tendinopathy Flashcards
where can tendinopathy occur in lower limb
achilles tendon, patella tendon, hamstring tendon, glut tendon, plantar problems
tendon structure
tendon originates from muscles, this goes into fascicles, within this you have fibres and fibrils, within the fibril is the tropocollagen- where crimping occurs (when stretching we elongated crimped tissue), within fascicles in interfasciular matrix- this is where lots of cells are stored- these cells can move out and cause issues
important of fascicles
each individual fascicles in continuous all the way down to insertion, important as if there is a diseased area in one area of fascicles, it can cause structural degradations, weaknesses and possibly snapping, they can be different sizes
what is tendinopathy
is a degree of inflammation, lots of collagen remodelling, lots of cell proliferation, neoangulinins, fibres of tendon should be continuous and linear, but with tendinopathy fibres become stringy, non-linear, not able to transfer force and stress tissue- mushy- may lead to rupture
what can lead to a tendon rupturing
this is caused by excess rest or exercise, if cells become over stimulate they degrade as they cant cope, if ypu under stimulate tissue, cells degrade tissue as it as seen as not needed
is tendinopathy degenerative or inflammation
there are components of inflammation with tendinopathy- low grade immune response (more immune cells), in ruptured tissue there is even more cells, immune system is targeting inflammation
is tendinopathy degenerative or inflammation- Adam and cooks and pardums model- 2009
if tissue is stressed, then it will adapt and will become more robust and resilient- too much of this can lead to tendon failing
structural changes with tendinopathy- alterations to cell population
increased number of tenocytes, increase tenocyte metabolism, increased immature tenocytes (can’t produce collagen that they should use), increased rate of apoptosis immunoactivity cells
structural changes with tendinopathy- disorganisation of collagen
reduced type 1 collagen, disorganised areas with higher concentrations of immature collagen bundles (increased type 3
structural changes with tendinopathy- ground substance
PG and GAG- these are natural lubricants around normal tissue, content alters, increased H20 (due to tenocytes producing more PG and GAG- but producing wrong type, they are bigger than normal and are hydrophilic- tendons absorb water and are weaker)
structural changes with tendinopathy- what does PG and GAG stand for
PG- proteoglycans
GAG- glucose amino glycans
structural changes with tendinopathy- chemical alterations
substance P, glutamate and lactate- all of these sensitive nerve tissue in tendons
structural changes with tendinopathy- neovascularization
influx of blood vessels into anterior surface and mid substance this is associated with various nerve fibres in growing into tendon- more nerves in areas where they should be, leads to them being sensitised, so when they are loaded pain is felt
tendinopathy of upper limb
RC- supraspinatus, Long head biceps, lateral/ medial epicondylagia, EPB/L
tendinopathy of lower limb
gluteal region, patella, achilles tendon, tibialis anterior/ posterior, peroneus longus/ brevis
when can the Achilles tendon rupture
can only occur when there is already underlying gross degeneration of achilleas tendon
who gets tendinopathy
endurance runners- 57%likely to get Achilles tendinopathy,
it is more common than OA
active groups in 40’s-
or groups of people in 60 with sedentary lifestyle
how does tendinopathy occur- wear
increased wear- more damage, training load, previous injury, muscle weakness, lower limb biomechanics, footwear training surfaces
how does tendinopathy occur- repair
tendon cannot recover properly- damage tendon, tendon structure, increased BMI or cytokines, diabetes, medication- antibiotics, steroids- make sin and tendons thinner, increase age, gender, genetic predisposition, sedentary behaviour, sleep, stress, eheumatological disorders
how does diabetes cause tendinopathy
increased cytokines due to increase glucose (also has advanced glycatin end product (ages)- alters flexibility of collagen (skin and CT)
how can tendinopathy be described
is an active process of degeneration that involves inflammatory pathways- transient tendon response to load
tendinopathy modifiable risk factors
tendon load, muscle power, obesity, cholesterol
tendinopathy non- modifiable risk factors
DM, genetic factors, early menopause, rheumatological disease, recent sciatica, recent injury
tendinopathy
homeostasis appears important, wear and repair balance is critical, inflammation and degeneration part of tendinopathy, changes in cells/ structure/ ground/ substance/ neovessels