IMMUNOCYTOCHEMICAL EXPRESSION OF GROWTH-FACTORS BY ODONTOGENIC JAW CYSTS

Citation
Tj. Li et al., IMMUNOCYTOCHEMICAL EXPRESSION OF GROWTH-FACTORS BY ODONTOGENIC JAW CYSTS, Journal of clinical pathology-Molecular pathology, 50(1), 1997, pp. 21-27
Citations number
44
Categorie Soggetti
Pathology
Volume
50
Issue
1
Year of publication
1997
Pages
21 - 27
Database
ISI
SICI code
Abstract
Aim-To determine the immunocytochemical pattern of expression of trans forming growth factor (TGF) a, epidermal growth factor (EGF), and TGF beta in the three most common types of odontogenic jaw cyst Methods-Gr owth factor expression was detected in paraffin wax sections of odonto genic cysts (27 odontogenic keratocysts, 10 dentigerous cysts, and 10 radicular cysts) using a streptavidin-biotin peroxidase technique with monoclonal antibodies directed against TGF alpha (clone 213-4.4) and TGF beta (clone TB21) and a polyclonal antibody directed against EGF ( Z-12). Results-The epithelial linings of all cysts showed reactivity f or TGF alpha which was mainly localised to basal and suprabasal layers . Odontogenic keratocyst linings expressed higher levels of TGF alpha than those of dentigerous and radicular cysts, with 89% (24/27) of odo ntogenic keratocysts exhibiting a strong positive reaction compared wi th 50% (five of 10) of dentigerous and radicular cysts, respectively. EGF reactivity was similar in all cyst groups, weaker than that for TG F alpha and predominantly suprabasal. TGF alpha and EGF were also dete cted in endothelial cells, fibroblasts and inflammatory cells within t he cyst walls. The most intense TGF beta staining in odontogenic cysts was extracellular within the fibrous tissue capsules, irrespective of cyst type. Conclusions-These results, together with previous studies of EGF receptor, indicate differential expression of TGF alpha, EGF an d their common receptor between the different types of odontogenic cys t, suggesting that these growth factors (via autocrine or paracrine, o r both, pathways) may be involved in their pathogenesis.