Cranial Cruciate Ligament and Meniscal Injuries in Dogs

Cranial cruciate ligament (CCL) rupture is one of the most common causes of lameness in adult dogs. The CCL plays a crucial role in limb function by maintaining stability of the stifle joint throughout the range of motion, thus injury to the CCL will result in joint instability and predispose the joint to degenerative changes. In dogs, the majority of CCL ruptures occurs under normal activity, likely owing to structural deterioration of the ligament and not because of a traumatic injury. Rupture of the CCL owing to degeneration can manifest acutely even in young dogs and eventually is often bilateral. Osteoarthritis, meniscal injury, and persistent lameness commonly occur with CCL rupture. Therefore, the debilitating pathologic condition related to CCL rupture is often referred to as "cruciate disease". Cranial cruciate ligament rupture is particularly common in large and giant breed dogs; however, any breed, size, or age of dog may be affected. Although clinical features and treatment options have been well discussed in the veterinary literature, the disease mechanisms for CCL rupture are poorly understood.

Cranial Cruciate Ligament

Anatomy

The cranial cruciate ligament is a dynamic structure and its anatomy and spatial arrangement are directly related to its function as a constraint of joint motion [1]. The CCL attaches proximally to the caudomedial part of the lateral condyle of the femur, within the intercondylar fossa of the femur, and courses cranially, medially, and distally across the joint as it passes from femur to tibia, and turns on itself in an outward lateral spiral of approximately 90° (Fig. 105-1). The CCL extends distally to attach to the cranial intercondylar area of the tibia, beneath the transverse intermeniscal ligament. The caudal cruciate ligament crosses the CCL medially in the middle of the joint. The CCL fans out proximally and distally at its attachments and is narrowest in the middle [2].

Figure 105-1. Normal anatomy of the canine stifle in flexion. A. long digital extensor tendon, B..caudal cruciate ligament, C. craniomedial band of CCL, D. caudolateral band of CCL, E. intermeniscal transverse ligament, F. distal part of tibial attachment of CCL.

The cranial cruciate ligament is a collection of parallel and twisted collagenous bundles, or fascicles (Fig. 105-1). These fascicles have been divided into two groups: the relatively thin craniomedial band that is rotated into an outward spiral (craniomedial spiral), and the caudolateral band that forms the bulk of the CCL (caudolateral bulk) (Fig. 105-1). The craniomedial band arises more proximally in the intercondylar fossa of the femur and inserts more cranially in the cranial intercondylar area of the tibia [1,2]. The caudolateral band is shorter and straighter.

When the stifle is extended, both craniomedial and caudolateral bands are tight, and when the stifle is flexed, the craniomedial band is tight and caudolateral band is relatively lax. However, the CCL is actually a continuum of collagenous fascicles, and a different portion of the CCL is taut throughout the range of motion; therefore, this grouping scheme may oversimplify the structure and function of the CCL [1].

Mechanics

Stifle mechanics are governed by muscular force and constrained by ligaments and joint capsule as well as by the geometry of the menisci and condyles [1]. The stifle is classified as a hinge joint with a combined motion primarily in two planes. Flexion and extension take place about the transverse axis, whereas rotary movement of the tibia on the femur occurs about the longitudinal axis. Slight craniocaudal and mediolateral movements also occur. The rotary motion is controlled by the condylar geometry and ligamentous constraints; internal rotation of the tibia is mainly limited by the anatomic relationship of cranial and caudal cruciate ligaments. The primary function of the CCL is to prevent cranial displacement of the tibia on the femur (cranial drawer), internal rotation of the tibia, and hyperextension of the stifle. Because the craniomedial band of the CCL is taut in both flexion and extension, it provides the primary check against cranial drawer motion, and because the entire CCL is taut in extension, it serves as the primary check against hyperextension of the stifle [1]. Together the cranial and caudal cruciate ligaments are responsible for craniocaudal stability of the stifle; the CCL prevents cranial drawer motion, and the caudal cruciate ligament prevents caudal displacement of the tibia on the femur (caudal drawer motion).

