8
Ligament Healing
1. Define and discuss the inflammatory response to injury.
2. Describe the phases of healing and sequence of events characteristic of each phase.
3. Identify the five cardinal signs of inflammation.
4. Describe the effects of immobilization on ligaments.
5. Discuss the effects of stress and exercise on ligaments.
6. Identify and discuss practical clinical applications of stress deprivation and protected motion during phases of ligament healing.
LIGAMENT ANATOMY
Interestingly, certain ligaments (e.g., ligamentum nuchae) contain greater amounts of elastin, which in turn contributes to different mechanical properties than those of ligaments with less elastin. Although considered hypovascular, ligaments demonstrate relative uniform microvascularity that originates from their origin and insertion sites.24
Ligaments have a rich sensory innervation of specialized mechanoreceptors and free nerve endings that contribute to proprioception and pain, respectively. Ligament attachment to bone is by direct or indirect transition. Direct ligament insertion into bone represents a gradual change from specific ligament fiber to fibrocartilage to calcified fibrocartilage to bone. With indirect insertion, the superficial layers of ligament fibers attach directly in the periosteum, whereas the deep fibers transition to bone by way of Sharpey’s perforating fibers.24
INJURY AND REPAIR
As with other vascular tissues, extraarticular ligaments heal in a highly structured, organized, and predictable fashion. Generally, the sequential cascade of events overlaps four stages of repair: Phase I, hemostasis and degeneration; Phase II, inflammation; Phase III, proliferation and migration; and Phase IV, remodeling and degeneration.11
In contrast, intraarticular ligaments, although demonstrating an intense vascular response to injury, do not heal spontaneously. The environment of intraarticular synovial fluid tends to dilute hematoma formation between the ends of the injured ligaments while preventing fibrin clot organization and ultimately limiting the intrinsic healing mechanism.24
Phase II is marked by a release of extremely potent chemical mediators of vasodilation, cell wall permeability, and pain in response to fibrin clot formation. Prostaglandins, histamine, bradykinins, and serotonin are mobilized to the trauma site to increase capillary permeability and profuse dilation of blood vessels. This action allows migration of specific inflammatory polymorphonuclear cells and lymphocytes to the injured tissue to initiate the action of ingestion (phagocytosis) to remove bacteria and dead tissue. The predominant cell types present during the acute inflammatory phase are neutrophils and lymphocytes. Monocytes are referred to as macrophages as they become phagocytes.24
The production of type III collagen, extracellular matrix, and, within 2 days, proteoglycans by fibroblasts initiate the beginning of Phase III matrix and cellular proliferation. Fibroblasts rapidly synthesize new extracellular matrix containing high concentrations of water; GAGs; and relatively weak, fragile, and immature type III collagen. Neovascularization (angiogenesis) begins as granulation tissue tenuously attaches to the damaged gap. Gradually the concentration of water, GAGs, and type III collagen decreases over several weeks. Inflammatory cytokines are slowly removed from the injured site. Fibroblastic activity synthesizes type I collagen during this highly cellular phase of repair. There is a marked decrease in vascularity within the repair tissue as the collagen concentration increases. Matrix organization continues as the fibrils of type I collagen slowly arrange and align in response to appropriately applied stress. As the density of collagen, elastin, and proteoglycans increase, the tensile properties of repaired tissue also increase.23
Important consideration must be given to the fact that intrinsically repaired extraarticular ligament does not return to normal, biochemically or biomechanically. Even after considerable time and remodeling of dense connective tissue, ultimate tensile strength may approach only 50% to 70% of normal ligaments up to 1 year after injury.16,24
The most common injury of joints are ligament sprains. The knee and ankle joints are common areas of sprains, with the incidence of knee ligament sprains, particularly those of the medial collateral ligament (MCL), occurring in as many as 25% to 40% of all knee injuries.7,19
Not all ligaments heal at the same rate or to the same degree.2 For example, the anterior cruciate ligament (ACL) does not appear to heal as well as the MCL of the knee.25 Factors affecting ligament healing include blood supply and function.12,25
Three key conditions must be present for ligaments to properly remodel or heal:2
1. Torn ligament ends must be in contact with each other.
2. Progressive, controlled stress must be applied to the healing tissues to orient scar tissue formation.
3. The ligament must be protected against excessive forces during the remodeling process.
The continuum of the healing process outlined here is ligament specific, and healing is related to blood supply, degree of injury, and mechanical stresses applied to the ligament.2
Nonsurgical Repair versus Surgical Repair
Ligaments can be repaired surgically or allowed to heal conservatively without surgery, depending on the degree of injury and involvement of supporting tissues. Investigators have shown that untreated ligaments heal by way of scar tissue proliferation rather than true ligament regeneration.8 Untreated ligament tears are biochemically inferior, possessing a large portion of type III immature collagen, and generally are not healed even at 40 weeks after injury.8
Grade I: Microscopic tearing of the ligament without producing joint laxity
Grade II: Tearing of some ligament fibers with moderate laxity
Grade III: Complete rupture of the ligament with profound instability and laxity
Grade I and II ligament sprains are most common, with only 15% of all knee sprains classified as grade III.3 Generally, grade I and II ligament sprains can be treated with protective bracing and comprehensive and progressive rehabilitation with appropriate strengthening to provide dynamic muscular support. With grade I and II ligament sprains of the knee (ACL, MCL, posterior cruciate ligament [PCL], and lateral collateral ligament [LCL]), good to excellent results can be anticipated in 90% of those cases treated nonsurgically.2
Repair versus Nonrepair
By virtue of its extracapsular anatomy, the MCL provides for a greater periarticular vascular response and the ability to protect the ligament from unwanted forces (e.g., varus, valgus, and internal and external rotation), and allows for an appropriate environment to stimulate healing and propagation of motion, collagen synthesis organization and orientation, proteoglycan concentration, and joint function. Therefore all three distinct grades (grades I, II, and III) of isolated MCL tears appear to heal uneventfully without surgical repair. Even though a fibrous repair gap may exist between torn ends of the ligament, resulting in inferior mechanical resistance to tensile loads, the greater cross-sectional area of the healed ligament provides for biochemical properties (e.g., ultimate tensile load to failure) that more closely resemble an uninjured ligament.24
Effects of Immobilization
Immobilization, surgery, injury, and rehabilitation of ligaments must take into consideration not only the healing response of the ligament itself, but also that of the ligament–bone interface. Stress deprivation of the ligament and ligament–bone complexes resulting from prolonged immobilization after injury or surgery can have significant and profound negative effects. Joint stiffness after immobilization is related to adhesion formation, active shortening of dense connective tissue (ligament),and decreases in water content.2 Studies show a gradual deterioration in ligament strength, loss of bone, weakening of cartilage and tendons, significant muscle atrophy, and negative effects on joint mechanics after periods of immobilization (Box 8-1).1
