Neer et al. [2] hypothesized that mechanical factors were at the origin of cuff arthropathy. According to this theory, loss of downward force performed by a healthy rotator cuff on the humeral head would result in a superior migration of the humerus. This might facilitate an erosion of the superior surface of the glenoid and of the antero-inferior aspect of the acromion. In addition, the upward migration of the humeral head could cause a joint instability, an eccentric work of the humeral head, and consequently, a premature wear of the articular cartilage in the areas of higher glenohumeral compression. Since 21 of the 26 patients cited in the paper had the rupture of the long head of the biceps tendon, Neer thought that this injury would help the upward migration of the humeral head.

Burkhart’s hypothesis [16] seems to support the mechanical theory. The author believes that the healthy inferior portion of the rotator cuff (below the center of rotation) creates a moment that must balance the deltoid moment (force coupling). Furthermore, the subscapularis is anteriorly balanced against the infraspinatus and teres minor posteriorly. Uncoupling of the essential force couples results in anterior superior translation of the humeral head with attempted elevation of the shoulder.

In 1997, Collins and Harryman [17] hypothesized that cuff arthropathy was initially due to supraspinatus tear and later to the infraspinatus lesion; the complex tendon tear would cause the upward migration of the humeral head and, consequently, the contact of articular cartilage of the humeral head against the antero-inferior margin of the acromion. Cartilage fragmentation results in particulate debris, which causes synovial thickening and effusion as well as calcium phosphate crystal formation. The enzymatic response to the crystals furthers the damage of the articular surfaces.

Concavity-compression mechanism, suggested by Hurov [18], further corroborates the mechanical theory. According to the author, the healthy cuff compresses the convexity of the humeral head against the pseudo-concavity of the glenoid; therefore, the cuff, with other periscapular muscles, would act as an important dynamic stabilizer of the joint. This action may be even more important in the presence of severe laxity of the static stabilizers of the shoulder (capsule, labrum, and glenohumeral ligaments).

Oh et al. [19] identified that critical tear sizes responsible for disrupted joint kinematics are those with full-thickness supraspinatus tears and 50 % detachment of the infraspinatus.

Neer et al. [1, 2] have also suggested that the osteoarthritis could depend on the loss of the “water tight” effect (loss of negative pressure normally existing inside the shoulder joint in normal conditions) due to the cuff tear.

This would cause dispersion of synovial fluid, normally contained in the joint, in the subacromial space. The dispersion would make the diffusion of synovial fluid into the joint cartilage difficult; consequently, the cartilage would be poorly nourished and would easily run into atrophy. Furthermore, diffusion of the fluid into the cartilage should be further hindered by the decrease in range of motion caused by the shoulder pain due to the cuff tear (loss of water and mucopolysaccharides content). In addition, decrease in mobility, resulting in pain, would lead the subchondral bone to be osteoporotic and more exposed to possible collapse.

It is known that cytokine and catabolic enzyme concentration increases in the early phases of osteoarthritis. Many studies have also proved that the rotator cuff tear leads to an increased production of interleukin 1β and TNF, which helps to explain the presence of pain and inflammation. It was also noted that the production of many cartilage matrix-specific matrix metalloproteinases (MMPs) increased, including MMP-1, MMP-2, MMP-3, MMP-8, and MMP-13 [20, 21]. The presence of MMP-3 is important because it is implicated in the proteolytic activation of the other MMPs. Yoshihara et al. [22] observed that there is a correlation between the concentration of these cytokines, collagenases, and aggrecanases and accelerated cartilage degeneration after a cuff tear.

These observations redimension the nutritional theory in the genesis of cuff tear arthropathy. In fact, with the evacuation of a part of the synovial fluid through the tendon lesion, inflammation factors and proteolytic enzymes should be removed and, thus, health status of articular cartilage should be preserved.

In 2012, Reuter et al. [23] sonographically assessed the articular surface of the glenohumeral joint in rats with a rotator cuff tear and observed a thickness decrease in the cartilage. Kramer et al. [24] histologically studied the glenohumeral cartilage of rats, respectively, submitted to detachment of the postero-superior rotator cuff and to suprascapular nerve root transection passing through the trapezoid (joint capsule was kept intact). The animals were killed 12 weeks after surgery. In the first case, if there had been degenerative changes of the cartilage, it would have been attributed, in accordance with the Neer’s hypotheses [1, 2], to the altered mechanical loading and to the nutritional theory, instead, in the second case, only to the mechanical hypothesis. Surprisingly, the amount of cartilage degeneration was similar between the groups. This result suggests that aberrant mechanical forces are the primary causes of articular cartilage degeneration in the setting of cuff tear arthropathy.

