Meniscus, Tendons, and Ligaments: Pathophysiology
Andrew O. Usoro, MD
Michael A. Kolosky, DO
Mark D. Price, MD, PhD
The menisci are two crescent-shaped fibrocartilaginous structures found on the medial and lateral aspects of the knee. The menisci enable effective articulation between the concave femoral condyles and the relatively flat tibial plateau.1,2 In cross section, they are triangular in shape starting with a thick peripheral rim, and then thinning to the central margin. The undersurface or inferior portion of the meniscus is convex, whereas the superior surface is more concave, mirroring the tibial and femoral articular surfaces, respectively. Each meniscus is made up of three sections: the anterior horn, meniscal body, and posterior horn; and the menisci are anchored to the subchondral tibial bone of the tibia through insertional fibers at the anterior and posterior horns called the meniscal roots. The anterior horns of the medial and lateral menisci are connected via a dense fibrous band called the anterior intermeniscal ligament in 50% to 90% of the population3,4,5 (Fig. 4-1).
MEDIAL MENISCUS
The medial meniscus is a C-shaped structure that is larger in radius compared to the lateral meniscus and covers roughly 50% of the medial tibial surface.2,6 The anterior horn has a robust attachment to the tibia near the intercondylar fossa anterior to the anterior cruciate ligament (ACL).2 The posterior horn whose cross-sectional area is larger than the anterior horn is anchored to the tibial plateau at the posterior intercondylar fossa, just anterior to the attachments of the posterior cruciate ligament (PCL) and posterior to the lateral meniscal root.2 Its entire peripheral border is attached to the tibial condylar ridge through the coronary ligament. Further anchoring the medial meniscus is its contiguous insertion to the deep medial collateral and capsular ligaments at the body, and to the posteromedial complex (posterior oblique ligament, oblique popliteal ligament, and semimembranosus tendon) at the posterior horn.1 There are no attachments to the capsule or fat pad at the anterior horn.7 The sum of these attachments is what accounts for the decreased mobility of the medial meniscus when compared to the lateral with the degree of movement in one study measured at 3 and 9 mm, respectively.8,9
LATERAL MENISCUS
Covering nearly 70% of the underlying lateral tibial plateau, the lateral meniscus is almost uniformly circular and in contrast to the medial meniscus, it is smaller and considerably more mobile, due to significantly fewer capsular and ligamentous attachments.6,8,10,11 The anterior horn of the lateral meniscus is attached to the intercondylar fossa, just lateral to the broad attachment site of the ACL. The posterior horn emanates just posterior to the lateral tibial spine and is in very close proximity to the broad PCL footprint.2 Unique to the lateral meniscus are two meniscofemoral ligaments that attach the meniscus to the medial femoral condyle. Individually, their existence within the knee is roughly 70%, whereas their prevalence found together is significantly lower at 4%.12,13,14,15 These fibrous bands are known as the ligament of Wrisberg and Humphrey and straddle the PCL posterior and anterior, respectively.13 Aiding in the mobility of the lateral meniscus is the lack of stout tibial and capsular attachments at the popliteal hiatus.14 The intra-articular portion of the popliteus tendon can be identified at the hiatus located between the posterolateral border of the lateral meniscus and the posterior knee capsule, aptly named the popliteal hiatus.16 Providing some stability to this area are the superior and inferior popliteomeniscal fascicules, which secure the posterolateral meniscus to the posterior joint capsule.14,16,17 Without these attachments, the lateral meniscus may become hypermobile and could require meniscocapsular repair.
