The Number of Injury Events Associated With the Critical Size of Bipolar Bone Defects in Rugby Players With Traumatic Anterior Shoulder Instability.

Background: The size of a glenoid bone defect is responsible for reduction in shoulder stability and is correlated with the number of instability events. Biomechanical studies have suggested that it should be considered concomitantly with the Hill-Sachs lesion as "bipolar" bone defects for assessing structural degradation, but the definitive number of instability events associated with the critical size has not been investigated.

Purpose: To (1) confirm that the number of instability events is the predictor of a critical size of bipolar bone defects and (2) demonstrate the cutoff value of the number of instability events for these defects in rugby players with traumatic anterior shoulder instability.

Study Design: Cross-sectional study; Level of evidence, 3.

Methods: One-hundred forty-four rugby players with anterior shoulder instability underwent morphologic evaluation for glenoid and Hill-Sachs lesions by computed tomography and determination of the critical (a glenoid bone defect of ≥25% or an off-track Hill-Sachs lesion) and subcritical (a glenoid bone defect of ≥13.5%) size of bipolar bone defects. In the primary analysis, the prevalence of the critical and subcritical size of bipolar bone defects was investigated. In the secondary analysis, the authors explored the predictors for these bone defects and determined the cutoff value correlating with the critical and subcritical size of bipolar bone defects by applying receiver operating characteristic curves.

Results: The primary analysis revealed that the prevalence of critical and subcritical size of bipolar bone defects was 20.8% and 61.8% of 144 shoulders, respectively. In the secondary analysis, multiple logistic regression analysis demonstrated that the total number of shoulder instability events and dominant shoulder were the significant factors associated with the critical and subcritical size of bipolar bone defects. The cutoff value for the number of instability events that correlated with critical bipolar bone defects was 6 for the dominant and 9 for the nondominant shoulder, whereas it was 4 for the dominant and 5 for the nondominant shoulder for subcritical bipolar bone defects.

Conclusion: The number of shoulder instability events and the dominant shoulder were the predictors for the critical and subcritical size of bipolar bone defects for a shoulder with traumatic instability. Four injury events should herald caution when treating rugby players with shoulder instability.