It has been suggested that the cranial cruciate ligament also functions to resist a force called "cranial tibial thrust" [3]. Cranial tibial thrust is hypothesized to occur during weight bearing by compression of the femoral condyles against the tibial plateau. The magnitude of cranial tibial thrust is dependent on both the degree of compression during weight bearing and the slope of the tibial plateau. The amount of tibial compression is variable and depends on the size, muscular force, and activity level of the dog. The tibial plateau slopes caudodistally and varies among dogs owing to anatomic and conformational differences. The CCL, together with the caudal horn of the medial meniscus and flexor muscle groups of the stifle, balances this force, preventing cranial translation of the tibia.

Histology

The cranial cruciate ligament is a complex structure consisting of an extracellular matrix and a diverse population of cells. The CCL has two histologically distinct regions: an epiligamentous region, composed of cellular synovial intima and loose connective tissue, and a core region, which is the major axial tissue component composed of collagen fiber bundles [4,5]. The collagen fibers are primarily composed of type I collagen and a smaller amount of type III collagen. Bundles of collagen fibers are longitudinally oriented, mostly running parallel to one another. Normal CCL collagen fibers have a recurrent undulating wave or crimped structure. During tensile loading of the ligament’s collagen fibers, the crimp is lost before the fiber ruptures. Crimping is a distinct structural feature of organized collagen fibers in dense connective tissue and is an important determinant of the biomechanical properties of the tissue. From a biomechanical standpoint, the loss of crimping reflects the viscoelastic properties of the cruciate ligament and corresponds to the "toe region" on a load/deformation curve.

The predominant cell type in the CCL is the fibroblast. Ligament fibroblasts are arranged in long parallel rows between collagenous fiber bundles. Three different types of fibroblasts have been described: fusiform or spindle-shaped, ovoid, and spheroid [5]. The cytoplasm of fusiform fibroblasts is intimately attached to the extracellular collagen and follows the crimped waveform of the fibers. Ovoid and spheroid fibroblasts are situated in the loose connective tissue between collagen fibers. It is currently unclear whether these cells represent differing metabolic states of the same cells or whether they are distinctly different fibroblasts.

The CCL has a relatively tenuous microvasculature, which arises predominantly from the infrapatellar fat pad and periligamentous tissue, as opposed to the proximal and distal attachment sites [1]. The CCL receives its blood supply from branches of the middle genicular artery, which forms a vascular synovial envelope around the ligament. The innervation of the CCL regulates vasomotor tone and proprioception. The greatest density of mechanoreceptors is found in the proximal region of the CCL. These may function to send impulses during flexion/extension and rotation. The role of these receptors in proprioception is unknown.

Histopathology

The cranial cruciate ligament appears to experience chronic and irreversible degeneration with aging [4]. Idiopathic degeneration is a common histologic finding of the intact CCL, despite its grossly normal appearance. Degenerative changes are generally characterized by a decreased number of normal ligament fibroblasts, chondroid metaplasia of ligament fibroblasts, and loss of the normal fibrous architecture of the extracellular matrix [4,5]. These changes result in a partial transformation of ligamentous tissue into fibrocartilage (Fig. 105-2). More severe changes such as hyalinization, mineralization, and cloning of chondrocyte-like cells can also occur; however, inflammatory or reparative responses are not observed. The degenerative changes can occur at a young age, particularly in large dogs, and progresses with aging. The severity of changes is usually similar in both stifle joints and affects the mechanical properties of the CCL.

Figure 105-2. Histology of ruptured CCL demonstrating loss of fibrous structure and decreased number of ligament fibroblast with chondroid metaplasia. Note the cloning of chondrocyte-like cells (center and top right corner) - (bar = 100 μm).

The interior "core region" of the CCL deteriorates earlier than the surface epiligamentous region, and the midportion of the CCL deteriorates earlier than areas close to bony attachments [4]. These findings may be related to the hypovascularity and ischemic environment of the core region of CCL. Histopathologic changes of CCL degeneration are more prominent in larger dogs weighing more than 15 kg; the onset of the degenerative changes occurs at an earlier age in these large dogs. Increasing body size may also exacerbate the rate and severity of the degenerative process.

