It has been suggested that heat-shock proteins (HSPs) might be involved in autoimmune disease mechanisms in humans, considering the high degree of sequence homology between bacterial and human HSPs. Several authors have postulated that HSPs might be involved in periodontal disease processes, but not specifically in peri-implantitis. Consequently, using immunohistochemical techniques, we studied the distribution of HSP25, HSP32, HSP60 and HSP72 in three groups of patients: (1) subjects with natural teeth (healthy periodontal tissue), (2) subjects with normal peri-implant mucosa and (3) subjects with clinically evident peri-implantitis. The immunolabelling for HSP25 and HSP60 was increased in the peri-implantitis group HSP32 immunolabelling slightly decreased in peri-implant and peri-implantitis gingiva. Labelling for HSP72 was undetectable in all three groups. In conclusion, we observed in peri-implantitis a clearly enhanced immunolabelling of two specific HSPs, HSP25 and HSP60, restricted to gingival epithelium and this could indicate a signal of local altered homeostasis.

Altered immunolocalization of heat-shock proteins in human peri-implant gingiva / E. Borsani, S. Salgarello, A. Stacchiotti, M. Mensi, R. Boninsegna, F. Ricci, L. Zanotti, R. Rezzani, P. Sapelli, R. Bianchi, L.F. Rodella. - In: ACTA HISTOCHEMICA. - ISSN 0065-1281. - 109:3(2007), pp. 221-227.

Altered immunolocalization of heat-shock proteins in human peri-implant gingiva

A. Stacchiotti;R. Bianchi
Penultimo
;
2007

Abstract

It has been suggested that heat-shock proteins (HSPs) might be involved in autoimmune disease mechanisms in humans, considering the high degree of sequence homology between bacterial and human HSPs. Several authors have postulated that HSPs might be involved in periodontal disease processes, but not specifically in peri-implantitis. Consequently, using immunohistochemical techniques, we studied the distribution of HSP25, HSP32, HSP60 and HSP72 in three groups of patients: (1) subjects with natural teeth (healthy periodontal tissue), (2) subjects with normal peri-implant mucosa and (3) subjects with clinically evident peri-implantitis. The immunolabelling for HSP25 and HSP60 was increased in the peri-implantitis group HSP32 immunolabelling slightly decreased in peri-implant and peri-implantitis gingiva. Labelling for HSP72 was undetectable in all three groups. In conclusion, we observed in peri-implantitis a clearly enhanced immunolabelling of two specific HSPs, HSP25 and HSP60, restricted to gingival epithelium and this could indicate a signal of local altered homeostasis.
2007
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/35307
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