MENISCUS STRUCTURE
The menisci are predominantly water (72%), collagen (22%), and other organic matter organized into a dense extracellular matrix.18 The extracellular matrix is composed primarily of collagen, glycosaminoglycans, and other adhesion molecules.12,19,20,21 The primary glycosaminoglycans involved are dermatan sulfate (20% to 30%), chondroitin-6 sulfate (40%), chondroitin-4 sulfate (10% to 20%), and keratan sulfate (15%).21,22 The highest concentration of these glycosaminoglycans can be found in the weight-bearing portion, along the inner half of the meniscus, and in the anterior and posterior horns. The
hydrophilic properties of the glycosaminoglycans play an important role and allow for water absorption and retention throughout the meniscus.23 The influx of water is paramount for the meniscal maintenance of structure while under compression during weight bearing. The degree of meniscal hydration is determined by the balance between the total swelling pressure and the constraining forces such as the Donnan osmotic pressure, defined as the extracellular osmotic pressure attributable to extracellular cations attached to the negatively charged surrounding proteoglycans. This additional pressure within meniscal tissue allows for increased resistance against compression loading. Consequently, the meniscus is able to maintain its structure without water extrusion during normal weight bearing. Additionally, due to small pore size within the meniscus, significant hydraulic pressures are required to force fluid outside the meniscal issue. Thus, the menisci are able to maintain their innate structure without water loss despite routine compression during weight bearing.21,24,25 Aggrecan is the major proteoglycan in the meniscus and largely responsible for this effect and its viscoelastic properties. Biglycan and decorin constitute the main smaller proteoglycans. As the meniscus transitions toward the inner free margin, the density of proteoglycans increases in order to allow for changes in the stress felt in the outer versus inner meniscus. Adhesion glycoproteins, primarily fibronectin, thrombospondin, and type VI collagen, link the extracellular matrix and provide structural support.23,26,27
hydrophilic properties of the glycosaminoglycans play an important role and allow for water absorption and retention throughout the meniscus.23 The influx of water is paramount for the meniscal maintenance of structure while under compression during weight bearing. The degree of meniscal hydration is determined by the balance between the total swelling pressure and the constraining forces such as the Donnan osmotic pressure, defined as the extracellular osmotic pressure attributable to extracellular cations attached to the negatively charged surrounding proteoglycans. This additional pressure within meniscal tissue allows for increased resistance against compression loading. Consequently, the meniscus is able to maintain its structure without water extrusion during normal weight bearing. Additionally, due to small pore size within the meniscus, significant hydraulic pressures are required to force fluid outside the meniscal issue. Thus, the menisci are able to maintain their innate structure without water loss despite routine compression during weight bearing.21,24,25 Aggrecan is the major proteoglycan in the meniscus and largely responsible for this effect and its viscoelastic properties. Biglycan and decorin constitute the main smaller proteoglycans. As the meniscus transitions toward the inner free margin, the density of proteoglycans increases in order to allow for changes in the stress felt in the outer versus inner meniscus. Adhesion glycoproteins, primarily fibronectin, thrombospondin, and type VI collagen, link the extracellular matrix and provide structural support.23,26,27
 FIGURE 4-1 Meniscal anatomy and attachments. |
Type 1 collagen is the main component of the extracellular matrix and varies in response to the region of the meniscus. It is collagen that is responsible for the tensile strength of the meniscus, which varies with age, injury, or pathologic condition.18,23,28 In the peripheral third of the meniscus, type I collagen accounts for 80% of the total collagen. This number dramatically drops to 40% in the avascular inner meniscal margin.29 There are noted to be smaller amounts of type II, III, IV, VI, and XIII collagen throughout the meniscus as well. In the deeper layers of the meniscus, collagen fibers are oriented circumferentially, parallel to the meniscal peripheral border. Superficially, radially oriented “tie” fibers are woven between the circumferential fibers to add structural integrity and prevent longitudinal tearing.30,31,32 These radial fibers prevent radial extrusion and allow the meniscus to maintain its structure during normal weight bearing of the knee.30,32 Radial tie fibers are more abundant in the posterior horn and decrease in concentration through the body, toward the anterior horn.32,33,34 Thus, in the meniscus, compressive force is transduced into a circumferentially directed tensile stress (known as the hoop stress) that is supported by the circumferential cross-linked collagen fibers.35,36 At the inner third of the meniscus, the collagen fibrils become heavily cross-linked by hydroxylpyridinium aldehydes in order to resist shear forces of the tibiofemoral articulation. Collagen type II (60%), glycosaminoglycans, and aggrecan predominate, leading to smaller fiber bundles and a structure more similar to articular cartilage37 (Figs. 4-2 and 4-3).