Pathogenesis and Epidemiology of CCL Rupture

Exact causes and disease mechanisms of CCL ruptures are undefined and remain controversial; therefore, cruciate disease has been referred to as the "enigma of the canine stifle" [1]. Although acute CCL rupture does occur with trauma, it is generally accepted that the majority of CCL lesions are the result of chronic degenerative changes in the ligaments themselves. Rupture of the CCL associated with major traumatic injury is usually unilateral and often involves multiple ligamentous injuries of the stifle and can lead to joint luxation. Isolated traumatic injury to the CCL is rare in dogs, is seen most often in puppies, and typically is associated with avulsion of the ligament at the tibial attachment site distally. In contrast, most pathologic cranial cruciate ligament ruptures are bilateral, midsubstance, incomplete or complete tears. Evidence is conflicting as to whether the degenerative changes seen in CCL are primary or secondary or a combination of multiple factors. Several risk factors have been proposed for CCL rupture; Table 105-1 summarizes the findings of recent epidemiologic studies [6-10].

Rupture of the CCL has significant association with breed, body weight, and neutering. Other factors, such as aging, gender, conformational variation, medial patellar luxation, inactivity, and obesity have also been associated with CCL rupture. Although the effect of the tibial plateau angle (TPA) on cruciate ligament stresses has been recognized in people, the effect of TPA on CCL rupture in dogs has yet to be established. The risk of CCL rupture is higher in certain breeds, such as the Rottweiler, Labrador and Chesapeake Bay retrievers, Newfoundland, Akita, Neapolitan mastiff, Saint Bernard, and Staffordshire bull terrier. Dog phenotype may have a significant effect on the structural properties of the CCL, as the CCL of certain breeds (e.g., Rottweiler) appears more vulnerable to mechanical overload. Material properties of the CCL from Rottweilers are inferior to those of rarely affected breed dogs (greyhounds), although craniocaudal laxity is similar in both breeds throughout the range of motion. Commonly affected breeds tend to have abnormal posture such as straight stifle, genu varum (bow-leg), or genu valgum (knock-knee). Larger dogs weighing more than 22 kg are at greater risk of cruciate disease and tend to develop CCL rupture at younger ages. It remains unclear whether obesity is a risk factor for the disease independent of the dog’s size. Neutering also increases the risk for cruciate rupture, particularly in female dogs, although the cause of this effect is not understood. The effect of hormonal status and endocrinopathy on CCL weakness and rupture are being investigated. The prevalence of CCL rupture increases with age and reaches a peak incidence at around 7 years.

The mechanism of traumatic CCL rupture can be related to its function as a constraint for joint motion. As stated above, the CCL serves to prevent cranial displacement of the tibia on the femur, to limit internal rotation of the tibia on the femur, and to prevent hyperextension of the stifle. Excessive forces during extremes of these motions can result in damage to the CCL. Common mechanisms of CCL injuries include sudden rotation of the stifle with the joint in 20° to 50° of the flexion, which can occur when the dog makes a sudden outward turn on the weight bearing limb, and hyperextension of the stifle, which can occur when a dog steps into a hole while running. Direct trauma to the stifle in any direction may cause damage to the CCL as well as to other joint structures.

Chronic degeneration and progressive weakening of the CCL appear to make it more susceptible to damage from minimal trauma, thereby predisposing the CCL to rupture. Despite extensive efforts in epidemiologic and clinical investigation, instigating causes of CCL degeneration and structural deterioration are not fully understood. Aging, hypovascularity of the CCL, abnormal conformation of the stifle, immune-mediated joint disease, and inflammatory joint disease have been proposed as contributing causes of CCL degeneration and rupture [11-13]. The degenerative changes in cellular and matrix components that develop in a ruptured CCL may result from the effects of remodeling and adaptation to various factors, such as ischemia, mechanical loading, and ligament microinjury.

Idiopathic degeneration of the CCL appears to begin within the central core portion and may be related to the ischemic nature of the tissue, complex mechanical environment (tension, compression, and shear) within the CCL, or both.

