5.2.1 Mechanisms of injury
Based on the biomechanical properties of normal ligaments, an understanding of the mechanisms of ligament injury can be gained. However, it must again be emphasized that all ligaments are not identical, and various ligaments are biomechanically adapted to their own unique environment. For instance, the ligamentum nuchae of the neck in animals must be able to allow repetitive cycles of elongation, but still be able to return to its original length (Davidson et al., 1992). This ligament has much greater quantities of elasticfibers than most skeletal ligaments, which are apparently able to protect it against permanent elongation.
On the other hand, as noted in the previous section, many ligaments, if loaded repeti-tively will either deform permanently or fail. At higher loads, all ligaments will either partially or completely fail. Interestingly, it has been shown that the failure strength of so-called normal ligaments actually increases slightly with training and exercise and decreases quite dramatically with long periods of immobilization (Cabaud et al., 1980;
Woo et al., 1982; Thornton et al., 2003).
Ligament injuries can be classified into two main categories: the first is repetitive microtrauma and the second can be called macrotrauma. Repetitive microtrauma causes the failure of a soft-tissue structure secondary to multiple exposures to forces, which are actually well below the normal ultimate tensile strength of that structure when exposed to a single load. Wilson (1996) for example, has suggested that the ultimate tensile stress of the rabbit patellar tendon decreased with increasing cycle number in vitro, supporting the concept that fatigue failures of these structures can occur. Fatigue failure has been shown to result from the propagation of microtears in materials, causing this type of structural failure at a lower-than-normal load. Importantly, a chronic state of inflammation and repair may be established in an attempt to heal microtears in living tissues, potentially leading to pain and disability for the patient (Safran, 1995). It has been hypothesized that if the rate of microtear production and propagation is more rapid than the rate of the repair in vivo, then persisting symptoms and signs of an injury will be manifested. This type of injury is common and well documented in tendon, since these structures tend to carry higher loads in vivo than ligaments (Woo et al., 1994a; Beynnon et al., 1995; Safran, 1995;
Screen et al., 2004). However, it has also been speculated that ligaments can also be injured
by this mechanism. For instance, the medial collateral ligament of the elbow has been diagnosed as one structure that may be damaged as a result of repetitive loading in throwing athletes (Safran, 1995; Cain et al., 2003).
By far the most clinically recognizable ligament injuries result from acute macrotrauma, in which forces are sufficient within a ligament to cause partial or complete rupture of its fibers. These injuries, which are generally known as ‘‘ligament sprains,’’ tend to occur in skeletally mature individuals with strong bone (Hurov, 1986; Matyas et al., 1990; Lam, 1988). Most tend to have well-documented mechanisms of injury and each is based on loads, which must be resisted by a specific ligament. For instance, the lateral collateral ligament of any joint is injured through a varus producing force, whereas the medial collateral ligament will be injured through a valgus producing force. The anterior cruciate ligament of the knee is torn commonly during a quick, turning (twisting) deceleration, producing anterior tibial external rotation (Dehaven, 1990; Olsen et al., 2004).
Ligament sprains have historically been graded according to the severity of a tear: grade 1 is an incomplete tear with no, or minimal, clinical laxity. This type of tear often involves only part of the ligament tearing (e.g., only one of its so-called bands). The band of the ligament that was tight when the joint was stressed will obviously tearfirst. Thus, the joint will only be seen to be unstable in that specific joint position. Note: a little known ‘‘trick’’ of physical examination is to test joint stability in multiple joint positions—until the position that it was in when injured is reached, where‘‘latent (minor) instability’’ may be revealed.
A grade 2 ligament sprain is also an incomplete tear with more obvious joint laxity, but an attainable ‘‘end-point’’ on physical examination; and grade 3 is a complete ligament tear resulting in significant joint laxity. Grade 2, and especially grade 3 tears, often involve more than one ligamentous structure, since the forces often progress through other ligamentous restraints.
Ligaments normally work in concert with each other and with other joint stabilizers to maintain stability throughout the range of motion of a joint. Therefore, after a particular ligament is injured, other joint stabilizers must assume the load that it was carrying (Frank et al., 1985). This redistribution of loads has considerable implications to subse-quent remodeling and adaptation or to failure of the other joint structures that assume these loads.
