Difference between revisions of "Shoulder:Biomechanics"

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=== Static stabilizers ===
 
=== Static stabilizers ===
 
Static stability of the glenohumeral joint is provided by the capsulolabral structures as well as the bony anatomy of the glenoid. Historically, significant effort was placed on understanding the importance of the anterior capsulolabral structures, due to the fact that these structures are classically torn in the case of anterior shoulder instability.6 The glenohumeral ligaments are a thickening of the joint capsule and represent the primary static stabilizers. To
 
Static stability of the glenohumeral joint is provided by the capsulolabral structures as well as the bony anatomy of the glenoid. Historically, significant effort was placed on understanding the importance of the anterior capsulolabral structures, due to the fact that these structures are classically torn in the case of anterior shoulder instability.6 The glenohumeral ligaments are a thickening of the joint capsule and represent the primary static stabilizers. To
allow a high degree of shoulder mobility they only become tight at the end-ranges of motion. The superior glenohumeral ligament is tight in adduction, the middle at 45 degrees of abduction and the inferior glenohumeral when the shoulder is brought to 90 degrees of abduction in
+
allow a high degree of shoulder mobility they only become tight at the end-ranges of motion. The superior glenohumeral ligament is tight in adduction, the middle at 45 degrees of abduction and the inferior glenohumeral when the shoulder is brought to 90 degrees of abduction in external rotation.7 The inferior glenohumeral ligament is therefore considered the strongest and most important soft tissue stabilizer. Structurally it can be avulsed from the glenoid side resulting in an antero-inferior labral lesion, as well as from the humeral side resulting in the less-frequent humeral avulsion of the glenohumeral ligament
external rotation.7 The inferior glenohumeral ligament is therefore considered the strongest and most important
+
(HAGL) lesion.8,9 The postero-inferior capsule and posterior inferior glenohumeral ligament are not as robust as their anterior counterparts,10 but it is often felt to be necessary to ‘balance’ both inferior ligaments during a soft tissue repair for instability. Laxity is a normal, physiologic
soft tissue stabilizer. Structurally it can be avulsed from
+
and asymptomatic finding, that corresponds to translation of the humeral head in any direction to the glenoid.11 Hyperlaxity is constitutional, multidirectional, bilateral and asymptomatic. Hyperlaxity of the shoulder is probably best defined as external rotation with the elbow at the side equal to or greater than 85 degrees.12 This nonpathological finding is a risk factor for instability but does not by itself demand treatment unless there is clear pathological laxity. Pathological laxity of the inferior glenohumeral ligament is observed when passive abduction in neutral rotation in the glenohumeral joint is above 105 degrees, there is apprehension above 90 degrees of abduction, or if a difference of more than 20 degrees between the two shoulders is noted.13,14 Pathological laxity is often multidirectional and associated with a redundant capsule leading to an increased glenohumeral volume.15 Biomechanical studies have focused on evaluating the effectiveness of soft tissue procedures to reduce capsular volume. Cadaveric models created by stretching the capsule 10–30% beyond the maximal range of motion, revealed that 1 cm capsular shifts were effective to reduce capsular volume by an average 33.7% (range, 25.3% to 44.6%).16–18 Ponce et al further reported a linear relationship between the number of 1 cm stitches and capsular volume, each plication reducing the volume by approximately 10%.19 Lastly, while both capsular plication and rotator interval closure have been reported to be effective in restoring intact range of motion after capsular stretching, the addition of an interval closure has the benefit of better restoring humeral head translation at 60 degrees of abduction.18,20
the glenoid side resulting in an antero-inferior labral
+
 
lesion, as well as from the humeral side resulting in the
+
The osseous glenoid is relatively flat, the biomechanical role of the glenoid cartilage and labrum is to double the depth of the glenoid socket and therefore enhance the contact area with the humeral head.21–23 This is further believed to stabilize the joint by helping to centre the humeral head when compressed against the glenoid by the rotator cuff muscles (concavity compression mechanism). A complete loss of the anterior labrum has been reported to decrease the contact area by 7% to 15%, and increase the mean contact pressure by 8% to 20%.24 A  biomechanical study by Hara et al identified the anteroinferior labrum as being the weakest point, with a mean force necessary to cause a rupture of 3.84 ± 1.00 kg/5 mm.25 Finally, it was postulated that an intact labrum could help create a negative intra-articular pressure (vacuum effect); this effect is, however, thought to be marginal when the rotator cuff muscles are contracted.26–28 Despite these important stabilizing effects, Itoi et al revealed that soft tissues alone play only a minor role in glenohumeral stability in mid-range of motion.29
less-frequent humeral avulsion of the glenohumeral ligament
+
 
