Dataset Information

Challenges to achieving low palatal fistula rates following primary cleft palate repair: experience of an institution in Uganda.

ABSTRACT:

Objective

To determine frequency of palatal fistula following primary cleft palate repair and the associated factors as a measure of cleft palate repair outcome and its challenges at a cleft centre in Uganda.

Results

Between May and December 2016, 54 children with cleft palate were followed up at Comprehensive Rehabilitation services of Uganda (CoRSU) hospital, from time of primary cleft palate repair until at least 3 months postoperative to determine whether they developed palatal fistula or not. Frequency of palatal fistula was 35%. Factors associated with increased fistula formation were cleft width wider than 12 mm (p = 0.006), palatal index greater than 0.4 (p = 0.046), presence of malnutrition at initial outpatient assessment (p = 0.0057) and at time of surgery (p = 0.008), two-stage palate repair (p = 0.005) and postoperative infection (p = 0.003). Severe clefting (palatal index greater than 0.4) was seen in 74% of patients and malnutrition (Low weight for age) seen in 48% of patients. Palatal fistula rates at our institution were high compared to reports in literature. The high proportions of severe clefting and malnutrition observed in our population that was also poor and unable to afford feeding supplements increased likelihood of fistula formation and posed challenges to achieving low fistula rates in our setting.

SUBMITTER: Katusabe JL

PROVIDER: S-EPMC5992877 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Publications

Challenges to achieving low palatal fistula rates following primary cleft palate repair: experience of an institution in Uganda.

Katusabe Josephine Linda JL Hodges Andrew A Galiwango George William GW Mulogo Edgar M EM

BMC research notes 20180607 1

<h4>Objective</h4>To determine frequency of palatal fistula following primary cleft palate repair and the associated factors as a measure of cleft palate repair outcome and its challenges at a cleft centre in Uganda.<h4>Results</h4>Between May and December 2016, 54 children with cleft palate were followed up at Comprehensive Rehabilitation services of Uganda (CoRSU) hospital, from time of primary cleft palate repair until at least 3 months postoperative to determine whether they developed palata ...[more]

PMID: 29880044

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Project description:BackgroundOverconsumption of retinoic acid (RA) or its analogues/derivatives has been linked to severe craniomaxillofacial malformations, such as cleft palate and midface hypoplasia. It has been noted that RA disturbed the proliferation and migration of embryonic palatal mesenchymal (EPM) cells in these malformations, yet the exact mechanisms underlying these disruptions remained unclear.MethodsA model of retinoic acid (RA)-induced cleft palate in fetal mice was successfully established. Histological alterations in the palate were evaluated using Hematoxylin and Eosin (H&E) staining and RNA in situ hybridization (RNAscope). Cellular proliferation levels were quantified via the Cell Counting Kit-8 (CCK-8) assay and EdU incorporation assay, while cell migration capabilities were investigated using wound healing and Transwell assays. Mitochondrial functions were assessed through Mito-Tracker fluorescence, mitochondrial reactive oxygen species (ROS) measurement, ATP level quantification, and mitochondrial DNA (mtDNA) copy number analysis. Differential gene expression and associated signaling pathways were identified through bioinformatics analysis. Alterations in the transcriptional and translational levels of Lhx6 and genes associated with mitophagy were quantified using quantitative PCR (qPCR) and Western blot analysis, respectively. Mitochondrial morphology and the mitochondrial autophagosomes within cells were examined through transmission electron microscopy (TEM).ResultsAbnormal palatal development in mice, along with impaired proliferation and migration of human embryonic palatal mesenchymal (HEPM) cells, was associated with RA affecting mitochondrial function and concomitant downregulation of Lhx6. Knockdown of Lhx6 in HEPM cells resulted in altered cell proliferation, migration, and mitochondrial function. Conversely, the aberrant mitochondrial function, proliferation, and migration observed in RA-induced HEPM cells were ameliorated by overexpression of Lhx6. Subsequent research demonstrated that Lhx6 ameliorated RA-induced dysfunction in HEPM cells by modulating PINK1/Parkin-mediated mitophagy, thereby activating the MAPK signaling pathways.ConclusionLhx6 is essential for mitochondrial homeostasis via tuning PINK1/Parkin-mediated mitophagy and MAPK signaling pathways. Downregulation of Lhx6 by RA transcriptionally disturbs the mitochondrial homeostasis, which in turn leads to the proliferation and migration defect in HEPM cells, ultimately causing the cleft palate.

Dataset Information

Challenges to achieving low palatal fistula rates following primary cleft palate repair: experience of an institution in Uganda.

Objective

Results

Publications

Challenges to achieving low palatal fistula rates following primary cleft palate repair: experience of an institution in Uganda.

Similar Datasets

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