Gene expression during palate fusion in vivo and in vitro

Failure of secondary palate fusion during embryogenesis is a cause of cleft palate. Disappearance of the medial epithelial seam (MES) is required to allow merging of the mesenchyme from both palatal shelves. This involves complex changes of the medial edge epithelial (MEE) cells and surrounding structures that are controlled by several genes whose spatio-temporal expression is tightly regulated. We have carried out morphological analyses and used a semi-quantitative RT-PCR technique to evaluate whether morphological changes and modulation in the expression of putative key genes, such as twist, snail, and E-cadherin, during the fusion process in palate organ culture parallel those observed in vivo, and show that this is indeed the case. We also show, using the organotypic model of palate fusion, that the down-regulation of the transcription factor snail that occurs with the progression of palate development is not dependent on fusion of the palatal shelves. Abbreviations: dsg1, desmoglein1; EMT, epithelial-mesenchymal transition; MEE, medial edge epithelium; MES, medial epithelial seam; RT-PCR, reverse-transcriptase polymerase chain-reaction

Dental procedures in children with severe congenital heart disease: a theoretical analysis of prophylaxis and non-prophylaxis procedures

OBJECTIVE—To estimate the cumulative exposure to bacteraemia from dental procedures currently recommended for antibiotic prophylaxis and compare this with cumulative exposure from dental procedures not recommended for prophylaxis.
DESIGN—Retrospective analysis.
SETTING—University and teaching hospital maxillofacial and dental department.
PATIENTS—136 children with severe congenital cardiac disease attending for dental treatment between 1993 and 1998 and for whom full records were available. Each dental procedure was tallied.
MAIN OUTCOME MEASURES—Cumulative exposure per annum to "non-prophylaxis procedures"; cumulative exposure per annum to "prophylaxis procedures".
RESULTS—Cumulative exposure to bacteraemia from prophylaxis procedures was not significantly greater than from non-prophylaxis procedures.
CONCLUSIONS—The data raise important questions about the appropriateness of current guidelines for antibiotic prophylaxis of bacterial endocarditis.


Keywords: congenital heart disease; dental treatment; cumulative risk; endocarditi

Bacteraemia following debanding and gold chain adjustment

The purpose of this research was to estimate the prevalence, intensity, and nature of bacteraemia following deband and gold chain adjustment. Forty-nine children, 25 males and 24 females, mean age 15.4 years, attending the Orthodontic Department at the Eastman Dental Hospital were recruited. A cannula was inserted into either the left or the right antecubital fossa using an aseptic technique. A 6 ml sample of blood was taken before treatment and another 6 ml, 30 seconds after either upper deband (n = 42) or gold chain adjustment (n = 7). McNewmar's test was used to determine differences in the proportion of positive blood cultures and Wilcoxon matched pairs test to compare continuous variables. There was no significant difference (P > 0.05) in the prevalence of bacteraemia between baseline (eight, 19 per cent) and following upper deband (11, 26 per cent) or between baseline (four, 57 per cent) and gold chain adjustment (four, 57 per cent). There was also no significant difference (P > 0.05) in the intensity of the anaerobic bacteraemia between baseline and following deband or gold chain adjustment. Although the number of subjects undergoing gold chain adjustment was small, the findings demonstrate that neither upper debanding nor gold chain adjustment is associated with a significant bacteraemia