Rotator Cuff Relevant Anatomy and Mechanics

7/29/2019 Rotator Cuff Relevant Anatomy and Mechanics

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Rotator Cuff Relevant Anatomy and

Mechanics.

Last updated Wednesday, January 26, 2005

The rotator cuff

The rotator cuff is the complex of four muscles that arise from the scapula and whose tendons blend in

with the subjacent capsule as they attach to the tuberosities of the humerus.

Anatomy of rotator cuff

The subscapularis arises from the anterior aspect of the scapula and attaches over much of the lesser

tuberosity. It is innervated by the upper and lower subscapular nerves. (Yung and Harryman, 1995) The

supraspinatus muscle arises from the supraspinatus fossa of the posterior scapula, passes beneath the

acromion and the acromioclavicular joint, and attaches to the superior aspect of the greater tuberosity.

It is innervated by the suprascapular nerve after it passes through the suprascapular notch. The

infraspinatus muscle arises from the infraspinous fossa of the posterior scapula and attaches to the

posterolateral aspect of the greater tuberosity. It is innervated by the suprascapular nerve after it passes

through the spinoglenoid notch. The teres minor arises from the lower lateral aspect of the scapula and

attaches to the lower aspect of the greater tuberosity. It is innervated by a branch of the axillary nerve.

Tendons

The insertion of these tendons as a continuous cuff around the humeral head (see figure 15-3)

permits the cuff muscles to provide an infinite variety of moments to rotate the humerus and tooppose unwanted components of the deltoid and pectoralis muscle forces. For an excellent

review of the anatomy and histology of the rotator cuff, the reader is referred to the works of

Clark and Harryman (Clark, 1988, Clark and Harryman II, 1992, Clark, Sidles, 1990) and

Warner's chapter on shoulder anatomy in The Shoulder: A Balance of Mobility and Stability.(Warner, 1993)

The long head of the biceps tendon may be considered a functional part of the rotator cuff. It

attaches to the supraglenoid tubercle of the scapula, runs between the subscapularis and the

supraspinatus, and exits the shoulder through the bicipital groove under the transverse humeral

ligament, attaching to its muscle in the proximal arm. Slatis and Aalto (Slatis and Aalto, 1979)

point out that the coracohumeral ligament and the transverse humeral ligament keep the bicepstendon aligned in the groove. Tension in the long head of the biceps can help compress the

humeral head into the glenoid. Furthermore, this tendon has the potential for guiding the head ofthe humerus as it is elevated, the bicipital groove traveling on the biceps tendon like a monorail

on its track. This mechanism helps to explain why the humerus is capable of substantial rotation

when it is adducted and allows very little rotation when it is maximally abducted (in which

position the tuberosities are constrained as they straddle the biceps tendon near its attachment tothe supraglenoid tubercle).


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Mechanics of cuff action

The mechanics of cuff action is complex. The humeral torque resulting from a cuff muscle's

contraction is determined by the moment arm (the distance between the effective point of

application of this force and the center of the humeral head) and the component of the muscleforce which is perpendicular to it (see figure 16). (Wuelker, Wirth, 1995).

The magnitude of force deliverable by a cuff muscle is determined by its size, health, andcondition as well as the position of the joint. The cuff muscles' contribution to shoulder strength

has been evaluated by Colachis and associates, (Colachis and Strohm, 1971, Colachis, Strohm,

1969) who used selective nerve blocks and found that the supraspinatus and infraspinatus

provide 45 per cent of abduction and 90 per cent of external rotation strength. Howell andcoworkers (Howell, Imobersteg, 1986) measured the torque produced by the supraspinatus and

deltoid muscles in forward flexion and elevation. They found that the supraspinatus and deltoid

muscles are equally responsible for producing torque about the shoulder joint in the functionalplanes of motion. Other estimates of the relative contributions of the rotator cuff to shoulder

strength have been published. (Bigliani, Morrison, 1986, Cofield, 1985, Van Linge and Mulder,

1963)
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Figure 16

Factors of analysis

There are at least three factors which complicate the analysis of the contribution of a given

muscle to shoulder strength:

1. the force and torque that a muscle can generate varies with the position of the joint:muscles are usually stronger near the middle of their excursion and weaker at the

extremes. (Lieber, 1992)

2. the direction of a given muscle force is determined by the position of the joint. Forexample, the supraspinatus can contribute to abduction and/or external rotation,depending on the initial position of the arm. (Otis, Jiang, 1994)

3. the effective humeral point of application for a cuff tendon wrapping around the humeralhead is not its anatomic insertion, but rather is the point where the tendon first contactsthe head, a point which usually lies on the articular surface (see figure 17).

