PURPOSE: the present study was conduced in order to analyse the molecular changes during the apoptotic cascade in knee articular cartilage of patients with OA. METHOD: articular cartilage specimens were assessed by histology (Haematoxylin and Eosin), histochemistry (Masson's Trichromic and Alcian Blue), immunohistochemistry through TRAIL, DR5 and Caspase-3, TUNEL and Hoechst staining in fresh isolated chondrocytes. RESULTS: histology results demonstrated the structural alterations in the articular knee cartilage with OA, and histochemistry results demonstrated the presence of matrix calcification and a proteoglycans reduction. Immunohistochemistry staining showed that structural alterations, matrix calcification and a proteoglycans reduction coincided with an increase in apoptotic cells when compared to normal cartilage; however, this cellular mechanism of death was demonstrated by TUNEL and Hoechst 33258 staining in fresh isolated chondrocytes. CONCLUSION: in this study, we demonstrated an apoptosis activation by the extrinsic pathway in OA cartilage. The apoptosis-positive cells might be due to a protection mechanism after sublethal injury, in particular, represented by an increased survival of chondrocytes that are able to participate in the repair process.
PURPOSE: the present study was conduced in order to analyse the molecular changes during the apoptotic cascade in knee articular cartilage of patients with OA. METHOD:articular cartilage specimens were assessed by histology (Haematoxylin and Eosin), histochemistry (Masson's Trichromic and Alcian Blue), immunohistochemistry through TRAIL, DR5 and Caspase-3, TUNEL and Hoechst staining in fresh isolated chondrocytes. RESULTS: histology results demonstrated the structural alterations in the articular knee cartilage with OA, and histochemistry results demonstrated the presence of matrix calcification and a proteoglycans reduction. Immunohistochemistry staining showed that structural alterations, matrix calcification and a proteoglycans reduction coincided with an increase in apoptotic cells when compared to normal cartilage; however, this cellular mechanism of death was demonstrated by TUNEL and Hoechst 33258 staining in fresh isolated chondrocytes. CONCLUSION: in this study, we demonstrated an apoptosis activation by the extrinsic pathway in OA cartilage. The apoptosis-positive cells might be due to a protection mechanism after sublethal injury, in particular, represented by an increased survival of chondrocytes that are able to participate in the repair process.
Authors: M J López-Armada; B Caramés; M Lires-Deán; B Cillero-Pastor; C Ruiz-Romero; F Galdo; F J Blanco Journal: Osteoarthritis Cartilage Date: 2006-02-21 Impact factor: 6.576
Authors: Ahmed Abdelmoniem Mousa; Hala Ali Ibrahim El-Gansh; Mabrouk Attia Abd Eldaim; Mostafa Abd El-Gaber Mohamed; Azza Hassan Morsi; Hesham Saad El Sabagh Journal: Environ Sci Pollut Res Int Date: 2019-10-15 Impact factor: 4.223
Authors: Laura A Smith Callahan; Anna M Ganios; Erin P Childers; Scott D Weiner; Matthew L Becker Journal: Acta Biomater Date: 2013-01-02 Impact factor: 8.947
Authors: Giuseppe Musumeci; Paola Castrogiovanni; Rosalia Leonardi; Francesca Maria Trovato; Marta Anna Szychlinska; Angelo Di Giunta; Carla Loreto; Sergio Castorina Journal: World J Orthop Date: 2014-04-18