Maxillary protraction to treat pediatric obstructive sleep apnea and maxillary retrusion: a preliminary report.

INTRODUCTION: Midface retrusion creates a size deficiency problem in the upper airway that has been improved in children using surgical midface advancement and orthopedic protraction of the maxilla. The results of these treatments have been mostly promising at enlarging the pharyngeal airway. Recently introduced bone anchored maxillary protraction (BAMP) uses implant inserted devices in the jaws to pull the maxilla forward against a backward pressure to the lower jaw. This is a pilot study that examines the use of BAMP as a strategy to treat maxillary retrusion, malocclusion and children with obstructive sleep apnea. METHODS: 15 children, ages 9-16 years with maxillary retrusion creating a skeletal malocclusion were treated with bone anchored maxillary protraction (BAMP) and the results were compared against an untreated control group. 8 children in the treatment group also had sleep disordered breathing/obstructive sleep apnea. All subjects had lateral cephalograms before and after BAMP therapy. The OSA cohort completed the pediatric sleep questionnaire (PSQ) and polysomnography prior to and at the end of BAMP. RESULTS: The majority of the OSA children (n = 5) showed improvement in their apnea-hypopnea index (AHI) and OSA symptoms after BAMP. Preliminary results of BAMP therapy show improvement in respiratory and airway parameters in OSA children with a highly significant change in the forward position of the upper jaw and enlargement in the nasopharyngeal to oropharyngeal junction as compared to an age and sex matched untreated control group. The outcomes were dependent on the age of treatment initiation and patient compliance. CONCLUSIONS: This preliminary work suggests that bone anchored maxillary protraction may be considered as an adjunctive treatment option in adolescents for improving midface retrusion and sleep apnea, but further work is needed to explore this therapy.

Comparative transcriptome of neurons after oxygen-glucose deprivation: Potential differences in neuroprotection versus reperfusion.

In the context of ischemic stroke, rescuing neurons can be theoretically achieved with either reperfusion or neuroprotection. Reperfusion works via the rapid restoration of oxygen and glucose delivery. Neuroprotection comprises molecular strategies that seek to block excitotoxicity, oxidative stress or various cell death pathways. Here, we propose the hypothesis that neurons rescued with reperfusion are different from neurons rescued with molecular neuroprotection. Neurons were subjected to oxygen-glucose deprivation (OGD) and then treated with "in vitro reperfusion" (i.e. energetic rescue via restoration of oxygen and glucose) or Z-VADfmk (to block apoptosis) or MK-801 (to block excitotoxicity). Levels of injury were titrated so that equivalent levels of neuronal salvage were achieved with reperfusion or neuroprotection. Gene arrays showed that OGD significantly altered the transcriptomic profiles of surviving neurons. Pathway analysis confirmed that a large spectrum of metabolic, inflammation, and signaling genes were perturbed. In spite of the fact that equal levels of neuronal salvage were achieved, energetic rescue renormalized the transcriptomic profiles in surviving neurons to a larger degree compared to neuroprotection with either Z-VADfmk or MK-801. These findings suggest that upstream reperfusion may bring salvaged neurons back "closer to normal" compared to downstream molecular neuroprotection.

Association between rs2294020 in X-linked CCDC22 and susceptibility to autoimmune diseases with focus on systemic lupus erythematosus.

Autoimmune diseases often share common susceptibility genes. Most genetic variants associated with susceptibility to systemic lupus erythematosus are also associated with other autoimmune diseases. The X-linked variant rs2294020 is positioned in exon 7 of the CCDC22 gene. The encoded protein functions in the regulation of NF-κB, a master regulator in immune response. The aim of this study is to investigate whether the rs2294020 polymorphism may be a general susceptibility factor for autoimmunity. We evaluated case-control association between the occurrence of rs2294020 and different autoimmune diseases, including new data for systemic lupus erythematosus and previous genome-wide association studies (GWAS) (though most did not analyse the X chromosome) of psoriasis, celiac disease, Crohn's disease, ulcerative colitis, multiple sclerosis, vitiligo, type-1 diabetes, rheumatoid arthritis, and ankylosing spondylitis. Cases from patients affected by amyotrophic lateral sclerosis and type-2 diabetes were also included in the study. We detected nominal significant associations of rs2294020 with systemic lupus erythematosus (additive model test: p=0.01), vitiligo (p=0.016), psoriasis (p=0.038), and in only one of two studies of multiple sclerosis (p=0.03). Our results suggest that rs2294020 is associated with the risk of several autoimmune diseases in European populations, specifically with diseases that present themselves, among else, in the skin.

A frequent phenotype for paediatric sleep apnoea: short lingual frenulum.

A short lingual frenulum has been associated with difficulties in sucking, swallowing and speech. The oral dysfunction induced by a short lingual frenulum can lead to oral-facial dysmorphosis, which decreases the size of upper airway support. Such progressive change increases the risk of upper airway collapsibility during sleep. Clinical investigation of the oral cavity was conducted as a part of a clinical evaluation of children suspected of having sleep disordered breathing (SDB) based on complaints, symptoms and signs. Systematic polysomnographic evaluation followed the clinical examination. A retrospective analysis of 150 successively seen children suspected of having SDB was performed, in addition to a comparison of the findings between children with and without short lingual frenula. Among the children, two groups of obstructive sleep apnoea syndrome (OSAS) were found: 1) absence of adenotonsils enlargement and short frenula (n=63); and 2) normal frenula and enlarged adenotonsils (n=87). Children in the first group had significantly more abnormal oral anatomy findings, and a positive family of short frenulum and SDB was documented in at least one direct family member in 60 cases. A short lingual frenulum left untreated at birth is associated with OSAS at later age, and a systematic screening for the syndrome should be conducted when this anatomical abnormality is recognised.