Mechanical joint laxity associated with chronic ankle instability: a systematic review

Lateral ankle sprains can manifest into chronic mechanical joint laxity when not treated effectively. Joint laxity is often measured through the use of manual stress tests, stress radiography, and instrumented ankle arthrometers.

To systematically review the literature to establish the influence of chronic ankle instability (CAI) on sagittal and frontal plane mechanical joint laxity.

Articles were searched with MEDLINE (1966 to October 2008), CINAHL (1982 to October 2008), and the Cochrane Database of Systematic Reviews (to October 2008) using the key words chronic ankle instability and joint laxity, functional ankle instability and joint laxity, and lateral ankle sprains and joint laxity.

To be included, studies had to employ a case control design; mechanical joint laxity had to be measured via a stress roentogram, an instrumented ankle arthrometer, or ankle/foot stress-testing device; anteroposterior inversion or eversion ankle-subtalar joint complex laxity had to be measured; and means and standard deviations of CAI and control groups had to be provided.

One investigator assessed each study based on the criteria to ensure its suitability for analysis. The initial search yielded 1378 potentially relevant articles, from which 8 were used in the final analysis. Once the study was accepted for inclusion, its quality was assessed with the PEDro scale.

Twenty-one standardized effect sizes and their 95% confidence intervals were computed for each group and dependent variable. CAI produced the largest effect on inversion joint laxity; 45% of the effects ranged from 0.84 to 2.61. Anterior joint laxity measures were influenced second most by CAI (effects, 0.32 to 1.82). CAI had similar but less influence on posterior joint laxity (effects, -0.06 to 0.68) and eversion joint laxity (effects, 0.03 to 0.69).

CAI has the largest effect with the most variability on anterior and inversion joint laxity measurements, consistent with the primary mechanism of initial injury.