The meniscus is sparsely populated with cells that are responsible for producing and maintaining the extracellular matrix. Early in development, the cells of the meniscus have a similar morphology with regional variations throughout the meniscus. These primary meniscal cells are categorized into two types: fibroblast-like cells with a fusiform appearance and chondrocyte-like cells with an ovoid appearance, found in the deep zones of the meniscus. They communicate with other cells via long cellular extensions.1,2,38 Cells in the inner, avascular portion of the meniscus resemble chondrocytes in morphology, whereas cells in the outer periphery are more fibroblastic in appearance and again account for the various stresses found in the different zones of the meniscus.1,38,39,40 Additionally, these cells are multipotent and are capable of trilineage differentiation (chondrogenic, adipogenic, and osteogenic).19 Because of their lack of proximity to each other and to the vascular supply of the meniscus, nutrition is obtained through diffusion.
 FIGURE 4-2 Microscopic view of meniscal collagen transition from peripheral type I collagen (dark) to inner margin type II collagen (light). |
 FIGURE 4-3 Biomechanical properties of the meniscus. A: Cross-sectional fiber patterns of the meniscus. B: Cross-sectional cut of meniscus. Note varying orientations of meniscal fibers. (Modified from Bullough PG, Munuera L, Murphy J, et al. The strength of the menisci of the knee as it relates to their fine structure. J Bone Joint Surg Br. 1970;52:564-567, with permission). |
Vascular Supply
The vascular supply to the medial and lateral menisci originates predominantly from the lateral and medial geniculate vessels (both with inferior and superior branches). Branches from these vessels give rise to a perimeniscal capillary plexus within the synovial and capsular tissue. This plexus is a tree-like network of vessels that supply the peripheral border of the meniscus throughout the synovial and capsular attachments. These vessels are oriented in a predominantly circumferential pattern with radial branches directed toward the center of the joint in a gradient fashion with the central most zone of the meniscus being avascular.41,42 Multiple studies have shown that the depth of peripheral vascular penetration is ˜10% to 30% of the width of the menisci42,43,44,45 (Fig. 4-4). Completing the vascular circuit are endoligamentous vessels arising from the anterior and posterior horns of the menisci forming terminal loops. The remaining portion of the menisci receive their necessary nourishment from the synovial fluid through diffusion and mechanical pumping (joint motion) similar to that of articular cartilage42,46 (Fig. 4-5). With the varying degrees of vascularity throughout the menisci, zones were created for easier classification and ultimately treatment. The “red-red” zone, named for its rich blood supply, is the peripheral third of the meniscus and consists of a high concentration of vascular channels, leading to its high healing potential. The middle third, known as the “red-white” zone, has less predictable healing after injury due to the intermediate density of vascular channels. Injuries in this zone tend to require ancillary procedures such as trephination, synovial abrasion, and a fibrin clot to increase vascularity. The “white-white” zone or inner third of the meniscus is named for its complete avascularity and demonstrates a poor healing potential.44 To provide nutrition to the inner periphery, knee range of motion assists with the passive diffusion of synovial fluid, which is the only method to obtain nutrition to this region of the meniscus47 (Fig. 4-6).
 FIGURE 4-4 Vascularity of the meniscus. Note the avascular inner third and highly vascular peripheral third. |
 FIGURE 4-5 Vascularity of the meniscus. Note the highly vascular periphery, anterior and posterior horns. |
 FIGURE 4-6 Relation of meniscus tear location to healing. (From Wiesel S. Operative Techniques in Orthopedic Surgery. Philadelphia: Wolters Kluwer; 2015.) |
Neurology
The central and medial portion of the tibiofemoral joint (and the meniscal tissue located therein) receives innervation from posterior articular branches of the posterior tibial nerve and terminal branches of the obturator and femoral nerves. The lateral meniscus and knee capsule receive innervation via the recurrent peroneal branch of the common peroneal nerve.48 These fibers follow the blood supply and are found primarily in the peripheral vascular zone covering the outer third of the meniscus as well as the anterior and posterior horns.45 The middle and inner third are innervated to a lesser degree. Three particular mechanoreceptors, Ruffini endings, Pacinian, and Golgi tendon organs, have been identified within the meniscus and may contribute to pain and proprioception during knee motion.49 These neural elements are important in deformation and pressure, tension changes, and neuromuscular inhibition, respectively, which may attribute for pain experienced after meniscal injury.48,50
Biomechanical Properties
