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Results for “Micrognathism”

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At least 19 recordsLinked to original sources
PubMed1985

Assessment of pharyngeal airway stability in normal and micrognathic infants.

A current hypothesis for obstructive sleep apnea states that 1) negative airway pressure during inspiration can collapse the pharyngeal airway, and 2) neural control of pharyngeal airway-dilating muscles is important in preventing this collapse. To test this hypothesis we performed nasal mask occlusions to increase negative pharyngeal airway pressures during inspiration in eight normal and five micrognathic infants. Both groups developed midinspiratory pharyngeal obstruction, but obstruction was more frequent in micrognathic infants and varied in some infants with sleep state. The airway usually reopened with the subsequent expiration. The occasional failure to reopen was presumably due to pharyngeal wall adhesion. If airway obstruction occurred in sequential breaths during multiple-breath nasal mask occlusions in normal infants, there was a breath-by-breath change in the airway pressure associated with airway closure (airway closing pressure); the airway closing pressure became progressively more negative. Micrognathic infants showed less ability to improve the airway closing pressure, but this ability increased with age. These findings suggest that nasal mask occlusion can test the competence of the neuromuscular mechanisms that maintain pharyngeal airway patency in infants. Micrognathic infants had spontaneous midinspiratory pharyngeal airway obstructions during snoring. Their episodes of obstructive apnea began with midinspiratory pharyngeal obstruction similar to that seen during snoring and nasal mask occlusions. These findings imply a similar pathophysiology for snoring, spontaneous airway obstruction, and obstruction during snoring.

Airway Obstruction↗
PubMed1989

Teratogenicity of 3,3-dimethyl-1-phenyltriazene in the rat: gross malformations including micrognathism.

3,3-Dimethyl-1-phenyltriazene (DMPT), an alkylating agent, has been reported to be teratogenic in chickens, mice, and rats. One of the most commonly affected structures is the mandible; however, a complete description and incidence rates of all malformations produced have not been published. Rats were treated on day 12 of gestation (day 0 = sperm in vaginal smear) with a single intraperitoneal injection of 30 mg DMPT/kg. Fetuses were examined on each subsequent day of gestation for external and skeletal abnormalities. Standard soft tissue examinations were performed on day-20 fetuses. A high percentage (greater than or equal to 80%) of treated litters contained numerous fetuses with micrognathism, cleft palates, syndactyly, adactyly, and misshapen digits and limbs. Lordosis, cerebellar and cerebral hypoplasia, decreased fetal size, and generalized delayed ossification were also observed. Dams exposed to DMPT had decreased food consumption and weight gains, although clinicopathologic and histopathologic evaluations failed to indicate other evidence of maternal toxicity. DMPT caused numerous permanent structural alterations that were not attributed to maternal toxicity.

Abnormalities, Drug-Induced↗
PubMed1986

Control of respiratory activity of the genioglossus muscle in micrognathic infants.

The genioglossus (GG) muscle activity of four infants with micrognathia and obstructive sleep apnea was recorded to assess the role of this tongue muscle in upper airway maintenance. Respiratory air flow, esophageal pressure, and intramuscular GG electromyograms (EMG) were recorded during wakefulness and sleep. Both tonic and phasic inspiratory GG-EMG activity was recorded in each of the infants. On occasion, no phasic GG activity could be recorded; these silent periods were unassociated with respiratory embarrassment. GG activity increased during sigh breaths. GG activity also increased when the infants spontaneously changed from oral to nasal breathing and, in two infants, with neck flexion associated with complete upper airway obstruction, suggesting that GG-EMG activity is influenced by sudden changes in upper airway resistance. During sleep, the GG-EMG activity significantly increased with 5% CO2 breathing (P less than or equal to 0.001). With nasal airway occlusion during sleep, the GG-EMG activity increased with the first occluded breath and progressively increased during the subsequent occluded breaths, indicating mechanoreceptor and suggesting chemoreceptor modulation. During nasal occlusion trials, there was a progressive increase in phasic inspiratory activity of the GG-EMG that was greater than that of the diaphragm activity (as reflected by esophageal pressure excursions). When pharyngeal airway closure occurred during a nasal occlusion trial, the negative pressure at which the pharyngeal airway closed (upper airway closing pressure) correlated with the GG-EMG activity at the time of closure, suggesting that the GG muscle contributes to maintaining pharyngeal airway patency in the micrognathic infant.

Cleft Palate↗
PubMed1991

Impaired mandibular growth and micrognathic development in children with juvenile rheumatoid arthritis. A longitudinal study of lateral cephalographs.

The present report is a longitudinal study of the craniofacial growth, based on lateral cephalographs of a group of 26 patients with juvenile rheumatoid arthritis (JRA), and a matched English control group. In the 26 matched pairs, the mean age at baseline was 8.4 years and at 6-year follow-up 14.7 years, female/male ratio was 3.3/1, and all patients had temporomandibular joint (TMJ) abnormalities. The study revealed obvious growth disturbances in the facial skeleton in the children with JRA. Compared with the controls, the patients showed a smaller mandible with an altered morphology and position. The mandible became more retruded by rotating posteriorly, around a centre in the molar region, and was characterized by appositional growth in the gonion area, vertical growth in the anterior part and proclination of the lower incisors. During the observation period the growth disturbances became more pronounced, reflecting the progressive nature of the abnormal development. Based on these findings, a future aspect of research in this field could be TMJ surgery and orthognathic surgery in an early stage, trying to avoid this unfavourable facial development.

Adolescent↗
PubMed1985

Mandibular skeletal dysmorphology in micrognathic mice.

The primary manifestations of micrognathia were microglossia, midline fusion of the right and left sides of the mandible, total absence of incisor and molar toothbuds and, in many cases, absence or perhaps premature resorption of Meckel's cartilage. In addition, there was altered osteogenesis as evidenced by disrupted trabecular patterns, as well as an overall dimensional reduction of the mandible both antero-posteriorly and laterally. Strikingly similar results were reported by Johnson (1926), who studied the progeny of x-irradiated mice. How specifically our results correlate with this much earlier work is a matter for further analysis. It seems clear that the critical factor in the development of micrognathia is not so much an abnormal formation of the bony mandible, but a deficiency of tongue development, specifically its intrinsic musculature. Thus, mandibular micrognathia involves not only a dysmorphology of the first branchial arch, but also the mesenchymal cell migration from the occipital somites. Taken together, the picture is one that suggests an underlying cause that may have its inception at a much earlier developmental stage, when ectomesenchymal migration from the region of the neural tube occurs. In any event, we can report confidently that spontaneous micrognathia in prenatal mice is not a simple dimensional reduction of the lower jaw, but a more complex morphological phenomenon.

Animals↗