We evaluated the influence of CT-free or CT-based computer assisted orthopaedic surgery (CAOS) on the alignment of total knee prostheses (TK) and micromotion of tibial components. This randomised study compared 19 CTfree, 17 CT-based CAOS TK, and a matched control group of 21 conventionally placed TK. Using Roentgen stereophotogrammetric analysis (RSA) the migration was measured. The alignment and component positions were measured on radiographs. No significant difference in leg and tibial component alignment was present between the three groups. A significant difference was found for micromotion in subsidence, with the conventional group having a mean of 0.16 mm, compared to the CT-free group at 0.01 mm and the CT-based group at −0.05 mm. No clinical significant difference in alignment was found between CAOS and conventionally operated TK. More subsidence of the tibial component was seen in the conventional group compared to both CAOS groups at two year follow-up.

Introduction Likely due to ignored heterogeneity in disease pathophysiology, osteoarthritis (OA) has become the most common disabling joint disease, without effective disease-modifying treatment causing a large social and economic burden. In this study we set out to explore responses of aged human osteochondral explants upon different OA-related perturbing triggers (inflammation, hypertrophy and mechanical stress) for future tailored biomimetic human models. Methods Human osteochondral explants were treated with IL-1β (10 ng/ml) or triiodothyronine (T3; 10 nM) or received 65% strains of mechanical stress (65% MS). Changes in chondrocyte signalling were determined by expression levels of nine genes involved in catabolism, anabolism and hypertrophy. Breakdown of cartilage was measured by sulphated glycosaminoglycans (sGAGs) release, scoring histological changes (Mankin score) and mechanical properties of cartilage. Results All three perturbations (IL-1β, T3 and 65% MS) resulted in upregulation of the catabolic genes MMP13 and EPAS1 . IL-1β abolished COL2A1 and ACAN gene expression and increased cartilage degeneration, reflected by increased Mankin scores and sGAGs released. Treatment with T3 resulted in a high and significant upregulation of the hypertrophic markers COL1A1 , COL10A1 and ALPL . However, 65% MS increased sGAG release and detrimentally altered mechanical properties of cartilage. Conclusion We present consistent and specific output on three different triggers of OA. Perturbation with the pro-inflammatory IL-1β mainly induced catabolic chondrocyte signalling and cartilage breakdown, while T3 initiated expression of hypertrophic and mineralization markers. Mechanical stress at a strain of 65% induced catabolic chondrocyte signalling and changed cartilage matrix integrity. The major strength of our ex vivo models was that they considered aged, preserved, human cartilage of a heterogeneous OA patient population. As a result, the explants may reflect a reliable biomimetic model prone to OA onset allowing for development of different treatment modalities. Supplementary Information The online version contains supplementary material available at 10.1007/s40744-021-00287-y.

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