Skin flap vascularity is a critical determinant of aesthetic results in autologous ear reconstruction. In this study, we investigate the use of intraoperative laser-assisted indocyanine green angiography (ICGA) as an adjunctive measure of skin flap vascularity in pediatric autologous ear reconstruction. Twenty-one consecutive pediatric patients undergoing first-stage autologous total ear reconstruction were retrospectively evaluated. The first 10 patients were treated traditionally (non-ICGA), and the latter 11 patients were evaluated with ICGA intraoperatively after implantation of the cartilage construct and administration of suction. Relative and absolute perfusion units in the form of contour maps were generated. Statistical analyses were performed using independent sample Student t test. Statistically significant differences in exposure and infection were not found between the 2 groups. However, decreased numbers of surgical revisions were required in cases with ICGA versus without ICGA (P = 0.03), suggesting that greater certainty in skin flap perfusion correlated with a reduction in revision surgeries. In cases of exposure, we found an average lowest absolute perfusion unit of 14.3, whereas cases without exposure had an average of 26.1 (P = 0.02), thereby defining objective parameters for utilizing ICGA data in tailoring surgical decision making for this special population of patients. Defined quantitative parameters for utilizing ICGA in evaluating skin flap vascularity may be a useful adjunctive technique in pediatric autologous ear reconstruction.

Background

Understanding long-term sequelae of cleft treatment is paramount in the refinement of treatment algorithms to accomplish optimized immediate and long-term outcomes. In this study, we reviewed sphincter pharyngoplasties as a method of velopharyngeal insufficiency (VPI) treatment in relationship to orthognathic surgery.

Methods

Cleft lip/palate and cleft palate patients, 15 years of age and older, were reviewed for demographics, VPI surgery, revisions, and subsequent orthognathic surgery at 2 institutions. Chi-square test, Student's t test, and logistic regression analyses were performed.

Results

In 214 patients reviewed (mean age, 19.5 years), 61.7% were male, 18.2% had isolated cleft palate, 61.2% had unilateral cleft lip and palate, and 20.6% had bilateral cleft lip and palate. A total of 33.6% were diagnosed with VPI and received a sphincter pharyngoplasty (mean age, 11.9 years). When subsequent orthognathic surgery was examined, sphincter pharyngoplasty was not associated with maxillary advancement (P = 0.59) but did correlate with an increase in mandibular surgery from 2.8% to 11.1% (P = 0.02). The indications for mandibular surgery in the pharyngoplasty population were related to congenital micrognathia. When cephalometric analyses were evaluated, sphincter pharyngoplasty resulted in a decreased sella-to-nasion-to-B point angle (mean, 79.0-76.3 degrees, P = 0.02) and a higher incidence of normal to class II maxillomandibular relationships as defined by A point-to-nasion-to-B point angles >0.5 (P = 0.02).

Conclusions

Sphincter pharyngoplasty decreases anterior mandibular growth and the discrepancy between maxillomandibular skeletal relationships because of the frequent predisposition of cleft patients to maxillary hypoplasia. In patients with congenital mandibular micrognathia, a small increase in mandibular surgeries may occur.

Ovarian cancer (OC) is most lethal malignancy among all gynecological cancer. Large bodies of evidences suggest that mitochondrial-derived ROS play a critical role in the development and progression of OC. Paraoxonase 2 (PON2) is a membrane-associated lactonase with anti-oxidant properties. PON2 deficiency aggravates mitochondrial ROS formation, systemic inflammation, and atherosclerosis. The role of PON2 in cancer development remains unknown. In this report, in human, we identified that PON2 expression is higher in early stages (but not in late stages) of OC when compared to normal tissue. Using a mouse xenograft model of OC, we demonstrate that overexpression of PON2 prevents tumor formation. Mechanistically, PON2 decreases OC cell proliferation by inhibiting insulin like growth factor-1 (IGF-1) expression and signaling. Intriguingly, PON2 reduces c-Jun-mediated transcriptional activation of IGF-1 gene by decreasing mitochondrial superoxide generation. In addition, PON2 impairs insulin like growth factor-1 receptor (IGF-1R) signaling in OC cells by altering cholesterol homeostasis, which resulted in reduced caveolin-1/IGF-1R interaction and IGF-1R phosphorylation. Taken together, we report for the first time that PON2 acts as a tumor suppressor in the early stage of OC by reducing IGF-1 production and its signaling, indicating PON2 activation might be a fruitful strategy to inhibit early stage ovarian tumor.