Tendon Pathology Flashcards
what are tendons made up of
collagen bundles arranged around a central elongated collection of tenocytes (tendon fibroblasts) and capillaries
what are tendons composed of at birth
cellular and vascular
what are tendons composed of in an adult
collagen fibrils form 80% of dry matter
what is the structure of collgen fibrils in collagen type 1
form a zigzag waveform in longitudinal orientation
what are tenocytes
elongated tendon fibrocyte/fibroblast
longitudinal rows alongside the collagen fibrils
how do tenocytes communicate
via gap junctions and respond to mechanical signals
what are the function of tenocytes
- synthesize and degrade all of the collagenous and non-collagenous matrix
- repair the tendon matrix when injured
- slow turn-over in normal tendon
what are the predisposing changes in the injury and repiar of tendon
cartilaginous metaplasia, ischemia, fibroblast proliferation
what are the predisposed sites for injury and repair of a tendon
anatomic weakness or disproportionate stretch
what are stretch lesions (3)
- fibrils pulled out of kink register
- ruptured collagen fibres
- rupture of capillaries
how are tendons repaired (3)
- tenocytes and peritenon cells form myofibroblasts
- collagen type III (immature collagen)
- maturation over time (collagen type I)
how are large lesions repaired
more necrosis, fibrin, malaligned, scar collagen, adhesions
what occures in the acute phase of injury
inflammatory cells
pro-inflammatory mediators and cytokines
commonly asymptomatic horses
what occurs in the subacute phase of injury
3-6 weeks post injury
inflammatory cells replaced by fibroblastic cells and small blood vessels (granulation tissue)
what cells are responsible for repair of tendons
fibroblastic cells (tenocytes)
what two sites do fibroblasts migrate into the tendon from
- tendon sheath (extrinsic repair)
- epitenon/endotenon (intrinsic repair)
what are the chronic phase of injury and repair
more than 3 months post injury
scar tissue
disorganized collagen fibrils
increased numbers of fibroblasts
enlarged endotendon
what occurs with maturation over time
decreased cellularity
alignment of collagen fibrils
what problems occur in tendon healing
- no regeneration: fascicles stuck together and destroyed by scar tissue
- ruptures may occur at margins of normal and scar tissue
- persistence of inflammatory cells (and blood vessels) in endotenon
what are the tendon pathologies
- vascular
- inflammatory
- traumatic
- anomaly
- metabolic/toxic
- idiopathic/iatrogen
- neoplastic
- degenerative
where are SDFT injuries most common
usually mid-metacarpal region
what occurs after a SDFT injury
microdamage
microscopic level
subclinical changes to the tendon
naturally present in tendons of older horses
accelerated accumulations in tendons of horses <10 years due to high intensity exercise
how does exercise accelerate the levels of microdamage
- mechanical overload
- hyperthermia
- hypoxia
- death or dysfunction of tenocytes –> poor tendon healing –> further presence/increase of microdamage
what occurs during mechanical overload in SDFT
high levels of force break collagen fibrils and alter microscopic structure of the tendon –> microdamage
how does the SDFT improve locomotion efficiency
SDFT converts both potential and kinetic energy into elastic energy
reduces muscle energy expenditure –> increases effeciency of locomotion
low mechanical safety marigin
what is hyperthermia in the tendon core
not all elastic energy is returned during recoil of tendon
5-10% lost as heat
inefficient dissipiation of heat within the tendon core due to its poor vascular supply
high temp leads to tenocyte death
what are the features of early microdamage in SDFT due to ageing
- decrease crimp angle (core) > 10 years
- decrease cellularity
- decreased gap junction communication
- increase in % type 1 tenocytes (and length)
what are the features of early microdamage in the SDFT due to exercise
- decreased crimp angle (core) < 10 years
- decreased collagen fibril diameter (core)
- decreased glycosaminoglycan content
what are the features of advanced microdamage in the SDFT
red core lesion
no clinical signs, no swelling
more type III collagen = immature (smaller, weaker fibrils)
what are parasitic diseases of tendons
horse and cattle
adult worms in tendon, tendon sheaths, connective tissue of brisket or abdominal walls
microfilariae migrate to skin, picked up by blood sucking parasite
low grade or no tissue reaction; asymptomatic
what is suspensory desmitis
degenerative diseases of tendons
changes in proteoglycan decomposition –> abnormal decorin and aggrecan
what occurs during suspensory desmitis
hyperextension of metacarpophalangeal/tarsophalangeal joint
what are the histological features of the tendon
tenocytes
vessels
not very cellular
what are these cells
