TENDON INJURY AND REPAIR y y y y Tendon injuries are secondary to direct trauma (lacerations) or tensile overload.

Tensile overload injuries are very common athletic injuries and can occur acutely or as a result of chronic overload. Acute tendon overload usually results in injury to the musculotendinous junction or a bony avulsion since tendons can withstand high tensile loads. Rarely does a normal tendon rupture midsubstance. Chronic tendon overload injuries are common overuse injuries and will be the focus of this section.

ANATOMY AND PHYSIOLOGY Tendons consist primarily of type I collagen fibrils, a proteoglycan matrix, and relatively few fibroblasts. 1. Type I collagen consists of two alpha-I polypeptide chains and one alpha-2 chain. These three chains are organized into a triple helix stabilized by hydrogen and covalent bonds (Wood et al, 2000). 2. The collagen triple helix molecules are aligned in a quarter-staggered arrangement to make up the collagen microfibril. This results in alignment of oppositely charged amino acids and contributes to the tendon s strength. 3. The microfibrils are then arranged in a parallel, well ordered, and densely packed fashion. This organization also contributes to the tendon s tensile strength. The microfibrils are combined with a proteoglycan and water matrix to form collagen fascicles. The tendon consists of groupings of these fascicles surrounded by connective tissue that contains blood vessels, nerves, and lymphatics (Wood et al, 2000). The insertion of tendons onto bone is usually via four zones: tendon, fibrocartilage, mineralized fibrocartilage, and bone. Tendons that bend at acute angles (flexor tendons in the hand) are enclosed in a distinct sheath that acts as a pulley (Wood et al, 2000). Synovial fluid within the sheath assists in tendon gliding. Tendons that are not enclosed in a sheath (Achilles tendon) are covered by a paratenon. Mechanical forces affect the characteristics of tendon. Tendons subjected to tensile loads have smaller densely packed collagen fibrils, increased collagen synthesis, smaller proteoglycans (Decorin), and a higher collagen to proteoglycan ratio. Tendons sustaining compressive loads exhibit increased proteoglycan levels, larger proteoglycan molecules, and larger less dense collagen fibrils (Hyman and Rodeo, 2000). Aging also affects the material characteristics of tendon with decreased collagen synthesis, increased collagen fibril diameter, decreased proteoglycan content, decreased water content, and decreased vascularity. This results in a stiffer, weaker tendon (Hyman and Rodeo, 2000).

CHRONIC TENSILE OVERLOAD INJURIES TERMINOLOGY

There is significant confusion regarding the terminology of chronic tendon injuries. Tendinitis, tendonitis, and tendinosis are frequently used terms to describe the clinical picture of pain, swelling, and stiffness in a tendon. Terminology based on pathology has been proposed (Jarvinen et al, 1997): a. Paratenonitis: Inflammation of the paratenon or tendon sheath. Peritendinitis and tenosynovitis are included in this category. b. Paratenonitis with tendinosis: Tendon degeneration with concomitant paratenon inflammation c. Tendinosis: Tendon degeneration without inflammation d. Tendinitis: Inflammation within the tendon Tendinopathy has been proposed as a generic term describing the clinical picture of pain, swelling, and impaired performance (Maffulli, Kahn, and Puddu, 1998). ETIOLOGY The etiology of chronic tendon injuries is multifactorial and involves a combination of intrinsic and extrinsic factors. Important intrinsic factors include anatomic abnormalities (malalignment, muscle weakness/imbalance, decreased flexibility, and joint laxity), age, gender, weight, and predisposing diseases (Almekinders, 1998; Kannus, 1997). Important extrinsic factors include excessive mechanical load (frequency, duration, and intensity), training errors (over training, rapid progression, fatigue, running surface, and poor technique), and equipment problems (footwear, racquets, and seat height) (Almekinders, 1998; Kannus, 1997). There are very few well-controlled studies that examine the etiologic factors involved in chronic tendon injuries. PATHOPHYSIOLOGY Repetitive load on a tendon that results in 4 8% strain causes microscopic tendon fiber damage. Continued load on the tendon at this level overwhelms the tendon s ability for repair. Damage occurs to the collagen fibrils, the noncollagenous matrix, and microvasculature (Hyman and Rodeo, 2000). Cellular damage results in inflammation of the surrounding paratenon (paratenonitis). Tissue edema, fibrin exudate, and capillary occlusion result in local tissue hypoxia. Audible crepitation may be noted on examination (Kannus, 1997). The paratenon becomes thickened as fibroblast proliferation and fibrotic adhesions develop. This results in decreased tendon gliding and triggering. Intrinsic tendon damage (tendinosis) may occur with continued tendon overload. Tendon degeneration may appear as a number of histologic entities (hypoxic degeneration, mucoid degeneration, fiber calcification, and the like) (Kannus, 1997).

