Clinical History: A 66 year-old man presents with persistent right shoulder pain, accompanied by painful clicking. (1A,B) T2-weighted fat-suppressed coronal MR images of the right shoulder are provided. What are the findings? What is your diagnosis?
Extensive chondral delamination involving the humeral head.
Low-grade intrasubstance delaminated tear of the supraspinatus tendon.
In the English language, a lamina is a thin layer or plate. A similar term, lamella, is defined as a thin plate-like layer or structure. Lamination is a process of manufacturing a material into multiple layers, and lamellation is an arrangement or structure in which there are thin layers or plates. Delamination, the subject of this web clinic, is defined as a mode of failure in which a material fractures or separates into layers. Of note, the word “delamellation” is not found in most English dictionaries.
Delamination is a well-known pattern of failure in composite material, related typically to the presence of weak adhesions between layers within that material, such as the failure of weak fiber polymers that are located between sheets of plastic. Delamination is recognized in cement, ceramics, and even in wood logs in which it is designated “shake”, representing failure of timber related to delamination along growth rings. The occurrence of delamination in many of these materials has been attributed to compression, shear, or tensile force, alone or in combination.
Delamination of human tissue is also well known. With regard to the musculoskeletal system, even a quick review of the recent scientific literature will confirm a large number of publications describing in detail delamination of cartilage and tendons. Although a similar process occurring in ligaments, menisci, and labra has received little or no attention, the term delamination can be used to describe certain patterns of failure in these tissues as well. An understanding of delamination in cartilage, tendons, ligaments, and menisci requires knowledge of the anatomic arrangement of the collagen framework in these tissues. Specifically, with regard to failure of human tendons, the plane of separation, or delamination, is along the longitudinal axis of the major collagen fibers, not through them, a situation that also occurs in ligaments. The collagen arrangement in articular cartilage and menisci, however, is more complex, creating confusion as to what represents true delamination in those tissues.
In most regions of the human body, articular cartilage is hyaline in type. Cartilage has low cellular content, with the chondrocytes constituting only about 2% of its total volume.1 The arrangement of the chondrocytes varies with depth. Near the articular surface, the chondrocytes are disc-shaped and oriented horizontally, while in the deeper portions of the cartilage, the chondrocytes are rounded in shape and arranged into columns.2,3 In the deep zone of cartilage, the highly ordered perpendicularly-oriented collagen fibers propagate around these columns of chondrocytes.3
The collagen framework of articular cartilage that, along with the proteoglycans, fulfills the mechanical role of the tissue, is painted on this cellular background. The lamina splendens is the most superficial layer of articular cartilage, being characterized by a high density of collagen fibers oriented parallel to the articular surface, loosely anchored to the underlying superficial zone.4 The collagen fibers in articular cartilage are arranged parallel to the surface in the superficial zone, arching through the transitional zone, and are oriented perpendicular to the surface in the deep zone (Figures 3 and 4).5,6 These arc-like columns of collagen are known as the arcades of Benninghoff. They extend through the entire thickness of the uncalcified cartilage to the tidemark and below, anchoring the cartilage to the subchondral bone plate.6,7 The tidemark represents the line between the uncalcified cartilage in the deep zone and the subjacent calcified cartilage.7 In the calcified zone, the collagen fibers maintain a perpendicular orientation, with deposits of calcification along their length.2
A review of the available literature indicates that cartilage delamination is generally described as occurring at the tidemark (Figure 5), where shear forces cause separation of the uncalcified articular cartilage superficial to the tidemark from the calcified cartilage and bone deep to the tidemark.8 The calcified cartilage, therefore, remains attached to the subchondral bone plate.
