Title: A Study on Molecular Biology and Pathology of Keloid
Authors: Dr S. Sudha, Dr M. Srinivaasan, Dr Kalesh S, Dr Krishna G
DOI: https://dx.doi.org/10.18535/jmscr/v6i2.74
Abstract
Introduction: Keloids are dermal fibro proliferative disorder characterized by excessive deposition of collagen in dermis and subcutaneous tissue after tissue injury or spontaneously. Angiogenesis inhibition has been shown to be effective in treatment of malignancy in both animal models and human beings. Recently, it has been reported that vascular endothelial growth factor (VEGF), a potent angiogenic factor, is over expressed in keloid tissue and may have a potential role in its evolution.
Materials and Methods: 40 cases of keloid were studied. Histopathological features were studied in Haematoxylin and eosin stained sections from paraffin block. Expression of VEGFR-2 was studied by Immunohistochemistry in 40 cases of keloid.
Results: The most common site observed was Ear lobe followed by sternum.52.5% cases had previous history of surgery or trauma. Family history of keloid was present only in 17.5% cases.62.5% cases presented to the clinic asymptomatically for cosmetic reasons.87.5% of Keloid case studied shows Normal thickness of epidermis with Rete pegs. Basal cell arrangement was regular in 97.5% of keloid. Basal cell Vacoulation was present in 87.5% of keloid. In 95% of Keloid collagen deposition was found in both papillary and reticular dermis. Haphazard arrangement of collagen fibres was found in 95% of keloid. Broad acellular glassy collagen was found in 57.5% of keloid. Moderate amount of Inflammation was found in 67.5% of keloid. In all cases of keloid, blood vessels was found aggregating below the epidermis.VEGFR-2 expression was increased involving all layers of epidermis, fibroblast and endothelial cells in 57.5% of keloid. Intense staining was noted in 32.5% of keloid whereas moderate staining in 25% of keloid.
Conclusion: Our findings demonstrates that overlying epidermis is the major source of VEGF, which suggests novel therapies for keloids by inhibiting the production and effect of keratinocyte-derived VEGF or by inhibiting keratinocyte-derived VEGF activity on its endothelial receptors.
Keywords: Keloid, VEGFR-2, Wound, Healing, Histopathology.
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