Once thought to be vestigial structures of the knee, the menisci serve many roles including secondary stabilization, proprioception, and load sharing of the tibiofemoral joint.51 The mechanism by which the menisci transmit load between the femur and tibia has been studied extensively. Biomechanical studies have demonstrated that approximately 50% to 70% of load acting on the extended knee joint is transmitted through the meniscus. This increases up to 85% in flexion.52 Also, during flexion the articular contact area is observed to decrease in size and shift posteriorly on the tibial plateau, placing more stress across the posterior horns.53 Throughout weight bearing, the femoral condyles provide an axial force, pushing the menisci away from the center of the joint, creating temporary radial meniscal extrusion and compression of the menisci.31 As the menisci become circumferentially displaced, tension among the meniscal fibers increases (hoop stress), thus creating a shock absorption-like effect of the tibiofemoral joint. Keeping the menisci located under the femur and not completely displacing are the strong tibial, meniscofemoral, and capsular attachment sites previously discussed.37
The menisci play an essential role in decreasing contact stresses throughout the knee joint. The biomechanics of how meniscus distributes contact stress have been extensively studied, through studies that examine knees that undergo partial or total meniscectomy. When a simulated total medial meniscectomy is performed, the tibiofemoral contact area decreases by 50% to 70%. This decrease was accompanied by a 100% increase in both peak pressure and pressure gradient at the edges of the contact area.37 Furthermore, this increase expands to 200% to 300% in the lateral compartment after a total lateral meniscectomy and sees a modest 40% to 50% decrease in contact area. With increasing compressive load, the contact stress rose more rapidly and to a significantly higher peak in the absence of menisci.54 Several cadaver studies of meniscectomies observed increased contact pressure of up to 80% to 90%, which increased with progressive larger amounts of meniscal resection.55,56,57 Moreover, resection of 75% of the posterior horn may increase contact stresses similar to those who undergo complete meniscectomy.54 Notably, a partial meniscectomy of the lateral meniscus leads to higher contact stresses due to the convex-convex relationship between the lateral femoral condyle and the lateral tibial plateau.10,11 With partial meniscectomy, the remaining peripheral rim of tissue continues to transmit a portion of the load although it should be noted that even with these meniscal-sparing procedures, contact stresses rise dramatically to upward of 350% with as little as 15% tissue resection58 (Fig. 4-7). Therefore, it is these changes in meniscal tensile properties that allow for more evenly distributed load bearing across the knee joint. These increases in contact pressures may lead to early cartilage wear and may contribute to the early onset of osteoarthritis.
In addition to the circumferential tensile forces seen across the meniscus, the menisci also see shear forces that vary depending on the articulation angle of the joint. As the knee moves through extension into flexion, the femoral condyles translate posteriorly onto the tibia as part of the femoral roll back phenomenon.59,60,61 The varying femoral condyle geometry as it moves through its arc of motion requires that the menisci change shape and slide relatively to the tibia. In extension, the menisci lie anterior-posterior, whereas in flexion, they lie more medial-lateral. Therefore, one of the important biomechanical properties of menisci is the low shear modulus, or modulus of rigidity which allows the surface of menisci to adapt easily to the changing geometry in the joint as it moves through its arc of motion. An increasing density of proteoglycans toward the inner regions of the menisci helps accommodate the changing stress throughout the meniscus.
It is therefore clear that the menisci play an essential role in load transmission. Additionally, the meniscus serves as
a secondary stabilizer of the knee. Although they are not primary stabilizers, they can assist in this role when the ACL’s function as a primary restraint is compromised. When the ACL has been transected, the meniscus aids to resist anterior translation of the tibia.62 This effect is primarily due to the posterior horn of the medial meniscus, which acts as a wedge between the femur and tibia to prevent anterior tibial translation.63,64 Prior data suggest a 58% increase in anterior tibial translation with meniscectomy when tested in ACL-deficient knees.65,66 The lateral meniscus also plays a significant role as a secondary stabilizer of the knee. While its role in sagittal translation is limited (likely due to the increased mobility of the lateral meniscus in this plane), it is much more significant in axial rotation of the knee. In particular, internal tibial rotation dramatically increases in dual ACL- and lateral meniscal-deficient knees. During a pivoting injury resulting in an ACL rupture, the lateral meniscus experiences significant shear forces due to this unstable rotary moment.67 This may explain the increased incidence of lateral meniscus tears in acute ACL injury. Even in the intact knee, the menisci appear to play an important role in rotary stability, providing additional and more subtle control of position and alignment beyond that provided by the primary restraints.68,69 It is therefore clear that the menisci play a key role in knee stability as well as load transmission.
