Injury and Repair

Damage to a ligament is technically termed a sprain.

Sprains are graded according to the amount of gross displacement of the joint appreciated on clinical examination and mi- croscopic findings. A grade 1 sprain is associated with pain but no joint instability on clinical examination. This represents intrafbrous injury to the ligament. A grade 2 sprain occurs when some but not all fibers have been torn; because some fibers are still in continuity, the joint is only minimally unsta- ble when the ligament is stressed. A grade 3 sprain is a complete tear of the ligament. Sprains can be caused both by contact or noncontact mechanisms (such as twisting); in fact, any mechanism that produces ten- sion on the ligament can cause injury. Liga- ment injuries are common, accounting for 25% to 40% of all knee injuries,8,9 and they are present, by definition, in all joint dislo- cations. Ligaments can be broadly divided into those that heal and those that do not, al- though the propensity for healing is more apt to be a function of the local environment rather than the ligament tissue itself. Liga- ments with potential to heal, such as the MCL of the knee, do so by progressing through three characteristic stages: inflammation, proliferation, and remodeling.10,11 The inflammatory phase begins within hours of the injury and predominates throughout the first 7 to 10 days after the injury.12,13 This phase is characterized by the presence of ne- crosis, inflammatory cells, and the growth of neovascular tissue on the surface of the liga- ment remnant.13 Corresponding injury to lo- cal capillaries causes hematoma formation and signals the continued migration of in- flammatory cells. Because inflammation ini- tiates the healing response, use of medica- tions that inhibit inflammation may impede the repair. The proliferative phase is characterized by an increase in cell density in the ligament remnants with ovoid cells and gradual neovascularization of the entire ligament remnant.12,13 New collagen formation—the provisional scar—and cell migration from the torn ligament ends into the granulation tis- sue are also seen during this phase.12 Thus, the space between the torn ends of the orig- inal ligament is filled with a matrix contain- ing disorganized proteins and many cells. In the rabbit MCL, this phase has started by 10 days and peaks at 21 days after rupture.13 The transition to the remodeling phase is characterized by a decrease in the prolifera- tive fibroblast response and an increase in matrix alignment.12,13 Thus, there is less cel- lularity and vascularity and denser collagen within the scar. Over time, this collagen be- comes more aligned with the natural tensile forces of the given joint. In the rabbit MCL, this phase starts at 21 days and continues for several years.

The progression from inflammation to proliferation to remodeling also has been re- ported in other dense, connective tissues, such as tendon and skin. The product of this process is a functional fibrovascular scar. Through the process of remodeling, this scar becomes like the original, uninjured tissue— but not perfectly so. Although remodeling begins as early as 6 weeks after injury, the final reorganization of the tissue (and thus recreation of normal mechanical properties) is not complete for up to 1 year after injury.

Some ligaments, especially intra-articular ligaments such as the ACL, fail to heal after rupture, even when they are sutured back together. It is not clear whether this lack of clinical healing is caused by an inability to initiate a healing response, an inhibition of the response, or simply a lack of nutrition to support healing. It is likely that the failure of these tissues to heal is the result of a combi- nation of factors.

Because of their healing potential, most injuries to ligaments found outside the joint, or extra-articular ligaments, can be treated successfully with immobilization or primary repair. Other treatments, such as ligament reconstruction, are used for intra-articular ligament injuries. For example, the ACL, which is an intra-articular ligament, is com- monly treated by removal of the torn liga- ment and replacement with a tendon graft that is secured in bony tunnels. This graft is only an approximation of the normal liga- ment, as it is currently impossible to recreate the complex geometry of the native ACL with an artificial ligament. Moreover, it is proba- ble that some of the neurologic function (ie, proprioception) is lost when the ligament is torn.

Even those ligaments that heal require well-conceived treatment. It is known that immobilization can lead to joint stiffness. This is because without the appropriate sig- nals provided by normal mechanical stress, the healing tissue fails to orient itself in the correct direction. This helter-skelter forma- tion of scar causes adhesions. Prolonged im- mobilization also weakens intact ligaments, as well as their insertion into bone. These processes are reversible, but reversing them takes time.