In order to understand the shear forces that act at the tidemark, we must first discuss compressive forces and introduce the concept of “buckling”. Buckling is a mode of failure that occurs in slender structural columns, such as collagen fibrils, in which compressive forces lead to lateral deflection, or bending, of the column.9 Buckling of collagen fibers occurs mostly in the transitional zone, with the collagen fibers in the deep zone demonstrating a greater stiffness.10 When the cartilage is compressed, it deforms, leading to bulk outflow of water through the extracellular matrix. As a result of the discrepancy in compressive stiffness between the noncalcified cartilage and the much stiffer underlying calcified cartilage and bone, the lateral deformation of the articular cartilage is constrained by the calcified cartilage bed, and resultant shear forces develop at the tidemark, causing delamination.11 Therefore, the tidemark delaminates much more easily than the deeper junctional region between cartilage and subchondral bone.12
With MRI, chondral delamination usually appears as a thin line of near-fluid signal intensity beneath the deep zone of articular cartilage, at the tidemark, separating the noncalcified cartilage from the underlying bone and calcified cartilage (Figures 6-9). In some cases, however, the zone of separation is thicker and even irregular in appearance, and marrow edema-like signal may be present in the subchondral bone.13 Whether the zone of separation is thin and regular or thick and irregular, it is critical to realize that the overlying cartilage surface may or may not be violated. Therefore, even with extensive delamination in the deeper region of the chondral coat, at the time of arthroscopy the surface of the articular cartilage may appear entirely normal, or there may only be a subtle bulge of the cartilage surface.14 Furthermore, when violation of the chondral surface does occur, the extent of delamination often extends beyond the margin of the superficial chondral defect.8
There are additional chondral abnormalities in both the medial and lateral facets of the patella and central region of the trochlea.
When one cartilage surface translates over another, shear stress develops at the articular surface. The normal articular cartilage surface has a coefficient of friction that is much lower than that of man-made materials, due to the smooth surface of the lamina splendens and the presence of specialized molecules in the surface layer that provide lubrication, such as lubricin.11 When excessive shear forces develop near the surface, surface-layer damage of the articular cartilage can occur, including fibrillation or fissuring (Figures 10 and 11). Fibrillation is defined as a process of forming fine fibers or fibrils. In articular cartilage, fibrillation results in surface irregularity of the cartilage, related to disorganization of the horizontally-oriented collagen bundles in the superficial cartilage layers.15 As the superficial collagen fibers have been described as layered or leaf-like in distribution, fibrillation can be considered a process of delamination, separating one surface layer of collagen from another. Fissuring is defined as a split or crack that is long and narrow. Chondral fissuring occurs primarily as a result of delamination between the obliquely and vertically oriented collagen fibrils, rather than by breakage of collagen fibrils.15 Specifically, a chondral fissure propagates by breaking bonds between the collagen fibrils.15,16
A transversely oriented region of failure in the midzone of articular cartilage is sometimes seen in association with chondral fissures on MRI (Figures 12 and 13). The interpretation of this finding and even its pathogenesis are not clear. One explanation might relate to the transverse nature of some of the cellular components of articular cartilage, appearing in rows. Thus, the process might be designated cartilage delamination of cellular rows, rather than collagen fibers, with the cellular architecture being used as the point of reference. Such a process, however, would intersect the classically described vertical arcades of collagen, unless these arcades have been modified as a response to a preexisting disorder. Specifically, in osteoarthrosis, extensive changes in the normal collagen organization have been reported, with the orientation of the collagen fibers demonstrating a wide range of angles, as well as regions with parallel collagen fibrils. There is also loosening of the collagen matrix, chondral fibrillation, and replacement of type II collagen with type I collagen in osteoarthritis.17 Therefore, it is possible that the transversely-oriented region of failure that is sometimes seen in the midzone of articular cartilage may represent delamination between pathologically disorganized collagen fibers. Until this process is better understood, however, there will be inconsistencies in the manner in which it is described and lack of agreement whether midzonal chondral failure should be designated as delamination.