a secondary stabilizer of the knee. Although they are not primary stabilizers, they can assist in this role when the ACL’s function as a primary restraint is compromised. When the ACL has been transected, the meniscus aids to resist anterior translation of the tibia.62 This effect is primarily due to the posterior horn of the medial meniscus, which acts as a wedge between the femur and tibia to prevent anterior tibial translation.63,64 Prior data suggest a 58% increase in anterior tibial translation with meniscectomy when tested in ACL-deficient knees.65,66 The lateral meniscus also plays a significant role as a secondary stabilizer of the knee. While its role in sagittal translation is limited (likely due to the increased mobility of the lateral meniscus in this plane), it is much more significant in axial rotation of the knee. In particular, internal tibial rotation dramatically increases in dual ACL- and lateral meniscal-deficient knees. During a pivoting injury resulting in an ACL rupture, the lateral meniscus experiences significant shear forces due to this unstable rotary moment.67 This may explain the increased incidence of lateral meniscus tears in acute ACL injury. Even in the intact knee, the menisci appear to play an important role in rotary stability, providing additional and more subtle control of position and alignment beyond that provided by the primary restraints.68,69 It is therefore clear that the menisci play a key role in knee stability as well as load transmission.
 FIGURE 4-7 Increased contact stress of the articular cartilage with reactive signal changes within the chondral surface. |
INJURIES
According to the American Academy of Orthopaedic Surgeons, arthroscopic knee surgery accounted for 636,000 cases per year in the United States as of 1999.25,70 Of these cases, treatment of meniscal injuries was the most commonly performed procedure and can account for upward of 20% of all procedures performed at some surgery centers.71 As one of the most common orthopedic injuries regardless of patient age, meniscal injury can greatly range in the degree of physical impairment. While the meniscus demonstrates amazingly resilient properties, injury may still occur if tension, compression, or shear forces exceed the strength of the meniscal matrix. Through improved understanding of etiology through epidemiologic data, we know that risk and prevalence is affected by age, activity level, gender, and patient comorbidities.72,73,74 Men are four times as likely to sustain a meniscal tear. Sports that require cutting and pivoting at various knee flexion angles such as basketball, soccer, gymnastics, football, wrestling, and skiing generate the highest risk for meniscal injury. Furthermore, lateral meniscal tears are less common than medial across all cohorts in an isolated setting.72,74
When clinically assessing for meniscal injury, a thorough and detailed history and physical are key. Clinical symptoms of catching, locking, pain, swelling, buckling, and decreased motion are some of the more common symptoms encountered. Pain is localized to the joint line of the affected side and unlike acute traumatic tears, degenerative tears are not associated with an acute effusion, but more intermittent symptoms and generalized discomfort. Provocative tests such as joint line tenderness to palpation, McMurray, Apley grind, and Thessaly test are used to help improve the physical exam diagnostic accuracy.75 Of these tests, Thessaly test has repeatedly demonstrated in the literature low false-positive and false-negative results with accuracy in the 95% range.76 While isolated meniscal pathology can be accurately diagnosed with history and physical examination alone, plain radiographs and MRI
should still be obtained to rule out other pathology, check mechanical alignment, and confirm the suspected diagnosis. Plain radiographs should include weight-bearing AP, Rosenberg, lateral, and merchant views. If there is suspicion for malalignment of the lower extremity, full-length standing, long cassette films should be obtained. MRI, the diagnostic imaging modality of choice for soft tissue pathology, has greatly improved the ability to diagnose a meniscal injury with an 88% sensitivity and a 94% accuracy.77,78 Normal meniscal structure will uniformly have low signal intensity throughout on both fat-suppressed and fast spin-echo images. If a nonfocal high signal is noted within the meniscal structure but does not extend to the meniscal surface, this is indicative of intrasubstance degeneration or grade I meniscal signal. Grade II is a focal linear high signal that again does not extend to the articular surface. Finally, grade III is a linear high-grade signal that extends to either the superior or inferior meniscal surface.79 In addition, blunting of the free margin of the meniscus is highly indicative of meniscal tear with a displaced fragment. Of particular note, it is also essential to view the meniscus in the sagittal, coronal, and axial planes to evaluate for displaced meniscal fragments in the gutters or intercondylar notch. For example, a displaced bucket-handle medial meniscal tear will take on the appearance of a “double PCL” on sagittal images as the displaced fragment runs in parallel with the native PCL creating a mirror image (Fig. 4-8).