Figure 17

Functions of cuff muscles

1. They rotate the humerus with respect to the scapula.2. They compress the head into the glenoid fossa, providing a critical stabilizing

mechanism to the shoulder, known as concavity compression. While in the past the cuffmuscles were referred to as head depressors, it is evident that the inferiorly directed

components of the cuff muscle force is small; instead the primary stabilizing function ofthe cuff muscles is through head compression into the glenoid (see figure 18). (Sharkey,

Marder, 1994, Wuelker, Roetman, 1994)
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Figure 18

They provide muscular balance, a critical function which will be discussed in some detail here. In

the knee, the muscles generate torques primarily about a single axis: that of flexion-extension. If the

quadriceps pull is a bit off-center, the knee still extends. By contrast, in the shoulder, no fixed axis

exists. In a specified position, activation of a muscle creates a unique set of rotational moments. For

example, the anterior deltoid can exert moments in forward elevation, internal rotation, and cross-

body movement (see figure 19). If forward elevation is to occur without rotation, the cross-body and

internal rotation moments of this muscle must be neutralized by other muscles, such as the

posterior deltoid and infraspinatus (see figure 20).(Sharkey, Marder, 1994) As another example, use

of the latissimus dorsi in a movement of pure internal rotation requires that its adduction moment

by neutralized by the superior cuff and deltoid. Conversely, use of the latissimus in a movement of

pure adduction requires that its internal rotation moment be neutralized by the posterior cuff and

posterior deltoid muscles.

Figure 19
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Figure 20

The timing and magnitude of these balancing muscle effects must be precisely coordinated toavoid unwanted directions of humeral motion. For a gymnast to hold her arm motionless above

her head, all the forces and torques exerted by each of her shoulder muscles must add up to zero.

Thus the simplified view of muscles as isolated motors, or as members offorce couplesmustgive way to an understanding that all shoulder muscles function together in a precisely

coordinated way: opposing muscles canceling out undesired elements leaving only the net torque

necessary to produce the desired action. (Rowlands, Wertsch, 1995)

This degree of coordination requires a preprogrammed strategy of muscle activation or engram

that must be established before the motion is carried out. The rotator cuff muscles are critical

elements of this shoulder muscle balance equation. (Basmajian and Bazant, 1959, DePalma,1967, Flanders, 1993, Grigg, 1993, Inman, Saunders, 1944, Jens, 1964, Joessel, 1880, Lieber and

Friden, 1993, Saha, 1971, Speer and Garrett, 1993, Symeonides, 1972, Walker, Couch, 1987)

Vascular anatomy

The vascular anatomy of the cuff tendons has been described by a number of investigators

(Brooks, Revell, 1992, Lohr and Uhthoff, 1990, Moseley and Goldie, 1963, Rathbun and

Macnab, 1970, Rothman and Parke, 1965) Lindblom (Lindblom, 1939a, Lindblom, 1939b)described an area of relative avascularity in the supraspinatus tendon near its insertion. Rothman

and Parke (Rothman and Parke, 1965) found contributions to the cuff vessels from the

suprascapular, anterior circumflex, and posterior circumflex arteries in all cases. Thethoracoacromial contributed in 76 per cent to the cuff's blood supply, the suprahumeral in 59 percent, and the subscapular in 38 per cent. These authors found the area of the supraspinatus just

proximal to its insertion to be markedly undervascularized in relation to the remainder of the

cuff. Uhthoff and coworkers (Uhthoff, Loehr, 1986 Oct 27) observed relative hypovascularity ofthe deep surface of the supraspinatus insertion as compared with its superficial aspect.


