The Effectiveness of Mandibular Distraction in Improving Airway Obstruction in the Pediatric Population
ABSTRACT Distraction osteogenesis is an effective technique for elongating the deficient mandible. The authors specifically evaluated its effectiveness in the treatment of airway obstruction in pediatric patients with mandibular hypoplasia.
A comprehensive literature review of the National Library of Medicine (PubMed) database was performed. English-language studies involving isolated distraction of the pediatric mandible (younger than 18 years) with descriptive reporting of airway changes were included. Extracted data included demographics, initial diagnosis, distractor type, distraction protocol, predistraction and postdistraction airway status, and complications.
Seventy-four articles met the inclusion criteria, resulting in 711 patients with craniofacial abnormalities who underwent mandibular distraction osteogenesis. Mean age at the time of distraction was 18.1 months. The most common diagnoses were isolated Pierre Robin sequence (52.9 percent), syndromic Pierre Robin sequence (7 percent), and Treacher Collins syndrome (6.8 percent). Mandibular distraction osteogenesis successfully treated airway obstruction in 89.3 percent of cases. Success was defined as either decannulation of tracheostomy, avoidance of tracheostomy or continuous positive airway pressure, or alleviation or significant improvement of obstructive sleep apnea symptoms. One hundred seventy-one (84.2 percent) of the 203 tracheostomy-dependent patients were successfully decannulated. Among the 181 patients with obstructive sleep apnea, mandibular distraction osteogenesis successfully allowed for either complete resolution or significant improvement of symptoms in 95.6 percent. A 23.8 percent overall complication rate was noted. The mean follow-up time was 28.7 months.
In addition to its positive effect on facial appearance, mandibular distraction osteogenesis is an effective procedure for the treatment of airway obstruction associated with congenital craniofacial defects involving mandibular hypoplasia in appropriately selected patients.
SourceAvailable from: Dongcheng Zhang[Show abstract] [Hide abstract]
ABSTRACT: The neural crest is the name given to the strip of cells at the junction between neural and epidermal ectoderm in neurula-stage vertebrate embryos, which is later brought to the dorsal neural tube as the neural folds elevate. The neural crest is a heterogeneous and multipotent progenitor cell population whose cells undergo EMT then extensively and accurately migrate throughout the embryo. Neural crest cells contribute to nearly every organ system in the body, with derivatives of neuronal, glial, neuroendocrine, pigment, and also mesodermal lineages. This breadth of developmental capacity has led to the neural crest being termed the fourth germ layer. The neural crest has occupied a prominent place in developmental biology, due to its exaggerated migratory morphogenesis and its remarkably wide developmental potential. As such, neural crest cells have become an attractive model for developmental biologists for studying these processes. Problems in neural crest development cause a number of human syndromes and birth defects known collectively as neurocristopathies; these include Treacher Collins syndrome, Hirschsprung disease, and 22q11.2 deletion syndromes. Tumors in the neural crest lineage are also of clinical importance, including the aggressive melanoma and neuroblastoma types. These clinical aspects have drawn attention to the selection or creation of neural crest progenitor cells, particularly of human origin, for studying pathologies of the neural crest at the cellular level, and also for possible cell therapeutics. The versatility of the neural crest lends itself to interlinked research, spanning basic developmental biology, birth defect research, oncology, and stem/progenitor cell biology and therapy. Birth Defects Research (Part C), 2014. © 2014 Wiley Periodicals, Inc.Birth Defects Research Part C Embryo Today Reviews 09/2014; 102(3). DOI:10.1002/bdrc.21081 · 3.87 Impact Factor