Medial Synovial Plica Irritation

Background

Medial synovial plicae are embryological structures that form within the knee. They are normal anatomical structures found within the joint capsule of the knee, appearing as thin, soft, and flexible structures that move with the knee during flexion and extension. Impingement of the plicae during motion of the knee can cause inflammation, resulting in medial knee pain. The medial suprapatellar plica of the knee is an intra-articular synovial fold on the medial aspect of the knee. This plica is one of the most common sources of knee pain in patients; however, a proper rehabilitation program allows most patients to recover from the symptoms associated with irritation of this structure.[1]

NextEpidemiologyFrequencyUnited States

No exact numbers on the incidence of patients with an irritated synovial plica are available; however, it is estimated that approximately 50% of patients who present with knee pain to a physician's office have some irritation of their patellofemoral joint. In this group of patients, most of them have some amount of suprapatellar plical irritation. Medial plica syndrome is seen in both young and old patients with a wide variety of activity levels.

PreviousNextFunctional Anatomy

The suprapatellar plica is an intra-articular synovial fold, which has its main component on the medial aspect of the knee. When the knee is in full extension, the suprapatellar plica commonly forms a shelf, which can be palpated by an examiner. Proximally, the plica is attached to the articularis genu muscle. Distally, it is attached to the anterior horn of the medial meniscus and the medial edge of the retropatellar fat pad. In some patients, this plical shelf can become fibrotic and may impinge on the medial edge of the medial femoral condyle. The distal synovial fold of the medial plicae is in close proximity with the tendon sheath of the gracilis, which could potentially explain gait abnormalities seen with plicae irritation.

PreviousNextSport-Specific Biomechanics

The quadriceps muscles and the articularis genu muscle dynamically control the medial suprapatellar plica. Good quadriceps tone seems to result in normal motion of this plica, whereas patients with poor quadriceps tone or tight hamstring muscles (antagonists of the quadriceps) commonly have irritation of their synovial plica.

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Quadriceps Injury

Background

Several types of quadriceps injuries can occur, the most common being the quadriceps contusion, which is painful and disabling. The usual cause of the quadriceps contusion is a direct blow to the anterior thigh from an object or another person (eg, helmet, knee). Very rarely, this injury can be severe enough to progress to an acute compartment syndrome.

Because the quadriceps is in contact with the femur throughout its length, it is susceptible to compression forces. The rectus femoris is the most commonly injured portion of the muscle because of its anterior location. Minimally, impact causes cellular edema of the muscle, but complete capillary disruption with localized hemorrhage leading to a tense anterior compartment can occur. The muscle is more resistant to injury if it is struck while in a contracted nonfatigued state. Other quadriceps injuries range from simple strains to more complex and disabling muscle ruptures. See the image below.

Modified treatment of quadriceps contusion. Used with permission courtesy of John Aronen, MD.

Other types of quadriceps injuries include strains of the quadriceps tendon, complete and partial tears of the quadriceps tendon, and fascial rupture of the quadriceps muscle. Specific areas of the quadriceps are affected for each of these diagnoses. The classic quadriceps strain occurs at the conjoined muscle tendon junction (jumper's knee). The partial tear of the quadriceps most commonly affects the indirect (distal) head of the rectus femoris. Fascial rupture usually occurs anteriorly at the mid thigh and causes a muscle hernia.

NextEpidemiologyFrequencyUnited States

Although quadriceps strains are common, minimal information about the frequency with respect to specific sports is available. As for quadriceps contusions, the most detailed frequency data came from the US Military Academy at West Point,[1] and the distribution per year was reported as follows: rugby 4.7%, karate and judo 2.3%, football 1.6%, and all other sports fewer than 1%. Quadriceps muscle hernias are believed to be more common in soccer, basketball, and rugby.

The incidence of jumper's knee at the quadriceps insertion onto the patella is less common than patellar tendinitis. One study reported that of all tendinopathies affecting the extensor mechanism, the frequency of patellar tendinitis at its insertion was 65%, quadriceps tendinitis was 25%, and patellar tendinitis at its insertion into the tibial tuberosity was 10%.

Rupture of the quadriceps tendon is more common in both older patients and younger athletes. Several studies show that the mean age of patients with quadriceps rupture is about 65 years. However, in athletes, the mean age cited ranges from 15 to 30 years. Sports associated with quadriceps rupture are high jump, basketball, and weight lifting. Rupture is also not uncommon in patients with renal failure.

PreviousNextFunctional Anatomy

The quadriceps femoris acts as a hip flexor and knee extender. The quadriceps femoris is composed of the following:

Rectus femorisVastus lateralisVastus medialisVastus interomedialis

Origins/insertions of quadriceps components include the following:

Rectus femoris - Ilium/tibial tuberosityVastus lateralis - Femur/tibial tuberosityVastus medialis - Femur/tibial tuberosityVastus interomedialis - Femur/tibial tuberosity

The 3 thigh compartments are as follows:

Anterior - Quadriceps muscles, femoral nerve and arteryPosterior - Hamstring muscles, sciatic nerveMedial - Adductor muscles, cutaneous branch of obturator nervePreviousNextSport-Specific Biomechanics

The function of the quadriceps is primarily that of tibial (knee) extension. One electromyography (EMG) study showed that the maximum extension moment and maximum quadriceps EMG activity were early in the kicking action, as the initial flexion changes to extension. This moment occurs before the foot makes contact with the ball. The peak activity of the hamstring occurs after the quadriceps peak, shortly before the ball is struck. The largest extension moment in this study was 260 Nm; this corresponds to a calculated tensile force in the patellar tendon of 7 times body weight.