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By contrast, Moseley and Goldie studied the vascular pattern in the cuff tendons including the

"critical zone" of the supraspinatus (i.e. the anterior corner of the tendon near its insertion which

is prone to ruptures and calcium deposits). They found a vascular network which receivedcontributions from the anterior humeral circumflex, the subscapular, and the suprascapular

arteries. (Moseley and Goldie, 1963) They concluded that the critical zone was not much less

vascularized than other parts of the cuff; rather, it was rich in anastomoses between the osseousand tendinous vessels. Rathbun and Macnab (Rathbun and Macnab, 1970) found that the fillingof cadaveric cuff vessels was dependent on the position of the arm at the time of injection. They

noted a consistent zone of poor filling near the tuberosity attachment of the supraspinatus when

the arm was adducted; with the arm in abduction, however, there was almost full filling ofvessels to the point of insertion. They suggested that some of the previous data suggesting

hypovascularity was, in fact, due to this artifact of positioning. Nixon and DiStefano (Nixon and

DiStefano, 1975) suggested that the "critical zone" of Codman corresponds to the area of

anastomoses between the osseous vessels (the anterolateral branch of the anterior humeralcircumflex and the posterior humeral circumflex) and the muscular vessels (the suprascapular

and the subscapular vessels).

Recently, the vascularity of the supraspinatus tendon has been reconfirmed by the laser Doppler

studies of Swiontkowski et al. (Swiontkowski, Iannotti, 1990) The laser Doppler assesses red cellmotion at a depth of 1 to 2 mm. These investigators found substantial flow in the "critical zone"of normal tendon and increased flow at the margins of cuff tears. Furthermore, Clark (Clark and

Harryman II, 1992) and Clark (Clark, 1988) and Clark et al (Clark, Sidles, 1990) found no

avascular areas on his extensive histological studies of the supraspinatus tendon.

Uhthoff and Sarkar (Uhthoff and Sarkar, 1991b) examined biopsy specimens obtained during

surgery on 115 patients with complete rotator cuff rupture. They found vascularized connectivetissue covering the area of rupture and proliferating cells in the fragmented tendons. They

concluded that the main source of fibrovascular tissue for tendon healing was the wall of the

subacromial bursa.

Supraspinatus insertion

The histology of the supraspinatus insertion has been studied in some detail. Codman (Codman,

1934a) observed that there were "transverse fibers in the upper portion of the tendon." He stated

that "the insertion of the infraspinatus overlaps that of the supraspinatus to some extent. Each ofthe other tendons also interlaces its fibers to some extent with its neighbor's tendons." In detailed

anatomical studies, Clark and Harryman (Clark and Harryman II, 1992) and Clark (Clark, 1988)

and Clark et al (Clark, Sidles, 1990) studied the tendons and capsule of the rotator cuffs from

shoulders aged 17 to 72 years. They found that the tendons splayed out and interdigitated to forma common continuous insertion on the humerus. The biceps tendon was ensheathed by

interwoven fibers derived from the subscapularis and supraspinatus. Blood vessels were noted

throughout the tendons with no avascular zones. When dissecting what initially appeared to be

an intact cuff, the authors frequently encountered a deep-substance tear in which fibers wereavulsed from the humerus.


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Benjamin and coworkers (Benjamin, Evans, 1986) have analyzed four zones of the supraspinatus

attachment to the greater tuberosity:

1. the tendon itself,2. uncalcified fibrocartilage,3.

calcifiedfibrocartilage, and4. bone.

Whereas there were blood vessels in the other three zones, the zone of uncalcified fibrocartilageappeared avascular. A tidemark existed between the uncalcified and calcified fibrocartilage that

was continuous with the tidemark between the uncalcified and calcified portions of articular

cartilage. The collagen fibers often meet this tidemark approximately at right angles. In thetendon of the supraspinatus there was an abrupt change in fiber angle just before the tendon

becomes fibrocartilaginous and only a slight change in angle within fibrocartilage. In interpreting

the significance of these findings, these authors point out that the angle between the humerus and

the tendon of the supraspinatus changes constantly in shoulder movement (see figure 35). While

the belly of the muscle remains parallel to the spine of the scapula, the tendon must bend to reachits insertion. This bending appears to take place above the level of the fibrocartilage so that the

collagen fibers meet the tidemark at right angles. The fibrocartilage provides a transitional zonebetween hard and soft tissues, protecting the fibers from sharp angulation at the interface

between bone and tendon. The fibrocartilage pad keeps the tendon of the supraspinatus from

rubbing on the head of the humerus during rotation, as well as keeping it from bending, splaying

out, or becoming compressed at the interface with hard tissue.

Figure 35

Loading environment

The loading environment of the cuff tendon fibers is complex, even in the normal shoulder.