Failure of the subchondral bone plate undermines the integrity of the overlying articular cartilage.11 As one final extension of the term delamination, in the presence of a process that weakens the subchondral bone plate or adjacent subchondral bone, shear forces could lead to delamination of the entire chondral layer and even portions of the subchondral bone plate (Figure 14). Some processes that might cause this include primary or secondary hyperparathyroidism with skeletal involvement and osteonecrosis. With hyperparathyroidism, subchondral resorption of bone is the culprit. In osteonecrosis, the situation is complicated as fractures, which manifest as the crescent sign, develop in regions of necrotic bone and may be located in the subchondral bone or in the subchondral bone plate itself, from where they may extend as a cleavage plane into the adjacent articular cartilage, even disrupting the chondral surface.
As classically described, cartilage delamination is considered a surgical lesion. If it is not appropriately recognized and treated, such delamination can result in significant morbidity. The process occurs most commonly in the young adult population and, without proper treatment, can lead to early-onset degenerative changes.13 Surgical options for treatment of chondral delamination include microfracture or bone marrow stimulation, osteochondral autograft or allograft transplantation, autologous chondrocyte implantation, particulated juvenile cartilage allograft transplantation, and cell-based and scaffold treatments.18,19 When the articular surface is intact, chondral delamination is effectively managed with bioabsorbable pin fixation to avoid propagation to a full-thickness chondral lesion.20
Delamination is a frequent complication after surgical repair of cartilage (Figure 15), and it occurs more commonly with autologous chondrocyte implantation.21 In delamination of surgically repaired cartilage, there is failure of the repair tissue to integrate with the subchondral bone, resulting in separation of the repaired cartilage from the underlying subchondral bone. The delaminated repair tissue may remain in situ or be displaced into the joint space. Delamination of the repaired cartilage often requires surgical revision.14
Structurally, tendons are composed of distinct fascicular subunits that contain bundles of collagen fibrils and constituent cells, the collagen bundles generally oriented along the long axis of the tendon (Figure 16).22 The cellular connective tissue lies between and separates adjacent collagen bundles. When tensile force is applied along the longitudinal axis of the tendon, the individual fascicles elongate to different degrees, leading to interfascicular movement (Figure 16). Histologic analysis has suggested that the lubricant protein lubricin facilitates such interfascicular sliding motion during loading. A deficit of this protein may contribute to tendon wear.23 One common pattern of tendon wear is designated a delaminating tear, which is defined as a separation oriented along the long axis of the tendon and located predominantly between and not through the collagen fibers. Thus, a purely delaminated tear is a collagen sparing tear of the tendon. The direction of delamination may be vertical, horizontal, or oblique, and the tear may be full-thickness or partial-thickness. Therefore, a delaminated tendon tear may violate one or more surfaces of the tendon or lie completely within its substance. Full-thickness delaminating tears are designated split tears (Figure 17), and these are most commonly encountered in the peroneus brevis tendon at the level of the ankle (Figure 18) and the biceps tendon at the level of the glenohumeral joint (Figure 19). A review of the available literature confirms that delaminated tendon tears have been studied predominantly with regard to the rotator cuff. Immunohistologic analysis of delaminated rotator cuff tendons has shown that delamination predominantly occurs between layers of the tendon with differing collagen fiber orientation, although delamination may also occur between collagen fibers of parallel orientation within the same layer of a tendon.24
On MRI, the appearance of tendon delamination is varied and related in part to whether the tear is full-thickness or partial-thickness. With regard to the rotator cuff, tendon delamination is suggested by the presence of an intrasubstance longitudinal fluid cleft separating articular and bursal fibers. In the presence of a full-thickness tear, delamination is also confirmed by differential retraction of the torn tendon fibers (Figure 20). With a partial-thickness intrasubstance delaminated tear, the plane of cleavage may be concealed at the time of arthroscopy (Figure 21). Alternatively, if the partial-thickness delaminated tear extends to the articular surface (Figure 22) or bursal surface, it can be detected by arthroscopy or bursoscopy, respectively. Delamination may also result in cysts at or adjacent to the myotendinous junction or within the muscle belly itself (Figure 23), the cysts being referred to as “sentinel cysts”.25 Sentinel cysts may occur with either full-thickness or partial-thickness delaminated tears, in relatively equal proportions.26
With full-thickness tears, delamination results in separation of the tendon into superficial and deep layers. The characteristic pattern of delaminated rotator cuff tendons is that the articular-sided (deep) layer is retracted more than the bursal-sided (superficial) layer (see Figure 20).27 Arthroscopic studies have demonstrated that the predominant direction of retraction of delaminated tears that involve both the supraspinatus and infraspinatus tendons is posteromedial if the superficial layer of tearing contains a larger amount of infraspinatus tendon than supraspinatus tendon, and is anteromedially directed if the superficial layer of tearing contains a larger amount of the supraspinatus tendon.28 Furthermore, the articular-sided (deep) layer of the delaminated tendon is more frequently thicker than the bursal-sided (superficial) layer, owing to muscle atrophy that is more often associated with the superficial layer.29
