Tendon Injuries

Introduction

  • Why do tendons degenerate/ rupture in the foot and ankle?
    • -40-50% are sports related
  • Statistics*
    • -53% wt bearing; forefoot pushoff
    • -17% sudden unexpected ankle dorsiflexion
    • -10% violent dorsiflexion/ plantarflexion of the foot; falling from height
    • -20% other

Extrinsic Causes of Tendon Degeneration or Rupture

  • Mechanical
    • -Sports/ Overuse:
  • Direct injection of steriods
    • -increased hypoxia leading to tendon degeneration
    • -decreased inflammatory response
  • Flouroquinolones
    • -inhibit tenoccyte metabolism
    • -reduces cell proliferation
    • -reduces matrix and collagen synthesis
  • Hyperthermia
  • Extrinsic Factors
    • -Biomechanical faults
  • Hyperpronation (excessive flat fleet)
  • Forefoot varus/ forefoot valgus
  • Pes Cavus (high arches)/ Pes Planus
  • (flat feet) genu valgum/ varum
  • Tibia vara
  • Femoral neck anterversion
  • LLD
  • Muscle weakness and imbalance
  • Decreased flexibility
  • Joint laxity

Intrinsic Factors to Tendon Degeneration or Rupture

  • Gender
  • Age
  • Overweight
  • Systemic conditions
    • -Rheumatoid Arthritis manifest itself in the Achilles to
    • -Other Conditions implicated in tendon rupture: SLE, Chronic renal failure, hyperurecemia, arterioslerosis, Diabetes Mellitus

Biomechanics

  • General Function of Foot and Ankle Tendons
    • -Transmit forces form muscle to bone
    • -Muscle protection; absorbs external forces
    • -tendon strength is related to thickness and collagen content
  • Achilles Tendon
    • -Strongest tendon in the human body
    • -calf muscle generates 3786N
    • -Peak loads when running 6.2-8.2 BW*

Stress Strain

  • At rest, tendon is a wavy configuration
  • >2% losses wavy configuration
  • intramolecular sliding of the collagen triple helices
  • returns to native position when unloaded
  • >4% tendon damage (microscopic failure)
  • >8% microscopic damage
    • -intrafibrilar damage by molecular slippage

Mechanical Theory of Tendon Degeneration or Rupture

  • tendon overuse
  • repetitive strain from 4-8%
    • -breaks cross linkage and causes tissue degeneration, leading to inflammation*
  • Increased cytokines and prostaglandins
  • Response depends on tendon anatomy
    • -Sheath tendons—> synovitis
    • -Nonsheath tendons–> degeneration of the tendon body

Tendon Blood Supply

  • Nutrition is through diffusion rather than vascular perfusion
  • intrinsic systems at the myotendinous junction
  • intstrinsic system at the osseotendinous junction
  • Extrinsic system
    • -paratenon- arterial branches penetrate the epitenon and forms intratendinous networks and anastamosis
    • -synovial sheath
  • Unsheath tendon- vessels pass through the paratenon then into any point along the tendon
  • Sheath tendon- better defined supply, enter at specific areas of the tendon
  • In general blood flow to tendons decrease with increases in age and mechanical load

Zones of Hypovascularity in Tendons

  • tendon blood flow usually decreases with increased age and mechanical loading
  • Regions of compromised blood flow
  • junctional zones
  • torsion
  • compression
  • friction

Zones of Hypovascularity

  • Tendons with suspected reduced vascularity
    • -Patellar, Achilles, biceps, posterior tibialis, supaspinatus, flexor digitorium perfundus
  • Supraspinatus and “Codmans Critical Zone”
    • -not avascular, intrinsic vessles become filled with blood once compression from the humeral head is removed
  • Zones of Avascularity may be due to extrinsic factors such as regions of compression, as opposed to a simple lack of blood supply*

Innervation

  • originates from the cutaneous, muscular, and peritendinous nerve trunks
  • most nerve fibers terminate as nerve endings on the tendon’s surface
    • -myelinated nerve ending- Golgi tendon organs
  • mechanoreceptors
  • Most numerous at the musculoteninous junction
    • -free nerve end fibers- nociceptors

