Chondromodulin‑I expression and correlation with angiogenesis in human osteoarthritic cartilage.

The present study aimed to evaluate the expression and localization of chondromodulin‑I (ChM‑I) in human osteoarthritic cartilage and its correlation with vascular invasion during osteoarthritis (OA) progression. Osteochondral specimens were collected from patients with OA, as well as from young and aged donors without joint diseases. The grade and the number of vascular channels terminating in non‑calcified cartilage of these collected specimens were assessed by Safranin‑O/Fast green staining. ChM‑I expression in articular cartilage was examined by immunohistochemistry, western blotting and reverse transcription‑quantitative polymerase chain reaction analyses. ChM‑I protein and mRNA levels in articular cartilage appeared to be consistent between the normal young and aged groups (P>0.05). In mildly degene-rated cartilage, ChM‑I expression decreased in the extracellular matrix (ECM) of the superficial zone and in the cytoplasm of the superficial and middle zone compared with normal cartilage (P<0.05). In moderately degenerated cartilage, ChM‑I protein expression was reduced in the ECM of all zones of articular cartilage, but the immunostaining intensity in the cytoplasm was increased. In severely degenerated cartilage, ChM‑I expression was detected primarily in the cytoplasm of the cluster‑forming chondrocytes. The density of vascular channels was correlated with the ChM‑I expression levels in cartilage ECM. ChM‑I expression was reduced in OA cartilage matrix, compared with normal cartilage (both young and aged), and correlated with angiogenesis, indicating that loss of ChM‑I may promote angiogenesis in OA cartilage. Expression of ChM‑I protein in the cytoplasm was decreased in mildly degenerated cartilage, whereas ChM‑I expression increased in moderately degenerated cartilage accompanied by chondrocyte proliferation. These findings suggested that attenuation of ChM‑I in the cartilage ECM may be due to decreased expression of ChM‑I in cytoplasm of early stage OA and increased depletion of ChM‑I in the ECM of advanced stage OA.