Synovitis & Degenerative Joint Disease, up to fetlock Flashcards

1
Q
  • two ways to get arthritis, broadly
A
  • abnormal stresses, normal cartilage
  • normal stress, abnormal cartilage
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2
Q

Synovitis & Capsulitis

A

Ø Trauma and inflammation of the synovial membrane and fibrous joint capsule.
> transient

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3
Q

Disruptive Articular Trauma
- causes

A

Ø Articular cartilage damage.
Ø Intra-articular fracture.
Ø Soft tossue injury (menisci, ligaments, etc.).
Ø Subchondral bone damage.

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4
Q

osteoarthritis (“DJD”) - nature of this disease

A

Ø Irreversible degradation & loss of articular cartilage.

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5
Q

Synovitis & Degenerative Joint Disease
Biochemical Mediators

A

Ø Matrix degrading enzymes > Metalloproteinases, Aggracanases
Ø Prostaglandins.
Ø Oxygen-derived free radicals.
Ø Inflammatory cytokines. > interleukin-1, TNFalpha

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6
Q

“recipe” for osteoarthritis

A

Athletic activity/trauma + biochemical “trauma” → osteoarthritis.

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7
Q

what two cytokines are common targets of osteoarthritis treatments

A

IL1, TNFa

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8
Q

Synovitis & Degenerative Joint Disease
clinical signs

A

Ø Joint effusion.
Ø Warmth.
Ø Pain on manipulation.
Ø Periarticular swelling.
Ø Lameness.

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9
Q

Synovitis & Degenerative Joint Disease
diagnostic steps

A

Ø Lameness examination.
Ø Diagnostic analgesia.
Ø Imaging.
> Radiographs
> Ultrasound
> CTorMRI
Ø ± Synovial fluid analysis.

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10
Q

Synovitis & Degenerative Joint Disease
treatment

A

Treatment
* rest
* Proper shoeing
* Various therapeutics
– Topical
– Systemic (oral or parenteral)
– Intraarticular

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11
Q

topical therapeutics for Synovitis & Degenerative Joint Disease

A

Ø Cold therapy
Ø Bandaging
Ø NSAIDs
Ø Dimethyl sulfoxide (DMSO)
Ø Extracorporeal shockwave therapy
Ø Therapeutic Laser
Ø Physiotherapy

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12
Q

oral therapeutics for Synovitis & Degenerative Joint Disease

A

Ø NSAIDs
Ø Neutraceuticals

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13
Q

parenteral therapeutics for Synovitis & Degenerative Joint Disease

A

Ø NSAIDs
Ø PSGAG
Ø Hyaluronic Acid
Ø Bisphosphonates

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14
Q

intra-articular therapeutics for Synovitis & Degenerative Joint Disease

A

Ø Corticosteroids
Ø Hyaluronic Acid
Ø (PSGAG)
Ø Autologous Conditioned Serum
> a.k.a. “IRAP”

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15
Q

Phenylbutazone for Synovitis & Degenerative Joint Disease
- what is it? duration of action? how long do effects last?

A

Systemic - NSAID
- 24 hours
– Better analgesia then ketoprofen
– Amelioration of lameness signs for 8 to 10 hrs & reduction of heat, effusion and synovial PGE2

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16
Q

flunixin for Synovitis & Degenerative Joint Disease
- admin route matters?
- effect timing, duration?

A

– 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

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17
Q

ketoprofen for Synovitis & Degenerative Joint Disease
- what is does
- advantage?

A

systemic NSAID
* Supposed to to inhibit also lipoxygenase, but has been proven not to be true
* Low toxicity in horses

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18
Q

naproxen for Synovitis & Degenerative Joint Disease
- what is this?
- use? comparison to others?

A

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

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19
Q

carprofen for Synovitis & Degenerative Joint Disease
- use? issues?

A

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

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20
Q

firocoxib for Synovitis & Degenerative Joint Disease
- what is this?
- comparison to others?
- efficacy?
- uses?

A

– 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

21
Q

Topical - Diclofenac cream for Synovitis & Degenerative Joint
- efficacy?

