A clinically friendly viscoelastic finite element analysis model of the mandible with Herbst appliance.

INTRODUCTION: As a powerful numerical approximation tool, finite element analysis (FEA) has been widely used to predict stress and strain distributions in facial bones generated by orthodontic appliances. Previous FEA models were constructed on the basis of a linear elastic phase of the bone response (eg, elastic bone strains to loading). However, what is more useful for clinical understanding would be predicting long-term strains and displacements of bone-segments responding to loading, yet tissue responses are (1) not promptly observable and (2) hard to predict in nature. METHODS: Viscoelastic property of the mandibular bone was incorporated into FEA models to visualize long-term, time-dependent stress and strain patterns in the mandible after being exposed to orthopedic stress. A mandible under loading by a Herbst appliance was modeled, and outcomes of the constructed elastic and viscoelastic models were compared. RESULTS: Patterns and magnitudes of the displacement throughout the mandible predicted by the viscoelastic model were exhibited in accordance with previous clinical outcomes of Herbst appliance therapy. The elastic models exhibited similar displacement patterns; however, the magnitude of the displacements in the models was invariably small (approximately 1 per 100) compared with those outputs of corresponding viscoelastic models. The corresponding maximum stress level in our viscoelastic mandible subjected to the Herbst appliance with the same loading was considerably low and relaxed in various regions when compared with the elastic model. CONCLUSIONS: We suggest that a viscoelastic model of the mandible mimics our general prediction of orthopedic treatment outcomes better than those by elastic models.

Gingival clefts revisited: Evaluation of the characteristics that make one more susceptible to gingival clefts.

INTRODUCTION: Orthodontic space closure after premolar extraction commonly results in the formation of a gingival cleft, which may contribute to orthodontic relapse and poor periodontal health. The purpose of this study was to examine clinical parameters that may predispose patients to gingival clefts. METHODS: Twenty-nine patients planned for treatment with premolar extractions (n = 87) and orthodontic space closure were evaluated in this prospective study. The clinical measures included width of keratinized buccal gingiva, thickness of buccal gingiva, thickness of buccal bone, time of space closure, and the occurrence (presence or absence) and severity (volume) of cleft formation. The association of the clinical measures with gingival cleft formation and severity was assessed separately for patients according to age group: young adolescent (≤13 years of age), adolescent (14-18 years of age), and adult (≥19 years of age). RESULTS: The overall incidence of gingival cleft formation was 73.2%, with a trend toward greater cleft formation in the young adolescents (79.4%) than in the adolescent and adult groups (69.2% and 68.2%, respectively). The mean severity of clefts exhibited a significant positive association with age group-young adolescent (26.6 mm2), adolescent (27.9 mm2), and adult (41.5 mm2). Buccal bone thickness was significantly correlated with gingival phenotype in the adolescent and adult groups (r = 0.42 and r = 0.52, respectively; both, P <0.05). Rate of space closure was significantly correlated with cleft formation (r = 0.71; P <0.001) in the adult group. CONCLUSIONS: The formation of gingival clefts is common after premolar extraction and space closure. Adults with a thinner gingival phenotype were more likely to develop gingival clefts of greater severity. The rate of space closure was significantly and inversely correlated with cleft formation in adults, reflecting a greater likelihood of cleft formation with slower space closure. Although various clinical parameters show a correlation to both severity and incidence of clefts, all patients undergoing postextraction space closure appear to be at risk and should be monitored.

Intermittent hypoxia in utero damages postnatal growth and cardiovascular function in rats.

Obstructive sleep apnea (OSA) is common in pregnancy and may compromise fetal and even postnatal development. We developed an animal model to determine if maternal OSA could have lasting effects in offspring. Pregnant Sprague-Dawley rats were exposed to reduced ambient O2 from 21 to 4-5%, approximately once per minute [chronic intermittent hypoxia (CIH)] for 8 h/day during gestation days 3-19. Similarly handled animals exposed to ambient air served as controls (HC). Offspring were studied for body growth and cardiovascular function for 8 postnatal weeks. Compared with HC, prenatal CIH led to growth restriction, indicated by smaller body weight and tibial length, and higher arterial blood pressure in both male and female offspring. Compared with same-sex HC, CIH males showed abdominal obesity (greater ratio of abdominal fat weight to body weight or tibial length), left ventricular (LV) hypertrophy (greater heart weight-to-tibial length ratio and LV posterior wall diastolic thickness), elevated LV contractility (increases in LV ejection fraction, end-systolic pressure-volume relations, and preload recruitable stroke work), elevated LV and arterial stiffness (increased end-diastolic pressure-volume relationship and arterial elasticity), and LV oxidative stress (greater lipid peroxide content). Compared with female CIH offspring, male CIH offspring had more profound changes in blood pressure (BP), cardiac function, myocardial lipid peroxidase (LPO) content, and abdominal adiposity. Rodent prenatal CIH exposure, mimicking human maternal OSA, exerts detrimental morphological and cardiovascular effects on developing offspring; the model may provide useful insights of OSA effects in humans. NEW & NOTEWORTHY Obstructive sleep apnea is common in human pregnancy. Following maternal exposure to chronic intermittent hypoxia, a hallmark of sleep apnea, both sexes of rat offspring showed growth retardation, with males being more vulnerable to hypertension and dysfunctional left ventricular changes. This model is useful to study detrimental effects of maternal obstructive sleep apnea on developing offspring in humans.