Analysis of gap formation at tooth-composite resin interface: effect of C-factor and light-curing protocol

OBJECTIVE: The aim of this study was to evaluate the effect of C-factor and light-curing protocol on gap formation in composite resin restorations. Material and METHODS: Cylindrical cavities with 5.0 mm diameter and three different depths (A=1.0, B=2.0 and C=3.0 mm) were prepared on the occlusal surface of 30 human molars and restored in a single increment with P 60. The composite resin was light-cured according to two protocols: standard - 850 mW/cm² / 20 s and gradual - 100 up to 1000 mW/cm² / 10 s + 1000 mW/cm² / 10 s. After storage in distilled water (37°C/7 days), the restorations were cut into three slices in a buccolingual direction and the gap widths were analyzed using a 3D-scanning system. The data were submitted to ANOVA and Student-Newman-Keuls test (alpha=0.05). RESULTS: ANOVA detected a significant influence for the C-factor and light-curing protocol as independent factors, and for the double interaction C-factor vs. light-curing protocol. Cavities with higher C-factor presented the highest gap formation. The gradual light-curing protocol led to smaller gap formation at cavity interfaces. CONCLUSIONS: The findings of this study suggest that the C-factor played an essential role in gap formation. The gradual light-curing protocol may allow relaxation of composite resin restoration during polymerization reaction

Histopathological Changes of the Heart After Neonatal Dexamethasone Treatment:Studies in 4-, 8-, and 50-Week-Old Rats

Dexamethasone (Dex), for prevention of chronic lung disease in preterm infants, showed potential negative long-term effects. Studies regarding long-term cardiovascular effects are lacking. We investigated possible histopathological myocardial changes after neonatal Dex in the young and adult rat heart. Rats were treated with Dex on d 1, 2, and 3 (0.5, 0.3, and 0. 1 mg/ka) of life. Control-pups received saline. At 4, 8, and 50 wk after birth rats were killed and anatomic data collected. Heart tissue was stained with hematoxylin and eosin, Cadherin-periodic acid schiff, and sirius red for cardiomyocyte morphometry and collagen determination. Presence of macrophages and mast cells was analyzed. Cardiomyocyte length of the Dex-treated rats was increased in all three age groups, whereas ventricular weight was reduced. Cardiomyocyte volumes were increased at 50 wk indicating cellular hypertrophy. Collagen content gradually increased with age and was 62% higher in Dex rats at 50 wk. Macrophage focus score and mast cell count were also higher. Neonatal Dex affects normal heart growth resulting in cellular hypertrophy and increased collagen deposition in the adult rat heart. Because previous studies in rats showed premature death, suggesting cardiac failure, cardiovascular follow-Lip of preterm infants treated with glucocorticoids should be considered. (Pediatr Res 66: 74-79, 2009

Neonatal glucocorticosteroid treatment causes systolic dysfunction and compensatory dilatation in early life:Studies in 4-week-old prepubertal rats

Glucocorticosteroid treatment is widely used to prevent chronic lung disease in premature infants, Recent studies in adult rats, treated with dexamethasone in the neonatal period, report negative long-term effects on the heart and severely reduced life expectancy. We treated neonatal rats with dexamethasone and studied cardiac function after 4 wk (prepubertal age) to investigate whether the late effects as previously described are preceded by detectable alterations in cardiac function at a younger age. Male rat pups (n = 12) were injected intraperitoneally with dexamethasone on d 1, 2, and 3 (0.5, 0.3, and 0.1 mu g/g) of life. Control pups (n = 10) received saline. At 4 wk the animals were anesthetized, and a pressure-conductance catheter was introduced into the left ventricle to measure pressure-volume loops. Cardiac function was measured and pressure-volume relations were determined to quantify intrinsic systolic and diastolic function. Subsequently, hearts were excised for histologic examination. Compared with saline-treated animals, dexamethasone-treated rats had a reduced ventricular weight (270 +/- 40 Versits 371 +/- 23 mg, p <0.001) and reduced systolic function (endsystolic elastance: 1.24 +/- 0.43 versus 2.50 +/- 1.39 min Hg/mu L, p = 0.028). Cardiac output was maintained and end-diastolic volume was increased (84 +/- 23 vervits 59 +/- 19 mu L p = 0.012) indicating it state of compensalory dilatation. Heart rate, diastolic function, and systemic vascular resistance were unchanged. Neonatal dexamethasone treatment causes cardiac alterations that can be detected in the prepubertal period and that may precede severe cardiac dysfunction later in life. If our findings are confirmed in humans. this may have consequences for a large patient population and cardiac screening at young age may be indicated to enable secondary prevention