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A U E R S & T > Chapter 80 - Medical treatment of joint disease > Flashcards

Chapter 80 - Medical treatment of joint disease Flashcards

1
Q
A

Figure 80-1. Schematic representation of inhibition
of the inflammatory cascade by nonsteroidal antiinflammatory
drugs (NSAIDs) and corticosteroids.

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2
Q
A

Figure 80-2. Schematic representation of effects associated with the administration of nonsteroidal antiinflammatory drugs (NSAIDs). MMP, Matrix metalloproteinase.

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3
Q
A

Figure 80-3. Schematic representation of the cyclooxygenase isoenzymes and target tissues. PGH2, Prostaglandin H2.

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4
Q

What are the two main goals of medical treatment for osteoarthritis in horses?

A

Reducing pain (lameness) and minimizing progression of joint deterioration.

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5
Q

What factors influence the optimization of a treatment plan for OA?

A

Accurate diagnosis, stage of disease, severity, available treatment modalities, and rehabilitation time.

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6
Q

What is the primary action of nonsteroidal anti-inflammatory drugs (NSAIDs) in treating joint disease?

A

Inhibiting the arachidonic acid cascade.

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7
Q

Which specific prostaglandin series is involved in pain and inflammation in damaged joints?

A

Prostaglandin E (PGE) series.

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7
Q

Why is long-term use of NSAIDs limited in treating joint disease?

A

Due to renal and gastrointestinal side effects.

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8
Q

What is a significant concern regarding the inhibition of PGE production?

A

Potential long-term unfavorable effects on cartilage metabolism.

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9
Q

What discovery in the early 1990s advanced the understanding of NSAIDs for OA treatment?

A

Identification of cyclooxygenase (COX) isoenzymes COX-1 and COX-2.

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10
Q

What role does COX-1 play in the body?

A

Associated with housekeeping functions and normal physiological functions of the gastrointestinal and renal systems.

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11
Q

How is COX-2 primarily involved in the body?

A

Associated with inflammatory events driven by macrophages and synovial cells.

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12
Q

What adverse effects are linked to NSAIDs that preferentially inhibit COX-1?

A

Damage to the gastroduodenal mucosa.

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13
Q

What has research indicated about topical NSAID applications?

A

They can be clinically beneficial and may reduce systemic side effects.

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14
Q

Which NSAID remains popular for musculoskeletal pain in horses, and why?

A

Phenylbutazone; due to its cost, ease of administration, and relatively few side effects in short-term use.

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15
Q

What were the findings when comparing phenylbutazone and diclofenac cream in horses with OA?

A

Phenylbutazone was associated with significantly more pathologic changes.

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16
Q

What effect does phenylbutazone have on μ-opioid receptor (MOR) expression in equine synovial membrane?

A

It attenuates the upregulation of MOR expression following synovitis.

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17
Q

What is the significance of firocoxib in the treatment of equine OA?

A

It is a selective COX-2 inhibitor approved for use in horses, effective in controlling inflammation associated with OA.

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18
Q

What concerns arise from stacking NSAIDs like phenylbutazone with flunixin meglumine?

A

Potential secondary side effects from combining NSAIDs.

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19
Q

How did lameness scores change during a study of firocoxib administration?

A

Scores improved rapidly within the first 7 days and continued to improve more slowly through 14 days.

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20
Q

What does ongoing research need to focus on regarding NSAIDs?

A

Determining appropriate dosages and durations of prescription.

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21
Q

How does the pharmacokinetics of firocoxib impact its clinical use?

A

A loading dose has been shown to maintain a constant drug concentration.

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22
Q

What is the current status of NSAIDs in treating joint inflammation associated with OA in horses?

A

Continued use is likely, with selective COX-2 inhibitors being utilized more frequently.

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23
Q

What enzyme do corticosteroids inhibit in the arachidonic acid cascade?

A

Phospholipase A2.

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24
Q

What is a selective action of corticosteroids aside from their effects on the arachidonic acid cascade?

A

They are selective COX-2 inhibitors.

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25
Q

What three corticosteroid preparations are currently available for equine clinicians?

A

Methylprednisolone acetate (MPA), triamcinolone acetonide (TA), and compounded betamethasone.

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26
Q

Which corticosteroid preparation showed the most beneficial effects in studies?

A

Triamcinolone acetonide (TA).

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27
Q

What detrimental effects were noted with methylprednisolone acetate (MPA)?

A

Detrimental effects on articular cartilage.

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28
Q

What does the lack of measured effects from compounded betamethasone suggest?

