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Objectives: The objective of the study was to quantify the 3‐D location of impacted canines by measuring their linear and angular deviations in relation to adjacent structures and further evaluate impaction severity. Methods: CBCT images of 314 impacted canines were analysed in the sagittal, coronal and axial planes. Linear and angular measurements were recorded. Canine inclination was identified in coronal and sagittal planes. An evaluation system was constructed for analysis. Upright canine was considered as the appropriate position for fully erupted maxillary canine. Outcomes were compared between right and left sides and by gender. For categorical variables, chi‐square tests were used while Mann‐Whitney U test was used for continuous variables. Regression models were used to measure severity. Results: Impactions were greater in females (119/207; 57.5%). No significant differences between unilateral (100/207; 49.3%) and bilateral (107/207; 51.7%) (P > 0.05). Out of 314 impactions, 105 (33.4%) were mild, 118 (37.58%) moderate and 91 (28.98%) severe. Severe impactions were primarily buccal (44/ 91; 48.3%), in the occlusal ½ of the adjacent incisor root (38/ 91, 41.7%), mesial to the distal border of central incisor (47/91, 51.6%), with sagittal angle value + >45 ̊ (46/ 91, 50.5%) and mesial tip + >30 ̊ (86/ 91, 94.5%). Conclusions: Severely impacted canines had their crowns buccal, closer to occlusal plane and mesial to the distal border of the central incisor with greater than 45‐degree buccal inclination and greater than 30‐degree mesial tip. The sagittal angle can have a significant impact on the severity of impaction. A new classification system was proposed to quantify severity. [ABSTRACT FROM AUTHOR]

Endothelin receptor blockade is an emerging therapy for pulmonary hypertension. However, hemodynamic and structural effects and potential changes in endogenous nitric oxide (NO)-cGMP and endothelin-1 signaling of chronic endothelin A receptor blockade in pulmonary hypertension secondary to congenital heart disease are unknown. Therefore, the objectives of this study were to determine hemodynamic and structural effects and potential changes in endogenous NO-cGMP and endothelin-1 signaling of chronic endothelin A receptor blockade in a lamb model of increased pulmonary blood flow following in utero placement of an aortopulmonary shunt. Immediately after spontaneous birth, shunt lambs were treated lifelong with either an endothelin A receptor antagonist (PD-156707) or placebo. At 4 wk of age, PD-156707-treated shunt lambs (n = 6) had lower pulmonary vascular resistance and right atrial pressure than placebo-treated shunt lambs (n = 8, P < 0.05). Smooth muscle thickness or arterial number per unit area was not different between the two groups. However, the number of alveolar profiles per unit area was increased in the PD-156707-treated shunt lambs (190.7 [+ or -] 5.6 vs. 132.9 [+ or -] 10.0, P < 0.05). Plasma endothelin-1 and cGMP levels and lung NOS activity, cGMP, eNOS, preproendothelin-1, endothelin-converting enzyme-1, endothelin A, and endothelin B receptor protein levels were similar in both groups. We conclude that chronic endothelin A receptor blockade attenuates the progression of pulmonary hypertension and augments alveolar growth in lambs with increased pulmonary blood flow. pulmonary heart disease; congenital heart defect

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