Auer Ch 83 Tendon Injury

Front 1

Composition of tendon:

Back 1

70% water, 30% is predominately type 1 collagen, with small contributions by ECM and tenocytes

Front 2

Composition of procollagen molecule:

Back 2

alpha helical chains, which have amino- and carboxy- terminal ends

Front 3

What is a collagen fibril?

Back 3

3 alpha helical chains

Front 4

How are collagen fibrils arranged?

Back 4

quarter-staggered

Front 5

What is a collagen fiber?

Back 5

bundle of collagen fibrils

Front 6

What is a fascicle?

Back 6

group of collagen fibers

Front 7

What delineates a fascicle?

Back 7

loose connective tissue surrounding it called the endotenon

Front 8

What is the tendon unit composed of?

Back 8

degrees of fascicles, each surrounded by endotenon

Front 9

Composition of endotenon?

Back 9

nervous and vascular supply to the tendon and has rounded mesenchymal source cells

Front 10

What surrounds the tendon unit?

Back 10

epitenon, a continuation of endotenon

Front 11

What is the paratenon?

Back 11

Surrounds the epitenon, in tendons outside of tendon sheaths

Front 12

Function of paratenon?

Back 12

reduces frictional forces between the tendon and surrounding soft tissues and supplies blood vessels and cellular elements for repair processes

Front 13

Composition of tendon sheath?

Back 13

outer fibrous wall and an inner synovial membrane lining the wall and the tendon

Front 14

What is mesotendon?

Back 14

divides the tendon sheath into compartments, is composed of 2 layers of synovium, and bring the intrathecal tendon a blood supply

Front 15

When is COMP most abundant?

Back 15

young tendon

Front 16

Function of COMP:

Back 16

organizing collagen molecules in the quarter-stagger arrangement of the fibril. Once the fibril is formed, COMP is displaced from the fibril

Front 17

What does the proteoglycan composition reflect?

Back 17

biomechanical environment of the tendon. Small proteoglycans are abdundant in tensile regions of the tendon and large proteoglycans are located in compressive areas of the tendon

Front 18

Where are tenocytes located?

Back 18

separate the collagen fibrils

Front 19

What does tenocyte shape represent?

Back 19

stage of activity or differently differenciated cells

Front 20

Shape & activity of type 1 tenocytes:

Back 20

spindle-shaped nuclei and are inactive

Front 21

Shape & activity of type 2 tenocytes:

Back 21

active in young, growing tendon and have oval nuclei

Front 22

Shape and activity of type 3 tenocytes:

Back 22

found in fibrocartilagenous regions of mature tendons in compressive region and have rounded nuclei similar to chondrocytes

Front 23

Blood supply to tendon:

Back 23

contributions from endotenon, paratenon, and mesotenon, from its muscular origin, osseous insertions, and accessory ligaments

Front 24

How does blood supply to the tendon differ by region?

Back 24

intratendinous blood supply is more abundant at the periphery of the tendon than the core of the tendon

Front 25

What do structural and material properties of tendon depend on?

Back 25

organization of the collagen fibrils and the fibril cross-linking

Front 26

What is crimp?

Back 26

Waveform of relaxed fascicles

Front 27

Function of crimp:

Back 27

partially responsible for tendon elasticity

Front 28

What is elongation of the tendon primarily due to?

Back 28

sliding of fascicles over one another rather than the fascicles stretching

Front 29

What contributes to fascicle sliding?

Back 29

loose nature of the endotenon

Front 30

How are structural properties of tendon reported?

Back 30

force-elongation curve (analogous to the load-deformation curve of bone structural properties)

Front 31

How are material properties of tendon reported?

Back 31

stress-strain curve (analogous to the stress-strain curve of bone material properties)

Front 32

What does the toe region of the force-elongation curve represent?

Back 32

elimination of the crimp in the fascicles

Front 33

What does the slope of the force-elongation curve in the linear region reflect?

Back 33

Stiffness of the tendon

Front 34

What is the yield point?

Back 34

associated with rupture of cross-linking and irreversible damage to the collagen fibril

Front 35

What is the ultimate tensile strength before rupture of the SDFT?

Back 35

12 kN or 1.2 ton

Front 36

What is ultimate tensile strain before SDFT rupture?

Back 36

10-12% of the length prior to rupture

Front 37

What is hysteresis?

