Abnormal Growth and Feeding Behavior in Upper Airway Obstruction in Rats

Tarasiuk, Ariel; Segev, Yael

doi:10.3389/fendo.2018.00298

Cited by 8 publications

(7 citation statements)

References 121 publications

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“…In this experiment, we found that intermittent nasal obstruction caused significant structural remodeling in rats and that these alterations were especially prominent in the early stage, during which the thickness of the condylar joint hyperplasia layer and the hypertrophic layer was reduced considerably. This finding is consistent with the previous study (Tarasiuk & Segev, 2018). This phenomenon does not occur in the intermittent hypoxia model.…”

Section: Discussionsupporting

confidence: 94%

Mouth breathing impairs the development of temporomandibular joint at a very early stage

Sun

et al. 2020

Oral Diseases

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Objectives The study aimed to explore the effects of mouth breathing and hypoxia on the condyle of temporomandibular joint (TMJ) via two animal models. Methods 24 four‐week‐old rats were randomly separated into three groups, consisting of eight control rats, eight intermittent hypoxia (IH) rats, and eight intermittent nasal obstruction (INO) rats. We use the IH model and the INO model to simulate children suffering from hypoxia and mouth breathing. After 16 days, the condyle of TMJ and surrounding white adipose tissue (WAT) and skeletal muscle tissue were obtained for further staining and qRT‐PCR. Finally, RNA‐seq was used to verify the results. Results The intermittent hypoxia cannot significantly change the overall structure in the cause of short‐term hypoxia stimulation, but the intermittent nasal obstruction can alter the condyle, WAT, and muscle, while also introducing noticeable structural changes in tissue hypoxia and macrophage infiltration. Sequencing data verified these findings and also suggested that this process might involve the Hif‐1α/Vegf axis. Conclusions Our findings reveal the very early structural impact of mouth breathing on condyle reconstruction in rat models, and hypoxia does not induce evident alteration on condyle. However, since these results are mainly focused on rats, further studies are needed to understand its effects on humans.

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Section: Discussionsupporting

confidence: 94%

Mouth breathing impairs the development of temporomandibular joint at a very early stage

Sun

et al. 2020

Oral Diseases

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“…OSA per se, independent from obesity, may increase the risk of metabolic syndrome 25 . OSA may upregulate inflammatory cascades that are associated with metabolic disorders and increased energy intake 26–30 . We found significantly higher levels of ferritin in adolescents with moderate/severe OSA compared to the no/mild OSA group, although no significant differences were found in hemoglobin or MCV.…”

Section: Discussionmentioning

confidence: 56%

Obstructive sleep apnea and metabolic disorders in morbidly obese adolescents

Haim

Daniel

Hershkovitz

et al. 2021

Pediatric Pulmonology

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Background Little known about the prevalence of obstructive sleep apnea (OSA) in morbid obese adolescents and the association between OSA and comorbid factors. Aim To examine the association between apnea–hypopnea index (AHI, a measure for OSA severity) and metabolic morbidity among morbidly obese adolescents. Methods We performed a population‐based retrospective cohort study by reviewing sleep study, metabolic indices, and comorbidity‐related data of a cohort (n = 106) of adolescents referred to a bariatric surgery clinic. We compared subjects with moderate/severe OSA (AHI ≥ 5) versus no/mild OSA (AHI < 5) OSA and three groups of subjects with increasing body mass index (BMI) concerning sleep‐study and metabolic indices using univariate analyses. To assess the link between AHI and ferritin levels a multivariate linear regression (adjusted for BMI and mean cell volume) was preformed. Results A total of 71 patients met the inclusion criteria. Subjects with moderate/severe OSA (n = 32, 45%) had higher BMI, cholesterol, cholesterol/high‐density lipoprotein (HDL) ratio, hemoglobin A1c, and serum ferritin levels (p < .05). AHI significantly increased across BMI strata (p = .02). Multivariate linear regression indicated that moderate/severe OSA was associated with higher levels of ferritin, unstandardized β = 49.1 (nIU/ml) (p = .025). Conclusions Morbidly obese adolescents with moderate/severe OSA versus no/mild OSA have a higher risk for metabolic complications. Therefore, OSA management should be considered in adolescents with morbid obesity, in addition to weight loss.

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“…However, there is controversy in whether the settings used to mimic IH in rodent experiments are clinically translatable to IH experienced in humans ( Farré et al, 2018 ). Mechanical obstruction of the airways or oxygen deprivation have also been used ( Almendros et al, 2011 ; Tarasiuk and Segev, 2018 ). The SRBD/OSA rodent models with ‘naturally occurring’ airway obstruction, such as the Zucker hooded rat ( Iida et al, 1996 ), exhibit loss of airway patency owing to excessive soft tissue or obesity.…”

Section: Discussionmentioning

confidence: 99%

Neural crest-specific loss ofBmp7leads to midfacial hypoplasia, nasal airway obstruction and disordered breathing, modeling obstructive sleep apnea

Baddam

Biancardi

Roth

et al. 2021

Disease Models &Amp; Mechanisms

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Pediatric obstructive sleep apnea (OSA), a relatively common sleep-related breathing disorder (SRBD) affecting approximately 1-5% of children, is often caused by anatomical obstruction and/or collapse of the nasal and/or pharyngeal airways. The resulting sleep disruption and intermittent hypoxia lead to various systemic morbidities. Predicting the development of OSA from craniofacial features alone is currently not possible and a controversy remains if upper airway obstruction facilitates reduced midfacial growth or vice-versa. Currently, there is no rodent model that recapitulates both the development of craniofacial abnormalities and upper airway obstruction to address these questions. Here, we describe that mice with a neural crest-specific deletion of Bmp7 (Bmp7ncko) present with shorter, more acute angled cranial base, midfacial hypoplasia, nasal septum deviation, turbinate swelling and branching defects, and nasal airway obstruction. Interestingly, several of these craniofacial features develop after birth during periods of rapid midfacial growth and precede the development of an upper airway obstruction. We identified that in this rodent model, no single feature appeared to predict upper airway obstruction, but the sum of those features resulted in a reduced breathing frequency, apneas and overall reduced oxygen consumption. Metabolomics analysis of serum from peripheral blood identified increased levels of hydroxyproline, a metabolite upregulated under hypoxic conditions. As this model recapitulates many features observed in OSA, it offers unique opportunities for studying how upper airway obstruction affects breathing physiology and leads to systemic morbidities.

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Abnormal Growth and Feeding Behavior in Upper Airway Obstruction in Rats

Cited by 8 publications

References 121 publications

Mouth breathing impairs the development of temporomandibular joint at a very early stage

Mouth breathing impairs the development of temporomandibular joint at a very early stage

Obstructive sleep apnea and metabolic disorders in morbidly obese adolescents

Neural crest-specific loss ofBmp7leads to midfacial hypoplasia, nasal airway obstruction and disordered breathing, modeling obstructive sleep apnea

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