Synovitis & Degenerative Joint Disease, up to fetlock Flashcards
- two ways to get arthritis, broadly
- abnormal stresses, normal cartilage
- normal stress, abnormal cartilage
Synovitis & Capsulitis
Ø Trauma and inflammation of the synovial membrane and fibrous joint capsule.
> transient
Disruptive Articular Trauma
- causes
Ø Articular cartilage damage.
Ø Intra-articular fracture.
Ø Soft tossue injury (menisci, ligaments, etc.).
Ø Subchondral bone damage.
osteoarthritis (“DJD”) - nature of this disease
Ø Irreversible degradation & loss of articular cartilage.
Synovitis & Degenerative Joint Disease
Biochemical Mediators
Ø Matrix degrading enzymes > Metalloproteinases, Aggracanases
Ø Prostaglandins.
Ø Oxygen-derived free radicals.
Ø Inflammatory cytokines. > interleukin-1, TNFalpha
“recipe” for osteoarthritis
Athletic activity/trauma + biochemical “trauma” → osteoarthritis.
what two cytokines are common targets of osteoarthritis treatments
IL1, TNFa
Synovitis & Degenerative Joint Disease
clinical signs
Ø Joint effusion.
Ø Warmth.
Ø Pain on manipulation.
Ø Periarticular swelling.
Ø Lameness.
Synovitis & Degenerative Joint Disease
diagnostic steps
Ø Lameness examination.
Ø Diagnostic analgesia.
Ø Imaging.
> Radiographs
> Ultrasound
> CTorMRI
Ø ± Synovial fluid analysis.
Synovitis & Degenerative Joint Disease
treatment
Treatment
* rest
* Proper shoeing
* Various therapeutics
– Topical
– Systemic (oral or parenteral)
– Intraarticular
topical therapeutics for Synovitis & Degenerative Joint Disease
Ø Cold therapy
Ø Bandaging
Ø NSAIDs
Ø Dimethyl sulfoxide (DMSO)
Ø Extracorporeal shockwave therapy
Ø Therapeutic Laser
Ø Physiotherapy
oral therapeutics for Synovitis & Degenerative Joint Disease
Ø NSAIDs
Ø Neutraceuticals
parenteral therapeutics for Synovitis & Degenerative Joint Disease
Ø NSAIDs
Ø PSGAG
Ø Hyaluronic Acid
Ø Bisphosphonates
intra-articular therapeutics for Synovitis & Degenerative Joint Disease
Ø Corticosteroids
Ø Hyaluronic Acid
Ø (PSGAG)
Ø Autologous Conditioned Serum
> a.k.a. “IRAP”
Phenylbutazone for Synovitis & Degenerative Joint Disease
- what is it? duration of action? how long do effects last?
Systemic - NSAID
- 24 hours
– Better analgesia then ketoprofen
– Amelioration of lameness signs for 8 to 10 hrs & reduction of heat, effusion and synovial PGE2
flunixin for Synovitis & Degenerative Joint Disease
- admin route matters?
- effect timing, duration?
– IV and PO plasma levels are similar
– IM associated with myonecrosis !!!!!
– Peak after 30 min
– Study comparing postOp analgesia , flunixin lasted 12.8, PBZ 8.4 and carprofen 11.7 hrs
ketoprofen for Synovitis & Degenerative Joint Disease
- what is does
- advantage?
systemic NSAID
* Supposed to to inhibit also lipoxygenase, but has been proven not to be true
* Low toxicity in horses
naproxen for Synovitis & Degenerative Joint Disease
- what is this?
- use? comparison to others?
Systemic - NSAIDs
– Oral
– No comparison to other NSAIDs regarding efficacy for OA
– In induced myositis naproxen was more effective then PBZ to provide analgesia (Jones 1978)
– Low toxicity
carprofen for Synovitis & Degenerative Joint Disease
- use? issues?
systemic NSAID
– Seems to have have disease modifying properties, but needs more work in equine
– 3/6 horses developed subQ edema after 1 week of twice the normal dose
firocoxib for Synovitis & Degenerative Joint Disease
- what is this?
- comparison to others?
- efficacy?
- uses?
