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Diagnosis of CGCGs of the jaws depends on both correct interpretation of clinical, radiographic and pathological data. Differentiation between aggressive and nonaggressive CGCGs should be considered to improve individual treatment planning.

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Macrophage infiltration has been implicated in infantile hemangioma (IH), the most common tumor of infancy. However, the exact role of macrophages in IH remains unknown. This study aims to clarify the functional significance of macrophages in the progression of IH. The distribution of macrophages in human IH was analyzed, and our results revealed that polarized macrophages were more prevalent in proliferating IHs than in involuting IHs, which was consistent with the increased macrophage-related cytokines in proliferating IHs. In vitro results further demonstrated that polarized macrophages effectively promoted the proliferation of hemangioma stem cells (HemSCs) and suppressed their adipogenesis in an Akt- and extracellular signal-regulated kinase 1/2 (Erk1/2)-dependent manner. Moreover, M2- but not M1-polarized macrophages promoted the endothelial differentiation of HemSCs. Furthermore, mixing macrophages in a murine hemangioma model elevated microvessel density and postponed fat tissue formation, which was concomitant with the activation of Akt and Erk1/2 signals. Cluster analysis revealed a close correlation among the macrophage markers, Ki67, vascular endothelial growth factor (VEGF), p-Akt, and p-Erk1/2 in human IH tissues. Collectively, our results suggest that macrophages in IH contribute to tumor progression by promoting the proliferation and endothelial differentiation while suppressing the adipogenesis of HemSCs. These findings indicate that targeting the infiltrating macrophages in IH is a promising therapeutic approach to accelerate IH regression.

Our previous study demonstrated that allograft inflammatory factor-1 (AIF-1) is present in the vessels of infantile hemangiomas but neither in the vessels of vascular malformations, pyogenic granulomas, normal skin, placental tissues nor in the neovessels of squamous cell carcinomas of the tongue. The purpose of this study was to explore the impact of AIF-1 alterations on endothelial cells (EC). Stable introduction of AIF-1 to the human umbilical vein EC line (HUV-EC-C) in vitro revealed that AIF-1 enhances the proliferation and migration of the EC and promotes G0/G1-to-S-phase transition, accompanied by up-regulation of basic fibroblast growth factor (p Ͻ 0.05). In contrast, AIF-1 did not affect the expression of granulocyte colony-stimulating factor, VEGF-a, monocyte chemoattractant protein-1, or tissue inhibitor of metalloproteinase-1. AIF-1 expression was not induced by hypoxia, VEGF-a, basic fibroblast growth factor, or insulin-like growth factor-2 in EC. Taken together, these findings suggest that the impact of AIF-1 on EC would stimulate angiogenesis and consequently affect the progression of infantile hemangiomas. (Pediatr Res 67: 29-34, 2010)