A

It has a less potent effect on joint tissues compared to TA and MPA.

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29
Q

In what context is the use of corticosteroids particularly recommended?

A

In high-motion joints.

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30
Q

What concerns arise regarding corticosteroids and catastrophic racetrack injuries?

A

Their ability to mask pain and potentially exacerbate injuries.

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31
Q

What recommendation did the International Federation of Horse Racing Authorities make regarding corticosteroid withdrawal?

A

A 14-day withdrawal period.

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32
Q

What was the role of corticosteroids in the study linking them to musculoskeletal injuries?

A

A positive association was identified but not a specific causal role.

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33
Q

What combination of substances was found to be most toxic to bovine articular chondrocytes?

A

Methylprednisolone acetate (MPA) combined with lidocaine.

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33
Q

How did the administration of mepivacaine affect the efficacy of TA?

A

It did not alter the potency or duration of action of TA.

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34
Q

What is a controversial aspect regarding the rest period following IA corticosteroid treatment?

A

Whether a rest period is necessary for better drug penetration and effectiveness.

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35
Q

What concerns are there regarding corticosteroids’ effects on chondrocyte metabolism?

A

They may transiently decrease anabolic metabolism, but the concern is considered overstated.

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36
Q

What has been noted about the effects of MPA on joint tissues?

A

Changes induced by MPA can last for more than 21 days.

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37
Q

What does clinical impression suggest about confinement after corticosteroid injection?

A

Confinement for 7 to 10 days can prolong the duration of action.

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38
Q

What association has been suggested between corticosteroids and laminitis?

A

A corticosteroid-induced laminitis association has not been directly proven.

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39
Q

What are the suggested maximum total body doses of TA to avoid laminitis?

A

18 mg for TA, 200 mg for MPA, and 30 mg for compounded betamethasone.

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39
Q

What did studies reveal about the incidence of laminitis following TA injections?

A

Very low incidence rates of 0.5% and 0.15% were reported.

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40
Q

Why is it difficult to establish a consistent model of laminitis following corticosteroid injection?

A

Due to variability in clinical reports and anecdotal suggestions.

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41
Q

What total body dose of TA does the author typically use in healthy athletic horses?

A

20 to 40 mg.

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42
Q

What should be considered regarding the frequency of corticosteroid treatment?

A

Higher total body doses should not be repeated frequently, especially in unfit horses.

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43
Q

What potential effects did the study on IA corticosteroids show regarding inflammatory cytokines?

A

A therapy attenuated the effects of IL-1 and TNF-α on cartilage.

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44
Q

Which matrix metalloproteinases’ expression was decreased by corticosteroids?

A

MMP-1, MMP-3, and MMP-13 mRNA.

45
Q

What finding suggests that corticosteroids might impede cartilage degradation?

A

Decreased expression of MMPs during inflammation.

46
Q

What type of joint is triamcinolone acetonide particularly recommended for?

A

High-motion joints.

47
Q

How can the effectiveness of corticosteroid injections be influenced post-treatment?

A

By the exercise or rest period that follows administration. box stall or paddock for 7 to 10 days, with a slow return to full work in the subsequent week can prolong the duration of action following injection,

48
Q

what are the maximal dosages of triam, methy and beta?

A

It has been suggested that the total body dose of TA should not exceed 18 mg, MPA should not exceed 200 mg, and compounded betamethasone should not exceed 30 mg.

49
Q

What are the two components that make up the disaccharide hyaluronan?

A

D-glucuronic acid and N-acetyl-D-glucosamine.

50
Q

Who produces HA for incorporation into synovial fluid?

A

Synoviocytes.

51
Q

What cells are responsible for producing HA that is incorporated into the extracellular matrix?

A

Chondrocytes.

51
Q

How do the concentration and molecular weight of HA affect its function?

A

They are important for its normal function and lubricating properties.

52
Q

What happens to the lubricating properties of HA during disease?

A

They are believed to decrease, leaving the joint unprotected.

53
Q

What anti-inflammatory activities has exogenous HA been documented to have?

A

Inhibition of chemotaxis, phagocytosis, and lymphocyte activity.

54
Q

What type of free radicals does HA scavenge?

A

Oxygen-derived free radicals.

55
Q

What is the half-life of exogenous HA when administered intraarticularly?

A

In the magnitude of hours.

55
Q

What is the hypothesized effect of exogenous HA administration on synoviocytes?

A

It may increase the synthesis of high-molecular-weight hyaluronate.

56
Q

What correlation has been established regarding HA and articular cartilage erosion?

A

A direct correlation between lubricating properties of HA and cartilage erosion.