– Selective COX 2 inhibitor
– Does not affect mucosal barrier as much as flunixin
– Reduced chronic lameness
– As effective as PBZ to reduce lameness & after 14 days better range of motion scores then PBZ
– Effective visceral analgesia
Topical - Diclofenac cream for Synovitis & Degenerative Joint
- efficacy?
– The horses treated with diclofenac showed significantly less lameness, decreased carpal bone sclerosis(MRI) and higher cartilage GAG content
topical DMSO for Synovitis & Degenerative Joint Disease
- what it does?
§ reduce edema
§ increase penetration of steroids
§ decrease superoxide radicals
§ However, the science behind it is shaky at best
Extracorporeal shockwave therapy for Synovitis & Degenerative Joint
- what is it?
- efficacy?
u Pulsed, high-energy acoustic waves.
u Exact MOA is unclear.
u Energy liberated at tissue interfaces.
u DJD study results are highly variable.
u Recognized analgesic affect.
Neutraceuticals - Glucosamine for Synovitis & Degenerative Joint
- what is it? what type should we use?
- Component of cartilage matrix
- Levels of glucosamine are low in equine serum and synovial fluid
- use glucosamine SULPHATE, it stays in synovial fluid longer
- shown to reduce needed application of IA medications in hock in the long term
Neutraceuticals -Chondroitin sulphate for Synovitis & Degenerative Joint
- what is it?
- use?
- efficacy?
- Component of cartilage matrix
- Used alone not beneficial
- Combination of chondroitin & glucosamine given to 15 veteran horses for 3 months – after 8 weeks, range of motion and stride length was significantly increased
Neutraceuticals - ASU for Synovitis & Degenerative Joint
- what is this?
- efficacy?
- ASUs (=avocado and soybean unsaponifiable extracts)
- Lameness scores, joint effusion, inflammatory
parameters were unchanged - Post mortem showed less cartilage erosion, and less synovial hemorrhage
- Total GAG content in cartilage higher
Systemic or IA -Hyaluronic acid for Synovitis & Degenerative Joint
- what is this? function?
- mechanism?
- Part of extracellular matrix (elasticity)
- Synthesized by chondrocytes & synoviocytes
- Function:
– Viscoelasticity of joint fluid & lubrication
– Reducing cell migration
– Decreasing rate of diffusion & flow of solutes
– Anti-inflammatory due to “steric hindrance” (slowing of chemical reactions) - reduce chemotaxis by increasing phagocytosis of activated neutrophils
- Clinical efficacy of IA HA demonstrated in multiple clinical reports
what molecular wiehgt of hyaluronic acid is most effective?
HA in the range of 0.5 to 2.0 x 106 d is ideal
is IV hyaluronic acid good?
- yes seems to be at least as an anti-inflammatory
- Reduced lameness, less synovial inflammation, lower TP, reduced PGE2 = effect on synoviocytes
- No effect on cartilage itself
Polysulfated glycosaminoglykan - Systemic (or IA)
- for Synovitis & Degenerative Joint
- what does it do?
- Mechanism of action – unknown
- Inhibits degradative enzymes involved in OA
- Anti-inflammatory role by reducing leukocyte migration & interleukin levels
- Biosynthetic role – increases HA, GAG, collagen content
Polysulfated glycosaminoglykan Systemic (or IA)
- can we give IM? what route is best? pros and cons?
- Evidence of IM efficacy not strong
- Efficacy demonstrated particularly for IA
- Drawback for IA administration is increased risk of sepsis
- Inhibits complement activity in the joint
- Incidence much lower when combined with amikacin
Systemic Biphosphonates - what do they do? uses?
- Decreases osteoclastic bone resorption
<><> - Clinical outcome subjectively improved for:
- navicular disease
- small (distal) hock joint OA
- DJD of the spine
Intra-articular Steroids
* Mechanism of action
– Reduce capillary dilatation, margination, migration & accumulation of inflammatory cells
– Inhibit synthesis & release of inflammatory mediators involved in development of OA (eg prostanoids, nitric oxide)
– Pain relief = reduction of prostaglandin due to inhibition phospholipase A2 and cyclooxygenase (COX) 2 inhibition
– Also disease modifying!!!!
* Suppress TNFα and IL1 at low concentrations – these are the most cartilage destructive enzymes
* Inhibit other mediators involved in OA at low doses
“Steroid arthropathy” - what are the concerns? solution?