5.2.2 Healing response
Just as the morphology and biomechanical properties of skeletal ligaments differ signifi-cantly, so do their responses to injury (Frank et al., 1983). The ligaments of the knee have been studied most extensively, and it has been well documented that the functional healing potential of the medial collateral ligament exceeds that of the anterior cruciate ligament (O’Donoghue et al., 1971; Frank et al., 1983; Inoue et al., 1987; Spindler et al., 2006). Many hypotheses have been postulated to explain these different healing potentials. These include differences in lattices to grow on, intrinsic ligamentfibroblastic response to injury, mechanical environment, intraarticular versus extraarticular environment (synovial fluid effects), blood supply, and inflammatory response. As of 2007, it appears that a combin-ation of these factors define the relative failure of unaided cruciate healing versus that of collateral healing.
The actual phases of ligament healing are analogous to healing in other connective tissues, such as the skin (Frank et al., 1983; Kondo, 2007). Specifically, ligaments generally appear to attempt to heal through scar-tissue production; scar formation is best explained by examining it in three specific phases: bleeding and inflammation, proliferation, and remodeling.
5.2.3 Bleeding and inflammation
When ligaments tear, there is immediate local pain (due to painfibers within the ligament) and bleeding (due to tearing blood vessels in and around the ligament). As with bleeding in any other injured structure, a rapid inflammatory response is initiated. A platelet and fibrin clot is produced, and a complex cascade of cytokines and growth factors are released, which promote and direct the inflammatory response. Local blood vessels dilate, acute inflammatory cells infiltrate, and fibroblastic scar cells begin to appear. This first phase of ligament healing lasts for hours to a few days.
5.2.4 Scar proliferation
The second phase of ligament healing involves the production of scar matrix by prolifer-ation of scarfibroblasts (Akeson et al., 1984; Broughton et al., 2006). The source of these cells is controversial; however, they are likely to be a combination of localfibroblasts and differentiating mesenchymal cells from the vasculature. Macrophages and other inflam-matory cells simultaneously remove damaged ligament, clot, and other cellular debris in an attempt to leave only the dense scar matrix. Although gaps may not befilled by scar in some cases (e.g., anterior cruciate ligament [ACL] of knee) the gap injury in most extra-articular ligaments probably does not becomefilled with a disorganized scar matrix within days (Figure 5.5). Neovascular ingrowth is then seen. This new matrix then rapidly increases in mass, and becomes less viscous and more elastic as the inflammation decreases and the scar matures over the next few weeks of healing. By 6 weeks most gaps are bridged and filled by new scar. This has prompted people in the distant past to conclude that
‘‘healing is complete by 6 weeks,’’ but that is not true.
5.2.5 Scar remodeling
The third and final phase of ligament healing is matrix remodeling. Once bridging has occurred, the scar matrix begins to contract, becomes less viscous, and becomes both denser and better organized. This process takes place over months to years. Histologic evidence reveals that biomechanical flaws within the scar matrix (debris, fat cells, loose matrix, hypercellular areas, and areas with matrix) are graduallyfilled in with collagenous matrix. This progressive removal of relative flaws has been shown to correlate with increased biomechanical strength (Shrive et al., 1995). Collagenfibers are also reorganized
Normal MCL Scar MCL
Figure 5.5 Scanning electron microscopic appearance of a normal medial collateral ligament (MCL) versus a 3 week MCL scar.
to become less random, and more aligned to resist tensile forces (Figure 5.6). Interestingly, however, normal crimp is never restored. In fact, it has also been shown that even after years of remodeling, ligament scar matrix remains different to normal ligament. The specifics of these differences have been well documented elsewhere (Frank et al., 1983;
Chimich et al., 1991).
Importantly, it has been shown in animal models of collateral ligament injury that even after one year of healing, the ligament is not normal histologically, biomechanically, or materially (Frank et al., 1983; Majima et al., 2006). Although the structural tensile strength of a rabbit or canine medial collateral ligament (MCL) at one year, for example, can reach nearly normal values (80%–90%) by virtue of being large, if corrected for its size, its material properties reach only about 30%–55% of that of a normal ligament (Woo et al., 1987b; Chimich et al., 1991).