Synovial hyperplasia between proliferation & reduced apoptosis : Immunohistochemical study for expression of bcl2 and p53 in rheumatoid synovium

Abstract EN

Objective: Defective apoptosis has been recently suggested as a pathogenetic mechanism for synovial hyperplasia in rheumatoid arthritis.

The underlying mechanism for the disturbed apoptotic machinery is not clearly understood and controversial results are presented about the level of these apoptosis related proteins in rheumatoid arthritis synovium.

Our study aimed at studying the expression of Bcl2 and P53 in rheumatoid arthritis synovium as compared to osteoarthritic and posttraumatic controls in order to clarify their role in the production of synovial hyperplasia.

Materials & Methods: Specimens were examined with light and electron microscopy for estimation of synovial hyperplasia and ultrastructural changes for apoptosis.

Immunohistochemical staining was done to the synovial tissue of 14 RA, 10 OA and 5 PT controls for the expression of the antiapoptotic protein Bcl2 and the tumor suppressor gene P53.

Results: Bcl2 although known for its antiapoptotic role was positive in 10 out of 14 cases, while P53 was positive for all RA samples.

There was a statistically insignificant difference in Bcl2 expression between RA and OA while it showed a statistically significant difference between RA and PT controls.

On the other hand P53 was significantly higher in RA versus OA controls while it was extremely negative in PT controls.

Conclusion: Defective apoptosis could be related to P53 expression while it is not always associated with increased expression of the antiapoptotic protein Bcl2.