INTRODUCTION
Osteoarthritis is a very common disease in our modern society. Up to 15% of the population worldwide is concerned by this uncurable chronic joint condition. Most of osteoarthritic cases are seen at the knee joint due to the intense daily repetitive mechanical stress resulting, at last, in cartilage deterioration, typically located at the weight-bearing areas. Paradoxically, a recent radiological study has shown that cartilage at the posterior aspect of the medial condyles but not the lateral condyles were significantly thicker in patients presenting advanced medial knee osteoarthritis. This study focuses on the histobiological characteristics of the cartilage at the non-weight-bearing areas in order to provide further information on the cartilage repair mechanisms in osteoarthritis.
METHODS AND MATERIALS
The study samples come from patients affected by medial knee osteoarthritis. The samples were
collected from 10 total knee replacement surgeries. Contrast-enhanced micro-CT imaging as well immunohistochemical methods were performed to analyze the region of interest.
RESULTS
The advanced imaging methods show that cartilage at the posterior aspect of medial condyles undergoes a severe repair response in consequence to the inflammatory environment resulting in a thickening process. It seems that the more advanced the osteoarthritic condition is, the more severe the remodeling mechanism is to be seen, as maximum cartilage thickness is positively correlated with the modified Mankin score. Signs of high cell proliferation associated with high cell apoptosis testify the repair mechanism that leads, in this articular area, to cartilage hypertrophy. The decreased concentration of the collagen content and the severe proteoglycan reduction as well as the typical advanced OA degrading signs, demonstrate the unhealthy cartilage state of the region of interest, despite the enhanced cartilage thickness.
DISCUSSION
In comparison to the current literature, the cartilage in the region of interest show to be rather hypertrophic, showing signs of high cell proliferation, than simply swollen. The reduced proteoglycan concentration and collagen content caused by the predominant cell apoptosis, not typically seen in hypertrophic states, show the distinct characteristics of this articular area. Furthermore, as the structural modifications seen at the non-weight-bearing areas vary drastically from one sample to another, assessing the posterior aspect of the condyles with advanced imaging methods as part of the individual approach to osteoarthritis, seems to be necessary in order to provide essential information for the introduction of an optimal therapy.
CONCLUSION
The cartilage at the posterior aspect of the medial femoral condyles thickens in result of the inflammatory environment caused by the biomechanical stress. The repair response leading to cartilage hypertrophy can only be observed at the non-weight-bearing areas because of the reduced mechanical strains. Further investigations of the cartilage at the widest range of articular motion remain necessary in order to fully understand the repair mechanisms in osteoarthritic conditions that leads to these particular molecular and structural modifications.