Current Concepts in the Pathogenesis and Management of Vascular Lesions - A Brief Review
Journal Title: Indian Journal of Dental Advancements - Year 2016, Vol 8, Issue 4
Abstract
Hemangiomas are considered to be benign tumors of infancy which show a rapid growth phase marked by endothelial cell proliferation, followed by gradual involution. On the other hand, vascular malformations are structural anomalies of blood vessels without endothelial cell proliferation. The pathophysiology of these lesions is still shroud in mystery. One etiologic hypothesis speculates that cells are "embolized" from the placenta. Another suggests that hemangiomas result from somatic mutations in a gene mediating endothelial cell proliferation. Recent data suggest an endothelial progenitor cell as the source of origin of the tumors. It has been speculated that hypoxia, either systemically (e.g., due to placental insufficiency) or in a specific "niche" area of poorly perfused tissue stimulates endothelial progenitor cells to proliferate inappropriately. The fetal endothelial cell precursor cells, possess specific histochemical markers (GLUT-1, Lewis Y Antigen, merosin), similar to those on placental blood vessels. Abnormal levels of matrix metalloproteinases (MMP-9) and proangiogenic factors (VEGF, b-FGF, and TGF-beta 1) play a crucial role. Genetic errors in growth factor receptors have also been shown to affect development of hemangiomas. Recent discoveries concerning hemangioma pathogenesis provide both an improved understanding and more optimal approach to workup and management like corticosteroid or propranolol therapy. Important detrimental associations can be seen with hemangioma, such as significant structural anomalies. Standards of care have dramatically changed evaluation and management of hemangiomas.Herein, we have briefly discussed the factors that contribute to the formation of hemangiomas and vascular malformations in general along with their management.
Authors and Affiliations
Snehanjan Sarangi, Debanjali Mukherjee
Keywords
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- EP ID EP474989
- DOI 10.5866/2016.8.10241
- Views 109
- Downloads 0
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