Reconsidering the evidence for muscle‐mediated rotational stability in the CCL ‐deficient stifle

I read with great interest the recent article by Natsios et al., “The role of muscle forces on rotational and cranio-caudal stability in the intact and CCL-deficient stifle: An ex vivo biomechanical study.”1 The authors used a cable-actuated cadaveric model capable of graded, multi-muscle activation. This is a meaningful advance over the fixed-tension surrogates used in earlier work. Periarticular muscle cocontraction nearly normalized internal tibial rotation in the cranial cruciate ligament (CCL)-deficient stifle, while cranio-caudal translation remained markedly elevated. The clinical implications, particularly regarding targeted biceps femoris strengthening, are appropriately emphasized. I would like to raise two points that may warrant clarification. First, each specimen underwent the full activation matrix—eight muscle conditions × seven activation levels, with triplicate repetitions for cranio-caudal translation testing—while intact. Only afterward was the CCL transected and the same matrix repeated on the same joint. Randomizing CCL status is clearly not feasible once the ligament is transected. However, no preconditioning protocol is reported to stabilize the viscoelastic behavior of the periarticular soft tissues before testing began. Recent systematic reviews applying validated risk-of-bias instruments to this category of cadaveric biomechanical studies report that even well-conducted investigations rarely achieve an ideal methodological quality score.2 This suggests that specimen handling and testing-protocol details are often incompletely reported in this literature. Given the substantial cumulative loading each joint underwent during the intact-condition series, accumulated creep or stress relaxation may have contributed to the reduction in internal rotation observed after transection, independent of CCL status itself. I would suggest that the authors report whether preconditioning cycles were performed, and whether cumulative loading history was assessed—for example, through a time-control condition or an analysis of drift across repeated trials. Second, I would welcome clarification of the non-significant comparison between intact and CCL-deficient internal rotation at 100% bodyweight three-muscle cocontraction (4.3° ± 2.3° vs. 2.8° ± 1.3°; p > .05). The Discussion interprets this as evidence that muscle activation restores rotational stability to near-intact levels. A non-significant p-value in a study of n = 8 does not, by itself, demonstrate equivalence. It may simply reflect limited statistical power, especially given the wide standard deviations relative to the means. Recent veterinary methodological literature has repeatedly cautioned against inferring “no difference” or “no effect” from non-significant results, and has called for effect estimates to be reported alongside confidence intervals instead.3, 4 Without such analysis, the clinical message that targeted strengthening can substantially normalize rotational laxity may overstate what the data support. I would recommend that the authors report a post hoc power calculation, or a formal equivalence analysis (e.g., two one-sided tests), for this comparison. I commend the authors for an elegant and clinically relevant experimental model. I believe these clarifications would strengthen confidence in the study's conclusions and their translation into clinical practice. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.