Levine (2000) — The Pathophysiology of Shoulder Instability

The Pathophysiology of Shoulder Instability

Levine, Flatow·Am J Sports Med·2000·182 citations·Shoulder & Elbow

This is a current-concepts review of the pathophysiology of glenohumeral instability. It walks through the normal static and dynamic stabilizers of the shoulder and the pathoanatomy that produces instability. The focus is on why labral detachment alone does not explain dislocation and what actually must be restored surgically.

Key Findings

The labrum doubles glenoid AP depth from 2.5 to 5 mm and deepens the concavity to 9 mm superior-inferior, acting as a chock-block. Labral resection cuts resistance to translation by 20% under compressive load, which is why preserving and repairing labral tissue matters.
An isolated Bankart lesion alone does not permit dislocation. A simulated Bankart in nine cadavers increased anterior translation by a maximum mean of only 3.4 mm, so additional capsular pathology is required for the head to escape.
When the IGHL is loaded to failure, it fails at three sites:
–Glenoid insertion (Bankart): 40%
–Intrasubstance: 35%
–Humeral insertion: 25%
–Even glenoid failures occurred only after significant elongation, establishing plastic deformation as a mechanism of subtle instability.
Arthroscopic Bankart repair failure rates range from 5% to 60%. The authors attribute much of this to unaddressed capsular stretch, since simply reattaching the labrum without retensioning the IGHL is doomed to fail.
Concavity-compression lets the intact labrum resist tangential forces up to 60% of the applied compressive load, showing how dynamic cuff loading contributes to stability across the mid-range where ligaments are lax.
An anteroinferior chondral-labral defect reduced effective glenoid height by roughly 80% and directional stability by 65%, quantifying why bony and labral loss critically compromises the socket.
Named variants must not be mistaken for pathology: the Buford complex (cord-like MGHL with absent anterosuperior labrum) and the sublabral foramen are normal, found in about 13.5% of shoulders in one series.

Board PearlAn isolated Bankart lesion alone is insufficient to dislocate the shoulder; loss of tension in the inferior glenohumeral ligament complex is the essential driver.

Clinical Relevance

The central teaching point: when you see a Bankart lesion, do not assume that reattaching the labrum fixes the problem. This review reframes the historical "essential lesion" as loss of tension in the inferior glenohumeral ligament complex, not labral detachment in isolation.

The IGHL undergoes plastic deformation before it detaches, so a stretched capsule can drive recurrent instability even after a technically clean labral repair. That mechanism explains the wide 5% to 60% arthroscopic failure range.

Practically, this is why capsular retensioning (capsulorrhaphy, shift) is combined with labral repair, and why unrecognized capsular stretch remains a leading cause of failed stabilization.

For boards, know the stabilizer roles by arm position (MGHL at 60 to 90 degrees abduction, IGHL as the hammock in abduction/external rotation) and distinguish normal variants (Buford complex, sublabral foramen) from true Bankart and ALPSA lesions.

Supplemental

The Pathophysiology of Shoulder Instability

Levine, Flatow·Am J Sports Med·2000·182 citations·Shoulder & Elbow

The Pathophysiology of Shoulder Instability

Key Findings

Clinical Relevance

Related Articles

The Pathophysiology of Shoulder Instability

Key Findings

Clinical Relevance

Related Articles

The Pathophysiology of Shoulder Instability

Key Findings

Clinical Relevance

Related Articles

The Pathophysiology of Shoulder Instability

Key Findings

Clinical Relevance

Related Articles