Tendon/Ligament Healing and Biomechanics Flashcards
introduce the hierarchical structure of tendon and ligaments and understand the functions of tendon
transfer strain from muscle to bone, maintain limb support and joint alignment
2 types:
1. positional (extensors): low strain, not as elastic, lower water content, lower collagen, lower sGAG
- energy storing (flexors): high strain/elasticity, high water content, higher collagen, greater collagen fiber diameter, higher sGAG
hierarchical structure: 1 collagen type I fiber triple helix into collagen fibril, 5 fibrils create a collagen fiber, which teams up with other collagen fibers to create a fascicle, which weaves together to form a tendon
endotenon: CT surrounding fiber bundles
epitenon: CT surrounding tendon
paratenon: loose CT outside epitenon, allows tendon to move against epitenon and other tissues
sheath: protective outer covering of tendon, produces synovial fluid
review relevant structure and function of clinically important soft tissue structure in the distal limb
- small cellular fraction but large extracellular matrix (collagen filaments and proteoglycan matrix)
-collagen type I: 95%
-collagen type II: 3%
-collagen fibers aligned along longitudinal axis (strength and stretch) - cellular portion: 90-95% is fibroblast-like cells (tenoblasts and tenocytes-produce ECM)
- proteoglycans: protein core with side chains for glycosaminoglycans (GAGs); large proteoglycans in areas with compressive forces, small proteoglycans in areas that provide structural support
- cartilage oligomeric matrix protein (COMP): glycoprotein, accumulates during growth, bind to collagen via zinc dependent mechanism, is structural and believed to provide strength
- CRIMP: wavy appearance, straightens with tension, allows for elasticity of tendon; age and exercise decreases decreased CRIMP angle (decreases buffer against strain and increases risk of tendon injury); larger collagen = stiffer CRIMP
- blood supply: either direct perfusion (less) or diffusion across tendon sheaths; increases with exercise and injury, decreases with age and mechanical loading
-extrinsic sources help with healing: from muscle origin, osseous insertion, and accessory ligaments (not as much to provide)
-intrinsic healing: paratenon (in non tendon sheath area), mesotenon (in tendon sheath area), intratendinous supply
describe the biomechanics of load
stance phase: flexor tendons under tensile stress, store much of kinetic energy when loaded from the first half of the stance phase as elastic energy, release this energy during the second half of stance phase to aid in propulsion (flexor tendons are energy saving elastic springs)
have a toe region, elastic region, and plastic region of load
-toe region: CRIMP straightens
-elastic region: tendons straighten
-plastic region: injury and leads to failure
describe safety margins
very low!
functional tensile strains are very close to failure strains
describe cyclic loading of the tendon
preconditioning: cyclical loading of a tendon to a level not reaching yield, leads to a more elastic, less stiff tendon
hysteresis: energy lost in form of heat during exercise or load as tendon becomes less stiff (but still needs time to recover)
when you condition a tendon with load or stress, need a signal to initiate some healing, and then need time to recover!
what changes occur with age?
- core region: decreased collagen CRIMP angle and decreased length = smaller buffer against strain (toe region almost gone); central fibers straighten, increased smaller fibrils, decreased GAG and COMP
- failure to repair damage: cellular senescence, absence of growth factor regulation or decreased response to growth factor
describe exercise’s effect on immature tendon
depends on type of tendon, age at exercise, and level of background exercise
-some degree of exercise IS necessary for proper function of tendon
-think about racehorses who race as baby 2 year olds; need to exercise them some as they grow and develop before asking them to train
-same for working dogs
describe exercise’s effect on mature tendon
- exacerbates the reduced CRIMP angle (already reduced bc age)
- increase in small fibrils with long term exercise (and age)
- CDET increases with exercise, SDFT does not
- exercise causes reduction in growth factors
- COMP in tensile regions peaks after growth then decreases
- if exercise results in injury may be much worse if older???
understand the risk factors (5) and causes (3) of tendon and ligament injury
3 causes
1. overstrain: sudden overload, overwhelming resistive strength, creeping/insidious onset, or not uniform pathology - lots of ways to overstrain basically
- trauma: overtraining, penetration/laceration
- degeneration: could have asymptomatic lesions, could be bilateral (but one limb more affected) due to various factors, or the association of age and exercise on decreased CRIMP angle
risk factors:
1. speed: faster = greater risk
2. surface: running in the rain, on the beach
3. weight carrying or obesity/pattern of movement
4. fatigue
5. shoes (equine)
understand the pathogenesis and endogenous healing response in tendon and ligaments (4 major stages)
- subclinical: injury itself
- inflammatory stage: intratendinous hemorrhage forms a hematoma, body increases blood supply and edema, infiltration of leukocytes (neutrophils first then macrophages)-owners usually notice this stage
- reparative phase: angiogenic response, accumulation of fibroblasts that are larger and more basophilic with larger nuclei, more similar to myofibroblasts than true tenocytes (lower quality), higher collagen type III content (also lower quality)
- remodeling phase: gradual transformation to collagen type I, collagen thickens, crosslinks increase, fiber alignment improves, fibrous tissue in/around tendon, increased stiffness; matrix is disrupted and there are more cells within ECM so less actual ECM
- scar tissue: different in composition to regular tissue, increased type III, eater, and GAG; not return to full function (decreased elasticity and prone to reinjury)
this process takes months to years!!!
what are factors that impair healing? (6)
- intrathecal location: poor healing, no paratenon (reduced extrinsic repair), adhesion
- increasing age
- immobilization (actually don’t rest as much as we’ve always said!)
- NSAIDs and corticosteroids
- decreased growth factors
- decreased expression of genes involved in tendon healing
describe the general properties of treatment in the various stages of healing
inflammatory phase: cryotherapy immediately after injury and then daily until inflam resolves
reparative phase: limited activity, massage, control pain
reparative/remodeling phase: gradual progression of strength exercises, joint mobilizations, PROM