(HAGL) lesion.8,9 The postero-inferior capsule and
+
=== Glenoid bone defects and morphology ===
posterior inferior glenohumeral ligament are not as robust
+
An important concept regarding glenohumeral joint stability is the concavity compression principle, which centres the humeral head on the glenoid. This centring mechanism is the result of the rotator cuff compressing the humeral head against the glenoid cavity, and is one  reason why an anterior glenoid rim defect predisposes to  recurrent anterior instability.30 While there is some controversy,  15% to 20% glenoid bone loss seems to be the cutoff value for soft tissue repair.31,32 Shin et al demonstrated that in case of an anterior defect ≥ 15%, a soft tissue procedure (Bankart) is unable to restore normal shoulder kinematics and even leads to postero-inferior translation of the humeral head in abduction and external rotation.32 On the other hand, bone grafting (glenoidplasty) can successfully reconstruct glenoid curvature and depth and therefore restore stability.30,33 Another key point is the reduced contact area and increased articular contact pressure induced by bony glenoid defects.24 While iliac bone graft (Eden-Hybinette), articular distal clavicle autografts
as their anterior counterparts,10 but it is often felt to be
+
and coracoid transfer (Latarjet or Bristow) can all restore normal values, the correct position and orientation of the bone graft is important.34,35 The Latarjet will, however, be limited by the amount of bone that can be harvested.
necessary to ‘balance’ both inferior ligaments during a
+
 
soft tissue repair for instability. Laxity is a normal, physiologic
+
Young et al reported mean values of 26.4 ± 2.9 mm and 9.3 ± 1.4 mm for length and thickness respectively.36 A graft placed in too lateral of a position will lead to an increased anterior-inferior peak contact pressure, whereas a recessed graft will lead to high edge loading. To avoid increased inferior contact pressure, the current evidence suggests orientating the coracoid bone graft in an inferior direction.37 The congruent-arc modification of the original Latarjet technique further allows the reconstruction of larger defects by matching the shape of the graft to that of the glenoid.38 The use of a distal tibial osteochondral allograft respects all these biomechanical principles and has been shown to be a valid alternative in the absence of reliable autograft.39
and asymptomatic finding, that corresponds to
+
 
translation of the humeral head in any direction to the glenoid.
+
During posterior shoulder dislocation, reverse Bankart lesions are only present in isolation in 51% of cases.40 They are, however, sufficient to increase posterior translation and inferior translation of the humerus in the sulcus position by 86% and 31% respectively.41 Additionally, glenoid  retroversion is more common in posterior instability and appears to predispose to posterior instability.42 Every five-degree increment of retroversion led to an additional posterior decentralization of the humeral head overall by (average ± standard deviation) 2.0 mm ± 0.3 in the intact and 2.0 mm ± 0.7 in the detached labrum condition. Bony alignment in terms of glenoid retroversion angle plays an important role in joint centration and posterior translation, especially in retroversion angles greater than 10 degrees.43 Labral injury from repetitive posterior loading or instability can range from a posterior labral tear to an incomplete, concealed avulsion of the postero-inferior labrum (also known as ‘Kim lesion’) to a reverse Bankart lesion. Glenoid retroversion beyond the average five degrees to 10 degrees has been shown to be a risk factor for developing subsequent posterior instability in a prospective study of healthy subjects. For every one degree increase in glenoid retroversion, the risk for posterior instability increase by 17%.44
11 Hyperlaxity is constitutional, multidirectional,
+
 
bilateral and asymptomatic. Hyperlaxity of the shoulder is
+
=== Humeral bone defects ===
probably best defined as external rotation with the elbow
+
A Malgaigne lesion45 also called a Hill–Sachs lesion46 describes the grooved defect of the humeral head. This frequently unrecognized complication of anterior dislocation of the shoulder joint is the result of compression of the posterolateral head upon the anterior glenoid rim. The presence of humeral bone loss has been linked with recurrent instability after open or arthroscopic shoulder stabilization. 47,48 Cadaveric studies have revealed that humeral bone defects as small as 12.5% of the humeral head diameter will affect joint stability, which can be restored with allograft reconstruction. However, an isolated 25% bone loss was not shown to be sufficient to explain recurrent instability on its own.49–51 In other words, glenoid bone loss is required as well. Clinically, the more common alternative to allograft reconstruction is the remplissage procedure, which insets the posterior capsule and infraspinatus tendon into the lesion. This procedure medializes the insertion of the posterior structures to prevent engagement and also decreases anterior translation of the
at the side equal to or greater than 85 degrees.12 This nonpathological
+
humeral head. A recent review identified 10 biomechanical studies of which only one reported persistent engagement after a remplissage procedure in the presence of a 25% humeral head defect.52 The same study further compared the remplissage to the Latarjet and found that 84% of specimens (27 of 32 testing scenarios) stabilized after remplissage, and 94% of specimens (30 of 32 testing scenarios)
finding is a risk factor for instability but does
+
stabilized after the Latarjet procedure. This was, however, not statistically significant and the authors concluded  that both techniques are effective.53 Nevertheless, at maximum external rotation at 60 degrees of abduction, remplissage altered the kinematics of the glenohumeral joint by shifting posteriorly and inferiorly the apex of the humeral head.54 Moreover, while often described as an inset of the infraspinatus tendon, the procedure is in fact a capsulomyodesis of the infraspinatus and teres minor;55 this has not only been proven in anatomic investigation, but also follows normal form as the tendon does not extend very far medially from its normal insertion.
not by itself demand treatment unless there is clear pathological
+
 