The mechanical properties of the quadriceps have been studied. The central aspect of 10-mm wide sections of the quadriceps was subjected to tensile loading and compared to a similar patellar tendon section. The ultimate load to failure of the unconditioned patellar tendon was higher (53.4 N/mm2) than the unconditioned quadriceps tendon (33.6 N/mm2). Strain at failure was also higher for the preconditioned patellar tendon (14.4%) than for the quadriceps tendon (11.2%).

Microscopic sections of human quadriceps tendon as it inserts into the patella show no crimping and no cement line. This is unlike other tendon insertion sites. The interdigitation between collagen fibers and the distinction between tendon and bone was least distinct along the anterior third of the patella.

A discussion of the biomechanics of specific injuries is as follows:

Strains, overuse, and rupture: The most common sites of injury correlate to the muscle tendon junctions both proximally and distally and to the muscle belly itself. Muscle strains are usually due to repetitive functional overload. Not surprisingly, quadriceps strains most commonly affect athletes who subject their knees to high levels of repeated loading of the extensor mechanism. The overuse trauma may range from microscopic failure of soft tissue with its associated inflammation or gross rupture. Gross rupture may be partial or complete. A large sudden load may cause the entire insertion to be compromised, leading to complete rupture. Repetitive loading, particularly eccentric loads, causes microfailure, usually at the muscle tendon junction. This microfailure can result in partial tears. Contusion: Direct trauma to the quadriceps may cause muscle fiber and connective tissue rupture and formation of a hematoma. Trauma to the quadriceps causes muscle fiber rupture, disruption of connective tissue, and hematoma formation. Inflammatory cells and macrophages enter the site of injury and begin clearing necrotic muscle cells. This process occurs over 2-3 days. Then, muscle cells attempt to regenerate at the same time scar tissue is being formed. A severe thigh contusion can lead to a compartment syndrome. Muscle hernia: The cause of this is not clear. It is usually associated with a sudden forceful kick, but it may be associated with a weakened or previously injured quadriceps fascia. PreviousProceed to Clinical Presentation , Quadriceps Injury

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Slipped Capital Femoral Epiphysis

Background

Slipped capital femoral epiphysis (SCFE) is one of the most important pediatric and adolescent hip disorders encountered in medical practice.[1, 2, 3, 4] Although SCFE is a rare condition, an accurate diagnosis combined with immediate treatment is critical.[5, 6] Despite the fact that the underlying defect may be multifactorial (eg, mechanical and constitutional factors), SCFE represents a unique type of instability of the proximal femoral growth plate. Clinically, the patient may report hip pain, medial thigh pain, and/or knee pain; an acute or insidious onset of a limp; and decreased range of motion of the hip.

On plain radiographs, the femoral head is seen displaced, posteriorly and inferiorly in relation to the femoral neck and within the confines of the acetabulum.[7] Treatment is primarily operative internal fixation. The goal is to prevent complications such as avascular necrosis (AVN).[2, 8, 9, 10]

A Klein line is a line drawn along the superior border of the femoral neck that would normally pass through a portion of the femoral head. If not, slipped capital femoral epiphysis is diagnosed. X-ray of a hip following operative percutaneous fixation of a slipped capital femoral epiphysis. NextEpidemiologyFrequencyUnited States

The overall incidence for SCFE in the United States is 10.8 cases per 100,000 children.[11] The incidence rate in boys (13.35 per 100,000) is higher than in girls (8.07 per 100,000). When compared with white children, black children have a higher incidence rate at 3.94 times, and Hispanic children have a 2.54 times higher incidence rate.

Rates of SCFE per 100,000 children are higher in the Northeast (17.15) and West (12.70) than in the Midwest (7.69) and South (8.12).[12] Evidence also points to a seasonal variation in SCFE occurrence. In areas north of 40º latitude, 57.4% of SCFEs occurred during the summer, whereas in areas south of 40º latitude, 57.3% of SCFEs occurred during the winter months.[11]

SCFE mainly occurs between the ages of 10 and 16 years.[1, 11] A slight downward trend has occurred for average ages over several years, with some data finding the average age for boys at 12.7 years and girls at 11.2 years. This change could be due to the phenomenon of children maturing at a younger age.[13]

In general, about 20% of patients have bilateral involvement at the time of presentation. It is felt that an additional 20-40% will subsequently progress to bilateral slips. When the presentation is sequential, the second hip usually presents within 18 months of the first SCFE.[14, 15]

The risk of SCFE is increased in children who are obese, as well as in children with other medical issues such as hypothyroidism, low growth hormone level, pituitary tumors, craniopharyngioma, Down syndrome, renal osteodystrophy, and adiposogenital syndrome.