The concept of delamination is also relevant in the discussion of so-called novel lesions of the infraspinatus tendon, which in general are regarded as a characteristic pattern of edema within the infraspinatus tendon anywhere from the distal tendon to the myotendinous junction.30 These lesions are associated with persistent tendon abnormalities on follow-up imaging, with or without muscle atrophy. Cadaveric studies of the infraspinatus muscle architecture have delineated two muscle bellies, a transverse portion and an oblique portion.31 The oblique portion contains a long and thick tendon that attaches to the greater tuberosity, and the transverse portion contains a thin and short tendon that attaches to the tendon of the oblique head (Figure 24).
Retrospective analysis of MRI studies demonstrating novel lesions has postulated that these novel lesions reflect a delaminating infraspinatus tendon injury with differential retraction of the transverse and oblique components (Figure 25).32 However, a review of the current literature demonstrates a lack of consensus on the precise location of this injury with regard to whether failure occurs at the myotendinous junction or distal tendon with tendon delamination. These lesions may be occult on arthroscopy when the deep oblique tendon fibers are intact, as well as on bursoscopy when the superficial transverse tendon fibers are intact.
Delaminated rotator cuff tears have been associated with impaired tendon healing following repair as compared to non-delaminated tears.33,34,35 However, the presence of delamination may be a confounding rather than an independent risk factor for the failure of cuff healing36 as some studies have shown similar clinical outcomes between repairs of delaminated and non-delaminated tears.35-36 Regardless, the identification of tendon delamination remains important whether it is accomplished by a radiologist at the time of interpretation of the MRI study or by an orthopaedic surgeon during arthroscopy as its presence may influence the surgical technique. Some delaminating tears have demonstrated a synovial lining, suggesting that curetting should be performed prior to suture repair to facilitate healing.24 Additionally, in the setting of delamination, some surgeons preferentially utilize mini-open rather than fully arthroscopic techniques37 or would perform a double layered repair of the superficial and deep tendon layers rather than a single row repair.28-29
Ligaments connect bone to bone, demonstrating a collagen architecture that is similar to that of tendons, with most of the collagen bundles oriented along the long axis of the ligament, in the general direction of the tensile forces applied to the ligament. The main differences in composition are a higher proteoglycan and water content and lower collagen content in ligaments relative to tendons. Additionally, the collagen structure in ligaments tends to be slightly less uniform, with more of a weaving pattern of the collagen bundles.38
At rest, ligaments demonstrate crimp, or slight laxity. Failure of ligaments can occur as complete tears or partial tears. These tears may be non-delaminated or delaminated, the latter leading to separation of adjacent collagen bundles. As one example, delamination of collagen fibers in ligaments forms the basis for what has been designated mucinous (cystic) degeneration (Figure 26). Although this process has been emphasized in the anterior cruciate ligament, occurring with increased frequency with advancing age, mucinous degeneration occurs in other ligaments as well, including the posterior cruciate ligament. Mucoid degeneration of the posterior cruciate ligament commonly coexists with mucoid degeneration of the anterior cruciate ligament.39 Histologically, mucoid degeneration reflects degradation of collagen and deposition of glycosaminoglycans between the collagen bundles, thereby reflecting a form of delamination between the collagen bundles, followed by progressive loss of collagen fiber structure and bundle integrity.40,41 While distorted, these collagen fibers remain uninterrupted and, therefore, mucoid degeneration does not truly represent a tear, although it may be misinterpreted as such when viewed with MRI.42
Typically, with MRI, mucinous degeneration of the anterior cruciate ligament (Figures 27-31) is characterized by thickening and increased intraligamentous signal, with intact fibers, often demonstrating a “celery stalk” appearance. Mucinous degeneration of the posterior cruciate ligament may manifest as the so-called “tram-track” appearance, with diffuse thickening and longitudinally increased signal intensity in the ligament and a peripheral rim of hypointense intact fibers (Figures 30 and 32).39 Paracruciate or intraosseous ganglion cysts, or both, are associated with mucinous degeneration of either cruciate ligament.42
Although mucinous degeneration is often regarded as a phenomenon of middle-aged and elderly persons, the MRI appearance of linear regions of altered signal and even enlargement of a ligament, especially in the anterior cruciate ligament, can be seen in children and young adults. Anecdotally, we have noticed this phenomenon in young athletes (Figure 29), especially soccer players, runners, and American football players, related to repetitive stress owing to vigorous activity rather than a single episode of trauma.