The causal link between initial inflammation (paratenonitis) and tendon degeneration (tendinosis) is unclear. Researchers have demonstrated that chronic paratenonitis can result in tendon degeneration in an animal model (Backman et al, 1990); however, a large clinical study showed no previous evidence of paratenonitis in over 60% of patients who sustained an Achilles tendon rupture (Kannus and Jozsa, 1991). The initial paratenonitis may be causative factor for tendon degeneration or may coexist independently. The exact cellular mechanism of tendon degeneration has not been completely defined. Important factors include tissue hypoxia, free radical induced tendon damage, and tissue hyperthermia (Kannus, 1997). DIAGNOSIS The history often reveals repetitive mechanical over- load. The athlete will usually be involved in either an endurance sport (running, cycling, and swimming) or a sport that requires repetition of a specialized skill (tennis, basketball, and baseball) (Hess et al, 1989). The athlete will frequently note an increase in the duration, frequency, or intensity of the training regimen. The pain is frequently worse after a period of rest following the training period. Changes in footwear, equipment, or training surface may be present. The physical examination may reveal swelling or crepitation along the tendon sheath. The degenerative tendon is often tender to palpation or painful with compression (impingement signs). Range of motion may be restricted (Almekinders, 1998). Diagnostic tests include radiographs to exclude stress fractures or osteoarthritis. Ultrasound or magnetic resonance imaging can be useful in tendons that are not easily palpated (rotator cuff). TREATMENT Removing or modifying the mechanical overload (relative rest) is the most important component of treating chronic tendon injuries. Correcting training errors and equipment problems should also be accomplished. Prolonged immobilization should be avoided. Immobilization results in deceased tendon strength and stiffness owing to proteolytic degradation of collagen (Hyman and Rodeo, 2000). Physical therapy is often prescribed for chronic tendon disorders. Stretching and strengthening (particularly eccentric exercises) are thought to be beneficial but there are few good studies that support this assertion. Modalities such as heat, ice, and ultrasound may also improve the patient s symptoms but there is little evidence that these techniques accelerate tendon healing. NSAIDs are frequently taken for chronic tendon disorders. A recent review of the literature stated that five of nine placebo-controlled studies demonstrated the efficacy of NSAIDs in the treatment of tendinopathy (Almekinders and Temple, 1998). There is no evidence that NSAIDs improve the healing process in tendon degeneration and there is evidence in muscle injury that NSAIDs may be harmful to tissue healing (Mishra et al, 1995). Short-term use of NSAIDs may be indicated to provide analgesia for the athlete. The use of corticosteroids injections in the treatment of tendinopathy is controversial. The rationale of using a local anti-inflammatory medication for a disease process that involves tissue degeneration is questionable.

Corticosteroids may decrease inflammation in the paratenon, reduce adhesions between the tendon and the peritendinous tissue, or block nociceptors in the damaged tendon (Paavola et al, 2002); however, only three of eight placebo-controlled studies in the literature demonstrate the efficacy of corticosteroid injections (Almekinders and Temple, 1998). Direct injections into the tendon substance should be avoided as they result in elevated tissue pressure and tissue damage. The use of corticosteroid injections around weight-bearing tendons such as the Achilles tendon and patellar tendon is controversial. There have been case reports of tendon rupture but there are no controlled studies and rupture of the tendon may have occurred without an injection. It is difficult to make recommendations on the use of corticosteroid injections owing to the paucity of scientific evidence regarding their use. The surgical treatment of chronic tendon injury is usually reserved for those cases that do not resolve with four to six months of nonsurgical treatment. The surgical procedures usually involve debridement of the degenerative tendon tissue. Occasionally complete resection and repair or grafting is required (Almekinders, 1998). Removal of the involved paratenon or release of the tendon sheath is occasionally necessary. Bony prominences may require removal (Haglunds, acromion). Clinical series in the literature demonstrate the success of surgical management but there are a very few controlled studies.

O Connor, F.G., Salis, R.E., Wilder, R.P., & Pierre, P.S. (2005). Sports Medicine Just the Facts. McGraw-Hill Companies