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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↗

PubMed1980

Cleidocranial dysostosis, severe micrognathism, bilateral absence of thumbs and first metatarsal bone, and distal aphalangia: a new genetic syndrome.

Five patients from three families have a new genetic syndrome. The features include cleidocranial dysostosis, bilateral absence of the thumbs and of the distal phalanges of the fingers, hypoplasia of the first metatarsus, absence of the distal phalanx and hypoplasia of the proximal phalanx of the big toe, pelvic dysplasia, bilateral hip dislocation, a constant facial dysmorphism with sparse hair, peculiar ears, severe micrognathism, and retracted and poorly delineated lips. The existence of consanguinity in two of the families, both with two affected siblings, as well as the lack of sex predilection, allow us to postulate that this syndrome is inherited in a recessive manner.

Abnormalities, Multiple↗

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↗

PubMed1998

Mandibular distraction in glossoptosis-micrognathic association: preliminary report.

Surgical treatment for glossoptosis-micrognathic association is indicated in the most severe cases. Usually, complications occur. We used mandibular distraction to pull the tongue away from the posterior pharyngeal wall. This procedure, used in 3 patients, was effective.

Humans↗

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↗

PubMed1997

[Histological study of micrognathic development in mouse fetus induced by 3,3-dimethyl-1-phenyltriazene].

The purpose of this study was to investigate the influence of 3,3-dimethyl-1-phenyltriazene (DMPT) on development of craniofacial structures in mouse fetus. (1) Pregnant C57BL/6 mice were treated with 30 mg/kg DMPT injection on days 10.5 approximately 13.5 of gestation. The fetuses were analyzed on day 15.0. The incidence of micrognathia was formed 100% in the treated group on days 10.5 and 11.0, and then decreased remarkably after day 11.5. This result suggested that the critical period of micrognathic development is days 10.5 approximately 11.0. (2) The fetuses, injected 30 mg/kg DMPT on day 10.5, were sacrificed on days 11.0 approximately 18.0. Their heads were used for the following histomorphological analyses: 1. clearing and Alcian blue-alizarin red double staining and 2. lateral graphic reconstruction using serial frontal sections. Dysmorphology of the anterior portion of Meckel's and nasal septal cartilage became evident after day 13.0, however, nasal capsule cartilage was hardly affected. It was concluded that hypoplastic Meckel's cartilage, caused by the administration of DMPT, induced mandibular dysmorphogenesis.

Animals↗

PubMed1998

[Observation of micrognathic development in mouse fetus induced by sulfadimethoxine].

The purpose of this study was to investigate the process of micrognathic development in mouse fetus induced by Sulfadimethoxine (SDM). SDM of 3,000 mg/kg was administered orally to pregnant ICR mice on days 8, 9, 10, 11, 12, and 13 of gestation. The fetuses were removed on day 15 to analyze the incidence of micrognathia. The incidence of micrognathia was the highest in the treated group on day 10. The fetuses, SDM-treated on day 10, were sacrificed on days 11, 12, 13, 14, 15, and 18 and prepared for histological and morphological analyses. Histomorphological analyses were performed by lateral and horizontal graphic reconstruction using serial frontal sections. It was also performed by clearing and alcian blue-alizarin red double staining. In the treated group, bilateral sigmoid buckling and shortening of Meckel's cartilage became evident after day 14, however, the nasal septal and capsule cartilage were less affected. It was concluded that remarkable hypoplastic and malformed Meckel's cartilage, caused by the administration of SDM, induced mandibular dysmorphogenesis.

Animals↗

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