**3. Shoulder disorders**

Pathogenesis of rotator cuff injuries is not completely clear, but it may arise from extrinsic factors, impingement by structures surrounding the cuff, and intrinsic alterations of the tendon itself [28].

On the tendinous portion of the rotator cuff impingement by the coracoacromial ligament and the acromion itself is responsible for the characteristic "impingement syndrome". A peculiar proliferative spur and ridge on the anterior lip and undersurface of the acromial anterior process has been found; furthermore, in many studies this area has shown erosions [4].

Anatomical changes may excessively narrow the subacromial space, in which rotator cuff tendons pass through, and include acromial shape variations (i.e. hooked acromion), orientation of the acromial angle or prominent osseous changes of the inferior portion of the acromionclavicular joint [29]. In 1986, Bigliani [30] described the important role of acromion shape, as an extrinsic mechanism, in rotator cuff tendinopathy; acromion classified into three types based on different shapes (**Figure 1**): Flat (Type I), Curved (Type II) and Hooked (Type III).

Association between acromion shape and severity of rotator cuff disorder has been well documented, with a greater prevalence of hooked acromion in subjects with subacromial impingement syndrome and full thickness tears. Alterations of shoulder kinematics, postural abnormalities, rotator cuff muscles deficits and decreased extensibility of pectoralis minor are biomechanical factors which can lead to rotator cuff tendons compression [4]. In addition,

**Figure 1.** Bigliani classification for acromial in different shapes.

shoulder kinematic alterations can cause a dynamic reduction of the subacromial space (compressing rotator cuff tendons) due to a superior shift of the humeral head [31] or an altered scapula biomechanics that leads acromion sliding downwards [32].

various combinations of changes like increase in upward rotation, decrease in posterior tilt and increase in internal rotation. However, the exact relationship between scapular dyskinesia and rotator cuff disorder is not completely clear; is dyskinesis a cause, an effect or a

Pathogenesis of rotator cuff injuries is not completely clear, but it may arise from extrinsic factors, impingement by structures surrounding the cuff, and intrinsic alterations of the tendon

On the tendinous portion of the rotator cuff impingement by the coracoacromial ligament and the acromion itself is responsible for the characteristic "impingement syndrome". A peculiar proliferative spur and ridge on the anterior lip and undersurface of the acromial anterior pro-

Anatomical changes may excessively narrow the subacromial space, in which rotator cuff tendons pass through, and include acromial shape variations (i.e. hooked acromion), orientation of the acromial angle or prominent osseous changes of the inferior portion of the acromionclavicular joint [29]. In 1986, Bigliani [30] described the important role of acromion shape, as an extrinsic mechanism, in rotator cuff tendinopathy; acromion classified into three types based on different shapes (**Figure 1**): Flat (Type I), Curved (Type II) and Hooked (Type III).

Association between acromion shape and severity of rotator cuff disorder has been well documented, with a greater prevalence of hooked acromion in subjects with subacromial impingement syndrome and full thickness tears. Alterations of shoulder kinematics, postural abnormalities, rotator cuff muscles deficits and decreased extensibility of pectoralis minor are biomechanical factors which can lead to rotator cuff tendons compression [4]. In addition,

cess has been found; furthermore, in many studies this area has shown erosions [4].

compensation? [26]

210 Advances in Shoulder Surgery

itself [28].

**3. Shoulder disorders**

**Figure 1.** Bigliani classification for acromial in different shapes.

Recent studies suggested that subacromial bursa is a pro-inflammatory membrane responsible for shoulder pain and other subacromial disorders. Blaine [33] demonstrated that inflammatory cytokines, such as Tumor necrosis factor (TNF), Interleukin 1 (IL-1), Interleukin 6 (IL-6), cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), increase in subacromial bursal in subjects suffering from bursitis and rotator cuff syndrome. It should also be pointed out that IL-1 and IL-6 play an important role as mediators of collagen catabolism [34].

Peritendinous alterations in rotator cuff disorders are thought to be a secondary phenomenon. Chandler [35] showed that the increased tension in the coracoacromial ligament, due to tendinopathy, stimulates the neoformation of bone on the underside of the acromion, which may result in an impingement syndrome leading to enthesopathy.

Acromial lateral sloping or glenoid version is structural features which play an important role in rotator cuff pathology as extrinsic factors. As mentioned in the previous paragraph, acromion shape influences supraspinatus tendon as it passes under the coracoacromial arch. Even a forward scapula posture, caused by forward head posture and increased kyphosis in combination, can reduce the subacromial space [36].