57
Q

What is the normal molecular weight range for HA found in synovial fluid?

A

0.5 to 3.0 million Daltons.

57
Q

What concentration range is normal for HA in synovial fluid?

A

0.33 to 1.5 g/L.

58
Q

What molecular mass is believed to have little effect when it comes to HA?

A

Less than 500 kDa.

59
Q

What was the dosage of HA administered in the randomized controlled trial involving knee OA?

A

20 to 25 mg of HA once a week for three treatments.

60
Q

What was the outcome of the HA treatment in the knee OA trial?

A

Reduced pain by up to 50% for 6 months post-treatment.

60
Q

What issue does the study raise about high molecular weight HA products?

A

It questions their cost/benefit ratio compared to mid-molecular weight products.

61
Q

What is the purpose of viscosupplementation?

A

To restore the elasticity and viscosity of synovial fluid.

62
Q

What advantage does cross-linked HA have over other forms?

A

Longer retention time and increased resistance to free radicals.

62
Q

What is Hylan G-F 20, and what are its reported benefits?

A

A cross-linked HA with effectiveness shown in clinical studies as a nonsteroidal medication.

63
Q

What was the outcome of the study on hylan in horses?

A

It failed to show beneficial effects, possibly due to differences in disease models.

64
Q

What dosing frequency has been suggested based on human clinical studies?

A

At least three doses, administered 1 week apart.

64
Q

What dosage of conventional HA was found effective in the equine fracture model?

A

20 mg per joint.

65
Q

In what conditions might HA be more effective?

A

In mild synovitis or capsulitis, rather than severe conditions.

66
Q

What outcomes were observed in a study of IV HA in Quarter Horses?

A

Horses treated with HA raced longer, had better performance metrics, and earned more money.

66
Q

What is the significance of the molecular weight of HA in its therapeutic effects?

A

Higher molecular weight is generally more effective, though exact correlations can vary.

67
Q

What are some unanswered questions regarding the mechanism of action for IV HA?

A

The specific mechanisms and long-term effects are not well understood.

68
Q

What are some examples of polysulfated polysaccharides (PSPs)

A

Polysulfated glycosaminoglycan (PSGAG; Adequan), GAG peptide complex (Rumalon), and pentosan polysulfate (Cartrophen Vet; Pentequin).

69
Q

What are chondroprotective effects, and how are PSPs related to them?

A

Chondroprotective effects refer to the ability to protect, retard, or reverse cartilage damage, which PSPs exhibit, although they are more specifically categorized as DMOAoaDs for their slow-acting effects on osteoarthritis.

70
Q

From what source is PSGAG primarily manufactured?

A

PSGAG is manufactured from bovine lung and trachea extracts containing chondroitin sulfate.

71
Q

Which key enzymes and cytokines have PSGAGs been shown to inhibit in some studies?

A

IL-1, matrix metalloproteinases (MMPs), and prostaglandin E2 (PGE2).

71
Q

What forms of PSGAG administration are mentioned in the text, and which is suggested to be more effective?

A

Intramuscular (IM) and intra-articular (IA) administration; IA administration appears to be more effective, particularly for acute synovitis and hemarthrosis.

72
Q

What were the findings of studies administering IA PSGAGs weekly in horses with induced osteochondral lesions?

A

IA PSGAGs significantly improved lameness, reduced radiographic progression of OA, and improved joint capsule parameters compared to untreated ponies.

73
Q

What was observed regarding PSGAG’s effectiveness when administered IM compared to shock wave therapy?

A

Shock wave therapy showed more impressive improvements than IM PSGAGs in treating joint conditions.

73
Q

How did the combination of PSGAG and triamcinolone acetonide (TA) perform compared to using each alone?

A

The combination was found to be less effective than using PSGAG or TA alone.

74
Q

For what conditions did practitioners find PSGAGs to be more effective than hyaluronic acid (HA)?

A

PSGAGs were deemed more effective for subacute osteoarthritis (OA) but less effective for idiopathic joint effusion and acute synovitis.

75
Q

What unique characteristic does pentosan polysulfate (PPS) have compared to PSGAG?

A

PPS is derived from beech wood hemicellulose, unlike PSGAG, which is sourced from animal extracts.

75
Q

Why is amikacin recommended when administering IA PSGAGs?

A

Amikacin is recommended because it lowers the risk of bacterial infection, which is increased with IA administration of PSGAGs.

76
Q

What type of joint therapy is PPS suggested to be beneficial for?

A

PPS could be useful for systemic treatment of mild or early-stage OA, especially in cases with multiple joint involvement.

