Sports Medicine: Just the Facts

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CHAPTER 10 • MUSCLE AND TENDON INJURY AND REPAIR 59


  • The insertion of tendons onto bone is usually via four
    zones: tendon, fibrocartilage, mineralized fibrocarti-
    lage, 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 sus-
    taining compressive loads exhibit increased proteo-
    glycan 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 con-
    tent, decreased water content, and decreased vascular-
    ity. 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 clin-
    ical 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 inflam-
    mation
    d. Tendinitis: Inflammation within the tendon

  • Tendinopathyhas 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 multifacto-
    rial and involves a combination of intrinsic and extrin-
    sic factors.
    •Important intrinsic factors include anatomic abnor-
    malities(malalignment, muscle weakness/imbalance,


decreased flexibility, and joint laxity), age, gender,
weight, and predisposing diseases (Almekinders,
1998; Kannus, 1997).
•Important extrinsic factors include excessive mechan-
ical load (frequency, duration, and intensity), training
errors (over training, rapid progression, fatigue, run-
ning surface, and poor technique), and equipment
problems (footwear, racquets, and seat height)
(Almekinders, 1998; Kannus, 1997).


  • There are very few well-controlled studies that exam-
    ine 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 col-
    lagen fibrils, the noncollagenous matrix, and
    microvasculature (Hyman and Rodeo, 2000).

  • Cellular damage results in inflammation of the sur-
    rounding 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 prolif-
    eration 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 calcifica-
    tion, and the like) (Kannus, 1997).

  • The causal link between initial inflammation (paratenon-
    itis) and tendon degeneration (tendinosis) is unclear.
    Researchers have demonstrated that chronic paratenoni-
    tis 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 rup-
    ture (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).

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