Interlayer formation and its effect on debonding polycrystalline alumina orthodontic brackets.

During the debonding of ceramic orthodontic brackets, there is a risk of causing fractures, cracks, or flaking of enamel or of the bracket itself. Preliminary work on the resin-enamel interface under bonded brackets with the indirect (modified Thomas) or the thermal-cured indirect bonding techniques revealed an interlayer of unfilled resin formed between the filled resin and the enamel surface. The direct bonding technique, on the other hand, showed no such layer. This study was designed to determine the effect of the interlayer on conventional debonding techniques for polycrystalline ceramic orthodontic brackets. Variables examined were bracket failure or fracture (BF), amount of remnant adhesive (ARI), and enamel damage. Brackets were bonded to 90 fresh bovine teeth. These were divided into three groups of 30 each, based on three methods of bonding, i.e., direct, indirect (modified Thomas), and an indirect technique that used a thermal-cured resin. Each bonding group was further divided into three groups of 10 each, based on the type of debonding technique used, i.e., lift off, delamination, and twisting. Brackets bonded by the indirect (modified Thomas, BF mean = 0.27, ARI mean = 0.93) and the indirect technique that used a thermal-cured resin (BF mean = 0.03, ARI mean = 0.43) resulted in an overall significantly lower failure (p < 0.01) and ARI score on debonding (p < 0.0001) compared with those bonded by the direct technique (BF mean = 1.03, ARI mean = 1.97). Specimens evaluated under the stereomicroscope revealed that the brackets bonded with the indirect techniques debonded at the filled-unfilled resin interface or within the interlayer of unfilled resin.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyclovir for chronic mucocutaneous herpes simplex virus infection in immunosuppressed patients.

Over 25 episodes of severe chronic and recurrent mucocutaneous herpes simplex virus infections in five immunodeficient patients were successfully treated with intravenous or oral acyclovir treatment. Acyclovir was shown to inhibit viral shedding rapidly, to be well tolerated, and to permit the complete healing of lesions. As expected, a course of acyclovir did not prevent later recurrences of the herpes virus infections. However, symptomatic recurrences were successfully suppressed during long (up to 65-day) courses of oral acyclovir.