Tendinopathy + principles of management Flashcards
(35 cards)
What are tendons?
- Anatomical structures between bone and muscles
- Transmit the force created in the muscle to the bone, and in this way they make joint movement possible
- Composed of dense, regular connective tissue and surrounded by dense irregular connective tissue sheaths
What are tendons made of?
Compromised of densely packed, parallel, slightly wavy type 1 collagen bundles, sparsely interspersed with tenocytes.
- Some lie within sheaths as they pass through areas of mechanical stress e.g. extensor tendons at wrist.
- Others surrounded by a paratendon e.g. Achiles tendon
What are tenocytes?
“tendon cells”
a specialised type of fibroblast responsible for secreting the components of the extracellular matrix
How is the collagen in tendons held together?
Held together with proteoglycan components
Both important for tendon’s mechanical properties:
COLLAGEN FIBRILS - allow tendons to resist tensile or stretching forces
PROTEOGLYCANS - allow tendons to resist compressive forces
What is the structure of a tendon?
Collagen fibril → Collagen fiber → Primary fiber bundle (sub fascicle) → Secondary → Tertiary (Endotendon surrounds each) → Tendon → Epitendon → Paratendon
How do tendons normally work?
- Tendons have to be able to withstand both tensile and compressive forces.
- When a muscle contracts, stretch is transmitted via tendon to bone to produce movement
- Some tendons have more of an energy storage and release function (like Achilles) - acts like a spring for propulsion (stretch shortening cycle).
Tendons are ‘ plastic’ structures capable of sustaining repeated tensile load.
How pathology can be manifested in tendons?
→ Overload of a tendon results in the development of pathology and a tendon that is less capable of sustaining repeated tensile load.
→ Slow metabolic rate/slow turnover of collagen - takes 50-100 days.
→ Prolonged resting of a tendon = stress shielding - can cause a mechanically weakened tendon.
What is a tendinopathy and who is likely to develop one?
An overuse tendon injury when the load placed on the tendon exceeds the tendons capacity.
→ some tendons in the body more likely to develop issues that others e.g. patella tendon, common extensor tendons, rotator cuff and achilles tendon.
→ highly prevalent + occurs in athletes + non-athletes
→ results in pain, decreased exercise tolerance of the tendon and impaired physical function.
Extrinsic risk factors for tendinopathy?
- changes in loading
- activity levels
- training errors
- recent injury
Intrinsic risk factors for tendinopathy?
- recent injuries
- age
- gender: male>female
- weight gain - effects circulating cytokine levels - creates cellular reaction and effects the tendon
- muscle power/strength
- previous lower limb tendinopathy
- altered biomechanics e.g. reduced ankle dorsiflexion
Who created the continuum model of tendon pathology (load induced tendinopathy)?
Cook + Purdam , 2009
What are components of Cook + Purdam’s continuum model?
Reactive tendinopathy
Tendon dysrepair (or failed healing)
Degenerative tendinopathy
Continuum model thus continuity between stages
Adding or removing load is the primary stimulus that drives a tendon fads or back along the continuum.
Reactive tendinopathy?
→ Can be due to overtraining/ sudden change in intensity/ blow
→ Non-inflammatory, proliferative response in the cells + matrix
→ Cellular proliferation + increased activation of tenocytes = increased deposition of proteaglycans by tenocytes
→ Resuts in matrix change - increased bound water associated with increased proteoglycans (hydrophilic)
→ Changes in ground substance in reactive tendinopathy + resulting tendon swelling occurs as quick adaptation necessary
→ Swelling/thickening happens to reduce stress- force per unit area - by increasing cross-sectional area and allows adaptation to occur (stiffness reduced).
Tendon disrepair? (or failed healing)
→ Attempt of tendon to heal with greater matrix breakdown
→ Overall increase in tenocytes and cellular metaplasia so cells change and become more like chondrocytes - from flat, elongated cells to rounded cells.
→ Marked increase in protein production
→ Type 1 + 3 collagen
→ Increase in proteoglycans results in separation of collagen and further disorganisation of the matrix
→ Increased vascularity of tendons of tendons + neural ingrowth into the tissue.
Degenerative tendinopathy?
If strain + individual factors continue, tendon becomes more pathological.
→ extensive matrix damage and cell changes
→ areas of cell death evident
→ tendon degenerative and some areas have hardly any cells present
→ large areas of matrix disorganised filled with blood vessels and nerve ingrowth
→ little collagen present - tendons susceptible to rupture
→ not much capacity for reversibility
→ islands of pathology
Features of a normal tendon?
flat elongated tendon cells (tenocytes)
parallel collagen fibres
smaller amount of proteoglycan
minimal vascularity within the tendon and minimal nerve fibres
Features of abnormal tendon disrepair?
change in cell appearance and activation (rounded tenocytes more like chondrocytes)
loss of collagen architecture
increased proteoglycan
increased vascularity + nerve ingrowth
Features of abnormal tendon degeneration?
areas of cell death evident
disorganised collagen matrix
increased proteoglycan and matrix breakdown products also evident
increased vascularity + nerve ingrowth
Clinical presentation of tendon problems?
Variable depending on the tendon affected and the site + stage of pathology.
Common clinical symptoms + signs:
- localised pain or swelling at site
- pain may develop after heavy or unaccustomed training/activity (or trauma)
- latent pain after exercise
- pain and some stiffness on rising/use of the tendon
What do cook and purdah suggest about tendon symptoms?
→ An older person with a thick, nodular tendon on palpation is likely to have a degenerative tendon.
→ A young athlete after an acute overload with a swelling of the tendon will have a reactive tendinopathy
What is the main goal of tendionopathy treatment?
To reduce pain, increase function and allow return to activity
How with tendinopathy rehabilitiation differ?
Varies depending on the perceived stage of the tendinopathy; functional assessment; activity status of the person and other contributing factors ( e.g. biopsychosocial).
What education and empowerment could be given to patients with chronic tendinopathy?
- basic education about condition
- explaining that not all pain is ‘harmful’ in tendinopathy
- discussing and explaining the pain felt through loading and resistance programmess may help address “fear-avoidance” and catastrophising beliefs.
- imported to bust misconceptions
Why do tendinopathies cause pain?
No clear explanation.
→ could arise from connective tissue sheaths
→ may be releated to ingrowth of blood vessels and nerves in chronic pts
→ chronic tendon pain can lead to central sensitisation
this is the increased reponsiveness of CNS neurons - due to continued afferent input from C-fibres.
changes in sensisitive thesholds @ dorsal horn + altered sensory processing = increased pain perception.