Tendon Composition

  • 95% Type I collagen
    • -hierarchical manner
  • collagen fibers–>fibrils–>fasicles–>tendon
  • Extracellular matrix
    • -transparent, colorless, homogenous, semi-fluid
    • -proteoglycans and water
    • -functions as a medium through which nutrients and waste products can diffuse
      between capillaries and cells
    • -allows for cell migration

Tenocytes

  • tendoblast- immature tendinocytes with high metabolic activity
  • tenocytes have a lower metabolic profile
    • -active in energy generation (krebs, anaerobic metabolism etc)
  • Oxygen consumption about 7.5 times lower than muscle cells
    • -essential to carry loads and maintain tension for long periods of time

Normal

  • Tenocytes lined up in an organized linear parallel fashion
  • flattened nuclei

Tendinopathy

  • disorder
  • haphazard healing without inflammatory cells
  • poor healing response
  • non-inflammatory intratendinous collagen degeneration

Mucoid Degeneration

  • Conversion of collagen into a gelatinous substance (glycosamine/ proteogycan )
  • proteinacous material left behind after cell death
  • less organized
  • large mucoid patches an vacuole between tendon
  • unconnected collagen fiber
  • unequal/ irregular crimping of the collagen fibers

Lipoid Degeneration

  • Cholesterol Clefts-clear spaces in stain
    • -foam cells
  • replaces degenerated or degraded tendon
  • sign of inflammation
  • Disruption of collagen structures

Neovascularizaton

  • Acute
    • -profuse and haphazard
    • -characterize by inflammatory cell reaction, edema, circulatory impairment
  • Chronic
    • -seen in painful tendon lesions apparently not associated with signs of attempted repair*
    • Increased nuclei, more chronic condition

Fibrinoid Degeneration

  • Acute tendinopathy
  • Fibrinous Proteination
    • -body trying to digest and organize
  • Also seen in the the walls of blood vessels and connective tissues in pts with
    • -SLE, Scleroderma, dermatomyosis

Cell Dropout

  • Acute inflammation
    • -secondary to ischemia
    • -prior to inflammatory reaction

Theories of Tendinopathy

  • Oxidative stress
    • -Factors affecting a cell’s sensitivity to hypoxia
  • ATP depletion
  • Ca+2 influx
  • Buffer free radical induced damage

Oxidative Stress

  • under maximal tensile load, tendons may become ischemic
  • hypoxia–> decreased ATP’s production–> tenocyte death
  • after reperfusion, generate oxygen free radicals–> tendinocyte death
    • -Peroxiredoxin concentrations increases in tendinopthy
    • -Induce Apoptosis?

Theories of Tendinopathy

  • Excessive Tendon apotosis
    • -Application of stress to tenocytes produce stress-activated protein kinases–> which in turn trigger apoptosis
    • -tendinopathic quadricep femoris tendon exhibit a spontaneous apoptotis 1.6 times greater than normal tendons
    • -more apoptotic cells in ruptured supraspinatus tendons than supscapularis tendon
  • Cytokines and Inflammatory prostaglandins
    • -PGE2, IL-6, and IL-1 beta all lead to increased synthesis of matrix metalloprotineinase (MMP)
    • -MMPs are a family of proteolytic
  • degrade the components of the extracellular network
  • facilitate tissue remodeling
    • -Fluoroquniolones induced MMP release
  • Hyperthermia
    • -repeated and prolonged exposure to heat may lead to degeneration over time

Phases of tendon healing

  • Inflammatory phase (0-few days)
    • -phagocytosis of necrotic debris
    • -increased vascular permeability
    • -angiogenesis
    • -tenocyte proliferation–> initiate type III collagen formation

Proliferative phase

  • peak production of type III collagen
    • -muffin et al, ruptured an tendinopathic achilles tendon produce greater amount of type III collagen
  • Remodeling phase (> 6wks)
    • -consolidation (6-10wks)
  • cellular–>fibrous
  • tenocytes and collagen fibers align themselves directions of stress
  • Higher proportion of Type-I collagen
  • Maturation phase (>10 wks-1year)
    • -fibrous–> scar-like tendon tissue