These fibers sustain concentric tension loads when the humerus is moved actively in the

direction of action of the cuff muscle (see figure 22). They sustain eccentric tension loads as they

resist humeral motion or displacement in directions opposite the direction of action of the cuff


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muscles (see figure 23). The tendon fibers are subjected to bending loads when the humeral head

rotates with respect to the scapula (see figure 21). As observed by Sidles (Matsen, Lippitt, 1994)

in MRI scans positioned with the arm positioned at the limits of motion, the glenoid rim canapply a sheering load to the deep surface of the tendon insertion (see figure 24). This abutment of

the labrum of the cuff against the cuff insertion may be a better explanation than acromial

impingement for the deep surface cuff detects seen in throwers (see figures 25 and 26). (Ferrari,Ferrari, 1994, Jobe, 1995, Liu and Boynton, 1993, Rossi, Ternamian, 1994, Tirman, Bost, 1994,Walch, Liotard, 1991)

Figure 21

Figure 22


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Figure 23

Figure 24

Figure 25
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Figure 26

Recently Ziegler et al (Ziegler, Matsen III, 1996) suggested that the superior cuff tendon alsoexperiences compressive loads as it is squeezed between the humeral head and the

coracoacromial arch when superiorly directed loads are applied to the humerus. In a cadaver

model, they found that the preponderance of an upward directed humeral load was transmittedthrough the cuff tendon to the overlying acromion. When the cuff tendon was excised the

humeral head moved cephalad 6 millimeters until the superior humeral load was applied directly

to the acromion (see figures 27 and 28). Using completely different methodologies Lazarus

(Lazarus, Harryman II, 1995, February 16-21) and Poppen and Walker (Poppen and Walker,

1976) also found that the humeral head translated 6 millimeters superiorly when the cuff tendonwas absent. Flatow et al (Flatow, Soslowsky, 1994) referred to this phenomenon as the spacereffect of the cuff tendon. Kaneko et al (Kaneko, DeMouy, 1995) found that superior

displacement of the humeral head was one of the most significant plain radiographic signs of

massive cuff deficiency (see figure 29). Sigholm and colleagues (Sigholm, Styf, 1988) found

evidence of this normal tendon compression in vivo. Using a micropipette infusion technique,they found that the normal subacromial resting pressure of 8 mm Hg was elevated to 39 mm Hg

by active shoulder flexion to 45 degrees and to 56 mm Hg by the addition of a one kilogram

weight to the hand in the elevated position. Recently, morphological evidence has emergedwhich supports the concept of compressive loading of the supraspinatus tendon. Okuda (Okuda,

Gorski, 1987) described fibrocartilaginous areas in areas of tendons subjected to compression.

Riley et al (Riley, Harrall, 1994 June) found such areas in the supraspinatus tendon and notedthat they had the proteoglycan/glycosaminoglycan of tendon fibrocartilage. They indicated thatthese morphological features were an adaptation to mechanical forces, including compression. It

has been questioned whether or not compression of the cuff by the acromion could produce the

type of cuff defects commonly seen in clinical practice. Recent investigations with a rat model(1996) demonstrated that increasing the loading and abrasion of the cuff tendon by the addition

of bone plates between the acromion and the tendon produced only bursal side lesions and never

the intratendinous or articular side cuff tendon defects which are most frequently seen clinically.


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Although young healthy tendons seem to tolerate their complex loading situation without

difficulty, structurally inferior tissue (Kumagai, Sarkar, 1994, Riley, Harrall, 1994 June), tissue

with compromised repair potential (Dalton, Cawston, 1995, Hamada, Okawara, 1994), ortendons frequently subjected to unusually large loads (as in an individual with paraplegia)

(Bayley, Cochran, 1987) may degenerate in their hostile mechanical environment. (Godsil and

Linscheid, 1970, Ozaki, Fujimoto, 1988, Riley, Harrall, 1994)

Figure 27

Figure 28

Tendon degeneration

Normal tendon is exceedingly strong. The work of McMasters (McMaster, 1933) is frequentlyquoted in this regard. He conducted experiments showing that loads applied to normal rabbit

Achilles tendons produced failure at the musculotendinous junction, at the insertion into bone, at

the muscle origin, or at the bone itself, but not at the tendon midsubstance. In his preparation,one-half of the tendon's fibers had to be severed before the tendon failed in tension. If the tendon


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was crushed with a Kocher clamp, pounded, and then doubly ligated above and below the injury,

rupture could be produced in half of the specimens when tested over four weeks later. Normal

tendon is obviously tough stuff!