In degenerate ligament, the numbers of typical fibroblasts (i.e., fusiform and ovoid cells) are decreased, and the numbers of cells exhibiting chondroid transformation (i.e., spheroid cells) are increased [5]. These cellular changes are associated with extensive disruption of the ligamentous matrix, transforming the ligament into cartilage-like structure. This type of tissue transformation is often attributed to altered oxygenation status and mechanical environment. Inadequate blood supply of the central region of the CCL may be exacerbated by the twisting of the cruciate ligaments on themselves during flexion. This, in turn, may reduce blood flow and may account for the CCL transformation. For ligament fibroblasts to persist under increasingly ischemic conditions, these cells may be undergoing metaplasia to form chondrocytes, which can survive by using anaerobic metabolic pathway. The complex mechanical environment within the CCL, which includes compression and shear, as opposed to simple tension, can also contribute to the tissue transformation. Cartilage-like tissue is more vulnerable to disruption under normal tensile forces; therefore, the degeneration with fibrocartilaginous transformation may predispose CCL to pathologic rupture. However, areas of fibrocartilage are observed in grossly normal CCL in rarely affected breeds (greyhounds), which may represent successful physiologic adaptation to ischemic environment [11]. It is currently unclear whether CCL degeneration and transformation into fibrocartilage constitute a pathognomonic condition causing CCL rupture.

Conformational variation such as straight stifle, narrow intercondylar notch, steep tibial plateau slope, MPL, valgus and varus deformities of the stifle, and repeated stress and microinjury can result in progressive degenerative joint disease and CCL rupture. These changes are frequently bilateral and have been referred to as "postural arthrosis". Postural abnormalities may also be a result of other orthopedic conditions. Straight stifle and narrow intercondylar notch, together with excessive rotation of the tibia and extension of the stifle, may cause constant impingement and abnormal compression of CCL against the cranial aspect of the intercondylar notch. Medial patellar luxation, genu varum, and excessive internal rotation of the tibia, or a steep tibial plateau slope may cause increased stress, micro injury, and degeneration of the CCL. These conformational variations and abnormalities may predispose the CCL to rupture. Although anatomic differences in the shape of the proximal tibia have been documented in dogs with cruciate disease, their role in cruciate disease is unclear because many dogs with a steep tibial plateau angle do not develop cruciate disease. Indeed, although the mean TPA in dogs varies between 23° and 25°, a wide range of TPA has been reported (13° to 34°) in normal dogs. Furthermore, because the functional TPA is approximately parallel to the ground in most dogs, the true effect of TPA on CCL stresses in vivo is unknown. Finally, although the correlation between CCL rupture and pathologic increases in TPA (> 55°), possibly secondary to gross plate injuries, seems established, the association between TPA and CCL rupture in a normal canine population remains controversial. Muscular force, body size, obesity, rapid weight gain, relative inactivity, and exercise can also modify the amount of stress sustained by the CCL. The beneficial effect of activity on ligament strength in dogs is well documented, although the roles of activity and inactivity in CCL rupture are not well understood.

Inflammatory disease may be involved in the initiation of CCL rupture [13,14]. Cruciate disease in dogs is often associated with infiltration of leukocytes into the synovial membrane of the stifle joint and the development of inflammatory changes in the synovial fluid. Anti-collagen antibodies, immune complex, and rheumatoid factors have been identified in synovial fluid of the joint with CCL rupture; therefore, involvement of immune-mediated disease has been proposed as a cause of CCL degeneration. However, anti-collagen antibodies are not likely the major factor of CCL degeneration and rupture, because the increase of anti-collagen antibodies is not specific for the type of joint disorder. More recently, collagenolytic enzyme expression has been found in the ruptured CCL and synovial fluid, and synovial macrophage-like cells that produce matrix-degrading enzymes have been identified. These findings suggest that inflammatory arthropathy predisposes the CCL to rupture, by release of proteolytic enzymes during inflammatory process. Release of collagenolytic proteases from the synovium into the stifle synovial fluid can significantly degrade the structural properties of the CCL and increase the likelihood of a pathologic midsubstance rupture. However, these inflammatory changes could be a secondary phenomenon, in response to the tissue damage during CCL rupture and osteoarthritis.

