• ABSTRACT
    • Normal asymptomatic glenohumeral motion is dependent on the coordinated function of dynamic and static stabilizers. Data from both selective sectioning studies of the capsuloligamentous components and tensile testing of the inferior glenohumeral ligament have provided important insights into the in situ function of these structures. However, little is known regarding the mechanism of microdamage accumulation in acquired shoulder instability. Recent findings suggest that cyclic subfailure loading of the inferior glenohumeral ligament may induce gradual stretching of the anteroinferior capsule, compromising its capacity to restrain excessive humeral translations. Further studies elucidating the mechanism of load transmission in the capsule during physiologic arm motion, as well as data on the intrinsic healing response of the capsular ligaments, are required to more fully characterize the pathoetiology of acquired shoulder instability.