Intrinsic factors, causing rotator cuff tendinopathy, affect tendon morphology and performance. There is growing evidence in literature supporting the fundamental role of these mechanisms in shoulder disorders.

Intrinsic mechanisms, such as aging processes, poor vascularity and altered biology, lead to tendon degradation also influencing tensile forces and altering loads [37–40].

A reduction in vascular supply of tendons is implicated in rotator cuff tears pathogenesis. In 1934, Codman described for the first time the "critical zone" (1 cm<sup>2</sup> area between the insertion of supraspinatus tendon at greater tubercle and myotendinous junction) which represents the most common site for tendon injury due to its reduced vascularity [4].

Tendon degeneration is the expression of an increased production by tenocytes of metalloproteinase enzymes (MMP); this means that tendon tears are an active and cell-mediated process. The hypothesis is that rotator cuff tears are the results of an imbalance between tendon synthesis and degradation, maybe due to the failed regulation of MMP activity in response of repeated mechanical strains. Tendon degeneration is further evident as it has demonstrated an increase in sulfated glycosaminoglycans (GAG) in supraspinatus tendinosis [41]. Sulfated GAG are associated with acute inflammation and new matrix formation, as well as amyloid production. A study conducted by Cole [42] demonstrated that supraspinatus chronic tears were characterized by 70% amyloid deposition on tendon context, unlike only 25% in patients suffering from acute traumatic injuries.

Another feature that may lead to shoulder disorders is genetics; it seems to be related to the polymorphism of genes which regulates collagen synthesis, like the one found in Achilles tendinopathy. However, this is just a hypothesis since no genes were identified till now as risk factors for rotator cuff diseases [43–45].

Other factors can influence mechanical properties and tensile loads response including tendon geometry, due to collagen fiber alignment. Among tendon alterations, it is important to highlight tendon irregularity and thinning, observed in subjects suffering from degenerative rotator cuff tendinopathy; these conditions influence mechanical properties. Even aging has been observed to be a negative factor for tendon degeneration. Biomechanical studies showed a reduced elasticity and a decreased tensile strength in tendons with aging [4]. Histological studies about rotator cuff tendons showed degenerative changes (calcifications and fibrovascular proliferation) in elderly in comparison to young people, both groups without history of shoulder disorders. Furthermore, aging causes a reduction in total sulfated GAG and proteoglycans in supraspinatus tendon [46].

with rotator cuff tendinosis: tendon fibers thinning and consequently ultrastructural alterations, cellular apoptosis, granulation tissue production and fibro-cartilaginous changes [50, 51]. The risk of progression, which can lead to full tendon rupture, is related to these histo-

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Hyaline and myxoid degeneration, which can affect collagen fibers, already occur in the degenerated tendon. The consequence of this is a reduction in tensile resistance that predis-

In degenerated tendon, healing processes are altered. In fact, the standard composition and structure of the osteotendinous insertion site, with the transition from non-mineralized to mineralized fibrocartilage, is not achieved. The causes of this poor healing process are multifactorial, but correlated to an inadequate and disorganized expression of the cytokines responsible for the formation of the complex structure and composition of the enthesis [52].

Other factors that may influence healing processes are the presence of inflammatory cells in the osteotendinous insertion site and a small number of stem cells in the tendon-bone inter-

An alteration during one of these phases leads to a bad regenerative process. Recent studies demonstrated the importance of the inflammatory phase, during which there is an increase of neutrophils, macrophages and mast cells in rotator cuff lesions in animal and human models. Millar et al. [54] evaluated rotator cuff tendon samples taken by biopsy during repairing phase. They observed significant infiltration of mast cells and macrophages in earlier phase of tendinopathy. Subsequently macrophages produce transforming growth factor-β1 (TGF-β1),

Fibrovascular scar is probably produced during this phase thanks to the action of macrophages. During the repairing phase of healing process, fibroblasts activation determines the expression of various cytokines, such as basic fibroblast growth factor (bFGF), insulinlike growth factor (IGF-1), platelet-derived growth factor-b (PDGF-b), vascular endothelial growth factor (VEGF), bone morphogenic protein-12 (BMP-12), BMP-13 and BMP-14 [4].

Calcific tendonitis can be potentially included in the sum of rotator cuff diseases. Its prevalence is estimated between 2.7 and 20% according to radiographies of asymptomatic adults. Usually occurs between the age of 40 and 50, with a higher prevalence in female sex and in sedentary workers. The probability of becoming symptomatic, both acute and chronic, has

pathological changes.

poses the tendon to rupture [4].

face, which hamper physiological scar formation [53].

which stimulates collagen formation and proteinase activity.

