Functionally aligned total knee arthroplasty: A lateral flexion laxity up to 6 mm is safe!

PURPOSE: Loose flexion gaps are associated with poor functional outcomes and instability in total knee arthroplasty (TKA). The effect of a trapezoidal flexion gap in a functionally aligned TKA remains unknown. The aim of this study was to investigate the effect of a larger lateral flexion gap in a robotic-assisted (RA), functionally aligned (FA) and cruciate-retaining (CR) TKA on clinical outcomes. METHODS: Data from 527 TKA in 478 patients from 2018 to 2020 were collected. All patients underwent an RA (MAKO, Stryker), FA and CR TKA. Gap measurements were collected intraoperatively. Patient-reported outcome measures (PROMs), pain Visual analogue score (VAS) and range of motion were collected postoperatively. Patients were also asked about the ease of stair ascent and descent and kneeling on a 5-point scale. The minimum follow-up was 2 years. Patients were stratified into three groups based on lateral flexion laxity. RESULTS: At 2 years postoperatively, the group with a looser gap (3-6 mm) had higher mean PROMs when compared with the group with a gap of 2-3 mm. There were no differences detected in any other outcomes at 2 years. A total of 70.9% of patients in the group with a 3-6 mm gap reported being able to walk down a flight of stairs 'easily', compared with 56.7% in the 2-3 mm group and 54% in the <2 mm group (p = 0.04). CONCLUSION: The study shows that a loose lateral flexion gap in functionally aligned CR TKA does not adversely affect outcomes in the short term. LEVEL OF EVIDENCE: Level III, retrospective cohort study.

Mitochondrial polymorphisms in rat genetic models of hypertension.

Hypertension is a complex trait that has been studied extensively for genetic contributions of the nuclear genome. We examined mitochondrial genomes of the hypertensive strains: the Dahl Salt-Sensitive (S) rat, the Spontaneously Hypertensive Rat (SHR), and the Albino Surgery (AS) rat, and the relatively normotensive strains: the Dahl Salt-Resistant (R) rat, the Milan Normotensive Strain (MNS), and the Lewis rat (LEW). These strains were used previously for linkage analysis for blood pressure (BP) in our laboratory. The results provide evidence to suggest that variations in the mitochondrial genome do not account for observed differences in blood pressure between the S and R rats. However, variants were detected among the mitochondrial genomes of the various hypertensive strains, S, SHR, and AS, and also among the normotensive strains R, MNS, and LEW. A total of 115, 114, 106, 106, and 16 variations in mtDNA were observed between the comparisons S versus LEW, S versus MNS, S versus SHR, S versus AS, and SHR versus AS, respectively. Among the 13 genes coding for proteins of the electron transport chain, 8 genes had nonsynonymous variations between S, LEW, MNS, SHR, and AS. The lack of any sequence variants between the mitochondrial genomes of S and R rats provides conclusive evidence that divergence in blood pressure between these two inbred strains is exclusively programmed through their nuclear genomes. The variations detected among the various hypertensive strains provides the basis to construct conplastic strains and further evaluate the effects of these variants on hypertension and associated phenotypes.