Equine Osteoarthritis Flashcards
1
Q
What is DJD
A
= degenerative joint disease
- most common joint disease in horses
- joints affected = hock, fetlcok, knee
- an arthritis, inflamation of surfave of joints caused by wear and tear
- process = inflamation affects more and more structures
- costly to industry in performance, treatments
2
Q
Joint capsule
A
- joint capsule contains hyaluronic acid which is rich in protein
- produced by sinovial sites which also produce chemical mediators (prostaglandins and interlukins)
- outermost fibrous layer of joint capsule that support synovial membranes
- inserts into the bone at the edge of the articular cartilage
- softer articular cartilage 75% water and collegen type 2, proteoglycans, chondrocytes
3
Q
Joint capsule - osteoarthritis
A
- deterioration of articular cartilage (break down), synovitis and changes in bone and soft tissue structures
- inflamation increase inflamtory and synovial fluids
- cartilage breakdown so much bone exposed, holes, cysts occur within surface
- joint cant glide, cause pain as it is crunching, swelling, trigger nerves and receptors
- Advanced = more swollen fibrous tissue around joint capsule and pressure, damage to articular surface continuing and forming calcified cartilage, bone deposits = osteophytes
4
Q
is equine osteoarthrits secondary to other causes?
A
Yes
- horse has a lot of work
- result of wear and tear, repeat concussion, inflamation due to joint damage
- trauma, fracture to joint, infectious within joints = arthritis, condition previously had in younger horse (OCD) = more predisposed to arthritis when older
5
Q
Age groups affected
A
- older age = more work when younger
6
Q
CS
A
- pain - vary lameness, reduced flexion
- joint effusion (swelling)
- soft tissue swelling
important to keep moving (sieses up feel worse)
7
Q
Normal articular cartilage compared to osteoarthritis (microscopically)
A
- chondrocytes = release cartilage matrix which embeded withing it
- chondrocytes not evenly spread, clustered
- fibrilation = breaking down surface of cartilage
8
Q
Process of cartilage destruction - inflamation
A
- inflamation (increased blood flow and swelling, heat increased vasodilation)
- affects synovial membrane
- congested, thickened
- ambormal increase in no. of synovicytes
- inflamatory cells infiltration into joint
- substances released e.g. interleukin 1 = a cytokine (messenger) regulate immune system and inflammatory response and main substance responsible for destruction of cartilage
- when antibodies produced against interleukin 1 = benefit stop cartilage damaged
~ metaloproteiniases
~ aggrecanases
~ prostaglandins
~ free radicles
~ tumour necrosis factor-a
9
Q
Process of cartilage destruction - fibrilation and loss of articular cartilage
A
- fibrilation = softening and cleft formations and start to break apart
- loss of cartilaginous extra cellular matrix
- chondrocyte apoptosis (increased by up to 8x) programed cell death
- cartilage fibrilation may extend as full depth cleft to sub-chondral bone
10
Q
Radiological changes
A
- osteophytes = put down bone to cope with extra pressure
- increased sub-chondral bone density (sclerosis)
~ occasional lysis or cyst like lesions in subchondral bone - joint space reduction
11
Q
Treating DJD - injections
A
- intra-articular low dose corticosteroid injection (anti-inflammatory product straight into joint) low dose = decrease severity of lesions and encourage heeling in joint
~ quick response to tratment (48 hours)
~ doesnt last long, repeat regulally, inject into joints difficult (precision, sterile environment = risk infection in joint very severe) - intra articular to stimulate endogenous HA production
~ hyaluronic acid to smooth joints, watered down if inflammation
~ may also be anti inflammatory - PSGAGs (polysulphated glycosamminoglycans) - chondroitin sulphates
~ chondroprotective - sustain/promote chondrocyte activity
~ inhibit effects of cytokines and prostaglandin on cartilage
~ may be anti-inflamatory in the synovia
~ intra articulally but marketed as intra muscually which reducs likely hood get into joints
12
Q
Treating DJD - NSAIDs
A
cant reverse it but slow it down and make horse comfortable
- NSAIDs
~ used in early stages
~ reduce inflamation and pain relief and easy to administer (oral, inject)
13
Q
Treating DJD - IRAP
A
- an autologous modified serum
= interleukin 1 receptor antagonist protein - to block IL-1 - made from horses own blood = little risk of rejection
~ spun down for serum
~ stimulate production of antagonist proteins
~ incubated and serum part is removed
~ serum into lots of syringes
~ inject into joints
~ potent anti-inflammatory going against interleukin 1 (causes damage to articular cartilage) encourage cartilage to heel - aids control of arthritis progression
14
Q
Treating DJD - Neutraceuticles
A
- bioavailability (amount med available to do job)via oral route not great
- 2% glucosamine and 22-32% chondroitin
- glucosamine - replace etra celluar matrix broken down
- chondrin sulphate - antiinflamatory properties, work with glucosamine (synergistic effect)
- MSM - no support for use in orthopaedic diseases
15
Q
Treating DJD - other possibilities
A
- avacado-soybean unsaponifiables
- oral hyaluroan gel
- green lipped mussle extract
- epiitalis
