbry P"]

METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.

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