International

In a study by Benson et al, the investigators reexamined the incidence of SCFE in New Mexico (previous studies had reported almost a 5-fold lower incidence of SCFE in New Mexico compared with Connecticut). The discharge databases for the 11 major medical centers in New Mexico from 1995 to 2006 were analyzed by comparison with the 2000 New Mexico census data. The incidence data are reported as cases per 100,000 boys aged 10-17 years and girls aged 8-15 years, as per the earlier study data.[16]

The investigators found an incidence rate of SCFE in New Mexico for the study period was 5.99, which was a statistically significant change that was more than double the reported incidence in the 1960s (2.13). Obesity was noted as a patient factor that changed since 1971 (tripled), although the national incidence of SCFE appeared to have remained fairly constant at 10.8 per 100,000. Benson et al theorized that "increased obesity in children and improved access to pediatric orthopaedic evaluation may have contributed to a significant increase in reported incidence of SCFE in New Mexico."[16]

PreviousNextFunctional Anatomy

SCFE results from a Salter-Harris type physeal fracture. In patients with SCFE, the epiphyseal growth plate is unusually widened, primarily due to expansion of the zone of hypertrophy. The hypertrophic zone, which constitutes 15-30% of the normal physis, can account for up to 80% of the width of the physeal plate in affected patients. Histologically, abnormal cartilage maturation, endochondral ossification, and perichondral ring instability occur. This leads to less organization of the normal cartilaginous columnar architecture. Slippage occurs through this weakened area.

The position of the proximal physis normally changes from horizontal to oblique during preadolescence and adolescence, redirecting hip forces from compression forces to shear forces. There is an association between femoral neck retroversion and a reduced neck-shaft angle with SCFE. These changes can increase the shear forces across the hip, leading to SCFE.[17] Other concomitant findings in the hip include inflammatory synovitis and disorganized collagen fibrils with accumulations of proteoglycans and glycoproteins within the growth plate; however, whether these changes are a cause or a result of SCFE remains undetermined.

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Rotator Cuff Injury

Background

Rotator cuff injuries are a common cause of shoulder pain in people of all age groups. They represent a spectrum of disease, ranging from acute reversible tendinitis to massive tears involving the supraspinatus, infraspinatus, and subscapularis. Diagnosis is usually made through detailed history, physical examination, and often, imaging studies.[1, 2, 3, 4, 5]

A normal rotator cuff and rotator cuff tear are shown below.

Rotator cuff, normal anatomy. Rotator cuff tear, anterior view.

Often, younger individuals with rotator cuff injuries relate a history of repetitive overhead activities involving the rotator cuff or, less commonly, a history of trauma preceding clinical onset of symptoms. In contrast, older individuals usually present with a gradual onset of shoulder pain and, ultimately, after radiographic testing is shown to have significant partial or full rotator cuff tears without a clear history of predisposing trauma. Nonoperative or conservative treatment is usually sufficient to heal the problem in the vast majority of individuals, with a few exceptions that are discussed.[1, 2, 3, 4, 5]

For excellent patient education resources, see eMedicineHealth's patient education articles Rotator Cuff Injury and Shoulder and Neck Pain.

NextEpidemiologyFrequencyUnited States

The frequency of full-thickness rotator cuff tears ranges from 5-40%, with an increasing incidence of cuff pathology in advanced age. Cadaveric studies by Bigliani et al found that 39% of individuals older than 60 years had full-thickness rotator cuff tears with an even higher incidence of partial tears.[6]

PreviousNextFunctional AnatomyNormal shoulder motion

The shoulder complex is comprised of several joints, including the sternoclavicular joint, acromioclavicular joint, glenohumeral (GH) joint, and scapulothoracic (ST) joint or pseudoarticulation. These articulations work together to carry out normal shoulder motion. The majority of motion occurs at the GH and ST joints. A rhythm between these 2 areas of motion has been described.[1, 3, 7, 8, 9, 10, 11, 12]

The GH–to–ST motion ratio of total shoulder motion is 2:1 (ie, 180° of abduction, consisting of 120° of GH motion and 60° of ST motion). The 2:1 ratio is an average over the entire arc of motion. This ratio changes through the arc of motion (ie, the 2:1 ratio is not constant throughout the entire range of motion [ROM]). In the initial portion of abduction, GH motion predominates and the ratio is 4:1 (GH:ST). As the shoulder moves above 90° of abduction, this ratio becomes 1:1° GH to 1° ST motion.

The importance of the scapula in normal shoulder motion cannot be overstated. The scapula, with the glenoid as its contact point, forms the platform for humeral head articulation and motion. A stable platform is essential for normal shoulder biomechanics in everyday activities and is crucial for high-demand activities (eg, overhead sports or work).[13]

The scapula must glide along the chest wall as it protracts and retracts during normal shoulder movements. Scapular winging results in glenoid antetilting, which results in functional elevation of the humeral head and impingement of the rotator cuff. In addition, without scapular motion, the origin and insertion of the deltoid approximate each other, resulting in a decreased optimal length-tension relationship and a decrease in force as the shoulder abducts. Normal scapular motion allows the deltoid to maintain its length-tension relationship and generate adequate force.

Stabilizers of the shoulder

The shoulder is considered a ball-in-socket joint, although the glenoid fossa is flat. In addition, the surface area of the glenoid is much smaller than that of the contacting humeral head (25-30%). The cartilaginous labrum provides much of the socket function and increases the surface area of contact for the humeral head.

Together, these components provide a great amount of shoulder mobility with limited stability. Shoulder stabilizers can be grossly categorized as static or dynamic. Dynamic stabilizers require an intact neuromuscular system to function, whereas static stabilizers help maintain congruity.