Healing process occurs in three steps:

Step 1. Inflammatory phase

Step 2. Repairing phase

**3.2. Calcific tendonitis**

been estimated to be higher than 50% [52].

Step 3. Remodeling phase

Other scientific researches demonstrated in elderly people a reduction of type I collagen and an increase in type III, weaker and more irregularly; however there is no consensus in literature whether these changes are related with aging or a secondary consequence of healing processes to repeated microtrauma (or overuse) [47].

An interesting classification is the one developed by Celli [48] that divides the old denomination "shoulder periarthritis" in four clinical presentations, depending on the type, localization and pain:


This classification has the advantage of easy application, but there is no immediate correlation with the cause of degeneration. The most common cause of shoulder pain is an inflammation of the bursae around the glenohumeral joint. The most affected is the subacromial bursa, located between the acromion and the tendons of rotator cuff, but also subdeltoid, subscapularis and subcoracoid bursae may be affected.

Pain is localized on the side of the proximal part of the arm, but it may also extend distally if the inflammatory process involves subdeltoid bursa, which often communicates with the subacromial one. Movements accentuate symptoms, particularly active abduction, that is markedly limited by pain.

#### **3.1. Rotator cuff tendinosis**

The incidence of rotator cuff tendinopathy and degenerative tears increases in aging and it is 40% in subjects over 70 years of age [49].

Rotator cuff tendinosis is due to disorganization in collagen fibers morphology and to alterations in tendon ultrastructure. Earlier studies showed histopathological changes associated with rotator cuff tendinosis: tendon fibers thinning and consequently ultrastructural alterations, cellular apoptosis, granulation tissue production and fibro-cartilaginous changes [50, 51]. The risk of progression, which can lead to full tendon rupture, is related to these histopathological changes.

Hyaline and myxoid degeneration, which can affect collagen fibers, already occur in the degenerated tendon. The consequence of this is a reduction in tensile resistance that predisposes the tendon to rupture [4].

In degenerated tendon, healing processes are altered. In fact, the standard composition and structure of the osteotendinous insertion site, with the transition from non-mineralized to mineralized fibrocartilage, is not achieved. The causes of this poor healing process are multifactorial, but correlated to an inadequate and disorganized expression of the cytokines responsible for the formation of the complex structure and composition of the enthesis [52].

Other factors that may influence healing processes are the presence of inflammatory cells in the osteotendinous insertion site and a small number of stem cells in the tendon-bone interface, which hamper physiological scar formation [53].

Healing process occurs in three steps:

Step 1. Inflammatory phase

Step 2. Repairing phase

Other factors can influence mechanical properties and tensile loads response including tendon geometry, due to collagen fiber alignment. Among tendon alterations, it is important to highlight tendon irregularity and thinning, observed in subjects suffering from degenerative rotator cuff tendinopathy; these conditions influence mechanical properties. Even aging has been observed to be a negative factor for tendon degeneration. Biomechanical studies showed a reduced elasticity and a decreased tensile strength in tendons with aging [4]. Histological studies about rotator cuff tendons showed degenerative changes (calcifications and fibrovascular proliferation) in elderly in comparison to young people, both groups without history of shoulder disorders. Furthermore, aging causes a reduction in total sulfated GAG and proteo-

Other scientific researches demonstrated in elderly people a reduction of type I collagen and an increase in type III, weaker and more irregularly; however there is no consensus in literature whether these changes are related with aging or a secondary consequence of healing

An interesting classification is the one developed by Celli [48] that divides the old denomination "shoulder periarthritis" in four clinical presentations, depending on the type, localization

**1.** Acute anterior shoulder: where inflammation is limited to the supraspinatus tendon and/

**2.** Global acute shoulder: pain is acute and inflammation compromised subdeltoid bursa.

**4.** Global chronic shoulder: even in this case the pain is chronic, but it affects the whole

This classification has the advantage of easy application, but there is no immediate correlation with the cause of degeneration. The most common cause of shoulder pain is an inflammation of the bursae around the glenohumeral joint. The most affected is the subacromial bursa, located between the acromion and the tendons of rotator cuff, but also subdeltoid, subscapu-

Pain is localized on the side of the proximal part of the arm, but it may also extend distally if the inflammatory process involves subdeltoid bursa, which often communicates with the subacromial one. Movements accentuate symptoms, particularly active abduction, that is mark-

The incidence of rotator cuff tendinopathy and degenerative tears increases in aging and it is

Rotator cuff tendinosis is due to disorganization in collagen fibers morphology and to alterations in tendon ultrastructure. Earlier studies showed histopathological changes associated

**3.** Chronic anterior shoulder: pain is chronic and localized on the anterior region.

glycans in supraspinatus tendon [46].

and pain:

212 Advances in Shoulder Surgery

shoulder.

edly limited by pain.