It is estimated that in normal activities, the force transmitted through the cuff tendon is in the

range 140 to 200 Newtons. (Laing, 1956, Liberson, 1937, Lohr and Uhthoff, 1990, Samilson,1980). The ultimate tensile load of the supraspinatus tendon in specimens from the sixth or

seventh decade of life has been measured between 600 and 800 Newtons. (Itoi, Berglund, 1995)

While cuff strength may be compromised by inflammatory arthritis (Cofield, 1987, McCarty,

Haverson, 1981) and steroids (Ellman, Hanker, 1986, Kennedy and Willis, 1976), the primary

cause of tendon degeneration is aging. Like the rest of the body's connective tissues, rotator cufftendon fibers become weaker with disuse and age; as they become weaker, less force is required

to disrupt them (see figure 30). (Chung and Nissenbaum, 1975, Neer, 1978, Rathbun and

Macnab, 1970, Swiontkowski, Iannotti, 1990) Hollis and associates (Hollis, Lyon, 1988) showed

that the anterior cruciate ligament of a 70-year-old is only 20 to 25 per cent as strong as that of a

20-year-old. Others have shown similar loss of tendon strength with age. (Codman, 1934b,DePalma, 1973, Lindblom, 1939a, Lindblom, 1939b, Lindblom and Palmer, 1939, Macnab,

1973, Neer, 1972, Neer, 1983, Nixon and DiStefano, 1975, Pettersson, 1942, Watson-Jones,1961) Uhthoff and Sarkar concluded that "Aging is the single most important contributing factor

in the pathogenesis of tears of the cuff tendons." (Uhthoff and Sarkar, 1993)

Pettersson (Pettersson, 1942) provides an excellent summary of the early work on the pathology

of degenerative changes in the cuff tendons. Citing the research of Loschke, Wrede, Codman,

Schaer, Glatthaar, Wells, and others, he builds a convincing case for primary, age-related

degeneration of the tendon manifested by changes in cell arrangement, calcium deposition,fibrinoid thickening, fatty degeneration, necrosis, and rents. He states that "the degenerative

changes in the tendon aponeurosis of the shoulder joint, except for calcification and rupture, giveno symptoms, as far as is known at present. On the other hand the tensile strength and elasticityof a tendon aponeurosis that exhibits such degenerative lesions are unquestionably less than in a

normal tendon aponeurosis."

The major role of tendon degeneration in the production of cuff defects was promoted as a

concept by Meyer (Meyer, 1924, Meyer, 1931) and corroborated by the studies of DePalma and

others (Cotton and Rideout, 1964, DePalma, 1983, DePalma, Gallery, 1949, DePalma, White,1950, Grant and Smith, 1948, Neer, 1990, Ozaki, Fujimoto, 1988, Uhthoff and Sarkar, 1991a,

Zuckerman, Kummer, 1992). Nixon and DiStefano, reviewing the literature on the microscopic

anatomy of cuff deterioration, (Nixon and DiStefano, 1975) found loss of the normal

organizational and staining characteristics of bone, fibrocartilage, and tendon without evidenceof repair. They summarized these degenerative changes as follows:

"Early changes are characterized by granularity and a loss of the normal clear wavy outline ofthe collagen fibers and bundles of fibers. The structures take on a rather homogenous

appearance; the connective tissue cells become distorted and the parallelism of the fibers is lost.

The cell nuclei become distorted in appearance--some rounded, others pyknotic or fasiculated.Some areas of the tendon have a gelatinous or edematous appearance with loosening of fibers


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that contain broken, frayed elements separated by a pale staining homogeneous material". This

histological picture is reminiscent of that described for tennis elbow, Achilles tendinitis and

patellar tendinitis.

