Analysis of the expression of heat-shock protein 27 in patients with oral lichen planus
Article first published online: 2 JUL 2012
© 2012 John Wiley & Sons A/S
Volume 19, Issue 1, pages 65–72, January 2013
How to Cite
García-García, V., Bascones-Martínez, A., García-Kass, A., Martinelli-Kläy, C., Küffer, R., Álvarez-Fernández, E. and Lombardi, T. (2013), Analysis of the expression of heat-shock protein 27 in patients with oral lichen planus. Oral Diseases, 19: 65–72. doi: 10.1111/j.1601-0825.2012.01951.x
- Issue published online: 7 DEC 2012
- Article first published online: 2 JUL 2012
- Accepted manuscript online: 31 MAY 2012 12:41PM EST
- Received 13 March 2012; revised 29 April 2012; accepted 24 May 2012
- oral precancer;
- heat-shock proteins;
- malignant transformation;
- oral cancer;
Oral Diseases (2012) 19, 65–72
Objective: Heat-shock protein 27 (hsp27) has been implicated in several biological events. In this experimental study, we aimed at analysing, for the first time, the expression of hsp27 in the diverse stages of oral lichen planus (OLP) lesions.
Materials and methods: Thirty-six biopsy specimens of patients with OLP and 10 of healthy patients were selected. OLP specimens were divided into three groups: G1 – moderate or mildly active OLP; G2 – active or moderately active atrophic OLP; G3 – mild or inactive atrophic OLP. Hsp27 expression was analysed by immunohistochemistry (staining intensity and percentage of stained cells), and results of staining were compared between the different groups. Gender, age and anatomical location were also studied.
Results: In the basal layer, an increase of hsp27 expression in both G2 and G3 was observed when compared to G1 and control group. In contrast, a decrease of hsp27 expression in the superficial layer was observed in all groups when compared to control group.
Conclusion: The increased expression of Hsp27 in the basal layer observed during the OLP evolution and the less staining in the superficial layers in all cases of OLP suggest that hsp27 may have a role in the OLP pathogenesis.