**3.1. Rotator cuff tendinosis**

40% in subjects over 70 years of age [49].

processes to repeated microtrauma (or overuse) [47].

or to the long head of the biceps tendon.

laris and subcoracoid bursae may be affected.

Step 3. Remodeling phase

An alteration during one of these phases leads to a bad regenerative process. Recent studies demonstrated the importance of the inflammatory phase, during which there is an increase of neutrophils, macrophages and mast cells in rotator cuff lesions in animal and human models. Millar et al. [54] evaluated rotator cuff tendon samples taken by biopsy during repairing phase. They observed significant infiltration of mast cells and macrophages in earlier phase of tendinopathy. Subsequently macrophages produce transforming growth factor-β1 (TGF-β1), which stimulates collagen formation and proteinase activity.

Fibrovascular scar is probably produced during this phase thanks to the action of macrophages. During the repairing phase of healing process, fibroblasts activation determines the expression of various cytokines, such as basic fibroblast growth factor (bFGF), insulinlike growth factor (IGF-1), platelet-derived growth factor-b (PDGF-b), vascular endothelial growth factor (VEGF), bone morphogenic protein-12 (BMP-12), BMP-13 and BMP-14 [4].

#### **3.2. Calcific tendonitis**

Calcific tendonitis can be potentially included in the sum of rotator cuff diseases. Its prevalence is estimated between 2.7 and 20% according to radiographies of asymptomatic adults. Usually occurs between the age of 40 and 50, with a higher prevalence in female sex and in sedentary workers. The probability of becoming symptomatic, both acute and chronic, has been estimated to be higher than 50% [52].

A 2009 study conducted by Maugars et al. [53] pointed out that between 7 and 17% of patients suffering from chronic shoulder pain was due to tendon calcification.

**3.3. Subacromial bursitis and impingement**

or a reparative tissue.

The subacromial bursa is the largest and most complicated bursa in human body. In a 1934 book [61], Codman affirmed that it behaves as a secondary scapula-humeral joint, although it is not composed of cartilage tissue. Therefore, he highlighted the functional issue of subacromial bursa. In 1972, Neer [62] further emphasized this point of view in his studies on impingement syndrome. Moreover, in other studies, he suggested that subacromial bursa is an inflammatory membrane that can lead to pain through nociceptors endings stimulation. Santavirta et al. [63] found a majority of CD-2 and CD-11b mononuclear cells in the bursa of patients suffering from subacromial bursitis. Yanagisawa [64] also demonstrated an increased expression of VEGF in patients with impingement syndrome, thus pointing out chronic inflammation and increased vascularity. Other studies [65] demonstrated the increased expression of pain mediators (substance P) in the subacromial space in subjects with impingement syndrome.

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Despite these evidences about subacromial bursa, the changes in biochemical mediators expression, implicated in subacromial impingement syndrome pathogenesis, have not yet completely identified. These investigations were carried on to determine the role of subacromial bursa in impingement syndrome; the question is if the bursa behaves as a pathological

During "bursitis" (**Figure 3**), there is a reduction of the overall subacromial space, which may lead to an increased compression of tissues inside. During subacromial impingement syndrome, it has been demonstrated tendons degeneration, due to inflammatory processes or

Impingement syndrome classification was first developed by Neer in 1983 [66] and it is based on histopatological damage of tissues. He defined this syndrome as a mechanical-compressive lesion of tissues of the subacromial space and he identified three progressive stages: first stage ("edema and hemorrhage stage") is typical in patients aged 25 or less with a history of overhead use of the upper limb during sport or work; second stage is defined by further deterioration of rotator cuff tendons and subacromial bursa, and it usually affects 25–40 years old patients; last stage, the third one, is characterized by bone spurs and partial or full-thickness

tension overload in shoulder mobilization (e.g. during work activities) [4].

tendon rupture affecting subjects aged 40 or more.

**Figure 3.** Subacromial bursitis: ultrasound imaging.

Calcific tendonitis is not simply a degenerative disorder, since calcification is not histologically associated with necrosis or tissue damage, but it is a cell-mediated process similar to an incomplete endochondral ossification.

One of the first authors to describe the calcium deposits cycle was Uhthoff [55] who divided it into two phases: a formative and resorptive one. Other authors subdivided the cycle into three phases: pre-calcification (asymptomatic), calcification (impingement) and post-calcification (acute) [56].

