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compared to CAS navigation was 1.5° (limit of agreement (1.96 SD) of 4.6°). Linear regression analysis showed that weight-bearing MLA measurements vary significantly from non-weight-bearing MLA measurements. Differences were more severe in patients with mediolateral instability (p = 0.010), age (p = 0.049) and ≥3° varus or valgus alignment (p = 0.008). Conclusion The clinical importance of this study lies in the finding that there are within-person differences between weight-bearing and non-weight-bearing measurement modalities. This has implications for preoperative planning, performing total knee arthroplasty (TKA), and clinical follow-up after TKA surgery using CAS navigation or patient-specific instrumentation. Level of evidence III.

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osteoarthritis presents as a change in the chondrocyte phenotype and an imbalance between anabolic and catabolic processes. Age affects its onset and progression. Small nucleolar RNAs (SnoRNAs) direct chemical modification of RNA substrates to fine-tune spliceosomal and rRNA function, accommodating changing requirements for splicing and protein synthesis during health and disease. Articular cartilage from young, old and OA knees was used in a microarray study to identify alterations in snoRNA expression. Changes in snoRNAs in osteoarthritis-like conditions were studied in chondrocytes using interleukin-1 and osteoarthritic synovial fluid. SNORD26 and SNORD96A knockdown and overexpression were undertaken using antisense oligonucleotides and overexpression plasmids. We identified panels of snoRNAs differentially expressed due to ageing (including SNORD96A, SNORD44) and osteoarthritis (including SNORD26 and SNORD116). In vitro experiments using osteoarthritis-like conditions affected snoRNA expression. Knockdown or overexpression of SNORD26 or SNORD96A resulted in changes in chondrogenic, hypertrophic, rRNA and osteoarthritis related gene expression. We demonstrate that snoRnA expression changes in cartilage ageing, and osteoarthritis and in osteoarthritis-like conditions, and when the expression of these snoRNAs is altered this affects chondrogenic and hypertrophic gene expression. Thus, we propose an additional dimension in the molecular mechanisms underlying cartilage ageing and osteoarthritis through the dysregulation of snoRNAs.