Brewer (Brewer, 1979) has demonstrated age-related changes in the rotator cuff. These changes

include diminution of fibrocartilage at the cuff insertion, diminution of vascularity,fragmentation of the tendon with loss of cellularity and staining quality, and disruption of the

attachment to bone via Sharpey's fibers. The bone at the insertion becomes osteoporotic and

prone to fracture. (Kannus, Leppala, 1995)

Recently Kumagai et al (Kumagai, Sarkar, 1994) studied the attachment zone of the rotator cuff

tendons to determine how degenerative changes affected the pattern of collagen fiberdistribution. Degenerative changes were found in all elderly tendons but not in tendons from

younger subjects. Changes in insertional fibrocartilage included calcification, fibrovascular

proliferation and microtears. In degenerative tendons, the normal distribution of collagen fiber

types was markedly altered with fibrovascular tissue containing type III collagen instead of the

usually predominant type II. The authors concluded that severe degenerative changes in the cufftendons of elderly individuals alter the collagen characteristic of the rotator cuff and that the

changes could be associated with impairment of biomechanical properties of the attachmentzone. Virtually identical findings were reported by Riley. (Riley, Harrall, 1994)

In all clinical reports, the incidence of cuff defects is relatively rare before the age of 40 andbegins to rise in the 50- to 60-year age group and continues to increase in the 70-year and over

age group. Of 55 patients with arthrographically verified cuff tears, Bakalim and Pasila (Bakalim

and Pasila, 1975) found only 3 who were under 40 years of age. Yamada and Evans found no

cuff tears in 42 shoulders under age 40. (Yamada and Evans, 1972) In Hawkins and coworkers'series of 100 cuff repairs, only 2 patients were in their third or fourth decade. (Hawkins,

Misamore, 1985) In their series of shoulder dislocations, Reeves (Reeves, 1966) and Moseley(Moseley, 1969) found the incidence of cuff tears among patients under 30 to be very low. Theseauthors found that the incidence of cuff failure in dislocated shoulders rose dramatically with the

age of the patient. As noted by DePalma, even massive injuries to young healthy shoulders

"seem more likely to produce glenohumeral ligament tears and fractures than ruptures of therotator cuff." Pettersson (Pettersson, 1942) states that "even in cases of traumatic rupture . . . the

age distribution indicates that changes in the elasticity and tensile strength are prerequisites for

the appearance of the rupture." Pettersson (Pettersson, 1942) reported further that in patients with

anteroinferior dislocations, the incidence of arthrographically proven partial- or full-thicknesscuff tears was 30 per cent in the fourth decade and 60 per cent in the sixth decade.

Many cuff defects occur in 50- to 60-year-old individuals who have led quite sedentary liveswithout a history of injury or heavy use. In one of his clinical series, Neer provided substantial

evidence for a degenerative etiology of cuff defects:(Neer, 1983)

1. 40 per cent of those with cuff defects have "never done strenuous physical work";2. cuff defects are frequently bilateral;3. many heavy laborers never develop cuff defects; and4. 50 per cent of patients with cuff defects had no recollection of shoulder trauma.


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In their 1988 report to the American Shoulder and Elbow Surgeons (ASES), Neer and coworkers

(Neer, Flatow, 1988) found that of 233 patients with cuff defects, all but 8 were over 40; 70 per

cent of the defects occurred in sedentary individuals doing light work, 27 per cent in females,and 28 per cent in the non dominant arm.

As expected, the deterioration in cuff quality is usually bilateral: Harryman found that 55% ofpatients presenting with cuff tears on one side had ultrasonographic evidence of cuff defects on

the contralateral side. (Matsen, Lippitt, 1994) Age related degeneration can also be observed by

MRI. (Tyson and Crues III, 1993)

The pattern of degenerative cuff failure is distinctive. E.A. Codman described the "rim rent" in

which the deep surface of the cuff is torn at its attachment to the tuberosity. (Codman, 1934b)Codman's wonderful book contains many photomicrographs of these rim rents, providing a

convincing argument that cuff tears most frequently begin on the deep surface and extend

outward until they become full-thickness defects (see figure 44). Codman pointed out that: "It

would be hard to explain this . . . by erosion from contact with the acromion process." Similarly,

McLaughlin (McLaughlin, 1944) observed that partial tears of the cuff "commonly involve onlythe deep surface of the cuff..." Wilson and Duff (Wilson and Duff, 1943) also described partial

tears near the insertion of the cuff. These occurred on the articular surface, on the bursal surface,and in the substance of the tendon. Cotton and Rideout (Cotton and Rideout, 1964) also

described "slight" tears on the deep surface of the supraspinatus adjacent to the biceps tendon in

their necropsy studies. Pettersson and DePalma noted that the innermost fibers of the cuff begin

to tear away from their bony insertion to the humeral head in the fifth decade and that thesepartial-thickness tears increase in size over the next several decades. (DePalma, 1973, Pettersson,

