ABSTRACT
Oral angiolipomas are exceedingly rare and little is known about their morphological and etiological features. Here, we report two cases of oral angiolipoma and discuss their clinicopathological and immunohistochemical features, focusing on endothelial markers. Both lesions presented mature adipocytes interspersed by small blood vessels containing fibrin thrombi. Immunohistochemical analysis showed numerous mast cells and expression of CD34, vascular endothelial growth factor, intercellular adhesion molecule-1, interferon-γ and interleukin 6 in most endothelial and stromal cells. Mast cell-endothelial cell interaction may be responsible for the reactive or neoplastic origin of the vascular proliferation of these entities.
Subject(s)
Angiolipoma/pathology , Mouth Neoplasms/pathology , Adipocytes/pathology , Adult , Antigens, CD34/analysis , Endothelial Cells/pathology , Endothelium, Vascular/pathology , Female , Fibrin/analysis , Follow-Up Studies , Humans , Immunohistochemistry , Intercellular Adhesion Molecule-1/analysis , Interferon-gamma/analysis , Interleukin-6/analysis , Male , Mast Cells/pathology , Microvessels/pathology , Middle Aged , Stromal Cells/pathology , Thrombosis/pathology , Vascular Endothelial Growth Factor A/analysisABSTRACT
Programming of fetal development is considered to be an important risk factor for noncommunicable diseases of adulthood, including coronary heart disease (CHD). Aiming to investigate the association between maternal nutrition and the development of the coronary arteries (CAs) in staged mice embryos, C57BL/6 mice embryos from Stages 16 to 23 were taken from mothers fed a normal protein (NP) or low protein (LP) diet, and the CA were studied. Although the LP embryos had lower masses, they had faster heart growth rates when compared with the NP embryos. The subepicardial plexuses were observed earlier in the NP embryos (Stage 20) than in the LP ones (Stage 22; P < 0.01). Apoptotic nuclei were seen around the aortic peritruncal ring beginning at Stage 18 in the NP and LP embryos. FLK1(+) (fetal liver kinase 1 = VEGF-r2 or vascular endothelial growth factor receptor 2) cells had a homogeneous distribution in the NP embryos as early as Stage 18, whereas a similar distribution in the LP embryos was only seen at Stages 22 and 23. Maternal protein restriction in mice leads to a delay in the growth of the heart in the embryonic period modifying the development of the subepicardial peritruncal plexus and the apoptosis in the future coronary orifice region.