Extrinsic Tendon Healing

  • healing by cell invasion from the surrounding sheath and synovium
  • loose granulation issue
  • disorganized
  • scar tissue and adhesions

Intrinsic Tendon Healing

  • Healing by proliferation of the epitenon and endotenon tenocytes (resident tenocytes)
  • Collagen deposition is organized like native collagen
    • -Hyaluronan levels may play a role in scarring vs. nonscarring
  • results in better biomechanics and fewer complications
    • -the normal gliding mechanism of the tendon sheath is preserved
  • larger and more mature collagen fibers

Translucent Zone

  • Cleavage of collagen fibers at wound edges produces fibrils
  • Areas of translucence-liberation of intact collagen fibril segment
    • -1st 14 days
  • Transluncent Zone
  • reincorrperated into growing tendon collagen fibers within the healing gap
  • Collagen fiber recovery involves the welding of newly deposited collagen and to residual collagen fibers at the edges of the tendon stumps
  • Reutilization of fibrils at the edges of healing tendons

Suturing Technique for Tendon Repair

  • include large margins of tendon on either side of the repair
    • -avoids excessive tension on the weakened areas

References

MuffuliN, Ewen SW et al. Tenocytes from ruptured and tendinpathic Achiles tendon produce greater amount of type III collagen than tenocytes from normal achilles tendon. An in vitro model of human tendon healing. American Journal of Sports Medicine 28(4): 499-505, 2000 Jul-Aug

Ehrlich, Paul et al. Dynamic Changes Appearing in Collagen Fibers During Intrinsic Tendon Repair. Annals Of Plastic Surgery 54 (2): 201-206, 2005 Feb

Linden, Van Der et al. Achilles Tendinitis Associated With Fluoroquinolnes. British Journal of Clinical Pharmacology 48 433-437

Yinger et al. Achilles Rupture in the Athlete Current Science and Treatment. Clinics in Podiatric Medicine and Surgery 19 231-250, 2002

Sharma Pankaj et al. Current Concepts Review. Tendon Injury and Tendinopathy: Healing and Repair. Journal Of Bone and Joint Surgery. 87A (1). 187-202. 2005 Jan

Paavola Mika et al. Current Concepts Review. Achilles Tendinopathy. Journal Of Bone and Joint Surgery. 84A (1). 2062-2076. 2002 Nov

Fenwick et al. The vasculature and its role in the damaged and healing tendon. Arthritis Research. Vol4, No4. 252-260.

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about his patients."

L. HARRIER

"Dr Deacon was an excellent human being, he treated me like a patient and not an number.... He was very sensitive and had good bedside manner....I am really upset that he is gone form the clinic where I live. I have nothing but good things to say about Dr. Deacon. He's Awesome!....I love the guy. He was an excellent individual plus an excellent doctor.
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Testimonials

"He was always very positive; he is a great doctor with wonderful communication. Dr Deacon suspected that I had a condition that went outside his expertise and encouraged me to get it checked out, his suspicion was correct, and because of him I am living a healthier happier life."

P. FERGUSON

"I really appreciate that Dr Deacon really took the time to listen to my concern, he took the time to explain the orthotics in detail and what is the best fit for me. I am a first time user for them and he really made me comfortable in my shoes!"

M. MISTRY

"Dr. Deacon was very pleasant and always put a smile on our faces. We loved seeing him."

B. MULLEN

"I have appreciated Dr. Deacon. He is very skilled at what he does. He cares a lot
about his patients."

T. HARPER

"Dr. Deacon is the best...he knows patient care and analysis. He is personable and gives
the right diagnosis."

H. HYMAN

"...Dr. Deacon is a very good doctor...you will be very lucky to have him as your doctor."

J. HEYWOOD

"Dr Deacon is a wonderful, kind doctor and is very concerned with
about his patients."

L. HARRIER

"Dr Deacon was an excellent human being, he treated me like a patient and not an number.... He was very sensitive and had good bedside manner....I am really upset that he is gone form the clinic where I live. I have nothing but good things to say about Dr. Deacon. He's Awesome!....I love the guy. He was an excellent individual plus an excellent doctor. He fixed
my feet very well."

A. THORNE

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