– Worry that pain free joint may accelerate cartilage degeneration
– High dose inhibits proteoglykan synthesis & negatively affect collagen organization
BUT only low levels needed for scavenging mediators
– REST is needed after injection (increased rest in people increased treatment efficacy by 70 %)
intra-articular steroids
- which are common used?
- key point for steroid dosing?
– Methylprednisolone acetate (Depomedrol)
– Triamcinolone acetonide
– Betamethasone acetate
<><><>
- for steroids, less is more
> want to avoid cartilage damage
Intraarticular IRAP
- what is this?
- use?
= Interleukin-1 Receptor Antagonist Protein
* In OA, interleukin 1(IL1) , a proinflammatory cytokine, induces matrix degeneration
* Healthy joint = balance between IL1 & IL1 antibody
- expensive but usually effective, if client wants to spend money do this instead of steroids
Common locations for DJD
High load – low motion joints
* Small hock joints (tarsometatarsal & distal intertarsal joints)
* Interphalangeal (Coffin/Pastern) Joints
<><>
High motion – lower load joints
* Fetlock
* Carpus
* Stifle (femorotibial joint)
Etiology of DJD in “high-load, low-motion” joints.
Ø Theory that nutrient and waste exchange less efficient in these joints because forces distributed over a smaller area (↑ pressure).
Ø May result in cartilage trauma (overload?) & perpetuated by trauma > INFLAMMATION
High load – low motion joints
> what we see with DJD > lesions, signs
Ø Cartilage necrosis
Ø Focal destruction of subchondral bone/ sclerosis
Ø Periosteal new bone & enthesiophyte production
Ø Ankylosis (complete/ partial) in advanced stages
Ø Advanced cases → bony enlargement
The Interphalangeal Joints - where we see DJD, names
Ø “High Ring Bone” = DJD pastern joint
Ø “Low Ring Bone” = DJD coffin joint
Interphalangeal DJD
- clinical signs
- Dx?
- Lameness → mild to severe. → acute or insidious onset.
<><> - Diagnostic Analgesia
Ø Abaxialsesamoid block.
Ø Synovial anesthesia of coffin or pastern joint
Interphalangeal DJD
Treatment
Ø Rest, NSAID’s and other medications as needed, initially.
Ø Intra-articular medications often quite helpful.
Ø Proper foot trimming and good shoeing.
Ø Surgical arthrodesis of PIP joint.
Ø Alcohol facilitated arthrodesis ???
DJD of the Distal Tarsal Joints
- other name?
- which joints?
- significance?
- clinical signs / classic history
- stride
- flexion tests
Ø a.k.a. Distal tarsitis or “bone spavin”.
Ø Tarsometatarsal (TMT) and distal intertarsal (DIT) joints.
Ø The most frequent and important cause of hind limb lameness in general.
Ø Typically, horses have an insidious onset of hind limb lameness, over a variable period.
Ø A “classic” history is that the horse “warms-out” of the lameness as exercise progresses.
Ø Horses tend to exhibit a shortened cranial phase of the stride and may stab or scuff the toe.
Ø Upper limb flexion positive
DJD of the Distal Tarsal Joints
Ø Radiographic Findings
- remodelling (subchondral sclerosis and osteolkysis) and osteophyte formation
- as the disease advances, decreases in joint space will become evident
- slab fractures of T-3 and T-C can be present.
DJD of the Distal Tarsal Joints
Ø Medical Treatment
§ Early: Rest, NSAID’s, systemic & IA medications.
§ The distal tarsal joints may be the most frequently injected joints in athletic horses.
DJD of the Distal Tarsal Joints
- facilitated ankylosis > whats this
§ Frequent IA corticosteroid therapy in certain horses?
§ IA 70% ethyl alcohol → initial clinical/experimental data encouraging.
DJD of the Distal Tarsal Joints
Ø Surgical Techniques
§ Transarticular drilling → 70-80% success rate.
§ Transarticular laser ablation.
§ Arthrodesis using small bone plates.
DJD of the Distal Tarsal Joints prognosis
§ Easily managed with IA medications in the early stages.
§ If you want to chemical arthrodese, more success if done early § Post operative success varies with each case and the horse’s use.
