Abstract
Aims: To evaluate the appearance and distribution of matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2) and tissue inhibitor of metalloproteinase-4 (TIMP-4) in lesional skin biopsies of psoriasis patients. Study Design: Observational study. Place and Duration of Study: Institute of Anatomy and Anthropology and Department of Infectology and Dermatology, Rīga Stradiņs University, between September 2013 and June 2014. Methodology: We included 40 patients (31 men, 9 women; age range 18-70 years) with Psoriasis vulgaris, with present characteristic psoriatic eruptions in typical localization sites and no treatment received. Skin samples were obtained using routine punch biopsy method. 10 clinically healthy skin samples obtained during nevus excision procedure were used as control material. All Short Research Article Sidhom et al.; BJMMR, 8(10): 883-890, 2015; Article no.BJMMR.2015.519 884 tissue specimens were stained with hematoxylin and eosin and by immunohistochemistry for MMP2, TIMP-2 and TIMP-4. The intensity of staining was graded semiquantitatively. Spearman’s rank correlation coefficient was calculated. Results: In psoriasis patients numerous MMP-2-containing keratinocytes were found in epidermis, MMP-2 positive dermal fibroblasts and inflammatory cells varied from few to abundant. Few epidermal cells and moderate to numerous dermal cells contained TIMP-2. Moderate to numerous epidermal and dermal cells contained TIMP-4. Statistically significant strong positive correlation was found between MMP-2 in epidermis and dermis (Spearman’s rank correlation coefficient = .878, P = .000). Statistically significant moderate positive correlation was found between TIMP-2 and TIMP-4 in dermis (Spearman’s rank correlation coefficient = .639, P = .000) and between TIMP-2 in epidermis and dermis (Spearman’s rank correlation coefficient = .564, P = .000). Conclusion: TIMP-4 seems to be most important inhibitor of psoriatic skin degeneration, richly raised by MMP-2. Its moderate correlation with TIMP-2 proves involvement of other tissue inhibitors in the degeneration inhibition and gives evidence about possible patterning between the tissue inhibitors of metalloproteinases.
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