Indeed, there are several theories regarding the pathogenesis of mucoid degeneration, including: (a) a theory of tissue degeneration that proposes an important causative role of aging; (b) a theory emphasizing injury, which highlights the fact that fibroblasts in the anterior cruciate ligament secrete glycosaminoglycans in the setting of trauma and, in response to joint and tissue motion, the deposited mucin substance dissects between the ligament fibers and causes fusiform dilatation of the ligament; and (c) a theory of “multiple microtrauma”, which states that multiple insignificant injuries result in formation of microcysts that merge into larger mucoid formations, probably as a result of injury to the protective synovium overlying the anterior cruciate ligament. The anatomy of the intercondylar notch may be a contributing factor, as a smaller and more vertically-oriented notch may predispose to ligamentous impingement and resultant microtrauma.43
Whether related to degeneration or repetitive stress, mucoid degeneration is associated with a stable ligament on physical examination. Mucoid degeneration has a predilection for the posterolateral bundle of the anterior cruciate ligament, and it may cause pain on terminal extension related to mechanical impingement of the hypertrophied ligament on the roof and lateral wall of the intercondylar notch.44 Mucoid degeneration of the anterior cruciate ligament is also associated with posterior knee pain and limited flexion. Some of the affected patients may be treated by partial or complete arthroscopic resection of the abnormal ligament, with resultant resolution of symptoms.45 At arthroscopy, there is a hypertrophic ligament with yellowish mucoid material along the length of its fibers; however, mucoid degeneration of the anterior cruciate ligament is frequently undetectable at arthroscopy using the standard anterior portal approach.42
Similar to tendons, partial tears of ligaments can occur, and sometimes such tears demonstrate delaminating components on MRI, with the delaminating component propagating parallel to the direction of the collagen fibers. Delaminating tears, or split tears, of the posterior cruciate ligament (Figures 33-35) have been documented in the literature, manifesting as increased linear signal intensity within the ligament. Although intrasubstance delamination of the posterior cruciate ligament has been associated with functional impairment or insufficiency in the majority of cases in one report, the true significance of this finding awaits further clarification through additional investigations.46
The menisci of the knee are crescent-shaped fibrocartilaginous structures, composed of approximately 70% water and 20% collagen interposed with fibrochondrocyte cells.47 The remaining dry weight is composed of proteoglycans, non-collagenous proteins, and glycoproteins. The interaction of water with the matrix framework influences the viscoelastic properties of the meniscus, and the collagens account for the meniscal tensile strength. Electron microscopic analysis of the collagen framework has revealed three layers (Figure 36).48 The superficial layer (1, Figure 36) is composed of a meshwork of thin fibrils without preferred orientation. The lamellar layer (2, Figure 36) is deep to the superficial layer and demonstrates radially oriented fibers peripherally and variably oriented fibers more internally. In simple terms, the collagen fibers, or bundles, in the central layer of the meniscus (3, Figure 36) are divided into two types based on their predominant orientation. The first of these are often designated longitudinal, or circumferential, collagen bundles. These bundles are found mainly in the outer two-thirds of the meniscus and extend in a circumferential pattern, connecting the anterior horn, midportion, and posterior horn of the meniscus. The second type are designated the radial tie fibers (blue, Figure 36), extending in from the periphery toward the apex of the meniscus, connecting the peripheral and central portions of the meniscus to provide structural integrity. The menisci serve important roles in load transmission, shock absorption, and stability.47 The longitudinal fibers of the central layer translate compressive loads into circumferential hoop stresses, and the anterior and posterior insertional, or root, ligaments of the menisci prevent peripheral meniscal extrusion during loading.