A more complete classification divided this cycle into four phases: pre-calcific phase, during which the fibrocartilaginous transformation occurs in the tendon context in a completely asymptomatic manner; formation phase that consists of the deposition of hydroxyapatite crystals within the tendon; re-absorbing phase, characterized by the release of these crystals and finally post calcific recovering phase.

It is therefore evident that there is currently no standardized histological classification for tendon calcifications in literature.

In concern to the radiographic aspects of calcification, many studies converge on Gartner's classification (1993), whereby three kinds of deposits can be identified. Type I refers to a well-defined and dense deposit, type II identifies a well-distinguished but radiotransparent deposit and finally, type III has a radiotransparent structure but with marginal margins [57].

In fact, the classification of the French Arthroscopic Society [58] also identifies three types of calcifications, indicating them with letters A, B and C (**Figure 2**), which reproduce the description of Gartner.

The authors discussed for a long time about the use of radiographic classification both to choose the most appropriate treatment and as an outcome to evaluate its beneficial effect. The fundamental concept is that radiographic classification is not sufficient on its own, but correlation with the clinical data is always necessary [59, 60].

**Figure 2.** Classification of calcifications by French Arthroscopic Society. A: Dense deposit and well-defined margins, C: nubecular deposit, margins not defined. B: intermediate between the two previous types.

#### **3.3. Subacromial bursitis and impingement**

A 2009 study conducted by Maugars et al. [53] pointed out that between 7 and 17% of patients

Calcific tendonitis is not simply a degenerative disorder, since calcification is not histologically associated with necrosis or tissue damage, but it is a cell-mediated process similar to an

One of the first authors to describe the calcium deposits cycle was Uhthoff [55] who divided it into two phases: a formative and resorptive one. Other authors subdivided the cycle into three phases: pre-calcification (asymptomatic), calcification (impingement) and post-calcification

A more complete classification divided this cycle into four phases: pre-calcific phase, during which the fibrocartilaginous transformation occurs in the tendon context in a completely asymptomatic manner; formation phase that consists of the deposition of hydroxyapatite crystals within the tendon; re-absorbing phase, characterized by the release of these crystals

It is therefore evident that there is currently no standardized histological classification for

In concern to the radiographic aspects of calcification, many studies converge on Gartner's classification (1993), whereby three kinds of deposits can be identified. Type I refers to a well-defined and dense deposit, type II identifies a well-distinguished but radiotransparent deposit and finally, type III has a radiotransparent structure but with marginal margins [57]. In fact, the classification of the French Arthroscopic Society [58] also identifies three types of calcifications, indicating them with letters A, B and C (**Figure 2**), which reproduce the descrip-

The authors discussed for a long time about the use of radiographic classification both to choose the most appropriate treatment and as an outcome to evaluate its beneficial effect. The fundamental concept is that radiographic classification is not sufficient on its own, but cor-

**Figure 2.** Classification of calcifications by French Arthroscopic Society. A: Dense deposit and well-defined margins, C:

nubecular deposit, margins not defined. B: intermediate between the two previous types.

suffering from chronic shoulder pain was due to tendon calcification.

incomplete endochondral ossification.

and finally post calcific recovering phase.

relation with the clinical data is always necessary [59, 60].

tendon calcifications in literature.

(acute) [56].

214 Advances in Shoulder Surgery

tion of Gartner.

The subacromial bursa is the largest and most complicated bursa in human body. In a 1934 book [61], Codman affirmed that it behaves as a secondary scapula-humeral joint, although it is not composed of cartilage tissue. Therefore, he highlighted the functional issue of subacromial bursa. In 1972, Neer [62] further emphasized this point of view in his studies on impingement syndrome. Moreover, in other studies, he suggested that subacromial bursa is an inflammatory membrane that can lead to pain through nociceptors endings stimulation. Santavirta et al. [63] found a majority of CD-2 and CD-11b mononuclear cells in the bursa of patients suffering from subacromial bursitis. Yanagisawa [64] also demonstrated an increased expression of VEGF in patients with impingement syndrome, thus pointing out chronic inflammation and increased vascularity. Other studies [65] demonstrated the increased expression of pain mediators (substance P) in the subacromial space in subjects with impingement syndrome.

Despite these evidences about subacromial bursa, the changes in biochemical mediators expression, implicated in subacromial impingement syndrome pathogenesis, have not yet completely identified. These investigations were carried on to determine the role of subacromial bursa in impingement syndrome; the question is if the bursa behaves as a pathological or a reparative tissue.