1942) The partial-thickness tears observed by Uhthoff and coworkers (Uhthoff, Loehr, 1986 Oct

27) were always on the articular side; none occurred on the bursal side in spite of the occasionalpresence of spurs or osteophytes on the acromion. Other authors also have described partial

thickness tears. (Bosworth, 1940, Bosworth, 1941, Codman, 1934b, Fukuda, 1980, Fukuda,

Mikasa, 1987, Kutsuma, Akaoka, 1982, Mikasa, 1979, Ozaki, Fujimoto, 1985, Strizak, Danzig,

1982, Tabata and Kida, 1983, Tabata, Kida, 1981, Tamai and Ogawa, 1985, Yamamoto, 1982,Yamanaka and Fukuda, 1981, Yamanaka, Fukuda, 1983) These observations suggest that the

deep fibers of the cuff near its insertion to the tuberosity are most vulnerable to failure, either

because of the loads to which they are exposed or because of their relative lack of strength orbecause of their limited capacity for repair.


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Figure 44

An important recent study by Fukuda et al documented the patterns of intratendinous tears andobserved that these lesions tend not to heal. (Fukuda, Hamada, 1994) Further evidence of the non

healing of cuff lesions was provided by Yamanaka and Matsumoto(Yamanaka and Matsumoto,

1994) who demonstrated progression of partial thickness tears. After initial arthrography, theyfollowed 40 tears (average patient age 61 years) managed without surgery. Repeat arthrograms

an average of one year later showed apparent healing in only 10%, reduction of apparent tear

size in 10%, and enlargement of the tear size in over 50% with over 25% progressing to fullthickness tears. Interestingly the clinical pain and function scores of these patients were

improved at followup. These observations lend proof to Codman's statement 60 years earlier, "Itis my unproved opinion that many of these lesions never heal, although the symptoms caused by

them usually disappear after a few months. Otherwise, how could we account for their frequentpresence at autopsy?" (Codman, 1934b) These studies also demonstrate the critical point that

scores based on clinical symptoms are an unreliable way of determining the integrity of the cufftendon.

Pathogenesis

The traumatic and the degenerative theories of cuff tendon failure can be synthesized into aunified view of pathogenesis. Through its life the cuff is subjected to various adverse factors

such as traction, compression, contusion, subacromial abrasion, inflammation, injections, and,

perhaps most importantly, age-related degeneration. Lesions of the cuff typically start where the

loads are presumeably the greatest: at the deep surface of the anterior insertion of thesupraspinatus near the long head of the biceps (see figures 31 and 32). Tendon fibers fail when

the applied load exceeds their strength. Fibers may fail a few at a time or en masse (see figure

33). Because these fibers are under load even with the arm at rest, they retract after their rupture.Each instance of fiber failure has at least four adverse effects:

1. it increases the load on the neighboring as yet unruptured fibers, giving rise to the zipperphenomenon,


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2. it detaches muscle fibers from bone (diminishing the force that the cuff muscles candeliver),

3. it compromises the tendon fibers' blood supply by distorting the anatomy contributing toprogressive local ischemia (see figure 34) and

4. it exposes increasing amounts of the tendon to joint fluid containing lytic enzymes whichremove any hematoma which could contribute to tendon healing (see figure 35).

Figure 31

Figure 32


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Figure 33

Figure 34

Figure 35

Even when the tendon heals, its scar tissue lacks the normal resilience of tendon and is,

therefore, under increased risk for failure with subsequent loading. These events weaken the

substance of the cuff, impair its function, and diminish its ability to effectively repair itself. Inthe absence of repair, the degenerative processtends to continue through the substance of the

supraspinatus tendon to produce a full thickness defect in the anterior supraspinatus tendon (see

figure 36). This full thickness defect tends to concentrate loads at its margin, facilitatingadditional fiber failure with smaller loads than those which produced the initial defect (see figure


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37). With subsequent episodes of loading, this pattern repeats itself, rendering the cuff weaker,

more prone to additional failure with less load, and less able to heal. Once a supraspinatus defect

is established, it typically propagates posteriorly through the remainder of the supraspinatus, theninto the infraspinatus (see figure 38).

