BACKGROUND: A previous cDNA-microarray analysis described constantly differentially expressed genes in wear particle induced and infectious SLIM (synovial-like interface membrane). This study aims to validate the cDNA microarray data in order to approve differences of the gene expression profiles of RNA and proteins. METHODS: Tissue from 16 wear particle induced and 20 infectious periprosthetic membranes were analyzed by RT-PCR and immunohistology with regard to the expression of inflammatoric associated genes. RESULTS: RT-PCR showed the genes cd9, cd11b, cd18, cd52 as well as pdgfrbeta in interface membranes. In the wear particle induced membrane the immunohistochemical analysis showed a significantly weaker gene expression of PDGFRbeta, whereas the differential overexpression of CD9, CD11b and CD52 was confirmed. For CD18, there was no difference in expression between wear induced and infectious periprosthetic tissue. CONCLUSION: Different pathomechanisms, which are reflected by different gene expression profiles, might produce different types of periprosthetic membranes. By RT-PCR and immunohistochemical analysis the micro array data of the genes cd9, cd11b, cd52 and pdgfrbeta could be validated. Identifying the gene products of cd9, cd11b and cd52 in blood or tissue may help to differentiate between wear induced and infectious loosening.
BACKGROUND: A previous cDNA-microarray analysis described constantly differentially expressed genes in wear particle induced and infectious SLIM (synovial-like interface membrane). This study aims to validate the cDNA microarray data in order to approve differences of the gene expression profiles of RNA and proteins. METHODS: Tissue from 16 wear particle induced and 20 infectious periprosthetic membranes were analyzed by RT-PCR and immunohistology with regard to the expression of inflammatoric associated genes. RESULTS: RT-PCR showed the genes cd9, cd11b, cd18, cd52 as well as pdgfrbeta in interface membranes. In the wear particle induced membrane the immunohistochemical analysis showed a significantly weaker gene expression of PDGFRbeta, whereas the differential overexpression of CD9, CD11b and CD52 was confirmed. For CD18, there was no difference in expression between wear induced and infectious periprosthetic tissue. CONCLUSION: Different pathomechanisms, which are reflected by different gene expression profiles, might produce different types of periprosthetic membranes. By RT-PCR and immunohistochemical analysis the micro array data of the genes cd9, cd11b, cd52 and pdgfrbeta could be validated. Identifying the gene products of cd9, cd11b and cd52 in blood or tissue may help to differentiate between wear induced and infectious loosening.
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