Managing obstructive sleep apnoea in children: the role of craniofacial morphology

Bozzini, Maria Fernanda Rabelo; Francesco, Renata Cantisani Di

doi:10.6061/clinics/2016(11)08

Cited by 15 publications

(15 citation statements)

References 31 publications

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“…The etiology of pediatric OSA is multifactorial. Craniofacial and neuromuscular factors along with lymphoid tissue hypertrophy and airway soft tissue inflammation are considered critical components contributing to pediatric OSA ( Bozzini and Di Francesco, 2016 ); however, controversy remains regarding the causes or consequences of these various manifestations. The resulting IH is considered a critical factor in the systemic pathogenesis of OSA ( Dewan et al, 2015 ).…”

Section: Introductionmentioning

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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Section: Introductionmentioning

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

View full text Add to dashboard Cite

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“…26,27 This suggests that pediatric OSAHS is the result of the interaction of multiple factors, including obesity, neuromuscular abnormalities, inflammatory mediator cascade activation, neurodegenerative diseases, and anatomical disorders; such as decreased mandibular and maxillary lengths, retromandibular ptosis, skeletal retrusion, and maxillary atresia. [28][29][30][31][32][33] The pan/core curve (Figure 1A) and rarefaction curves (Figure 1B,C) proved that the sample size of this study was sufficient, the sequencing depth met the requirements, and the data could reflect the real situation of the gut microbiota. We found that the OSAHS group had more sequences than the control group.…”

Section: Predictive Function Analysismentioning

confidence: 69%

Gut microbiota dysbiosis in 4‐ to 6‐year‐old children with obstructive sleep apnea–hypopnea syndrome

Cai

et al. 2022

Pediatric Pulmonology

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Objective Several experiments on animals have reported the relationship between obstructive sleep apnea–hypopnea syndrome (OSAHS) and gut microbiota. We investigated the gut microbiota composition of children aged 4–6 years with OSAHS to complement the pathogenesis and clinical screening methods of OSAHS. Methods We collected feces from 43 children with OSAHS and 45 controls aged 4–6 years. We extracted total bacterial DNA from feces and analyzed the composition of gut microbiota through 16S ribosomal RNA sequencing. Results There were significant differences in bacteria producing short‐chain fatty acids (SCFAs) between OSAHS children and controls, including Faecalibacterium, Roseburia, and a member of Ruminococcaceae. A gut microbiota model for pediatric OSAHS screening showed that the receiver operating characteristic‐area under the curve (ROC‐AUC) was 0.794 with 79.1% and 80.0% sensitivity and specificity, respectively. Functional analysis of the gut microbiota revealed several alterations in metabolism. Conclusion The composition of gut microbiota in OSAHS children is partially changed. The altered intestinal flora may provide a new screening method for the diagnosis of children with OSAHS. The prediction of gut microbiota function suggests that intestinal metabolic function may be altered in OSAHS children.

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“…Craniofacial modifications are widely studied for their association with OSA ( 15 – 17 ). The optimal functioning of the upper airway (i.e., proper suction and swallowing, as well as nasal breathing) depend on many factors among which normal growth of the facial structures is one of the most important ( 18 ).…”

Section: Discussionmentioning

confidence: 99%

The Ogival Palate: A New Risk Marker of Sudden Unexpected Death in Infancy?

et al. 2022

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ObjectiveOgival palate (i.e., a narrow and high-arched palate) is usually described in obstructive breath disorder but has been found in infants unexpectedly deceased. We studied the association between ogival palate and sudden unexpected death in infancy (SUDI) on the basis of a computed tomography (CT) evaluation.MethodsWe conducted a monocentric case-control study of children under 2 years of age who died of SUDI, for which a head CT scan and an autopsy were performed between 2011 and 2018. Each case was matched by sex and age (± 30 days) to two controls selected among living children in the same center who benefited from a cranio-encephalic CT scan. Four parameters of the hard palate were measured by CT: height, width, length, and sagittal angle; the height/width ratio was calculated. The presence of an ogival palate was also subjectively evaluated by the radiologists, independently from the measurements. Standardized odds ratios (OR) were calculated using conditional logistic regression models, all expressed for +1 standard deviation (SD).ResultsThirty-two deceased children were matched to 64 living control children. Mean ages were 5.0 and 5.3 months, respectively. Twenty-eight cases were considered to have died as a result of SIDS. The mean heights of the hard palate were significantly higher in the deceased children [4.1 (± 0.7) millimeters (mm)] than in the living children [3.2 (± 0.6) mm], with OR (+1SD) = 4.30 (95% confidence interval [CI], 2.04–9.06, P = 0.0001). The mean widths of the hard palate were 21.0 (± 1.9) mm and 23.2 (± 2.1) mm, respectively, with OR = 0.15 (95% CI, 0.06–0.40, P = 0.0001). The mean sagittal angles were significantly more acute in deceased children [134.5° (± 9.3)] than in living children [142.9° (± 8.1)], with OR = 0.28 (95% CI, 0.14–0.56, P = 0.0003). The mean height/width ratios were 19.8 (± 3.7) and 14.1 (± 3.3), respectively, with OR = 6.10 (95% CI, 2.50–14.9, P = 0.0001). The hard palate was subjectively considered as ogival in 59.4% (19/32) of the cases versus 12.5% (8/64) of the controls.ConclusionRadiological features of the ogival palate were strongly associated with SUDI. This observation still needs to be confirmed and the corresponding clinical features must be identified.

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Managing obstructive sleep apnoea in children: the role of craniofacial morphology

Cited by 15 publications

References 31 publications

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

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

Gut microbiota dysbiosis in 4‐ to 6‐year‐old children with obstructive sleep apnea–hypopnea syndrome

The Ogival Palate: A New Risk Marker of Sudden Unexpected Death in Infancy?

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