Figure 36

Figure 37


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Figure 38

With progressive dissolution of the cuff tendon, the spacer effect of the cuff tendon is lost,

allowing the humeral head to displace superiorly (see figures 29 and 39), placing increased load

on the biceps tendon. As a result, the breadth of the long head tendon of the biceps is often

greater in patients with cuff tears in comparison to uninjured shoulders (see figure 40). (Ting,Jobe, 1987) In chronic cuff deficiency, the long head tendon of the biceps is frequently ruptured.

Figure 29


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Figure 39

Figure 40

Further propagation of the cuff defect crosses the bicipital groove to involve the subscapularis,starting at the top of the lesser tuberosity and extending inferiorly. As the defect extends across

the bicipital groove, it may be associated with rupture of the transverse humeral ligament and

destabilization of the long head tendon of the biceps allowing its medial displacement (see figure

41). (Slatis and Aalto, 1979)


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Figure 41

The concavity compression mechanism of glenohumeral stability (see figure 18) is compromisedby cuff disease. Beginning with the early stages of cuff fiber failure, the compression of the

humeral head becomes less effective in resisting the upward pull of the deltoid. Partial thickness

cuff tears cause pain on muscle contraction similar to that seen with other partial tendon injuries(such as those of the Achilles tendon or extensor carpi radialis brevis). This pain produces reflex

inhibition of the muscle action. In turn, this reflex inhibition along with the absolute loss of

strength from fiber detachment makes the muscle less effective in balance and stability.

However, as long as the glenoid concavity is intact, the compressive action of the residual cuffmuscles may stabilize the humeral head (see figure 42). When the weakened cuff cannot prevent

the humeral head from rising under the pull of the deltoid, the residual cuff becomes squeezed

between the head and the coracoacromial arch. Under these circumstances, abrasion occurs with

humeroscapular motion, further contributing to cuff degeneration (see figure 43). Degenerativetraction spurs develop in the coracoacromial ligament which is loaded by pressure from the

humeral head (analogous to the calcaneal traction spur that occurs with chronic strains of the

plantar fascia) (see figure 39). Upward displacement of the head also wears on the upper glenoidlip and labrum (see figure 44), reducing the effectiveness of the upper glenoid concavity. Further

deterioration of the cuff allows the tendons to slide down below the center of the humeral head,

producing a "boutonniere" deformity (see figure 41). (Norris, Fischer, 1983) The cuff tendonsbecome head elevators rather than head compressors. Just as in the boutonniere of the finger, the

shoulder with a buttonholed cuff is victimized by the conversion of balancing forces into

unbalancing forces. Erosion of the superior glenoid lip may thwart attempts to keep the humeral

head centered after cuff repair (see figure 42). Once the full thickness of the cuff has failed,

abrasion of the humeral articular cartilage against the coracoacromial arch may lead to asecondary degenerative joint disease known as cuff tear arthropathy (see figures 39 and 47).

(Neer, Craig, 1983)


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Figure 41

Figure 42

Figure 43


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Figure 44

Figure 45

Figure 46


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Figure 47

The cuff muscle deterioration which inevitably accompanies chronic cuff tears is one of the mostimportant limiting factors in cuff repair surgery. Atrophy, fatty degeneration, retraction, loss of

excursion are all commonly associated with chronic cuff tendon defects. (Leivseth and Reikeras,

1994, Nakagaki, Tomita, 1994) To a large extent, these factors are irreversible.(Goutallier,Postel, 1994) These changes increase with the duration of the tear and do not rapidly reverse

after cuff repair. (Goutallier, Postel, 1995)

Disclaimer

This resource has been provided by the University of Washington Department of Orthopaedics

and Sports Medicine as general information only. This information may not apply to a specificpatient. Additional information may be found athttp://www.orthop.washington.eduor by

contacting the UW Department of Orthopaedics and Sports Medicine.
http://www.orthop.washington.edu/http://www.orthop.washington.edu/http://www.orthop.washington.edu/http://www.orthop.washington.edu/uw/tabID__3337/Default.aspxhttp://www.orthop.washington.edu/uw/tabID__3337/Default.aspxhttp://www.orthop.washington.edu/uw/tabID__3376/ItemID__822/mid__10357/wversion__Staging/index__False/DesktopModules/Pictures/PictureView.aspxhttp://www.orthop.washington.edu/uw/tabID__3337/Default.aspxhttp://www.orthop.washington.edu/

Rotator Cuff Relevant Anatomy and Mechanics

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