The coracohumeral ligament (CHL) arises from the lateral base and dorsal surface of the coracoid process and inserts into the anterior rotator cuff via two bands: the anterior band inserting on the lesser tuberosity (blending with the subscapularis tendon and the SGHL) and the posterior band inserting on the greater tuberosity (blending with the supraspinatus anterior fibres). The CHL forms the superior boundary of the rotator interval and is the primary passive restraint to inferior glenohumeral translation in the adducted position.
Limits inferior translation of the glenohumeral joint in the adducted arm; stabilises the biceps tendon at the rotator interval as part of the biceps pulley; with the SGHL forms the primary passive constraint against inferior subluxation in the adducted and neutral rotation position; becomes fibrotic and contracted in adhesive capsulitis.
CHL contracture is the primary pathology in adhesive capsulitis (frozen shoulder), producing the characteristic loss of external rotation in the adducted position. The CHL and SGHL at the rotator interval are the first structures to become inflamed and fibrotic in adhesive capsulitis, and their release is the first step in arthroscopic capsular release for frozen shoulder — releasing the rotator interval restores external rotation immediately. CHL integrity is assessed in the biceps pulley complex: tears of the CHL allow medial biceps subluxation at the bicipital groove entrance.
The coracohumeral ligament at the rotator interval becomes fibrotic and contracted in the inflammatory phase of adhesive capsulitis, producing the hallmark loss of external rotation in the adducted arm as the CHL physically blocks ER; arthroscopic rotator interval release dividing the CHL immediately restores ER and is the first capsular release step in frozen shoulder surgery.
