Ligament or tendon injury occurs when the load acting on the tissue is over its own capacity. When the load is over phase III in the above-mentioned stress-strain curve, tissue failure occurs. As soon as the ligament starts to heal up after the injury, usual healing process will proceed namely: 1. inflammatory; 2. cellular and matrix proliferation (regeneration); and 3. remodeling.(Hildebrand and Frank 1998, Reid 1992)
In the following, changes in the tissues structures as well as their mechanical properties during the healing processes will be discussed.
A. Healing response within tendon and ligament toward injury
I. Inflammatory phase
At the cellular level, alteration of structural makeup starts.
• Formation of fibrin clot (Hildebrand and Frank 1998, Reid 1992).
• Fibroblasts proliferation (Hayman and Rodeo 2000, Liu et al 1995, Reid 1992).
• Ligament: High Type III collagen (loosely packed thin fibrils), low Type I collagen (densely packed thick fibrils)
Tendon: Similar amount of Type I & III production (Liu et al 1995).
II. Regeneration
At cellular level:
• Type I collagen fibrins bridge up the gap between the torn ends (Hildebrand and Frank 1998).
• Spare collagen framework formed (Reid 1992).
• Formation of scar with Type I collagen comprises large percentage of scar tissue (Frank 1996, Liu et al 1995).
• Fibroblast remains predominant cell.
III. Remodeling
1. At cellular level:
• There is an increase of collagen density & cross link, alignment of collagen fibers in the axis of ligament (Hayman and Rodeo 2000, Liu et al 1995).
• Histological normal ligament after 7 months, mechanical properties still not fully returned to normal state.
• Still high type III collagen percentage in repaired ligament (Liu et al 1995)
• Alignment of collagen fibers is longitudinally along lines of stress in tendon, minimal histological difference from normal tendon after 20th week.
2. Mechanical properties of an healed injured tendon and ligament
• The tensile strength shows dramatic reduction (Reid 1992).
• Ligamentous strength after repair is in the region of 60 to 70% normal after 6 weeks of healing (Reid 1992).
• It takes up 3 months before 80% of the original strength is acquired (Reid 1992).
• Intra-articular ligaments usually gain tensile strength more slowly, 3 months 50% of normal strength & 6 months 70% functional strength. (Reid 1992).
• Strength and stiffness restore to 40 – 90% of normal values in animal studies, only about 30 – 70% of the material strength has returned (Frank 1996).
• Viscoelastic properties appear to return to 70 – 90% of normal values (Frank 1996).
• Ligament (using MCL) heals structurally 70 – 80% of the strength and structural stiffness of a normal MCL. The scar reaches a maximum of only about 30% of normal MCL strength, even after months to years of healing (Frank et al 1999, Frank 1996).
3. Formation of scar tissue
• Scar development: inflammation and formation of granulation tissue, scar proliferation and scar remodeling (Frank 1996).
• Comparison between ligament scar and normal ligament properties (Table 1.)
| Normal ligament | Ligament Scar |
| Collagen aligned | Collagen disorganized |
| Collagen densely packed | Defects between collagen fibers |
| Large collagen fibrils | Small collagen fibrils |
| Mature fiber cross-links | Immature cross-links |
| Primarily collagen type I (< 10% type III) | More collagen type III |
| Small proteoglycans | Some large proteoglycans |
| Other components minor | Excesses of other components |
| Cell metabolism low | Cell metabolism high |
| Low cell density | Increased cell density |
| Low vascularity | Increased vascularity |
• 3 major reasons for scar weakness – “flaws”, smaller than normal collagen fibril sizes and abnormal collagen cross-linking (Frank et al 1999, Hayman and Rodeo 2000).
• Normal ligaments Densely packed nearly parallel arrangements of a range of sizes of collagen fibers, cross-links are stable and resistant to breakdown. However the scar tissue has poorer cross-links and needs months to realign and abnormal collagen cross-linking (Frank et al 1999, Hayman and Rodeo 2000).
B. Effects of Immobilization and Mobilization
• Immobilization protects some ligament repairs grossly, causes isolated ligament scars to be less stiff and significantly less strong than scars in the joint that have been allowed to move, decreases ligament strength, has potential minimization of scar length which leads to ligament laxity (Frank 1996).
• Study in rabbit’s ACL showed changes in the shape and intracellular structure of fibroblasts from the ligament after immobilization, ligament switches progressively from an anabolic to a more catabolic state (Boorman et al 1998).
• Mobilization with some degree of mechanical load appears to be essential to the normal maturation and maintenance of the structural and mechanical properties of ligaments (Boorman et al 1998).
• Mobilization with controlled movement has been shown to improve scar stiffness and strength without compromising scar length, shown to stimulate collagen synthesis, matrix remodeling, production of better quality scar when compared with those produced with immobilization, production of increased scar mass to resist the tensile stresses involved (Frank 1996).
• Movement creates tension that increases fibroblast proliferation, migration and collagen synthesis, aligns the fibroblast & collagen fibrils parallel to the direction of the force. Therefore a healing ligament will have a high tensile strength (Liu et al 1995).
• In tendon, passive mobilization can prevent adhesion between the sheath and the healing tendon that restricts motion.
• In conclusion, mechanical stimulus (mobilization) has a significant affect on ligament and tendon structure.
Overview on management of tendon / ligament injuries
Grade I injury
| Signs | Management |
| – Minimal loss of structural integrity | – Minimal functional loss |
| – No abnormal motion | – Early return to training – some protection may be necessary |
| – Little or no swelling | |
| – Localized tenderness | |
| – Minimal bruising |
Grade II injury
| Signs | Management |
| – Significant structural weakening | – Tendency to recurrence |
| – Some abnormal motion | – Need protection from risk of further injury |
| – Solid end feel to stress | – May need modified immobilization |
| – More bruising and swelling | – May stretch out further with time |
| – Often associated hemarthrosis & effusion | – Dramatic reduction of tensile strength, a ware of the dangers of unduly stretching healing structures at this point. |
Grade III injury (complete rupture)
| Signs | Management |
| – Loss of structural integrity | – Needs prolonged protection |
| – Marked abnormal motion | – Surgery may be considered |
| – Significant bruising | – Often permanent functional instability |
| – Hemarthrosis |