Mylène Jansen

Cartilage collagen structure after KJD and HTO using T2-mapping 313 15 KJD patients, goes paired with an increase in cartilage volume. Alternatively, the collagen orientation of newly formed cartilage could be simply be similar to the more superficial tissue that had been lost before, as T2 values are short in the deep layer, where the collagen is oriented perpendicular to the subchondral bone, and longer in the superficial layer, where the collagen fibers are oriented more parallel to the cartilage surface. 9 Either way, while it is tempting to draw direct conclusion on paired T2 value and volume increases, it is important to realize that the T2 values represent the entire cartilage and not just newly formed tissue. In HTO-indicated KJD patients and HTO patients a significant increase in T2 values is seen, but no significant changes in cartilage volume, which corresponds with previous cartilage thickness results. 18 Although the increase in T2 values was significantly larger than in matched OAI patients, case-control matching between a late OA cohort (patients who need surgical treatment) and an early OA cohort (OAI) is not perfect, and the T2 value increase might still be the result of natural progression. The fact that a higher age and BMI had a positive influence on the T2 value increase is consistent with other studies showing natural progression. 10,36,37 Also, in patients treated with an autologous chondrocyte transplantation for a cartilage defect, an increase in T2 values of 2.8 ms in a 1–2 year period was seen in the healthy (control) cartilage. 7 It might be that any surgical intervention, or a change in weight-bearing as a result, already affects cartilage content or structure, regardless of what intervention is performed. The difference between the KJD groups is somewhat surprising. In the larger MRI cartilage thickness study in the original RCT, it was shown that mild OA patients (KLG ≤2) did not show significant changes in cartilage thickness or denuded bone areas, while severe OA patients (KLG ≥3) showed significant regeneration. In the current study, mild and severe OA could not be compared, since by this definition only 2 KJD patients in the current study had mild OA. The original indication of TKA or HTO might still reflect a difference in somewhat more or less severe OA, as indicated by the significant baseline difference in MAC cartilage volume as well. As such, the different responses in the 2 groups might be because more severely affected patients show a better response to KJD. Anecdotally, the 2 KJD patients with a KLG of 1 and 2 showed a higher than average T2 value increase combined with a much higher than average decrease in cartilage volume. A clear limitation of this study was sample size. While it provides interesting exploratory results that despite the small sample size could reach statistical significance, and correspond well previous results, a larger sample size would likely allow for stronger conclusions. It would be worthwhile to perform imaging studies in a larger group of patients, either 3T T2-mapping or more advanced sequences on a 7T scanner, and add more time points, including a scan immediately post-treatment. HTO patients could be included as well, although that may require changes to the treatment protocol. Imaging studies could be combined with synovial biomarker analyses to better interpret imaging analysis results.