A

– The horses treated with diclofenac showed significantly less lameness, decreased carpal bone sclerosis(MRI) and higher cartilage GAG content

21
Q

topical DMSO for Synovitis & Degenerative Joint Disease
- what it does?

A

§ reduce edema
§ increase penetration of steroids
§ decrease superoxide radicals
§ However, the science behind it is shaky at best

22
Q

Extracorporeal shockwave therapy for Synovitis & Degenerative Joint
- what is it?
- efficacy?

A

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.

23
Q

Neutraceuticals - Glucosamine for Synovitis & Degenerative Joint
- what is it? what type should we use?

A
  • 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
24
Q

Neutraceuticals -Chondroitin sulphate for Synovitis & Degenerative Joint
- what is it?
- use?
- efficacy?

A
  • 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
25
Q

Neutraceuticals - ASU for Synovitis & Degenerative Joint
- what is this?
- efficacy?

A
  • 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
26
Q

Systemic or IA -Hyaluronic acid for Synovitis & Degenerative Joint
- what is this? function?
- mechanism?

A
  • 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
27
Q

what molecular wiehgt of hyaluronic acid is most effective?

A

HA in the range of 0.5 to 2.0 x 106 d is ideal

28
Q

is IV hyaluronic acid good?

A
  • 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
29
Q

Polysulfated glycosaminoglykan - Systemic (or IA)
- for Synovitis & Degenerative Joint
- what does it do?

A
  • 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
30
Q

Polysulfated glycosaminoglykan Systemic (or IA)

  • can we give IM? what route is best? pros and cons?
A
  • 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
31
Q

Systemic Biphosphonates - what do they do? uses?

A
  • Decreases osteoclastic bone resorption
    <><>
  • Clinical outcome subjectively improved for:
  • navicular disease
  • small (distal) hock joint OA
  • DJD of the spine
32
Q

Intra-articular Steroids
* Mechanism of action

A

– 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

33
Q

“Steroid arthropathy” - what are the concerns? solution?

A

– 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 %)

34
Q

intra-articular steroids
- which are common used?
- key point for steroid dosing?

A

– Methylprednisolone acetate (Depomedrol)
– Triamcinolone acetonide
– Betamethasone acetate
<><><>
- for steroids, less is more
> want to avoid cartilage damage

35
Q

Intraarticular IRAP
- what is this?
- use?

A

= 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

36
Q

Common locations for DJD

A

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)

37
Q

Etiology of DJD in “high-load, low-motion” joints.

A

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

38
Q

High load – low motion joints
> what we see with DJD > lesions, signs

A

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

39
Q

The Interphalangeal Joints - where we see DJD, names

A

Ø “High Ring Bone” = DJD pastern joint
Ø “Low Ring Bone” = DJD coffin joint

40
Q

Interphalangeal DJD
- clinical signs
- Dx?

A
  • Lameness → mild to severe. → acute or insidious onset.
    <><>
  • Diagnostic Analgesia
    Ø Abaxialsesamoid block.
    Ø Synovial anesthesia of coffin or pastern joint
41
Q

Interphalangeal DJD
Treatment

A

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 ???

42
Q

DJD of the Distal Tarsal Joints
- other name?
- which joints?
- significance?
- clinical signs / classic history
- stride
- flexion tests

A

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

43
Q

DJD of the Distal Tarsal Joints
Ø Radiographic Findings

A
  • 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.
44
Q

DJD of the Distal Tarsal Joints
Ø Medical Treatment

A

§ Early: Rest, NSAID’s, systemic & IA medications.
§ The distal tarsal joints may be the most frequently injected joints in athletic horses.

45
Q

DJD of the Distal Tarsal Joints
- facilitated ankylosis > whats this

A

§ Frequent IA corticosteroid therapy in certain horses?
§ IA 70% ethyl alcohol → initial clinical/experimental data encouraging.

46
Q

DJD of the Distal Tarsal Joints
Ø Surgical Techniques

A

§ Transarticular drilling → 70-80% success rate.
§ Transarticular laser ablation.
§ Arthrodesis using small bone plates.

47
Q

DJD of the Distal Tarsal Joints prognosis

A

§ 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.