laxity. Pathological laxity of the inferior glenohumeral
+
For posterior instability, the McLaughlin procedure56 using the detached subscapularis tendon has been described for locked posterior instability in presence of a  reverse Malgaigne (Hill–Sachs) lesion. This technique has been subsequently modified as either a reverse remplissage57 or an osteotomy of the lesser tuberosity with the attached subscapularis (Hughes and Neer method) to allow additional bone support to articular cartilage with satisfactory  outcome both in acute and chronic setting.58,59
ligament is observed when passive abduction in
 
neutral rotation in the glenohumeral joint is above 105
 
degrees, there is apprehension above 90 degrees of
 
abduction, or if a difference of more than 20 degrees
 
between the two shoulders is noted.13,14 Pathological laxity
 
is often multidirectional and associated with a redundant
 
capsule leading to an increased glenohumeral
 
volume.15 Biomechanical studies have focused on evaluating
 
the effectiveness of soft tissue procedures to reduce
 
capsular volume. Cadaveric models created by stretching
 
the capsule 10–30% beyond the maximal range of motion,
 
revealed that 1 cm capsular shifts were effective to reduce
 
capsular volume by an average 33.7% (range, 25.3% to
 

Revision as of 21:20, 2 July 2020

Bullet Points

  • The stability of the glenohumeral joint depends on soft tissue stabilizers, bone morphology and dynamic stabilizers such as the rotator cuff and long head of the biceps tendon.
  • Shoulder stabilization techniques include anatomic procedures such as repair of the labrum or restoration of bone loss, but also non-anatomic options such as remplissage or tendon transfers.
  • Rotator cuff repair should restore the cuff anatomy, reattach the rotator cable and respect the coracoacromial arch whenever possible. Tendon transfer, superior capsular reconstruction or balloon implantation have been proposed for irreparable lesions.

„„

  • Shoulder rehabilitation should focus on restoring balanced glenohumeral and scapular force couples in order to avoid an upward migration of the humeral head and secondary cuff impingement. The primary goal of cuff repair is to be as anatomic as possible and to create a biomechanically favourable environment for tendon healing.

Keywords

Anatomy; glenohumeral instability; humerus; ligaments; rehabilitation; rotator cuff; scapula; therapeutic implications.

Introduction

The biomechanics of the shoulder are highly complex. First, it is composed of four joints (glenohumeral, acromioclavicular, scapulothoracic, and sternoclavicular). The glenohumeral joint has six degrees of freedom and is the most mobile joint in the human body, allowing the hand to reach a wide range of positions. This mobility can be further enhanced by translation of the humeral head on the glenoid, but the consequence of this tremendous mobility is perhaps a predisposition to instability and impingements. Second, mobility is assumed by 18 muscles that act in synergy. Consequently, decoupling/isolating them is impossible, making precise kinematic analysis and clinical examination difficult. Third, the glenohumeral joint has the characteristics of an active non-weight-bearing joint, leading to major bony and muscular modifications and frequent tendon overuse.

When looking at the shoulder as a functional unit, it appears that several factors need consideration. To function normally, the shoulder needs all the anatomic structures to work in a chain. Form will allow function.1 First, the central nervous system provides a signal to the muscletendon unit. By contracting, the muscle transmits its tension to the tendon, which then acts as a lever arm on the joint. To be efficient, such a system requires a stable fulcrum. The necessary stability is provided by static and dynamic factors such as bony contours, ligaments, labrum, capsule, etc.