The static stabilizers have been studied well in cadaver specimens to understand their stabilizing effects. Static stabilizers continue to function in the setting of neurologic or intrinsic muscle pathology in conditions such as hemiplegia, spinal cord injury, brachial plexus injury, suprascapular nerve injury, and myopathies. This is not true for the dynamic stabilizers (eg, rotator cuff muscles). With neuromuscular injury or intrinsic muscle damage, the dynamic stabilizers lose their ability to exert dynamic motor control of the humeral head, ultimately leading to GH laxity and shoulder pain.

Static stabilizers

Static stabilizers include the bony structures, labrum, GH ligaments, and joint capsule. Unlike the hip joint, the bony articulation of the shoulder offers little stability. This is due to the limited contact area of the glenoid with the humeral head, flattened architecture, and retroverted positioning. The labrum is a fibrous structure that attaches to the glenoid to increase the contact area and deepen the socket of the glenoid up to 50%, forming a concave surface. Three GH ligaments exist, as follows: superior, middle, and inferior. The inferior GH ligament is the most important for shoulder stability and has 3 components, anterior, inferior, and posterior, therefore, it is more appropriately referred to as the inferior GH complex.

Dynamic stabilizers

Dynamic stabilizers[14] include the rotator and scapular stabilizers (ie, teres major, rhomboids, serratus anterior, trapezius, levator scapula). The rotator cuff is composed of 4 muscles: the supraspinatus, infraspinatus, subscapularis, and teres minor. The supraspinatus is the principal supporting and kinetic muscle of the shoulder. The primary function of the rotator cuff muscles is to stabilize the GH joint so that the larger shoulder movers (eg, deltoid, latissimus dorsi) can carry out their function without significant motion of the humeral head on the glenoid. Increased movement results in shearing forces across the joint (to the labrum, in particular) and may result in humeral head migration and impingement upon the rotator cuff muscles and tendons.

The rotator cuff muscles are associated and assist with some shoulder motion; however, their main function is to provide stability to the joint by compressing the humeral head on the glenoid. The supraspinatus assists in shoulder abduction by maintaining the humeral head centered on the glenoid, with the middle deltoid acting as the primary mover. These muscles act as force couples, because they work synergistically to carry out a particular movement.

Electromyography (EMG) studies have demonstrated a high degree of supraspinatus activity during the initial 30° of abduction. This has been misinterpreted to imply that the supraspinatus initiates shoulder abduction and acts to abduct the shoulder in the first 30°. In actuality, the supraspinatus fires to stabilize the GH joint as the deltoid abducts the arm.[15, 16, 17, 18, 19]

Increased EMG activity in the supraspinatus during the initial 30° is a reflection of increased firing requirements of this muscle to stabilize the GH joint as the deltoid is activated. The infraspinatus and teres minor muscles assist in external rotation of the shoulder and also provide an inferior pull upon the humeral head, assisting in its centering during overhead activity. The subscapularis muscle participates in this centering but also acts with the pectoralis muscles and latissimus dorsi as an internal rotator of the shoulder, serving as the main internal rotators of the shoulder.

Weakness or insufficiency of the rotator cuff muscles results in increasing demands on the static stabilizers. If these demands are long term or recurrent, static stabilizers may begin to fail. This can result in stretching or attenuation of the capsule, which results in even greater shoulder laxity and greater demands on the already weak rotator cuff muscles. Humeral head migration may occur with capsule laxity and result in rotator cuff impingement and pain. Pain may inhibit rotator cuff muscle firing, leading to disuse and further weakening of the dynamic stabilizers with greater demands placed on the static stabilizers.

Increased humeral head translation can also lead to shearing and injury to the glenoid labrum. Rotator cuff impingement, tendinitis, and labral pathology are commonly encountered injury patterns in athletes and workers who perform overhead motions. Focusing solely on the static stabilizers in treatment neglects the dynamic structures that probably initiate and perpetuate the cycle.

PreviousNextSport-Specific Biomechanics

A similar type of motion is involved in a number of overhead sports activities (eg, serving in tennis, spiking in volleyball, throwing a football or baseball). The baseball throwing motion has been studied in detail and can be divided into 5 stages.

Stage 1 is the wind-up phase. EMG studies have determined that the rotator cuff muscles are inactive during this initial stage.Stage 2 is the early cocking stage and involves shoulder external rotation and abduction supplied primarily by the deltoid.Stage 3 is the late cocking stage, which continues until maximal external rotation is achieved. The rotator cuff muscles are very active during this stage, especially the subscapularis, which eccentrically contracts and acts as a dynamic stabilizer. Stage 4 is the acceleration stage, which begins with internal rotation of the humerus and ends with release of the baseball. During this phase, the pectoralis major and the latissimus dorsi are very active, whereas the muscles of the rotator cuff are inactive. Stage 5 is the follow-through of the baseball pitch, where deceleration takes place. During this phase, the rotator cuff muscles and the posterior deltoid are most active. The supraspinatus eccentrically contracts to decelerate internal rotation of the limb.

Proper balance between the concentrically contracting muscles that generate force and the eccentrically contracting muscles that control movement is important. Imbalance between these opposing muscle groups results in overuse of muscles and, ultimately, overuse injuries of the shoulder. Note that a great deal of the force generated in overhead sports occurs in the trunk and lower extremity, and these areas should be targeted in any conditioning program for athletes who throw.