Genetic and breed predisposition have recently been implicated in the pathogenesis of CCL rupture [15,16]. Early studies suggest that 1) collagen turnover may be increased in dogs predisposed to CCL rupture (Labrador retrievers) compared with dogs not predisposed to CCL rupture (greyhounds); 2) collagen fibril of greyhounds are larger than those of Labrador retrievers; and 3) craniocaudal joint laxity is greater in Labrador retrievers compared with greyhounds. Whether cranial cruciate ligament weakness could be part of generalized collagen abnormality remains uncertain because weakness in other ligaments and joints is not commonly seen in dogs with CCL rupture. These differences may be influenced by genetics and may account for the differential predisposition of the two breeds to CCL rupture. Further studies have revealed the high incidence of CCL rupture in Newfoundlands (22%) and suggested that CCL rupture has a potential recessive mode of inheritance with 51% penetrance in a population of Newfoundlands. A genetic association was also determined between CCL rupture status and a large number of statistically significant microsatellite markers on canine chromosomes 3, 10 and 23 in this population.

Cruciate Ligament Pathology

Pathology of CCL disease appears to involve a gradual degeneration of the CCL itself, inflammatory disease in the stifle joint, partial rupture, progressive rupturing, complete rupture, and secondary disease such as progressive osteoarthritis and meniscal injury. Partial ruptures can occur at any part of the CCL, although it has been suggested that the relatively thinner craniomedial band of the CCL is more susceptible to rupture. Complete ruptures appear to occur near the tibial attachment, although location of the rupture is often indeterminable.

An initial pathology with slight weakening or stretching of the CCL may not cause lameness, but can produce mild instability within the joint and, therefore, initiate the osteoarthritis process. Dogs with early cruciate disease (i.e., minor partial CCL rupture) may have little or no palpable instability, but they are often presented with lameness, effusion of the stifle joint, and mild osteoarthritis. Major partial or complete CCL ruptures produce marked instability of the stifle joint, resulting in pain, lameness, and progressive degenerative changes within the joint. Clinical observations have demonstrated that these changes consist of periarticular osteophyte formation, capsular thickening, and meniscal degeneration. As these changes progress, the joints become less unstable. Advanced or end-stage cruciate disease may have little palpable stifle instability because of extensive periarticular fibrosis.

After a partial or complete CCL rupture, some degree of tissue repair responses arise in the periligamentous region of the ligament. Distinct phases of tissue repair, including an inflammatory phase, a periligamentous repair phase, a proliferative phase, and a remodeling phase, occur after rupture of the anterior cruciate ligament in humans. Whether similar phases exist in dogs is unknown. Expansion of the volume of the periligamentous tissue does occur in the dog during a repair phase that lasts many weeks; however, a bridging scar does not form in the rupture site. Eventually, synovial tissue covers the ruptured ends of the CCL. The extracellular matrix of ruptured CCL has an increased turnover indicated by increased collagen and glycosaminoglycan synthesis, and increased levels of proteolytic enzymes. This response may represent a degrading and remodeling phase of the CCL after rupture.

Rupture of the CCL causes various degrees of inflammation in the stifle. The inflammatory changes within synovium are variable even within the same joint. Plasma cells, lymphocytes, and macrophages are commonly seen in the synovium, although the infiltrate is not noticeable in some cases. Although partial CCL rupture has been associated with moderate synovial fluid inflammatory changes, synovial fluid analysis in dogs with CCL rupture generally shows a non-inflammatory process. This suggests that CCL rupture is a progressive condition with an early inflammatory component. Several studies have investigated osteoarthritic parameters associated with CCL rupture [17]. Proinflammatory factors, cytokines, nitric oxide, degradation products of matrix, epitopes of cartilage matrix, and degrading enzymes have been shown to increase with osteoarthritis in the stifle with CCL rupture; however, no specific marker for CCL rupture is known.