There is no uniformly accepted classification system for meniscal tears. One system, introduced by the International Society of Arthroscopy, Knee Surgery and Orthopaedic Sports Medicine (ISAKOS), classifies meniscal tears based on seven factors: tear depth; rim width; radial location; central to the popliteal hiatus; tear pattern; quality of tissue; and length of tear.49 With regard to tear pattern, longitudinal, horizontal, radial, and flap tears are the categories that are used. For our discussion of meniscal delamination, it is useful to look at three of these tear patterns: longitudinal tears, horizontal tears; and radial tears. Identification of these tear patterns aids in management as longitudinal vertical tears are more likely to heal when compared to longitudinal horizontal or radial tears.50
Longitudinal (circumferential) vertical tears, frequently simply referred to as longitudinal or vertical tears, (Figure 37) are generally related to axial loading and are found in the outer half or two-thirds of the meniscus. They extend for a variable distance from a more anterior position to a more posterior position, and they often do so along the path of least resistance, parallel to the long axis of the longitudinal collagen bundles. Such extension represents one pattern of meniscal delamination. If these tears deviate from this path, becoming oblique in direction, violation of some of these collagen fibers is required, the tear pattern being designated longitudinal (circumferential) vertical oblique in direction. Furthermore, longitudinal vertical tears that extend for a considerable distance in an anteroposterior direction will violate radial tie fibers along their course. Longitudinal (circumferential) horizontal tears (Figure 38), often simply described as horizontal tears or cleavage tears, are generally related to shear forces. These tears generally begin at or near the inner apex of the meniscus and propagate in a peripheral direction, sometimes violating the outer surface of the meniscus and accompanied by parameniscal cysts. These tears often extend along the path of least resistance, between and not through the longitudinal (circumferential) collagen fibers, representing a second pattern of meniscal delamination. If these tears have a large anteroposterior component, they too will violate the radial tie fibers. Radial meniscal tears (Figure 39) also begin in the inner margin of the meniscus. Their path of least resistance is parallel to and not through the radial tie fibers, as they extend to the periphery of the meniscus, a pathway that represents a third pattern of delamination. Radial tears that extend into the outer half of the meniscus will violate some of the longitudinal (circumferential) collagen fibers. Further, those radial tears that are obliquely oriented, so-called parrot beak tears, will violate some of the radial tie fibers. Of note, one can use this same rationale to illustrate that some multidirectional meniscal tears are associated with interlayer and intralayer delamination (Figure 40).
Delamination is a mode of failure in which a material separates into layers, and it is a process that is commonly seen in human tissues including articular cartilage, tendons, ligaments, and menisci. Knowledge of the collagen architecture of these tissues is important for understanding how delamination occurs. Delamination of cartilage and tendons is well-described in the literature, and both are of significance to the orthopaedic surgeon. In particular, chondral delamination occurring at the tidemark is a surgical lesion. As delamination of the deeper zone of articular cartilage may be concealed at the time of arthroscopy, recognition of this pattern of failure becomes an important diagnostic exercise for the radiologist. Tendon delamination alters surgical management, particularly when it occurs in the rotator cuff tendons. A similar process of tissue delamination may occur in ligaments and menisci, a process that has received little or no attention in the literature.
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