Back 37

difference between the stress-strain relationship of an unloaded and a loaded tendon

Front 38

What does the area between the hysteresis curves represent?

Back 38

energy lost as heat, raising the temperature of the core of the tendon

Front 39

How does a repeatedly loaded tendon moves the hysteresis curve?

Back 39

to the right to reach as steady state in a process of conditioning, indicating that the repeatedly loaded tendon is more elastic

Front 40

Relationship of tendon loading to stiffness:

Back 40

Rapidly loaded tendon is more stiff (less elastic) and a repeatedly loaded tendon is less stiff (more elastic)

Front 41

How do tendon injuries occur?

Back 41

overstain or by direct trauma

Front 42

Methods of overstain injuries?

Back 42

either a sudden overloading of the structure, overwhelming its resistive strength or an accumulation of tendon degeneration, progressively weakening the tendon

Front 43

How does age affect the tendon?

Back 43

Overall reduction in tendon strength, core crimp shortens, COMP and GAG content decreases in the core

Front 44

How does exercise affect the tendon?

Back 44

Overall reduction in tendon strength, core crimp shortens, decrease COMP and GAG in the core

Front 45

How does tendon microdamage occur?

Back 45

tendon matrix degeneration and failure of the resident cell population to repair the damage

Front 46

Why does tenocyte failure occur?

Back 46

reduced cell numbers and reduced gap junctions that would enable a coordinated anabolic response and absence of appropriate growth factors

Front 47

What causes the most microdamage?

Back 47

Higher number of loading cycles and the highest loading rates (i.e. galloping)

Front 48

How do loading cycles and high loading rates cause damage?

Back 48

induce upregulation of proteolytic enzymes. Physical energy directly disrupts fibers, cross-linking, and matrix proteins. increasing the temperature of the core, may also damage matrix proteins or affect cellular metabolism

Front 49

What is the first phase of tendinopathy?

Back 49

Degeneration

Front 50

When does clinical tendon injury occur?

Back 50

stress overwhelms the structural integrity of the tendon, resulting in disruption of tendon matrix, breaking cross-links, fibrillar rupture, and ultimately complete separation of tendon tissue

Front 51

What does the repair phase involve?

Back 51

extrinsic repair mechanisms by infiltration of angiogenic and fibroblastic factors. It results in the formation of scar tissue, which is predominately type 3 collagen

Front 52

What does the remodeling phase invove?

Back 52

type 3 collagen is transformed to type 1, but incompletely, resulting in an inferior structure, which is less stiff than the original and predisposing to reinjury

Front 53

Possible mechanisms for production of core injury:

Back 53

lack of vascular supply to the core vs the periphery of the tendon, increase in temperature that occurs with release of energy with repeat loading, and the difference in crimp angle in the core vs the periphery of the tendon. The central fibers are straightened first under loading

Front 54

Examples of molecular markers:

Back 54

COMP, Carboxy-terminal propeptide of type 1 collagen (PICP) is a marker of collagen synthesis and cross-linked carboxy-terminal telopeptide of type 1 collagen (ICTP) is a marker of tendon degradation

Front 55

When is synovial COMP used diagnostically?

Back 55

shown to be more useful than ultrasound in detecting intrathecal tendon injuries within the DFTS

Front 56

When is serum COMP used diagnostically?

Back 56

may be useful for detecting joint disease or determining whether training levels are excessive

Front 57

Effect of cold therapy:

Back 57

anti-inflammatory and analgesic effects by increasing vasoconstriction, decreasing enzymatic activity, reducing inflammatory mediators, and slowing nerve conduction

Front 58

Effect of ESWT:

Back 58

mediate tendon healing by inducing analgesia through an effect on sensory nerves

Front 59

Effect of therapeutic ultrasound:

Back 59

conversion of sound energy to thermal energy to increase vascularization and fibroblast proliferation

Front 60

Effect of low-level laser light therapy:

Back 60

stimulate cellular metabolism and enhance fibroblast proliferation and collagen synthesis

Front 61

Effect of intralesional PSGAG:

Back 61

anti-inflammatory effects by inhibiting collagenases, MMPs, and macrophage activation

Front 62

Effects of intralesional HA:

Back 62

decreases the extent of adhesion formation when used intrathecally in DFTS, and decreases inflammatory cell infiltration and intratendinous hemorrhage

