Effects of unilateral premature fusion of the zygomaxillary suture on the growth of nasomaxillary complex.

Unilateral premature fusion of the zygomaxillary suture was produced in 2-week-old guinea pigs by immobilization with methyl-cyanoacrylate adhesive. The effects of sutural fusion on the growth of the nasomaxillary complex were evaluated by radiographic cephalometry with implants, and histologic assessment. The immobilization successfully constrained the anteroinferior displacement of the maxilla and zygomatic bone on the fused side. Compensatory responsive remodeling at adjacent sutures and in certain regions of the nasomaxillary complex was observed. Developmental asymmetry was found when the fused side was compared with the nonfused side. No gross anatomic asymmetry of the facial complex as a whole, however, was detected. Adaptive compensation involving periosteal bone deposition occurred at the junction of the lower maxillary process and the maxilla proper on the fused side. This, together with periosteal bone resorption in corresponding areas on the nonfused side served to offset any developmental asymmetry that might have occurred, thus leading to a compensatory preclusion of gross anatomic asymmetry.

Mechanism of hypocalcemia induced by intraperitoneal, intragastric, and intravenous administration of ethanol to the rat.

Acute hypocalcemic effects of intraperitoneal administration of 3 and 5 g ethanol/kg body weight; intragastric administration of 3, 5, and 7 g ethanol/kg body weight; and intravenous administration of 2.5 a ethanol/kg body weight were investigated in 20 h fasted female Wistar rats. Dose-dependent hypocalcemia was similarly induced by intraperitoneal and intragastric routes of administration. Net calcium efflux from plasma, as indicated by the plasma 45Ca activity, was unaffected by 3 g ethanol/kg body weight but was delayed at higher doses of ethanol. Intragastric, but not intraperitoneal, administration of ethanol increased the gastrointestinal luminal calcium content partly by enhancing calcium secretion. Significantly increased tissue 45Ca content 30 min after ethanol administration was evident in the duodenum (31%), jejunum (27%), and colon (33%) in the intragastric ethanol-treated group and in the duodenum (40%), jejunum (38%), ileum (45%), colon (39%), and liver (25%) in the intraperitoneal ethanol-treated group. Thus, the hypocalcemia induced by both intraperitoneal and intragastric administration of ethanol could be partly accounted for by the suppression of calcium efflux from some soft tissues. In contrast, intravenous administration of ethanol was found to enhance the calcium efflux from plasma without affecting the net 45Ca content in the soft tissues. The mechanism(s) by which ethanol affects calcium transport has yet to be elucidated.