Ultrastructural study of chondrocytes from fibrillated and non-fibrillated human osteoarthritic cartilage

Abstract

Knee articular cartilage samples obtained by arthroscopy from ten patients with well defined knee osteoarthritis (OA) were studied by light and transmission electron microscopy. The morphological phenotype of cells from fibrillated and non-fibrillated regions of OA cartilage was characterized. Three different cell sub-populations were identified. Type 1 cells were found in the superficial and upper middle zones and comprised single chondrocytes and cells organized in aggregates or "clones' that showed a typical chondrocyte phenotype. Type 2 cells displayed a secretory phenotype. Type 3 cells comprised chondrocytes undergoing a degenerative process and were distributed throughout all zones of the cartilage. Changes in the cytoskeletal arrangement, presence of abundant filopodia, peripheral localization of centrioles, and presence of primary cilia were found in many chondrocytes suggesting that they are active motile cells. No mitotic figures were found in this study. Morphometrical analysis was performed to determine the total number of cells and the number of chondrocytes per lacuna in the superficial and upper middle zones of fibrillated and non-fibrillated OA cartilage. There were no statistically significant differences in the total number of cells. In contrast, fibrillated OA cartilage contained a statistically significantly higher percentage of lacunae containing four of more chondrocytes than non-fibrillated OA cartilage samples. The absence of mitotic figures and the presence of motile elements in many chondrocytes raise the possibility that cell aggregates or "clones' in damaged OA cartilage originate by an active process of cell migration rather than by cellular division.

Depletion of SIRT6 causes cellular senescence, DNA damage, and telomere dysfunction in human chondrocytes

“…*Statistically significant difference (n ¼ 3, P ¼ 0.03 and P ¼ 0.01 respectively). progression of OA, and the chondrocytes in these clusters are proliferating clonal chondrocytes 29 . It has been suggested this is a self-reparatory process 30 , which implies that SIRT6 plays a role in the proliferation of chondrocytes.…”

The role of the cytoskeleton in the viscoelastic properties of human articular chondrocytes

“…The cytoskeleton may therefore serve an important biomechanical function in governing cellmatrix interactions in articular cartilage, and may also play a role in regulating the response of the chondrocyte to mechanical stimuli. Therefore, changes in mechanical properties of chondrocytes that occur with hip osteoarthritis may reflect changes in the structure and composition of these cytoskeletal proteins [30]. At this point, it is not possible to determine whether these changes are causally related to osteoarthritis, or simply phenomena that occur secondary to the disease process.…”

Chemotaxis of human articular chondrocytes and mesenchymal stem cells

“…A morphological analysis of chondrocytes in human osteoarthritic cartilage identified changes in the cytoskeletal arrangement such as the presence of abundant filopodia, peripheral localization of centrioles, and presence of primary cilia suggesting that they are actively motile cells. 24 In some animal models of cartilage injury cells migrate to the defects, proliferate, and form a repair tissue, 25 but these cells are thought to originate from synovium and the subsynovial space.…”