In orthopedic literature, almost simultaneously to Neer’s hypotheses, a nosologic entity similar to the cuff arthropaty has been described: the “Milwaukee syndrome” [25]. Although it is responsible for a clinical condition similar to that of the cuff arthropaty, this disease has been attributed to the presence in the synovial fluid of basic calcium phosphate crystals encapsulated into microspheroids without apparent inflammatory cell response. Indeed, an altered capsular degenerated cartilage and synovium, possibly with a macrophage response and subsequent release of collagenase and neutral proteases, are associated with this condition, resulting in the attack and subsequent destruction of the joint.

In 1985, Dieppe and Watt [26] noted that basic calcium phosphate crystals could be found in arthritic and neuropathic joints and in apparently healthy joints of elderly subjects. In addition, the apatite crystals are found especially in the most destructive atrophic situations. Therefore, the authors hypothesized that the crystals are produced by the processes that are secondary to joint degeneration. This hypothesis redimensions the inflammatory theory and suggests that the syndrome is a form of cuff arthropathy.

Cuff arthropathy could be considered an autoimmune rheumatic disease. As well as for scleroderma or systemic lupus erythematous, patients with cuff tear arthropathy are frequently females. No study has ever confirmed this hypothesis. We are conducting a study to verify the reliability of this hypothesis; however, available data do not allow us to formulate conclusions.

It is possible that the cuff arthropathy is the result of a fortuitous coincidence between rotator cuff tear, which is frequently found in elderly patients [27, 28], and idiopathic glenohumeral arthropathy. In other words, arthropathy would occur regardless of cuff tear.

Upward migration of the humeral head consequent to the cuff tear would only be responsible for the fast evolution of the arthritic process, and it would only cause a more precocious wear of the upper portion of the glenoid surface. If this hypothesis is correct, the cuff arthropathy should not have a clear preference for sex and patients should have an average age similar to that of patients with concentric arthropathy; instead, the cuff arthropathy is predominantly found in females and in older patients.

Since cuff tear arthropathy and youth joint laxity are significantly more frequent in females, we hypothesized that these two conditions are associated with each other. If the rotator cuff tear occurs in patients who have/had joint laxity, it is possible that the involved shoulder could develop a severe static instability that might be responsible for a premature wear of the cartilage of the superior glenoid. This assumption justifies the evident difference in the prevalence of cuff arthropathy due to gender.

In order to verify this theory, we are administering a questionnaire to patients with glenohumeral arthritis to detect joint hypermobility [29, 30]. The questionnaire investigates, using major and minor criteria, patient’s ability to perform uncommon activities, the presence of joint diseases, or the tendency to dislocation.

At our knowledge, no studies have been conducted regarding histological differences between shoulder arthropathy with or without cuff tear. Actually, the vast majority of the studies have considered histological and ultrastructural characteristics of the idiopathic arthritis, assuming that there were no differences between the two conditions. In both, articular cartilage layer is thinned or, as in the areas submitted to higher mechanical stress, has deep and broad splits or is completely absent, leaving wide exposition of the subchondral bone. In the most severe cases, cells are arranged in clusters in the deeper layer of the cartilage; sometimes chondrocyte lacunae are empty, surrounded by thickened collagen fibers [31]. The living cells are in intense activity and have well-developed cytoplasmin granules. They are enclosed in lacunae that contain numerous fibrils and mature collagen fibers. Matrix is represented by thickened collagen fibers, arranged in all directions, often perpendicularly disposed with respect to articular surface. Colloidal iron staining shows the presence of mucopolysaccarides around the living chondrocytes.

Neer [2] histologically described 26 shoulders with cuff arthropathy. Authors observed three consistent findings: areas with atrophic cartilage and osteoporotic subchondral bone in the humeral head; areas where cartilage is denuded and subchondral bone is sclerotic; and fragments of articular cartilage in the subsynovial layer. An histological study performed by Jensen et al. [14] on specimens of patients with cuff arthropathy revealed foci of calcific deposits in synovial microvilli.

Kramer et al. [24] performed an elegant study on rats whose cuff tendons were previously excised. The histological analysis was performed 12 months after surgery. Authors observed significant cartilage changes in the humeral head compared with the control side. Applying the modified Mankin score [32] (widely used for histologic evaluation of osteoarthritis), they obtained a value of 5.7 ± 1.9 in the involved shoulder and 2.0 ± 1.0 in the control side (p < .001). The score considers the structure, cellularity, safranin O staining, and tidemark integrity. Analogously, glenoid values were 5.1 ± 1.9 and 2.4 ± 0.8 (p < .001).