Front 63

Effect of intralesional methylprednisolone:

Back 63

dystrophic mineralization and tissue necrosis

Front 64

Effect of intralesional IGF-1:

Back 64

stimulates extracellular tendon matrix synthesis and is a mitogen, but showed no difference in quantities and type of collagen synthesized in a collagenase model of tendinopathy

Front 65

Effect of intralesional PrP:

Back 65

source VEGF, TGF beta, and PDGF, which can stimulate cell proliferation and matrix synthesis

Front 66

Effect of intralesional bone marrow concentrate:

Back 66

supplies a source of GF but is low in MCS

Front 67

Effect of MCS for tendon injury:

Back 67

potential to stimulate tissue regeneration rather than heal by tissue repair processes

Front 68

Indications for tendon splitting:

Back 68

acute tendon injuries to decompress the core lesion of serum and blood and facilitate vascular ingrowth

Front 69

Indication for desmotomy of the accessory ligament of the SDFT:

Back 69

produce a functionally longer musculoskeletal unit and reduce strain on the SDFT, although in a cadaver model it was shown to increase strain during loading

Front 70

Approaches to desmotomy of ALSDFT:

Back 70

open or tenoscopic

Front 71

Describe open approach to desmotomy of ALSDFT:

Back 71

medial 10 cm skin incision between the cephalic vein and the caudal radius at the level of the medial malleolus of the radius. The flexor carpi radialis sheath is incised and retracted caudally to expose the ALSDFT, which is sharply transected. The sheath and fascia are closed in 2 layers and the skin is closed

Front 72

Describe tenoscopic approach to desmotomy of ALSDFT:

Back 72

scope portal created on the lateral aspect of the limb 2 cm proximal to the distal radial physis, into the carpal sheath. With the limb at 90 degrees, the ALSDFT is transected

Front 73

Approach to DFTS tenoscopy:

Back 73

scope portal just distal to the PSB and 1-2 cm palmar-plantar to the neurovascular bundle

Front 74

Treatment of manica lesions:

Back 74

Debridement of manica lesions is associated with a poorer outcome than removal of the manica and its attachments medial, lateral and proximally

Front 75

Describe approach for fasciotomy- neurectomy of deep branch of the lateral plantar nerve for chronic SL desmitis:

Back 75

4-6 cm incision is made on the lateral aspect of the limb, adjacent to the lateral border of the SDFT, extending distally from the level of the chestnut

Front 76

Indications for desmotomy of the ALDDFT:

Back 76

adhesions or flexural deformity

Front 77

Describe desmotomy of ALDDFT:

Back 77

skin incision is made in the proximal MC region to expose the ALDDFT, which is sharply transected. The fascia and skin are closed in 2 layers. A tenoscopic approach through the carpal sheath has been described

Front 78

Goal of tendon laceration repair:

Back 78

restore gliding function of the tendon, minimize gap formation and adhesions, and preserve functional vasculature

Front 79

Describe tenorrhaphy:

Back 79

monofilament absorbable suture, either 3-loop pulley pattern or interlocking loop pattern

Front 80

Why is absorbable suture used for tendon repair?

Back 80

Non-absorbable materials result in shearing between healed tissues and the suture material and can cause lameness

Front 81

Benefit of 3-loop pulley:

Back 81

prevents distraction of the ends of the tendon under load

Front 82

Benefit of interlocking loop:

Back 82

has little suture material outside of the tendon, preferred for intrathecal repair

Front 83

Material options for tendinoplasty?

Back 83

carbor fiber, polyester, autologous extensor tendon grafts, and poly-L-lactic acid

Front 84

Disadvantages of carbon fiber implants:

Back 84

associated with persistent lameness from shear forces created by the inelastic carbon fibers

Front 85

Benefits of poly-L-lactic acid implants?

Back 85

supports fibroblast growth, loses strength over several months, matching the mechanical properties of the tendon

Front 86

Complications associated with flexor tendon lacerations:

Back 86

necrotic tendinopathy, concurrent synovial sepsis, cast complications, adhesions, exuberant granulation tissue, flexural deformity, and reinjury

Front 87

Complications of extensor tendon lacerations:

Back 87

exuberant granulation tissue, sequestrum formation, and flexural deformity