Due to demographical changes with a prolonged life experience in the aging active population, the prevalence of anterior traumatic shoulder dislocations has increased [9]. There is an increasing incidence of shoulder dislocations starting with 12.89 (50–59 years)–28.38 (>90 years) per 100.000 person years at risk affecting more women than men, and a recurrence rate in patients older than 60 has been reported to be 11–22% [5, 7, 18]. In this population the active and passive stabilizers are both affected once the shoulder was dislocated [4]. The pathophysiology of anterior shoulder dislocation between a young and active population and the older population is different and is related to changes due to the loss of elasticity in capsulo-labral complex as well as degenerative changes to the rotator cuff tendon with distribution of the glenohumeral rhythm [10]. Basically, there are two described mechanisms: The anterior mechanism leads to lesion of the anterior labrum-ligament complex with a sudden eccentric load to the posterior aspect of the rotator cuff. This induces a refectory contracture and over-tensioning of the posterior cuff tendon, which can cause a partial or total rupture of a preexisting injury of a degenerated infraspinatus and supraspinatus tendon [1, 10]. Additionally, there are also ruptures to the upper part of the subscapularis tendon, commonly seen with a humeral avulsion of the inferior glenohumeral ligament [17]. The posterior mechanism popularized by Craig [3] on the contrary can be explained by a dislocation with the arm in maximum abduction, flexion, and external rotation. This leads to an impact of the infraspinatus and supraspinatus on superior glenoid rim and subsequently causes a rupture to a degenerative posterior-superior tendon structure. This mechanism can be seen with and without damages to the anterior capsulo-labral complex.

Whereas the young population dislocates because of failure to the anterior capsulo-labral complex (anterior mechanism), the older patient commonly dislocates because of loss of posterior active stabilizing structures, especially the posterior aspect of the rotator cuff (posterior mechanism) [10]. A cadaveric study investigating the influence of rotator cuff muscle activity and stability showed a 50% increase of dislocations in all positions of the glenohumeral joint examined with a 50% decrease of muscle activity [14]. Furthermore, a cuff-deficient model showed that a smaller lesion of the ligamentous-labral complex was needed to cause instability in comparison to an intact shoulder [13]. The frequency of rotator cuff tears after an anterior shoulder dislocation has been reported to be between 7 and 32% and is rising with aging [2, 6, 16]. Additionally, it has been shown that 50% of patients older than 60 years with a primary shoulder dislocation had a rotator cuff tendon tear and even over 70% if they had recurrent dislocations [7].

There is still no consensus about whether a symptomatic degenerative ruff tendon with a lesion to the tendon structure may lead to an abnormal active stabilization and can be seen as the cause of dislocation or if the dislocation itself induces a cuff injury [15, 17]. But a hint for a preexisting rotator cuff lesion can be seen in those patients with shoulder dislocation with a trivial trauma compared to forces needed to dislocate a shoulder in a young population [8, 11, 12]. Therefore, the purpose of the following chapters will focus on treatment of shoulder instability in the older patient, aimed to point out the specifics in regard to a lesion to the anterior capsulo-labral complex as well as a damage to the rotator cuff tendon.