Indian journal of dermatology, venereology and leprology · 2018
Reduced immunohistochemical expression of CCN3 in vitiligo.
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Faria Adriane Reichert, Jung Juliana Elizabeth, Silva de Catro Caio Cesar, de Noronha Lucia
Аннотация
BACKGROUND: Defective adhesion seems to be involved in the chronic loss of melanocytes observed in vitiligo. Recent findings showed an association of genetic variants of an adhesion gene with vitiligo and reduced immunohistochemical expression of some adhesion molecules in vitiligo skin.
AIMS: To compare CCN3 immunohistochemical expression in lesional and non-lesional epidermis of individuals with vitiligo.
METHODS: A total of 66 skin specimens from 33 volunteers with vitiligo were analyzed by immunohistochemistry using anti-CCN3 antibodies. Absence of topical or systemic treatment for vitiligo over the previous 30 days and availability of an area of non-lesional skin for biopsy at least 15 cm away from any vitiliginous macules were the main inclusion criteria.
RESULTS: A significant reduction of CCN3 expression was observed in lesional skin as compared to non-lesional skin (P = 0.001).
LIMITATIONS: Paraffin embedded skin samples do not allow investigation by molecular biology methods. Not all samples allowed analysis due to the lamina preparation technique. Complete clinical data was not available for all patients.
CONCLUSION: Our results support the hypothesis of impaired cell adhesion in vitiligo suggested by genetic studies. The pattern of immunohistochemical expression suggests that vitiligo might be an epithelial disease and not just a melanocyte disorder.
AIMS: To compare CCN3 immunohistochemical expression in lesional and non-lesional epidermis of individuals with vitiligo.
METHODS: A total of 66 skin specimens from 33 volunteers with vitiligo were analyzed by immunohistochemistry using anti-CCN3 antibodies. Absence of topical or systemic treatment for vitiligo over the previous 30 days and availability of an area of non-lesional skin for biopsy at least 15 cm away from any vitiliginous macules were the main inclusion criteria.
RESULTS: A significant reduction of CCN3 expression was observed in lesional skin as compared to non-lesional skin (P = 0.001).
LIMITATIONS: Paraffin embedded skin samples do not allow investigation by molecular biology methods. Not all samples allowed analysis due to the lamina preparation technique. Complete clinical data was not available for all patients.
CONCLUSION: Our results support the hypothesis of impaired cell adhesion in vitiligo suggested by genetic studies. The pattern of immunohistochemical expression suggests that vitiligo might be an epithelial disease and not just a melanocyte disorder.