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Acromioclavicular Joint Injury

Background

Injuries in and around the shoulder are common in today's athletic society. Proper knowledge of the different problems and treatment options for shoulder disorders is necessary to get patients back to their preinjury state.

Acromioclavicular (AC) joint injuries are common and often seen after bicycle wrecks, contact sports, and car accidents. The acromioclavicular joint is located at the top of the shoulder where the acromion process and the clavicle meet to form a joint. Several ligaments surround this joint, and depending on the severity of the injury, a person may tear one or all of the ligaments. Torn ligaments lead to acromioclavicular joint sprains and separations.[1]

The distal clavicle and acromion process can also be fractured. Injury to the acromioclavicular joint may injure the cartilage within the joint and can later cause arthritis of the acromioclavicular joint.

This article discusses the anatomy of the acromioclavicular joint, the diagnosis of disorders of this joint, and the different treatment options.

For excellent patient education resources, see eMedicineHealth's First Aid & Injuries Center. Also, see eMedicineHealth's article on Shoulder Dislocation.

NextEpidemiologyFrequencyUnited States

Injuries to the acromioclavicular joint are the most common reason that athletes seek medical attention following an acute shoulder injury. Glenohumeral dislocations (see Shoulder Dislocation) are the second most common injuries seen. Men in their second through fourth decades of life have the greatest frequency of acromioclavicular joint injuries, which are most often incomplete tears of the ligaments.[1]

PreviousNextFunctional Anatomy

The normal width of the acromioclavicula joint is 1-3 mm in younger individuals; it narrows to 0.5 mm or less in individuals older than 60 years.

The acromioclavicular joint is made up of 2 bones (the clavicle and the acromion), 4 ligaments, and a meniscus inside the joint.

The acromioclavicular joint is surrounded by a thin joint capsule and 4 small ligaments. These ligaments mostly give joint stability to anterior and posterior translation, as well as provide horizontal stability to the joint.

Another set of ligaments also provides vertical stability to the acromioclavicular joint. These ligaments are called the coracoclavicular ligaments, which are found medial to the acromioclavicular joint and go from the coracoid process on the scapula to the clavicle.

Different injuries result in different tears of the 2 coracoclavicular ligaments (the conoid and the trapezoid). Torn acromioclavicular joint ligaments and/or torn coracoclavicular ligaments are seen in acromioclavicular joint sprains. The meniscus that lies in the joint may also be injured during sprains or fractures around the acromioclavicular joint. The acromioclavicular capsular ligaments provide most of the joint stability in the anteroposterior (AP) direction. The conoid and trapezoid ligaments aid in providing superior-inferior stability to the joint. Compression of the joint is restrained mainly by the trapezoid ligament.

PreviousNextSport-Specific Biomechanics

When a person falls onto their shoulder, the force pushes the tip of the shoulder down. The clavicle is usually kept in its anatomic position, whereas the shoulder is driven down, which injures the different ligaments or causes a fracture. When the ligaments are injured they are either sprained or, in more severe cases, torn.

Acromioclavicular joint sprains have been classified according to their severity. In a type I sprain, a mild force applied to these ligaments does not tear them. The injury simply results in a sprain, which hurts, but the shoulder does not show any gross evidence of an acromioclavicular joint dislocation. Type II sprains are seen when a heavier force is applied to the shoulder, disrupting the acromioclavicular ligaments but leaving the coracoclavicular ligaments intact. When these injuries occur, the lateral clavicle becomes a little more prominent.

In type III sprains, the force completely disrupts the acromioclavicular and coracoclavicular ligaments. This leads to complete separation of the clavicle and obvious changes in appearance. The lateral clavicle is very prominent. A few more types of acromioclavicular joint sprains have been classified, but types I–III are the most common (see below).

Classification of acromioclavicular joint injuries.

An acromioclavicular joint sprain is more common than a fracture after an injury. However, fractures of the distal clavicle and the acromion process may occur, so the healthcare provider must be aware of such injuries and ready to diagnose and treat them as well (see Clavicular Injuries).

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Supraspinatus Tendonitis

Background

Supraspinatus tendonitis is often associated with shoulder impingement syndrome. The common belief is that impingement of the supraspinatus tendon leads to supraspinatus tendonitis (inflammation of the supraspinatus/rotator cuff tendon and/or the contiguous peritendinous soft tissues), which is a known stage of shoulder impingement syndrome (stage II) as described originally by Neer in 1972.[1]

The causes of supraspinatus tendonitis can be broken down into extrinsic and intrinsic factors.[2, 3] Extrinsic factors are further broken down into primary impingement, which is a result of increased subacromial loading, and secondary impingement, which is a result of rotator cuff overload and muscle imbalance. In athletes whose sport involves stressful repetitive overhead motions, a combination of causes may be found.

Recent studies

Lewis et al demonstrated the presence of neovascularity in individuals with a clinical diagnosis of rotator cuff tendinopathy and, to a lesser extent, in asymptomatic shoulders. Twenty patients (mean age, 50.2 y; range 32-69 y) with a clinical diagnosis of unilateral rotator cuff tendinopathy received a clinical examination then underwent bilateral grey scale and color Doppler ultrasound assessment.

