Mylène Jansen

Summary and general discussion 401 19 Apart from bone-to-bone JSWmeasured on weight-bearing radiographs as an indirect measure for cartilage restoration, cartilage thickness can be measured directly on non-weight-bearing MRI scans. Strangely, these 2 techniques have always shown a poor correlation in longitudinal changes over time. In chapter 12 , bone-to-bone JSW measured on non-weight-bearing CT is introduced to investigate whether the poor correlation is because of the difference in weight- bearing or because of measuring bone-to-bone distance versus cartilage thickness. Only CT 3D JSW and MRI cartilage thickness showed a significant longitudinal correlation, pointing towards the difference in weight-bearing as the cause of the weak correlation between changes in radiographic JSW and MRI cartilage thickness. Potentially this is because of the influence of cartilage resilience, although more research on this topic is warranted. The MRI cartilage thickness up to 10 years after KJD treatment is reported in chapter 13, using a 3-dimensional whole-joint approach. At 1- and 2-years post-treatment, cartilage in the most affected weight-bearing region was significantly thicker than before treatment. Male patients and those with more severe OA showed somewhat enhanced benefit. From 5 years post-treatment the cartilage started gradually thinning again, likely the result of natural progression. Even 10 years after treatment an increase in cartilage thickness was still observed, especially in the less affected parts of the joint. Thus, an initial boost of cartilaginous tissue repair after KJD treatment provides long-term tissue structure benefit. Subsequently, MRI cartilage thickness changes after KJD were compared with those after HTO treatment, as described in chapter 14 . Two years after treatment, TKA-indicated KJD patients showed not only a significant increase in cartilage thickness, but also a decrease in denuded bone areas. HTO-indicated KJD patients showed no significant change, while patients treated with HTO even showed significant deterioration on MRI despite an increased radiographic JSW. OA severity most strongly predicted MRI cartilage restoration, and significant cartilage restoration was seen only after KJD in severe OA patients. It appeared that in patients with severe OA, KJD may be more effective in restoring cartilage thickness than HTO. With the cartilage thickness changing after treatment, the next step was to evaluate the cartilage quality, which is presented in chapter 15 using T2-mapping MRI, representing cartilage collagen structure. After treatment with KJD or HTO, cartilage T2 relaxation times increased more than might be expected in natural OA progression, which could indicate loss or reorganization of collagen structure integrity. In TKA-indicated KJD patients, this increase was limited to the first year after treatment, after which the collagen content or structure improved. As these same patients showed a significant cartilage volume increase as well, increasing T2 values may partly be the result of maturation of newly formed cartilage and reorganization of the matrix in the first period after treatment.