Meniscal Injury

Pathophysiology

Primary lesions of the meniscus are rare in dogs, however meniscal injuries secondary to rupture of the cruciate or collateral ligaments are common. Most frequently the medial meniscus is affected following cranial cruciate ligament rupture. Damage to the menisci can be either acute or degenerative and usually involves the caudal and medial portions of the medial meniscus [18]. A general understanding of the anatomy and biomechanics of the menisci is important in understanding the pathophysiology of injury.

Anatomy

Each stifle contains a medial and lateral meniscus, which are C-shaped fibrocartilaginous disks interposed between the articulating surfaces of the femur and tibia. In cross section, menisci are wedge shaped with a thin, concave central edge and a thick periphery. The lateral meniscus forms a slightly greater arc and is more concave than the medial meniscus, corresponding to the articular surfaces of the femur and tibia. The menisci are anchored to the tibia and femur via five meniscal ligaments and to each other by the intermeniscal ligament (Fig. 105-3). The lateral and medial menisci are each firmly anchored to the tibia by a cranial and caudal meniscotibial ligament. The caudal horn of the lateral meniscus is also attached to the lateral aspect of the medial femoral condyle by the meniscofemoral ligament. The medial meniscus is not directly linked to the femur, however. Because of extensive fibrous attachments to the joint capsule and medial collateral ligament, it is intimately attached to the tibia. In contrast, the lateral meniscus is more mobile in part because of the popliteal hiatus (imprint of the popliteal tendon and bursa on the lateral edge of the lateral meniscus) and subsequent lack of peripheral connection with the lateral joint capsule and/or collateral ligament. The intermeniscal ligament lies just cranial to the tibial attachment of the cranial cruciate ligament and joins together the cranial portions of the lateral and medial meniscus [19,20].

Figure 105-3. Drawing of the dorsal aspect of the tibia showing the menisci and their attachments.

The meniscus is a fibrocartilage that is composed of 60 to 70% water. Collagen accounts for 60 to 70% of the dry weight (15-25% wet weight), with type I collagen predominating (> 90%). Type II collagen, proteoglycans, matrix glycoproteins and small amounts of elastin make up the rest of the dry weight [21]. The articulating surface of the meniscus is composed of fine fibrils arranged in a random mesh-like woven matrix. This random distribution is effective against shear stresses. Immediately below the meniscal surface, large collagen fiber bundles are arranged circumferentially, which optimizes meniscal resistance against hoop stresses. Finally, smaller radially oriented fibers are found throughout the meniscal tissue, tying the large circumferential bundles together. This fibrillar orientation provides the structure to the meniscus and predominates throughout the peripheral two thirds of the tissue. In contrast, the inner third of the region resembles hyaline cartilage in that it contains smaller collagen fibers arranged in a more random pattern [22]. Unlike the meniscal body, which is relatively avascular, the meniscal horns have an abundant blood supply, which arises from branches of the medial and lateral genicular arteries. Further branching supplies the joint capsule, which provides vessels to the periphery of the meniscus. However, vessels penetrate the menisci for only 10 to 25% of their width, the remainder of the meniscus being totally avascular [21,23]. The clinical relevance of this vascular distribution has led to the recognition of three zones with decreasing healing potential, namely - from the periphery to the center - the red, red-white, and white zones [23]. Owing to the meager blood supply, meniscal injuries occurring axial to the peripheral rim rarely heal. In addition, a layer of vascular synovial tissue, apparently continuous with the sheath that surrounds the cranial cruciate ligament, covers the cranial and caudal horn attachments of both menisci. The caudolateral portion of the lateral meniscus, adjacent to the popliteal tendon and the inner aspects of both menisci, lacks vessels and relies on diffusion of synovial fluid for nutrition. The innervation of the menisci follows the vascularization pattern, with the meniscal horns being more richly innervated with mechanoreceptors and free nerve endings than the body of the menisci.

