Dataset Information

Mechanism of posterior malleolar fracture of the ankle: A cadaveric study.

ABSTRACT:

Objectives

Ankle fracture treatment involves reduction of the bone fragments and stabilization of the joint by reversing the mechanics of injury. For posterior malleolar fracture however, the true mechanism is not understood, leading to a lack of consistent guidance on how to best treat this injury.

Methods

Fifteen cadaver ankles were subjected to fracture loading that replicated the Lauge-Hansen pronation-external rotation mechanism. An axial load was applied to each specimen, which was mounted on a materials testing machine, and the foot was rotated externally to failure. Digital video cameras recorded the failure sequence of specific anatomic structures.

Results

Posterior malleolar fracture occurred in 7 specimens. Of these, 1 was an intra-articular fracture, another was a fracture involving the entire posterior tibial margin consisting of 2 fragments: that of the posterior tubercle and that of the posteromedial margin of the tibial plafond, with the former judged to be a consequence of avulsion by the posterior inferior tibiofibular ligament and the latter a consequence of axial loading from the talus. In the remaining 5 specimens, the posterior malleolar fracture was a small extra-articular avulsion fracture.

Conclusions

Fractures at the posterolateral corner of the distal tibia were shown to be avulsion fractures attributed to the posterior inferior tibiofibular ligament and produced by external rotation of the talus. A fracture involving the entire posterior tibial margin consisting of 2 fragments can be produced by a combination of avulsion by the posterior inferior tibiofibular ligament and axial loading from the talus.

SUBMITTER: Haraguchi N

PROVIDER: S-EPMC8022911 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionIntra-articular fractures are the leading etiology for posttraumatic osteoarthritis (PTOA) in the ankle. Elevation of proinflammatory cytokines following intra-articular fracture may lead to synovial catabolism and cartilage degradation. We aimed to compare cytokine levels in injured and healthy ankle joints, examine the longer-term cytokine levels in fractured ankles, and investigate the association between cytokine levels in fractured ankles and plasma.Materials and methodsIn this cross-sectional study, synovial fluid (SF) and plasma of forty-seven patients with acute intra-articular ankle fractures and eight patients undergoing implant removal were collected prior to surgery. We determined concentrations of sixteen inflammatory cytokines, two cartilage degradation proteins, and four metabolic proteins and compared the levels in acutely injured ankles with those of the healthy contralateral side or during metal removal. Cytokine levels in injured ankles were also compared to serum cytokine levels. Nonparametric Wilcoxon rank-sum and Spearman tests were used for statistical analysis, and a p value below 0.05 was considered significant.ResultsCompared to the healthy ankles, the synovial fluid in ankles with acute intra-articular fracture had elevated levels of several proinflammatory cytokines and proteases (IL-1β, IL-2, IL-6, IL-8, IL-12p70, TNF, IFNγ, MMP-1, MMP-3, and MMP-9) and anti-inflammatory cytokines (IL-1RA, IL-4, IL-10, and IL-13). The levels of cartilage degradation products (ACG, CTX-2) and metabolic mediators (TGF-β1 and TGF-β2) were also significantly higher. Synovial concentrations of ACG, IL-12-p70, IFNγ, IL-4, and bFGF correlated with serum levels. While most of the examined synovial cytokines were unchanged after implant removal, IL-4 and IL-6 levels were upregulated.ConclusionsWe show that an acute ankle fracture is followed by an inflammatory reaction and cartilage degeneration. These data contribute to the current understanding of the protein regulation behind the development of PTOA and is a further step towards supplementing the current surgical treatment. This cross-sectional study was "retrospectively registered" on the 31th October 2017 at ClinicalTrials.gov (NCT03769909). The registration was carried out after inclusion of the first patient and prior to finalization of patient recruitment and statistical analyses: https://clinicaltrials.gov/ct2/show/NCT03769909?term=NCT03769909&draw=2&rank=1.