The specificity of biomechanically relevant parameters, such as, for example, joint reaction forces, is that they cannot be measured in vivo without invasive procedures.2 Our knowledge therefore mainly relies on experimental cadaveric studies3 or computational modelling.4 These simulations have become more sophisticated in recent years, allowing the inclusion of an increasing number of variables with the ability to adjust both pathology and patient-specific characteristics.5 This ongoing process will without doubt call into question prior assumptions and allow further insights into shoulder biomechanics. It is crucial to understand the basic principles of shoulder biomechanics and their modifications in the most common pathologies encountered in daily practice.

Instability

Static stabilizers

Static stability of the glenohumeral joint is provided by the capsulolabral structures as well as the bony anatomy of the glenoid. Historically, significant effort was placed on understanding the importance of the anterior capsulolabral structures, due to the fact that these structures are classically torn in the case of anterior shoulder instability.6 The glenohumeral ligaments are a thickening of the joint capsule and represent the primary static stabilizers. To allow a high degree of shoulder mobility they only become tight at the end-ranges of motion. The superior glenohumeral ligament is tight in adduction, the middle at 45 degrees of abduction and the inferior glenohumeral when the shoulder is brought to 90 degrees of abduction in external rotation.7 The inferior glenohumeral ligament is therefore considered the strongest and most important soft tissue stabilizer. Structurally it can be avulsed from the glenoid side resulting in an antero-inferior labral lesion, as well as from the humeral side resulting in the less-frequent humeral avulsion of the glenohumeral ligament (HAGL) lesion.8,9 The postero-inferior capsule and posterior inferior glenohumeral ligament are not as robust as their anterior counterparts,10 but it is often felt to be necessary to ‘balance’ both inferior ligaments during a soft tissue repair for instability. Laxity is a normal, physiologic and asymptomatic finding, that corresponds to translation of the humeral head in any direction to the glenoid.11 Hyperlaxity is constitutional, multidirectional, bilateral and asymptomatic. Hyperlaxity of the shoulder is probably best defined as external rotation with the elbow at the side equal to or greater than 85 degrees.12 This nonpathological finding is a risk factor for instability but does not by itself demand treatment unless there is clear pathological laxity. Pathological laxity of the inferior glenohumeral ligament is observed when passive abduction in neutral rotation in the glenohumeral joint is above 105 degrees, there is apprehension above 90 degrees of abduction, or if a difference of more than 20 degrees between the two shoulders is noted.13,14 Pathological laxity is often multidirectional and associated with a redundant capsule leading to an increased glenohumeral volume.15 Biomechanical studies have focused on evaluating the effectiveness of soft tissue procedures to reduce capsular volume. Cadaveric models created by stretching the capsule 10–30% beyond the maximal range of motion, revealed that 1 cm capsular shifts were effective to reduce capsular volume by an average 33.7% (range, 25.3% to 44.6%).16–18 Ponce et al further reported a linear relationship between the number of 1 cm stitches and capsular volume, each plication reducing the volume by approximately 10%.19 Lastly, while both capsular plication and rotator interval closure have been reported to be effective in restoring intact range of motion after capsular stretching, the addition of an interval closure has the benefit of better restoring humeral head translation at 60 degrees of abduction.18,20

The osseous glenoid is relatively flat, the biomechanical role of the glenoid cartilage and labrum is to double the depth of the glenoid socket and therefore enhance the contact area with the humeral head.21–23 This is further believed to stabilize the joint by helping to centre the humeral head when compressed against the glenoid by the rotator cuff muscles (concavity compression mechanism). A complete loss of the anterior labrum has been reported to decrease the contact area by 7% to 15%, and increase the mean contact pressure by 8% to 20%.24 A biomechanical study by Hara et al identified the anteroinferior labrum as being the weakest point, with a mean force necessary to cause a rupture of 3.84 ± 1.00 kg/5 mm.25 Finally, it was postulated that an intact labrum could help create a negative intra-articular pressure (vacuum effect); this effect is, however, thought to be marginal when the rotator cuff muscles are contracted.26–28 Despite these important stabilizing effects, Itoi et al revealed that soft tissues alone play only a minor role in glenohumeral stability in mid-range of motion.29

Glenoid bone defects and morphology

An important concept regarding glenohumeral joint stability is the concavity compression principle, which centres the humeral head on the glenoid. This centring mechanism is the result of the rotator cuff compressing the humeral head against the glenoid cavity, and is one reason why an anterior glenoid rim defect predisposes to recurrent anterior instability.30 While there is some controversy, 15% to 20% glenoid bone loss seems to be the cutoff value for soft tissue repair.31,32 Shin et al demonstrated that in case of an anterior defect ≥ 15%, a soft tissue procedure (Bankart) is unable to restore normal shoulder kinematics and even leads to postero-inferior translation of the humeral head in abduction and external rotation.32 On the other hand, bone grafting (glenoidplasty) can successfully reconstruct glenoid curvature and depth and therefore restore stability.30,33 Another key point is the reduced contact area and increased articular contact pressure induced by bony glenoid defects.24 While iliac bone graft (Eden-Hybinette), articular distal clavicle autografts and coracoid transfer (Latarjet or Bristow) can all restore normal values, the correct position and orientation of the bone graft is important.34,35 The Latarjet will, however, be limited by the amount of bone that can be harvested.

