Pathology · 2003
Differential expression of transforming growth factors-beta 1, -beta 2, -beta 3 and the type I, II, III receptors in the lining epithelia of inflamed gingiva.
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Ye Ping, Simonian Mary, Chapple Cheryl C, Gibbins John R, Kumar Rakesh K, Hunter Neil
Аннотация
AIMS: To investigate the distribution of transforming growth factor-beta isoforms in chronically inflamed periodontal tissues.
METHODS: The present study determined, by immunohistochemistry, the expression patterns of TGF-betas and their receptors in the lining epithelia of inflamed gingiva. Frozen sections were obtained from 22 human gingival biopsies.
RESULTS: TGF-beta 1 was not detected in gingival epithelial cells in examined sections. Detection of TGF-beta 2 indicated a progressive reduction of staining from the external oral epithelium through to gingival sulcus and the gingival attachment or pocket epithelium. TGF-beta 3 showed intense staining in all domains of both minimally inflamed gingiva and advanced periodontitis tissues. TGF-beta RI was visualised as focal staining of the spinous layer in the external oral epithelium of both periodontitis lesions and minimally inflamed tissues. TGF-beta RII was present throughout the strata, but with progressive reduction in intensity from the oral epithelium to gingival attachment or pocket epithelium respectively while, conversely, TGF-beta RIII showed an increase in diffuse staining intensity from external oral epithelium to pocket epithelium.
CONCLUSIONS: A distinct expression profile was observed within different individuals for TGF-betas and the corresponding receptors. These findings provide a basis for evaluation of the role of these growth factors in the pathogenesis of periodontitis.
METHODS: The present study determined, by immunohistochemistry, the expression patterns of TGF-betas and their receptors in the lining epithelia of inflamed gingiva. Frozen sections were obtained from 22 human gingival biopsies.
RESULTS: TGF-beta 1 was not detected in gingival epithelial cells in examined sections. Detection of TGF-beta 2 indicated a progressive reduction of staining from the external oral epithelium through to gingival sulcus and the gingival attachment or pocket epithelium. TGF-beta 3 showed intense staining in all domains of both minimally inflamed gingiva and advanced periodontitis tissues. TGF-beta RI was visualised as focal staining of the spinous layer in the external oral epithelium of both periodontitis lesions and minimally inflamed tissues. TGF-beta RII was present throughout the strata, but with progressive reduction in intensity from the oral epithelium to gingival attachment or pocket epithelium respectively while, conversely, TGF-beta RIII showed an increase in diffuse staining intensity from external oral epithelium to pocket epithelium.
CONCLUSIONS: A distinct expression profile was observed within different individuals for TGF-betas and the corresponding receptors. These findings provide a basis for evaluation of the role of these growth factors in the pathogenesis of periodontitis.