Journal of Pediatric Orthopaedics - 2026-06-18 - Journal Article
The Coronal Lateral Collateral Ligament Sign Occurs Independent of Generalized Joint Hyperlaxity in Children and Adolescents With ACL-Deficient Knees.
Pedrick EG, Mitchell BC, Bomar JD, Edmonds EW
Topics
Key Takeaway
The coronal LCL sign was present in 64% of pediatric ACL-deficient knees and occurred at equal rates in hyperlax (Beighton ≥6, 62%) versus normal-laxity (64%) patients (P=1.0), confirming it as an ACL-specific instability marker independent of generalized ligamentous laxity.
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Summary
This study asked whether generalized joint hyperlaxity (Beighton ≥6), ramp lesions, or Segond fractures drive the coronal LCL sign in pediatric ACL-deficient knees. One hundred patients under 19 years old undergoing ACL reconstruction were stratified by Beighton score; LCL sign presence was determined on MRI. The LCL sign was present in 64% overall with no difference between lax and normal cohorts (P=1.0), no association with ramp lesions (55% vs. 42%, P=0.211), and no association with Segond fractures.
Key Limitation
The lax cohort (n=13) is critically underpowered, making all negative findings in that subgroup statistically unreliable and limiting conclusions about hyperlax patients specifically.
Original Abstract
BACKGROUND
The lateral collateral ligament (LCL) sign is known to be correlated with greater anterior tibial translation (ATT) and internal tibial rotation in the setting of anterior cruciate ligament (ACL) tear. The LCL sign has also been correlated to risk for graft failure following ACL reconstruction, but its association with global joint hyperlaxity or concomitant injury such as ramp lesions or Segond fractures has not been assessed. This study aims to determine whether generalized joint hyperlaxity, ramp lesion, or Segond fractures are associated with a higher incidence of the coronal LCL sign in pediatric ACL-deficient knees.
METHODS
A retrospective review of ACL reconstruction patients less than 19 years old with clinically reported Beighton scores was performed over 8 years. The presence of the LCL sign was determined from magnetic resonance imaging, and cohorts were developed based on Beighton scores into a "lax" cohort (Beighton ≥6) or "normal" cohort (Beighton <6).
RESULTS
A total of 100 children met criteria (42% female, mean age 14.6±2.1 y, range: 9.0 to 18.5 y) with 87 normal and 13 lax patients. The LCL sign was identified in 64% of patients with a similar presence in the lax (62%) and normal (64%) cohorts (P=1.0). There was no significant difference in the proportion of ramp lesions in the positive LCL sign (55%) and negative LCL sign cohorts (42%) (P=0.211). Further, there was no significant difference in the proportion of Segond fractures in the lax (0%) and normal (6%) cohorts (P=1.0).
CONCLUSIONS
The LCL sign appears to be an independent predictor of ACL pathology that is not affected by generalized ligamentous laxity, presence of ramp lesions, or Segond fractures. In combination, these results suggest that the LCL sign may be specific to the type of instability introduced by an ACL tear, independent of other concomitant sources of knee instability (traumatic or atraumatic). Moreover, the LCL sign is potentially an independent predictor of potential ACL graft failure.
LEVEL OF EVIDENCE
Level IV-case series.