Neovascularity was found in the symptomatic shoulder in 13 of 20 patients (35%) as well as in the asymptomatic shoulder in 5 of the 20 patients (25%).[4] Of 6 other patients who withdrew from the study before entering the trial, 1 withdrew due to cessation of symptoms and did not have neovascularity in either shoulder; 5 withdrew due to bilateral symptoms, of whom 2 had signs of bilateral neovascularity, 1 had unilateral neovascularity, and the remaining 2 did not have neovascularity in either shoulder.[4] No association was identified between the presence of neovascularity and pain, duration of symptoms, and neovascularity and shoulder function. The investigators noted more research is needed to evaluate the relevance of their findings.

In another study, Millar et al suggested proinflammatory cytokines may have a role in supraspinatus tendinopathy.[5] The investigators used custom micro-arrays to assess rat supraspinatus tendinopathy produced by running overuse. In addition, samples of torn supraspinatus tendon and matched intact subscapularis tendon from patients undergoing shoulder surgery for rotator cuff tears, as well as control samples of subscapularis tendon from 10 individuals with normal rotator cuffs undergoing arthroscopic shoulder stabilization, were collected and examined with semiquantitative reverse transcription polymerase chain-reaction (RT-PCR) and immunohistochemistry.[5] The presence of significant upregulation of proinflammatory cytokines and apoptotic genes was found in the rat samples (P = 0.005) as well as in the supraspinatus and subscapularis tendons obtained from the patients with rotator cuff tears (P = 0.0008).

NextEpidemiologyFrequencyUnited States

Supraspinatus tendonitis is a common cause of shoulder pain in athletes whose sports involve throwing and overhead motions.

PreviousNextFunctional Anatomy

The shoulder consists of 2 bones (ie, humerus, scapula), 2 joints (ie, glenohumeral, acromioclavicular), and 2 articulations (ie, scapulothoracic, acromiohumeral). Several interconnecting ligaments and layers of muscles join these bones. The relative lack of bony stability in the shoulder permits a wide range of motion. Soft tissue structures are the major glenohumeral stabilizers.

The static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. The dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles such as the pectoralis major, latissimus dorsi, and serratus anterior.

The rotator cuff consists of 4 muscles, which control 3 basic motions: abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor for controlling external rotation, and the subscapularis for controlling internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. It is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed by the acromion, coracoacromial arch, and acromioclavicular joint on the upper rim and the humeral head and glenoid below. It accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been identified as a cause of impingement syndrome and rotator cuff tendonitis.

Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described that variations in acromial size and shape can contribute to impingement. From cadaveric studies, 3 different variations in the morphology of the acromion are described. Type I is flat, type II is curved, and type III is anteriorly hooked. Although the curved configuration is the most common (43% prevalence, compared with 17% for flat and 40% for hooked), the hooked configuration is associated most strongly with rotator cuff pathology.

Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament, where thickening can occur, and the undersurface of the acromioclavicular joint, where osteophytes can form. Only rarely is the medial coracoid involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch.

Nonoutlet impingement can also occur. The causes may be loss of normal humeral head depression either from a large rotator cuff tear or weakness of the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. Another way this may occur is with thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.

PreviousNextSport-Specific Biomechanics

Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff tendonitis. Shoulder pain and rotator cuff tendonitis are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, tennis).

Secondary impingement

Supraspinatus tendonitis is often attributed to impingement, which is seldom mechanical in athletes. Rotator cuff tendonitis in this population may be related to subtle instability and therefore may be secondary to such factors as eccentric overload, muscle imbalance, and glenohumeral instability or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint.

Secondary impingement may be the most common cause in young athletes who use overhead motions and who frequently place repetitive large stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures and leading to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendon. These increased demands may lead to rotator cuff pathology such as partial tearing or tendonitis, and, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging on the coracoacromial arch, which leads to rotator cuff inflammation. In these patients, treatment should be directed at the underlying instability.

Glenoid impingement

Recently, the concept of glenoid impingement has been suggested as an explanation for partial-thickness rotator cuff tears in throwing athletes, particularly those tears involving the articular surface of the rotator cuff tendon. Such tears might occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon either from abnormal motion of the glenohumeral joint or from increased forces on the rotator cuff necessary to stabilize the shoulder.

Arthroscopic studies of these patients have noted impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position, abducted and externally rotated. Lesions are noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement and rotator cuff tendonitis.

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Superior Labrum Lesions

Background

Before the use of shoulder arthroscopy and magnetic resonance imaging (MRI) in the diagnosis and management of shoulder problems, glenoid labrum lesions were underappreciated. More specifically, superior labrum lesions about the insertion of the long biceps tendon were typically noted or managed using standard open surgical techniques. An improved understanding of the surgical anatomy and the biomechanical contributions of the superior labrum have demonstrated its significance in shoulder stability and its role in the pathogenesis of shoulder pain.