During "bursitis" (**Figure 3**), there is a reduction of the overall subacromial space, which may lead to an increased compression of tissues inside. During subacromial impingement syndrome, it has been demonstrated tendons degeneration, due to inflammatory processes or tension overload in shoulder mobilization (e.g. during work activities) [4].

Impingement syndrome classification was first developed by Neer in 1983 [66] and it is based on histopatological damage of tissues. He defined this syndrome as a mechanical-compressive lesion of tissues of the subacromial space and he identified three progressive stages: first stage ("edema and hemorrhage stage") is typical in patients aged 25 or less with a history of overhead use of the upper limb during sport or work; second stage is defined by further deterioration of rotator cuff tendons and subacromial bursa, and it usually affects 25–40 years old patients; last stage, the third one, is characterized by bone spurs and partial or full-thickness tendon rupture affecting subjects aged 40 or more.

**Figure 3.** Subacromial bursitis: ultrasound imaging.

#### **3.4. Rotator cuff tears**

Rotator cuff tears represent approximately one-third of medical visits for shoulder pain, but sometimes it is a problem difficult to diagnose. Among patients suffering from shoulder pain, rotator cuff tears are the most common cause, especially in subjects aged 60 or more [67]. The incidence of this pathology increases with age; moreover, studies on cadavers have noticed 30% of cases with rotator cuff tears [68]. As mentioned, literature agrees that the incidence increases with age. In particular, a study [69] noted that the incidence of asymptomatic tears in patients aged 50–59 years was 13%, between 60 and 69 years the incidence was 20%, among 70–79 years was 31% and over 80 years was 51%. Yamamoto et al. [67] observed a prevalence of full-thickness tears of 20.7% in a sample population, mean age 57.9 years, with or without symptoms. In a 2006 review of autopsy studies, evaluating 2553 shoulders (mean age 70.1 years), it observed a prevalence of 18.5% for partial-thickness tears and 11.8% for full lesions [68]. Rotator cuff tears are very common, so the pathological history and the clinical examination play a critical role, especially in subclinical cases.

or 50% of thickness; grade III involves more than 6 mm or more than 50% of thickness. In full-thickness tears a complete fibers disruption brungs to a direct communication between

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The greater the size of the lesion, the extent of retraction and the quantity of fatty muscle atrophy, the less the chance of healing from rotator cuff tear. The natural history of the lesion is the further increase in size over time. Therefore, for example, partial thickness tears become total lesions and, referring to Cofield's classification (**Table 1**), small-sized tears tend to evolve

Frozen shoulder, or adhesive capsulitis, is a painful and disabling condition of unknown etiology caused by a spontaneous contracture of the glenohumeral joint in absence of an evident previous event, resulting in reduction of joint motion [71]. This debilitating condition affects from 2 to 5% of the general population [72] and its prevalence increases to 10–38% in patients with comorbidities, such as hypothyroidism [73], diabetes, increased body mass index and cervical spondylosis [74]. This condition is more common in women and in non-dominant

The currently recognized classification (**Table 4**) identifies as a primary frozen shoulder a condition with any clearly identifiable etiopathogenetic cause, and as secondary a condition triggered by a well-defined cause. The last one, is further subdivided into intrinsic, extrinsic

Neviaser describe this state as *adhesive capsulitis* to emphasize the inflammatory component affecting the capsule, multiregional areas of synovitis and synovial angiogenesis [77].

Further classifications of rotator cuff tears [4] are shown in **Tables 1**–**3**.

**Figure 4.** Ellman classification of rotator cuff tears. A: grade I; B: grade II; C: grade III.

subacromial and glenohumeral spaces.

shoulders. The mean age of onset is 50–55 years [75].

Small <1 cm Medium 1–3 cm Large 3–5 cm Massive >5 cm

**Table 1.** Cofield classification (by tear size).

toward massive lesions.

**3.5. Frozen shoulder**

and systemic [76].

Pathogenesis of rotator cuff tears is complex and multifactorial. For this reason, there are two different schools of thought, according to which tendon injuries can be due to intrinsic or extrinsic factors. Codman [61] had already described the intrinsic theory according to which tendon degenerates in the critical area of hypovascularity; this area is 1 cm from the insertion of supraspinatus to the humeral head. Besides this, due to its low vascularization, it is also an area with low healing capacity. According to extrinsic theory, the cuff tendons, flowing into the subacromial space (i.e. between the acromion, the coracoacromial ligament and the humeral head) can be compressed and then injured.

The majority of rotator cuff tears affected supraspinatus and infraspinatus tendons; these are described as postero-superior cuff tears. On the contrary, antero-superior tears are less common and typically extend anteriorly involving rotator interval or subscapularis tendon. Partial tears consist of a partial disruption of tendon fibers without communication among bursal and articular spaces.