Function

The menisci are thought to participate in four main functions: namely shock absorption, joint stability, sensation, and hydrostatic lubrication [19,20]. The menisci distribute approximately 65% of the joint force through load transmission (shock absorption). The circumferential arrangement of the collagen fibers and the strong ligamentous attachments of the menisci help convert compressive loads across the joint into hoop stresses, thus absorbing most of the energy generated during weight bearing. The viscoelastic behavior of the meniscal tissue further contributes to the shock absorption function of the menisci, thereby sparing the articular cartilage of the tibia and femur from excessive stresses. The menisci also act as elastic movable washers and contribute to joint stability by improving congruity between the femur and tibia. Because of their firm attachment to the tibia and/or femur, the menisci further contribute to limiting the relative motion of the femur with regard to the tibia. The sensory function of the meniscus is achieved via an abundant nerve supply to its periphery. In addition, because mechanoreceptors located in the cranial and caudal horns can detect pressure changes within the joint, it is believed that the menisci can receive and transmit proprioceptive information. Additionally, due to a feedback mechanism to myotactic receptors, the menisci allow specific muscle actions to occur in response to acute changes in intra-articular stresses, which in turn contribute to the protection of intra-articular structures during extreme range of motion. The menisci are also thought to provide hydrostatic lubrication of the articular cartilage. It has been shown that following meniscectomy the intra-articular friction coefficient is increased by up to 20%. As a minor function, the menisci act as space fillers, preventing synovial entrapment between the weight-bearing articular surfaces of the femur and tibia [19].

Mechanism of Meniscal Injury

The stifle functions as a hinge joint with axial rotation of the tibia on the femur through the range of motion. During range of motion, the displacement of the menisci within the joint is dictated in part by their specific attachment to the tibial plateau and (for the lateral meniscus) to the femur. During extension, the menisci slide cranially on the tibial plateau then return to a more caudal position as the stifle flexes. With extreme flexion the excursion of the medial meniscus is such that the caudal horn may protrude beyond the caudal aspect of the tibial plateau. In such cases, the caudal horn of the medial meniscus may be acutely crushed between the femoral condyle and the tibial plateau. Because the lateral meniscus is more mobile (less firmly attached to the tibia), the lateral meniscus undergoes considerably more displacement than does the medial meniscus during range of motion.

Excessive compressive and/or shear stresses, resulting from stifle instability, whether acute or chronic, lead to meniscal degeneration [24,25]. The degenerative process is associated with structural alteration of the meniscal tissue such as mucoid degeneration of the cartilage matrix, fragmentation of the collagen bundles, and fibrillation. This alteration in fibrocartilage microstructure makes the menisci more vulnerable to injury and tear after minimal trauma. In chronic cases, calcification within the fibrocartilage can also occur secondary to degenerative change. In addition, modification of the biochemical composition of the meniscal tissue characterized by an increase in water content and a decrease in collagen content has also been reported and seems to correlate with the degradation of its biomechanical properties, including a decrease in compressive stiffness to ~ 60% of normal. It has been suggested that the extent of theses changes correlates with the loading of the meniscal tissue and, therefore, varies between the cranial, central, and caudal regions of the meniscus. Interestingly, shifts in weight bearing following CCL rupture also affect the mechanical properties on the contralateral normal medial meniscus. As the weight-bearing forces increase on the sound limb, so do loads to which the healthy meniscus is subjected. Adaptative remodeling is reflected by an increased compressive stiffness of the normal meniscus.