Andrews et al published a study that examined glenoid labrum lesions related to the long head of the biceps (LHB) in 73 throwing athletes.[1] The authors observed that the LHB was contiguous with the superior labrum and that most of these patients had avulsed the anterosuperior labrum off the glenoid in conjunction with the biceps tendon. Subsequently, Snyder et al defined the pattern of superior labral injury in 27 patients who were described as having superior labrum anterior posterior (SLAP) lesions.[2] The authors described the SLAP lesion as a labral detachment originating posterior to the long biceps insertion and extending anteriorly. These lesions were subsequently categorized as types I-IV, as follows:

SLAP classification[2] Type I: The glenoid labrum demonstrates degenerative changes and fraying at the edges but remains firmly attached to the glenoid rim. No avulsion of the biceps tendon is present (see the image below, upper left). Type II: Degenerative changes and fraying are present in type II lesions. The glenoid labrum is detached completely from the anterosuperior to the posterosuperior glenoid rim. This portion of the labrum is lifted by the long biceps tendon, and the attachment of the biceps tendon is unstable (see the image below, lower right). Upper left - Type I superior labrum anterior posterior lesion. Lower right - Type II superior labrum anterior posterior lesion. Type III: With type III lesions, the free margin of the superior labrum is displaced into the joint (bucket handle), whereas the labral attachment to the glenoid rim and biceps tendon remains intact. The insertion of the biceps tendon is not unstable (see the image below, upper left). Type IV: The superior portion of the labrum is displaced into the joint (bucket handle) in type IV lesions. In contrast to type III tears, the long biceps tendon is also affected, involving partial rupture in the direction of the fibers (see the image below, lower right). Upper left - Type III superior labrum anterior posterior lesion. Lower left - Type IV superior labrum anterior posterior lesion.

Superior labral pathology is now recognized as a potential sources of considerable pain and disability in active patients. The goal of this article is to familiarize the reader with the anatomy, pathophysiology, diagnosis, and management of labral tears of the superior glenoid.

For patient education materials, see the Hand, Wrist, Elbow, and Shoulder Center, as well as Rotator Cuff Injury and Shoulder Separation.

Related Medscape Reference topics:

Multidirectional Glenohumeral Instability

Posterior Glenohumeral Instability

Rotator Cuff Injury

Superior Labral Lesions [in the Orthopedic Surgery section]

NextEpidemiologyFrequencyUnited States

Snyder et al reported the result of over 140 patients who were treated operatively for superior labral lesions.[3] The authors noted a 6% incidence of SLAP lesions in persons undergoing shoulder arthroscopy for all diagnoses over an 8-year period. The percentages of the types of SLAP lesions encountered were as follows: type I, 21%; type II, 55%; type III, 9%; type IV, 10%; and complex lesions, 5%. Associated lesions included Bankart lesions (22%) and lesions of the rotator cuff (11%). Only 28% of SLAP lesions were found without associated pathology.

Kim et al reported that of 544 shoulder arthroscopy procedures, 139 (26%) demonstrated a SLAP lesion.[4] Of the SLAP lesions, 103 (74%) were type I, 29 (21%) were type II, 1 (0.7%) was type III, and 6 (4%) were type IV. Most (123) of the SLAP lesions were found to be associated with other intra-articular lesions.

Most recently, Kampa and Clasper evaluated the presentation and incidence of SLAP lesions in military and civilian populations.[5] Of 178 patients who underwent arthroscopy for complaints of either pain, instability, or pain and instability, 39 (22%) SLAP lesions were found. According to the Snyder classification (see Introduction, SLAP classification), 20.5% were type I, 69.3% were type II, 5.1% were type III, and 5.1% were type IV. The authors found that patients with a history of trauma or symptoms of instability were more likely to have a SLAP lesion than patients presenting with atraumatic etiologies. Military patients also had a higher incidence of these lesions relative to civilian patients.

Collectively, these data suggest that patients who suffer traumatic injuries of the shoulder are at increased risk for sustaining an injury to the superior labrum, and that the severity of the resulting lesion is variable. Traumatic SLAP lesions are often associated with other intra-articular shoulder injuries, and the examining physician must have a high index of suspicion for coexisting pathology.

PreviousNextFunctional Anatomy

Grossly, the glenoid labrum surrounds the entire circumference of the glenoid surface. Moseley and Overgaard[6] in 1962 and Detrisac and Johnson[7] in 1986 described the labrum as a redundant fold of capsular (fibrous) tissue. Superiorly, the labrum is contiguous with the tendon insertion of the LHB as it attaches to the supraglenoid tubercle. The anterior labrum fibers may insert into the middle glenohumeral ligament (joint capsule). The superior labrum is more meniscuslike in structure because its fibers are loosely attached to the glenoid rim and may overlap the superior glenoid surface, whereas the inferior labrum is attached more tightly to the glenoid rim and is typically round in appearance.

The entire labral complex is attached at all points to either the bony glenoid rim or joint capsule about the glenoid, except in the anterosuperior margin. A sublabral foramen is present in most individuals; this labral foramen may be confused on MRI or at arthroscopy with a labral tear.

The Buford complex represents another anatomic variant and is described as a cordlike thickening of the middle glenohumeral ligament and absence of the anterosuperior labrum. This anatomic finding must be recognized as a normal variant because attempts to repair or debride this region may result in abnormal capsular constraint, shoulder stiffness, or glenohumeral instability. Interestingly, a retrospective review suggested that the presence of a Buford complex may correlate with the presence of a SLAP lesion in patients.[8]

Histology

Cooper et al examined the anatomy and histology of the glenoid labrum.[9] The authors noted an existing fibrocartilaginous transition zone at the superior glenoid margin between the fibrocartilaginous labrum and the hyaline cartilage of the glenoid surface. This study also confirmed the gross observation that the superior labrum fibers insert directly into the fibers of the LHB, distal to the biceps insertion into the supraglenoid tubercle. Histologic examination also revealed that the labrum consists of densely packed collagen bundles and fibrochondrocytes.

