Tendon

Tendon 

• Structure and composition

  • Composition

    • Water: 50%–60% of total tendon weight

    • Collagen: 75% of dry weight

      • 95% type I collagen, also type III collagen

    • Elastin: 1%–2% of dry weight

      • Highly elastic protein that allows tendon to resume its shape after stretching

         

         

        FIG. 1.44 Tendon and ligament architecture.

        From Brinker MR, Miller MD: Fundamentals of orthopaedics,

        Philadelphia, 1999, Saunders, p 15.

         

      • Also responsible for “toe region” of stress-strain curve

    • Proteoglycans

      • Decorin—most predominant proteoglycan in tendons. Regulates tendon diameter and provides cross-links between collagen fibers. Also shown to have antifibrotic properties via inhibition of TGF-β1.

      • Aggrecan—present at points of tendon compression

      • Biglycan

    • Tenocytes (fibroblasts):

      • Derived from mesoderm

      • Function to synthesize ECM, collagen, and proteoglycans

      • Assemble early collagen fibrils and produce matrix-degrading enzymes (MMPs)

      • Detect strain during tendon loading though deflection of cell cilia

      • Tenocyte production of collagen increases tendon healing and reduces repair ruptures.

      • Role in tendinopathy (due to inflammatory

         

  • Structure

    mediator production)

    • Tenocytes produce type III collagen in response to rupture.

    • Greater proportion of type III collagen, naturally seen in Achilles tendon, predisposes tendons to rupture.

      • Strands of collagen (triple helix of two α1 chains and one α2 chain) organized into microfibrils, which in turn make up fibrils, fascicles, and tendon

      • Fascicles surrounded by endotendon (contiguous with epitendon covering entire tendon)

        • Carry the neurovascular and lymphatic supply of tendons

        • Composed of type III collagen

        • With aging, more type I collagen strands interdigitate between type III collagen strands.

      • Covered by paratenon (Achilles, patellar tendons) versus synovium (digital flexor tendons)

        • Higher vascularity of paratenon leads to increased healing.

      • Sheathed tendons

        • Vincula (extension of synovium) carry blood supply to one tendon segment ( Fig. 1.45 ).

        • Some nutrition from synovial fluid (found between the two layers of the synovial sheath) via diffusion

      • Myotendinous junction

        • Actin microfilaments extend from the last Z line

        • These are linked to the sarcolemma, which in turn connects to the collagen fibril–rich matrix of the tendon.

      • Bone-tendon junction (direct vs. indirect)

        • Direct (fibrocartilaginous) insertion

          • Usually in areas subject to high tensile load

          • Four layers: tendon, fibrocartilage, mineralized fibrocartilage, and bone

        • Indirect Insertion

          • Fibers insert directly into periosteum through Sharpey fibers

• Mechanical properties

  • Anisotropic: properties vary depending on direction of applied force

  • Viscoelastic: properties vary depending on rate of force application

     

     

     

     

     

    FIG. 1.45 (A) India ink specimen demonstrating the vascular supply of the flexor tendons via vincula. (B) Close-up of the specimen.

    From Simon SR, editor: Orthopaedic basic science, ed 2, Rosemont, IL, 1994, American Academy of Orthopaedic Surgeons, p 51.

     

    • Creep: increasing deformation under constant load

    • Stress relaxation: decreasing stress with constant deformation (elongation)

    • Hysteresis: during loading and unloading, the unloading curve is different from the loading curve. The difference between the two represents the amount of energy that is lost during loading.

  • Stress-strain curve

    • Rest: collagen fibers are “crimped.”

    • Toe region: flattening of crimp; nonlinear; tendon stretched easily

    • Linear region: intermediate loads

    • Failure

• Injury and healing

  • Three stages of tendon healing

    • Inflammation

      • Hematoma formation following by resorption

      • Type III collagen is produced at the injury site by tenocytes.

      • Weakest stage of repair

    • Proliferation: maximal type III collagen production

    • Remodeling:

      • Begins at 6 weeks

      • Decreases cellularity

      • Type I collagen predominates

  • Two mechanisms:

    • Intrinsic: recruitment of local stem/progenitor cells from endotenon and epitenon

    • Extrinsic: cells from surrounding tissue invade damaged area.

      • Faster but primary source of adhesions

  • Achilles, patellar, and supraspinatus tendons are prone to rupture at

    hypovascular areas.

    • Achilles tendon is hypovascular 4–6 cm proximal to calcaneal insertion.

  • Responsive to different cytokines and growth factors

    • PDGF genes transfected into tenocytes show collagen formation.

    • VEGF genes transfected into tenocytes show TGF-β upregulation and adhesion formation.

    • When exposed to PMNs (as with inflammation), tenocytes upregulate genes for inflammatory cytokines, TGF-β, and MMPs while suppressing type I collagen expression.

  • Surgical tendon repairs: weakest at 7–10 days

    • Maximum strength achieved at 6 months, reaching two-thirds of original strength.

    • No evidence in favor of a trough (exposing tendon to cancellous bone) over direct repair to cortical bone.

  • Motion and mechanical loading have beneficial effects on tenocyte function.

  • Immobilization decreases strength at tendon-bone interface.