Young et al reported mean values of 26.4 ± 2.9 mm and 9.3 ± 1.4 mm for length and thickness respectively.36 A graft placed in too lateral of a position will lead to an increased anterior-inferior peak contact pressure, whereas a recessed graft will lead to high edge loading. To avoid increased inferior contact pressure, the current evidence suggests orientating the coracoid bone graft in an inferior direction.37 The congruent-arc modification of the original Latarjet technique further allows the reconstruction of larger defects by matching the shape of the graft to that of the glenoid.38 The use of a distal tibial osteochondral allograft respects all these biomechanical principles and has been shown to be a valid alternative in the absence of reliable autograft.39

During posterior shoulder dislocation, reverse Bankart lesions are only present in isolation in 51% of cases.40 They are, however, sufficient to increase posterior translation and inferior translation of the humerus in the sulcus position by 86% and 31% respectively.41 Additionally, glenoid retroversion is more common in posterior instability and appears to predispose to posterior instability.42 Every five-degree increment of retroversion led to an additional posterior decentralization of the humeral head overall by (average ± standard deviation) 2.0 mm ± 0.3 in the intact and 2.0 mm ± 0.7 in the detached labrum condition. Bony alignment in terms of glenoid retroversion angle plays an important role in joint centration and posterior translation, especially in retroversion angles greater than 10 degrees.43 Labral injury from repetitive posterior loading or instability can range from a posterior labral tear to an incomplete, concealed avulsion of the postero-inferior labrum (also known as ‘Kim lesion’) to a reverse Bankart lesion. Glenoid retroversion beyond the average five degrees to 10 degrees has been shown to be a risk factor for developing subsequent posterior instability in a prospective study of healthy subjects. For every one degree increase in glenoid retroversion, the risk for posterior instability increase by 17%.44

Humeral bone defects

A Malgaigne lesion45 also called a Hill–Sachs lesion46 describes the grooved defect of the humeral head. This frequently unrecognized complication of anterior dislocation of the shoulder joint is the result of compression of the posterolateral head upon the anterior glenoid rim. The presence of humeral bone loss has been linked with recurrent instability after open or arthroscopic shoulder stabilization. 47,48 Cadaveric studies have revealed that humeral bone defects as small as 12.5% of the humeral head diameter will affect joint stability, which can be restored with allograft reconstruction. However, an isolated 25% bone loss was not shown to be sufficient to explain recurrent instability on its own.49–51 In other words, glenoid bone loss is required as well. Clinically, the more common alternative to allograft reconstruction is the remplissage procedure, which insets the posterior capsule and infraspinatus tendon into the lesion. This procedure medializes the insertion of the posterior structures to prevent engagement and also decreases anterior translation of the humeral head. A recent review identified 10 biomechanical studies of which only one reported persistent engagement after a remplissage procedure in the presence of a 25% humeral head defect.52 The same study further compared the remplissage to the Latarjet and found that 84% of specimens (27 of 32 testing scenarios) stabilized after remplissage, and 94% of specimens (30 of 32 testing scenarios) stabilized after the Latarjet procedure. This was, however, not statistically significant and the authors concluded that both techniques are effective.53 Nevertheless, at maximum external rotation at 60 degrees of abduction, remplissage altered the kinematics of the glenohumeral joint by shifting posteriorly and inferiorly the apex of the humeral head.54 Moreover, while often described as an inset of the infraspinatus tendon, the procedure is in fact a capsulomyodesis of the infraspinatus and teres minor;55 this has not only been proven in anatomic investigation, but also follows normal form as the tendon does not extend very far medially from its normal insertion.

For posterior instability, the McLaughlin procedure56 using the detached subscapularis tendon has been described for locked posterior instability in presence of a reverse Malgaigne (Hill–Sachs) lesion. This technique has been subsequently modified as either a reverse remplissage57 or an osteotomy of the lesser tuberosity with the attached subscapularis (Hughes and Neer method) to allow additional bone support to articular cartilage with satisfactory outcome both in acute and chronic setting.58,59