ABSTRACT
In the present study, 25% EDTA, in gel form, was used to analyse its micromorphological effects on tooth surfaces with the objective to see the effectiveness of EDTA in etching so as to replace phosphoric acid as an etchant. EDTA has neutral pH (6.4 - 7.4) and is known to open & widen the dentinal tubules as well as remove the smear layer. An in vitro study was conducted on orthodontically extracted premolars with 25% EDTA as an etchant which was applied on prepared tooth surfaces for 15 seconds, 1 minute and 3 minutes. The effects of EDTA gel was observed under SEM and results tabulated and evaluated. There was statistically significant differences between the 3 etching time groups and the results indicate that etching with 25% EDTA for 15 seconds is inadequate. The best results were obtained in the 3 minute time etch group. The results so obtained can be attributed to the fact that EDTA acts selectively and/or requires more time for action.
Subject(s)
Acid Etching, Dental/methods , Bicuspid , Chelating Agents/administration & dosage , Dental Enamel/drug effects , Dentin/drug effects , Edetic Acid/administration & dosage , Humans , Hydrogen-Ion Concentration , Microscopy, Electron, Scanning , Smear Layer , Time FactorsABSTRACT
Female BALB/c strain of mice fed on Zn deficient diet for 2-, 4- and 6- weeks exhibited prolonged diestrous phase with only VII types of follicles instead of VIII as compared to their respective control and pairfed. Light microscopic studies displayed increased atresia, cessation of oogenesis and ovulation, degeneration of follicular cells of zona granulosa, clumped chromatin of oocyte and disrupted zona pellucida and corona radiata. Ultrastructural studies of peripheral follicular and theca interstitial cells of type VI and VII follicles revealed swollen mitochondria, dilated ERs (free of RNP particles), increased lysosomes, several necrotic areas of cytoplasm and pyknotic nuclei. Conclusively, Zn deficiency may lead to (1) reduction in energy, protein intake and in secretion of GnRH by hypothalamus and LH and FSH by hypophysis, (2) increased synthesis and/or secretion of prolactin. (3) reduced output of estrogen, and (4) eventually slow growth or arrest of ovulation or atresia of the growing follicles in the ovary.