The primary labrum vascular supply originates from the suprascapular, circumflex scapular, and posterior humeral circumflex arteries. Only the periphery of the labrum appears to be vascularized, and no contribution to the labral blood supply is derived from the underlying bone. Prodromos et al observed that fetal and newborn shoulders possess an extensive blood supply throughout the labrum, whereas adult specimens have only sparse peripheral vasculature.[10] Apparently, labral vascularity, much like the meniscus, recedes with advanced age.

As previously mentioned, the LHB brachii muscle is also anatomically important in the discussion of SLAP lesions (see Introduction, Background). This LHB tendon arises from the supraglenoid tubercle, and fibers from the superior labrum attach to the biceps tendon in this region. Following the examination of over 100 cadaver specimens, Vangsness et al estimated that approximately 50% of the biceps tendon originates from the superior labrum.[11] The most common labral origin of the biceps is the posterior-superior region.

PreviousNextSport-Specific Biomechanics

Long before the advent of shoulder arthroscopy, labral tears were described in association with anterior shoulder subluxation and dislocation, suggesting a role for the labrum in glenohumeral stability maintenance. McGlynn and Caspari described the intra-articular findings of subluxating shoulders noted at the time of arthroscopy.[12] As suggested by previous studies, fraying, tearing, or detachment of the glenoid labrum was a common finding in this group of 19 unstable shoulders.

In defining the relevant factors contributing to anterior shoulder stability, Turkel et al noted that the inferior glenohumeral ligament, which attaches to the glenoid via the labrum, is essential in preventing anterior shoulder instability.[13] The glenoid labrum increases the area and depth of the glenoid cavity, contributing to articular stability of the glenohumeral joint. The labrum has been suggested to act as a chock block to the humeral head as it attempts to translate anteriorly or posteriorly upon the glenoid surface.

Andrews et al demonstrated that superior labrum lesions were observed in a group of overhead throwing athletes who underwent arthroscopic examination of the shoulder.[1] On the basis of observed lesions in this group of athletes, the authors suggested that the biceps tendon is subjected to large forces during the act of throwing. Intraoperative stimulation of the biceps during arthroscopic shoulder surgery also revealed that the LHB tends to pull the labrum off the superior glenoid rim (especially in the presence of a SLAP lesion). Therefore, excessive forces generated by the biceps tendon during overhead throwing activities may lead to the generation of superior labral tears.

In a study from the University of Pittsburgh, Rodosky et al analyzed the role of the LHB and superior labrum in anterior shoulder instability.[14] A dynamic cadaveric shoulder model was used to simulate the forces of the late-cocking phase of the throwing motion. Strain gauges were placed in the inferior glenohumeral ligaments of 7 nonembalmed cadaver shoulders. Tests of anterior glenohumeral translation were made with and without the presence of superior labral lesions (analogous type II lesions). Varying forces were applied to the biceps tendon (0-100% extrapolated maximum force) in all tested specimens.

In normal shoulders (ie, no SLAP lesion), peak torque increased 22% and peak torsional rigidity increased 32% in shoulders with maximal biceps (loading versus unloaded shoulders).[14] In shoulders with a simulated SLAP lesion and no biceps loading, the observed peak torque was 12% lower than that of normal specimens, and a 120% increase in inferior glenohumeral ligament strain was observed. In shoulders with simulated SLAP lesions and 100% biceps loading, the observed peak torque was 7% lower than that of normal specimens. Torsional rigidity was also decreased by the creation of a SLAP lesion with and without biceps loading. In this study, torsional rigidity represented a measure of the tested shoulder to resist rotational forces.

In another study, Pagnani et al examined the effect of superior glenoid labrum lesions on glenohumeral translation.[15] In this cadaveric study, the investigators applied sequential anterior, posterior, superior, and inferior forces of 50 Newtons (N) to the proximal humerus. A 22-N compressive force was also applied. During the application of the described loads, a 55-N force was applied to the LHB tendon. The shoulders were tested in 7 positions of glenohumeral elevation and rotation. Each specimen was tested with a normal superior labral complex, a partial superior labral tear, and a complete tear (including the biceps insertion on the supraglenoid tubercle).

The authors found that a partial tear of the superior labrum had no significant effect upon superoinferior or anteroposterior translation[15] ; however, the creation of a complete SLAP lesion resulted in significant increases in anterior and inferior translation at all arm elevations. Increased glenohumeral translation persisted even after the application of a 55-N force to the biceps tendon. Pagnani et al suggested that the LHB tends to stabilize the joint by generating joint compressive forces and by acting as a physical restraint to translation.

These data suggest that in external rotation and abduction, the forces generated by the biceps muscle result in an increase in torsional rigidity. These findings suggest that increased loads applied to the biceps tendon may protect the shoulder from anterior subluxation during the throwing motion.

Related Medscape Reference topics:

Elbow and Forearm Overuse Injuries

Overuse Injury

Rotator Cuff Injury

Related Medscape topic:

Resource Center Exercise and Sports Medicine

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