The average normal thickness of rotator cuff tendons is between 8 and 12 mm. The depth of tear defines the degree of lesion. Codman classified tendon tears in three types [61]:


Another classification proposed by Neer [62] divided the condition of pain, inflammation, oedema and hemorrhage as stage I, tendinous fibrosis as stage II and fibers rupture as stage III.

Taking into account the average thickness of supraspinatus tendon, Ellman [70] classified rotator cuff tears (**Figure 4**): grade I consists of a tear depth lower than 3 mm (or involving less than 25% of tendon thickness); grade II characterized by a depth between 3 and 6 mm

**Figure 4.** Ellman classification of rotator cuff tears. A: grade I; B: grade II; C: grade III.

or 50% of thickness; grade III involves more than 6 mm or more than 50% of thickness. In full-thickness tears a complete fibers disruption brungs to a direct communication between subacromial and glenohumeral spaces.

Further classifications of rotator cuff tears [4] are shown in **Tables 1**–**3**.

The greater the size of the lesion, the extent of retraction and the quantity of fatty muscle atrophy, the less the chance of healing from rotator cuff tear. The natural history of the lesion is the further increase in size over time. Therefore, for example, partial thickness tears become total lesions and, referring to Cofield's classification (**Table 1**), small-sized tears tend to evolve toward massive lesions.

#### **3.5. Frozen shoulder**

**3.4. Rotator cuff tears**

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subclinical cases.

bursal and articular spaces.

stage III.

humeral head) can be compressed and then injured.

Rotator cuff tears represent approximately one-third of medical visits for shoulder pain, but sometimes it is a problem difficult to diagnose. Among patients suffering from shoulder pain, rotator cuff tears are the most common cause, especially in subjects aged 60 or more [67]. The incidence of this pathology increases with age; moreover, studies on cadavers have noticed 30% of cases with rotator cuff tears [68]. As mentioned, literature agrees that the incidence increases with age. In particular, a study [69] noted that the incidence of asymptomatic tears in patients aged 50–59 years was 13%, between 60 and 69 years the incidence was 20%, among 70–79 years was 31% and over 80 years was 51%. Yamamoto et al. [67] observed a prevalence of full-thickness tears of 20.7% in a sample population, mean age 57.9 years, with or without symptoms. In a 2006 review of autopsy studies, evaluating 2553 shoulders (mean age 70.1 years), it observed a prevalence of 18.5% for partial-thickness tears and 11.8% for full lesions [68]. Rotator cuff tears are very common, so the pathological history and the clinical examination play a critical role, especially in

Pathogenesis of rotator cuff tears is complex and multifactorial. For this reason, there are two different schools of thought, according to which tendon injuries can be due to intrinsic or extrinsic factors. Codman [61] had already described the intrinsic theory according to which tendon degenerates in the critical area of hypovascularity; this area is 1 cm from the insertion of supraspinatus to the humeral head. Besides this, due to its low vascularization, it is also an area with low healing capacity. According to extrinsic theory, the cuff tendons, flowing into the subacromial space (i.e. between the acromion, the coracoacromial ligament and the

The majority of rotator cuff tears affected supraspinatus and infraspinatus tendons; these are described as postero-superior cuff tears. On the contrary, antero-superior tears are less common and typically extend anteriorly involving rotator interval or subscapularis tendon. Partial tears consist of a partial disruption of tendon fibers without communication among

The average normal thickness of rotator cuff tendons is between 8 and 12 mm. The depth of

Another classification proposed by Neer [62] divided the condition of pain, inflammation, oedema and hemorrhage as stage I, tendinous fibrosis as stage II and fibers rupture as

Taking into account the average thickness of supraspinatus tendon, Ellman [70] classified rotator cuff tears (**Figure 4**): grade I consists of a tear depth lower than 3 mm (or involving less than 25% of tendon thickness); grade II characterized by a depth between 3 and 6 mm

tear defines the degree of lesion. Codman classified tendon tears in three types [61]:

**1.** bursal-side tear (BT) confined to the bursal surface of the tendon;

**3.** joint-side tear (JT) located on the joint side of the tendon.

**2.** intratendinous tear (IT), which is localized within tendon thickness and

Frozen shoulder, or adhesive capsulitis, is a painful and disabling condition of unknown etiology caused by a spontaneous contracture of the glenohumeral joint in absence of an evident previous event, resulting in reduction of joint motion [71]. This debilitating condition affects from 2 to 5% of the general population [72] and its prevalence increases to 10–38% in patients with comorbidities, such as hypothyroidism [73], diabetes, increased body mass index and cervical spondylosis [74]. This condition is more common in women and in non-dominant shoulders. The mean age of onset is 50–55 years [75].