should still be obtained to rule out other pathology, check mechanical alignment, and confirm the suspected diagnosis. Plain radiographs should include weight-bearing AP, Rosenberg, lateral, and merchant views. If there is suspicion for malalignment of the lower extremity, full-length standing, long cassette films should be obtained. MRI, the diagnostic imaging modality of choice for soft tissue pathology, has greatly improved the ability to diagnose a meniscal injury with an 88% sensitivity and a 94% accuracy.77,78 Normal meniscal structure will uniformly have low signal intensity throughout on both fat-suppressed and fast spin-echo images. If a nonfocal high signal is noted within the meniscal structure but does not extend to the meniscal surface, this is indicative of intrasubstance degeneration or grade I meniscal signal. Grade II is a focal linear high signal that again does not extend to the articular surface. Finally, grade III is a linear high-grade signal that extends to either the superior or inferior meniscal surface.79 In addition, blunting of the free margin of the meniscus is highly indicative of meniscal tear with a displaced fragment. Of particular note, it is also essential to view the meniscus in the sagittal, coronal, and axial planes to evaluate for displaced meniscal fragments in the gutters or intercondylar notch. For example, a displaced bucket-handle medial meniscal tear will take on the appearance of a “double PCL” on sagittal images as the displaced fragment runs in parallel with the native PCL creating a mirror image (Fig. 4-8).
With the rise in the aging population, we have also seen an increase in prevalence of asymptomatic meniscal pathology. Previous studies have demonstrated that there is a 5.6% incidence of asymptomatic meniscal tears in a younger patient population (mean age of 35).80 As the population increases, these incidental findings increase as well. At an average age of 65, the prevalence is an astonishing 76%.81 In the setting of concomitant injury, specifically an ACL tear, there is a 57% and 36% prevalence of lateral and medial meniscal tear, respectively. Of these, the lateral meniscus is more commonly identified in acute ACL injuries, whereas medial meniscal injuries are more common with chronic ACL tears.82
 FIGURE 4-8 “Double PCL” sign with the arrow pointing to the displaced medial meniscal bucket-handle tear. |
DEGENERATIVE TEAR
Degenerative meniscal tears are very commonplace and may be attributed to normal aging of the knee. They occur more commonly in older people and in addition to aging, may be related to intrinsic collagen breakdown and “wear and tear” of the knee joint.23,83 Over time, degenerative changes seen in the meniscus include decreased cellular density, mucoid degeneration with disruption of collagen fiber orientation, and the appearance of acellular zones. Oftentimes, degenerative meniscal tears occur in the setting of potential osteoarthritis of the knee.84,85,86,87 In patients with osteoarthritis, 70% to 90% are noted to have concomitant degenerative meniscal pathology.18,23
Degenerative tears are typically horizontal-cleavage or complex tears with frayed, macerated edges. Degenerative tears may be unstable and complex or simple and stable. Cells in the superficial meniscus layer can be hyperplastic, and the collagenous bundles are separated by degenerative mucoid changes. In stable tears, there may be minimal meniscal displacement and patients may be asymptomatic. As a result, degenerative meniscal tears are often noted as incidental findings when advanced imaging of the knee is obtained.23,85
The hallmark of degeneration of the meniscus is loss of proteoglycan and collagen from the meniscus extracellular matrix.18,88,89,90 Two specific classes of degradative enzymes, metalloproteinases (MMPs) and aggrecanases (ADAMTS), are primarily responsible for degradation of meniscal extracellular matrix proteins. As a result, many studies have utilized these two proteins as potential biomarkers for meniscal degeneration.91,92,93 Specifically, elevated levels of MMP-1, MMP-2, MMP-3, and MMP-13 have been associated with meniscal injury and development of osteoarthritis.18
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