Prolonged immobilization-induced stress delays alveolar bone healing. A histometric study in rats.

The purpose of the present study was to investigate the effect of prolonged immobilization-induced stress on reparative bone formation, using the rat alveolar healing as an experimental protocol. Stress was attained by immobilization for 2 hours a day, beginning three days before extraction of the upper right incisors and continuing until sacrifice. The stress condition was assayed on the basis of plasma corticosterone concentration (measured by double-antibody radioimmunoassay), which increased by 2.5 to 4 times in rats submitted to immobilization. The volume density of neoformed bone filling the alveolar socket was quantified by a histometric differential point-counting method 7 to 21 days following tooth extraction. Stress caused a significant delay in reparative bone increment, somewhat related to impairment of coagulum remission and/or organization.

Increased plasma levels of soluble vascular cellular adhesion molecule-1 in patients with chest pain and angiographically normal coronary arteries.

AIMS: To assess plasma levels of vascular cellular adhesion molecule-1, a marker of endothelial dysfunction, in patients presenting with coronary syndromes submitted to coronary angiography. METHODS AND RESULTS: Plasma levels of soluble vascular cellular adhesion molecule-1 were measured by enzymatic immunoabsorbent assay in eight patients with angina-like chest pain and angiographically normal coronary arteries; in 14 patients with stable angina and in 18 patients with unstable angina, both with coronary lesions by angiography, and in 10 healthy volunteers. Levels of soluble vascular cellular adhesion molecule-1 were higher in unstable angina patients (1777+/-161 SE pg ml(-1)) compared to patients with stable angina (1178+/-206 SE pg ml(-1), P<0.05). Moreover, patients with angina-like chest pain and normal coronary arteries had significantly higher soluble vascular cellular adhesion molecule-1 levels (2307+/-295 SE pg ml(-1)) compared to stable angina patients (P<0.05), but similar levels compared to unstable angina patients. Patient groups had higher values of soluble vascular cellular adhesion molecule-1 compared to the control group (734+/-97 SE pg ml(-1)). CONCLUSIONS: Increased levels of soluble vascular cellular adhesion molecule-1 are associated with coronary artery disease in patients with anatomically established lesions. In patients free of flow-limiting lesions and angina-like chest pain, high levels of this marker may indicate endothelial dysfunction.