The currently recognized classification (**Table 4**) identifies as a primary frozen shoulder a condition with any clearly identifiable etiopathogenetic cause, and as secondary a condition triggered by a well-defined cause. The last one, is further subdivided into intrinsic, extrinsic and systemic [76].

Neviaser describe this state as *adhesive capsulitis* to emphasize the inflammatory component affecting the capsule, multiregional areas of synovitis and synovial angiogenesis [77].


**Table 1.** Cofield classification (by tear size).


**Table 2.** Patte classification (by cuff tears retraction).


accumulation that in part differentiate into myofibroblasts. They exert tractions on new col-

**Figure 5.** Frozen shoulder at MRI. Coronal PD (A): thickening of the axillary recess of the glenohumeral joint; sagittal PD

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The diagnosis is essentially clinical, based on the evidence of the reduction of the ROM (range of motion) in particular in extrarotation, elevation and intrarotation of the glenohumeral joint, in the absence of X-ray lesions. This is accompanied by pain at the insertion of the deltoid and muscular weakness [80]. Radiographic images are not helpful, unless in the case of associated pathologies, such as fractures, arthritis and metallic implants. In selected cases, with suspected association with rotator cuff tendinopathy or impingement syndrome, we can refer

According to Neviaser et al. [80], the clinical presentation is indicative of the stage of the

Stage 1, preadventive stage: patients have mild pain at the end of the range of motion and this

Stage 2, "freezing" stage: is often characterized by a high level of discomfort and a high level

Stage 4, "thawing" stage: in this phase we have painless stiffness and motion that typically

The diagnosis is based essentially on clinical examination, exclusion of other pathologies and normal glenohumeral radiographs. Initial evaluation of global postural assessment should be perform before focusing on the shoulder, because shoulder pain is often associated with thoracic

condition is often mistakenly diagnosed as impingement syndrome.

Stage 3, "frozen" stage: is characterized by significant stiffness, but less pain.

lagen deposits with stiffening of the capsule [79].

(B): inflammation in the rotator cuff interval.

to magnetic resonance imaging (**Figure 5**) [81].

of pain and a progressive loss of ROM.

adhesive capsulitis:

improves by remodeling.

**4. Clinical presentation**

**Table 3.** Goutallier classification: by extent of fatty muscle degeneration.


**Table 4.** Frozen shoulder classification.

Histological findings attribute to neoangiogenesis the growth of new nerves in the capsuloligamentous complex of these patients and this may be the explanation of the pain associated with capsulitis.

Immunocytochemical analysis on arthroscope biopsy material revealed the presence of chronic inflammatory cells predominantly made up of mast cells, T cells, B cells and macrophages, as well as the presence of fibrosis that results from mast cell infiltrate, which typically regulate the proliferation of fibroblasts [78].

Frozen shoulder seems to be the result of failure of the healing process after an initial inflammatory phase, characterized by an excess of cytokines and growth factors with fibroblasts

**Figure 5.** Frozen shoulder at MRI. Coronal PD (A): thickening of the axillary recess of the glenohumeral joint; sagittal PD (B): inflammation in the rotator cuff interval.

accumulation that in part differentiate into myofibroblasts. They exert tractions on new collagen deposits with stiffening of the capsule [79].

The diagnosis is essentially clinical, based on the evidence of the reduction of the ROM (range of motion) in particular in extrarotation, elevation and intrarotation of the glenohumeral joint, in the absence of X-ray lesions. This is accompanied by pain at the insertion of the deltoid and muscular weakness [80]. Radiographic images are not helpful, unless in the case of associated pathologies, such as fractures, arthritis and metallic implants. In selected cases, with suspected association with rotator cuff tendinopathy or impingement syndrome, we can refer to magnetic resonance imaging (**Figure 5**) [81].

According to Neviaser et al. [80], the clinical presentation is indicative of the stage of the adhesive capsulitis:

Stage 1, preadventive stage: patients have mild pain at the end of the range of motion and this condition is often mistakenly diagnosed as impingement syndrome.

Stage 2, "freezing" stage: is often characterized by a high level of discomfort and a high level of pain and a progressive loss of ROM.

Stage 3, "frozen" stage: is characterized by significant stiffness, but less pain.

Stage 4, "thawing" stage: in this phase we have painless stiffness and motion that typically improves by remodeling.
