RESUMEN
Intense pulsed light (IPL) is used for aesthetic and therapeutic purposes. According to recent literature, utilizing IPL may boost upregulation of anti-inflammatory cytokines, and downregulation of pro-inflammatory cytokines. Concerns have been raised about potential thermal damage to the soft and hard tissues in the oral cavity. Therefore, the aim of this study was to determine the safety of using IPL of various intensities in the tissues of the oral cavity. METHODS: Three adult pigs were included in the trial. The oral cavity was divided into four quadrants and projected with a wide range of IPL settings. Alveolar bone, buccal mucosa, and gingival tissue samples were taken immediately and after 24 h. In each animal, one quadrant of the jaw was left untreated and served as a control. All samples were processed and stained with H&E. RESULTS: Clinical examination showed no evidence of changes in the integrity of the examined tissues. Histological examination of the different tissues did not demonstrate significant thermal damage or changes in the characterization of the cells compared to the control tissues. CONCLUSIONS: The use of IPL in the oral cavity is safe and does not negatively affect the tissues.
RESUMEN
BACKGROUND: Osteosarcoma (OS) mortality is attributed to lung metastases. Endothelial progenitor cells (EPCs) mediate the angiogenic switch in several cancers. The spatial proximity between EPCs and OS in the bone led to the hypothesis that EPCs-osteosarcoma interactions may possibly promote OS progression and aggressiveness. METHODS: A PI3K inhibitor, Bevacizumab (an anti-VEGF-A antibody), and an anti-FGF2 antibody were added to the EPCs' conditioned medium (EPC-CM), and their impacts on OS cell (U2-OS and 143B) proliferation, migration, invasion, MMP9 expression, and AKT phosphorylation were determined. The autocrine role of VEGF-A was assessed using Bevacizumab treatment and VEGF-A silencing in OS cells. Toward this end, an orthotopic mouse OS model was established. Mouse and human tumors were immunolabeled with antibodies to the abovementioned factors. RESULTS: EPC-CM enhanced osteosarcoma MMP9 expression, invasiveness, and migration via the PI3K/AKT pathway. The addition of Bevacizumab and an anti-FGF2 antibody to the EPC-CM diminished OS cell migration. The autocrine role of VEGF-A was assessed using Bevacizumab and VEGF-A silencing in OS cells, resulting in decreased AKT phosphorylation and, consequently, diminished invasiveness and migration. Consistently, OS xenografts in mice displayed high VEGF-A and FGF2 levels. Remarkably, lung metastasis specimens derived from OS patients exhibited marked immunolabeling of CD31, VEGF-A, and FGF2. Conclusions: EPCs promote OS progression not only by physically incorporating into blood vessels, but also by secreting cytokines, which act via paracrine signaling. EPCs induced in vitro MMP9 overexpression, invasion, and migration. Additional animal studies are warranted to further expand these results. These findings may pave the way toward the development of novel EPCs-targeted therapeutics aimed at blocking OS metastasis.