Most commonly, meniscal injuries occur secondary to stifle instability resulting from CCL rupture, with injury to the medial meniscus being reported in at least 50% of cases [24-26]. Although acute meniscal injuries can happen, delayed lesions occurring weeks to months after cruciate rupture are far more typical. Instability in the cruciate-deficient stifle results in a combination of excessive internal tibial rotation and cranial tibial translation. This combined motion induces disproportionately high compressive and shear stresses on the relatively immobile medial meniscus. With cranial displacement of the tibia/medial meniscus complex, the concave inner border of the meniscus may be stretched to the point of creating a transverse tear. It has been estimated that normal meniscal tissue fails at strain levels exceeding 5% and that degenerative menisci could likely tear at lower strain levels. Eventually, shear stresses generated at the surface of the meniscus by the repetitive sliding of the tibia are transmitted to the meniscal stroma, creating a deep horizontal cleavage. Ultimately, this pathologic cleavage plane propagates toward either surface of the meniscus, creating a grossly visible longitudinal tear (Fig. 105-4). The term bucket-handle tear has been used to describe the displaced medial portion of a longitudinal tear. Alternatively, the caudal horn of the medial meniscus may become crushed or pushed cranially between the medial femoral and tibial condyles as cranial translation of the tibia occurs during weight bearing. In such cases, the caudal meniscotibial ligament may be severed, which in turn allows the caudal horn of the medial meniscus to move freely between the caudal and cranial compartments of the joint. In some cases, the caudal meniscotibial ligament remains intact and the caudal horn alone is damaged. The alternate motion of the caudal horn is initially associated with a characteristic clicking or snapping sound when the dog is walking or the joint is manipulated. Eventually, the degenerate horn may become fibrotic and even calcified and may interfere with complete range of motion.

Figure 105-4. Arthroscopic views of a normal medial meniscus immediately following experimental transection of the cranial cruciate ligament (left) and 8 months postoperatively (right). The normal meniscus is viewed from the tibial plateau eminences toward the medial aspect of the joint (along the transverse plane). The torn meniscus is viewed in a cranial to caudal direction (along the sagittal plane). Note the circumferential tear at the limit of the "red-white" zone (arrow heads). Also note the extent of the synovial reaction compared with a normal stifle. MFC: medial femoral condyle, CaH: caudal horn, MTL: meniscotibial ligament, MTP, medial tibial plateau, CaCL: caudal cruciate ligament, ICN: intercondylar notch, MM: medial meniscus.

In contrast, damage to the lateral meniscus has seldom been reported. However, with the increased popularity of arthroscopic stifle exploration, lateral meniscal lesions are being recognized [26]. In a retrospective evaluation of 100 cruciate-deficient stifles, 77% of the joints had gross structural alteration of the lateral meniscal structure, generally observed as a series of small radial tears of the cranial horn (Fig. 105-5). The clinical significance of these minor tears is unknown. Because of the lack of connection between the lateral meniscus and the joint capsule or collateral ligament, severe lesions of the lateral meniscus seem unlikely and have yet to be reported. Isolated injuries to either meniscus, in the absence of a cruciate rupture, are rare although theoretically possible following sudden compressive force directly on the meniscus, such as jumping from a height and landing with the stifle in full extension.

Figure 105-5. Arthroscopic view of normal lateral menisci (A & C) and 8 months following experimental transection of the CCL (B & D). Note (B) the series of small radial tears at the free edge of the meniscus (arrow heads) and the damage to the articular cartilage of the femoral condyle (chondromalacia*) and of the tibial plateau (fibrillation °). Also note (D) the presence of a cartilaginous nodule (open arrow) at the level of the caudal horn and the severe synovial proliferation (#). CaH: caudal horn, LM, lateral meniscus.

Menisectomy

The relative benefit of partial versus total removal of either meniscus remains controversial because both result in gross and microscopic degenerative changes of the articular surfaces of the femur and tibia [27-29]. Although a partial meniscectomy may have a protective effect on articular surfaces, it has been associated with limited tissue regeneration, particularly if the resected segment is entirely located within the avascular center (white zone) of the meniscus. Furthermore, experimental studies in humans have demonstrated that, after partial meniscectomy, the femorotibial articular contact area decreased by approximately 10%, while peak local contact stresses increased by 65%. Conversely, total meniscectomy lead to a 75% decrease in contact area and an approximately 235% increase in peak local contact stresses [25]. The reported advantages of a complete meniscectomy, however, include a more extensive regeneration of the resected meniscus if the excision line runs through the peripheral vascularized (red zone) portion of the meniscal tissue. In such cases, the regenerated meniscal tissue, derived from the synovial membrane, is generally formed within 3 to 6 months. Unfortunately, the regeneration process is somewhat inconsistent and the regenerated fibrocartilage is ineffective in preventing the development of secondary osteoarthritis, which will occur in almost 100% of cases.