76
Q

How did an oral HA product perform when tested for PGE2 levels in a model of equine OA?

A

Oral HA led to a significant reduction in PGE2 levels in OA joints compared to placebo-treated horses.

76
Q

What potential benefits of extracorporeal shock wave therapy (ESWT) in treating osteoarthritis (OA) in horses have been suggested by clinical studies?

A

Improvements in clinical lameness, decreased synovial fluid protein, and reduced GAG release into the bloodstream

77
Q

What mechanisms were proposed for ESWT’s effects in reducing OA progression in rabbit models?

A

Decreased chondrocyte apoptosis and a reduction in nitrous oxide (NO) levels in synovial fluid.

78
Q

What specific experimental approach was used to evaluate ESWT’s effects on OA in equine models?

A

An osteochondral fragment was created to induce OA, with treatments initiated 14 days later.

79
Q

How was the administration of shock waves scheduled in the study using ESWT for equine OA?

A

2000 shock waves at energy level E4 were applied on day 14, and 1500 shock waves at E6 on day 28.

80
Q

In the ESWT study, which joint area was the primary target for energy delivery, and how much energy was focused on the site of fragmentation?

A

The middle carpal joint capsule attachment was the primary target, with approximately 20% of energy directed at the fragmentation area.

81
Q

What specific improvements were observed in ESWT-treated horses compared to controls?

A

Significant improvements in lameness, lower synovial fluid protein levels, and reduced GAG release.

82
Q

Which bisphosphonate (BP) is FDA-approved for treating navicular disease in horses, and what age restriction applies?

A

Clodronate (OSPHOS) is approved for horses over four years of age.

83
Q

What primary concerns exist regarding the use of BPs in treating OA in horses?

A

Inconsistent pharmacological effects, uncertain dosing regimens, and potentially harmful routes like intra-articular administration.

84
Q

What adverse effects are associated with BPs in equine treatments?

A

Acute side effects include colic-like symptoms and renal toxicity.

85
Q

What promising effects have studies shown for the use of IA stanozolol in OA treatment models?

A

Reduced osteophyte formation, less subchondral bone reaction, and cartilage regeneration.

86
Q

What limitation is highlighted in the study of IA stanozolol for joint health?

A

Long-term joint health effects and cartilage regeneration stimulation remain unclear.

87
Q

What type of polymer-based materials are currently researched for mimicking articular cartilage properties?

A

Hydrogels, especially gelatin methacrylamide (gelMA) hydrogels, are investigated.

88
Q

Which ECM components are added to gelMA hydrogels to improve their chondrogenic potential?

A

HA (hyaluronic acid) and CS (chondroitin sulfate).

89
Q

What are the benefits of IL-1 and TNF inhibition in treating OA, according to recent findings?

A

Clinically beneficial effects, especially in reducing inflammation and slowing disease progression.

90
Q

What advantage does autologous conditioned serum (ACS) offer in equine OA treatment?

A

It increases IL-1Ra levels and shows beneficial symptoms and disease-modifying effects.

91
Q

What findings suggest that IRAP II may be more effective than IRAP in ACS treatment?

A

IRAP II sera contain significantly higher levels of IL-1Ra and other cytokines.

92
Q

What is a primary reason for the clinical preference for PRP over ACS in joint treatments?

A

PRP requires less preparation time and is more convenient for in-stall use.

93
Q

How does platelet activation with CaCl₂ affect PRP’s inflammatory response in normal horses?

A

Activation with CaCl₂ resulted in lower WBC release, reducing the inflammatory response.

94
Q

What component concentrations are high in the “autologous protein solution” (APS) used for joint disease treatment?

A

WBCs, platelets, and various proteins are concentrated.

95
Q

What significant outcome was observed with APS treatment in client-owned horses with natural OA?

A

Reduced lameness within 14 days and high client satisfaction at 12 and 52 weeks.

96
Q

What makes MSCs valuable in joint disease treatment according to early studies?

A

They localize to and assist in the repair of damaged joint tissues like cartilage and menisci.

97
Q

What findings regarding MSCs suggest potential limitations in OA treatment?

A

MSCs alone may not counteract OA progression due to enzymatic degradation and joint debris.

98
Q

What specific challenge in MSC treatment outcomes does the equine study highlight?

A

The effectiveness of MSC treatment may depend on the severity of joint fibrillation.

99
Q

What outcome was reported in a prospective multicenter trial for MSC-treated horses with joint damage?

A

A 76% return-to-work rate with 43% achieving full performance.

100
Q

What were the observed benefits of MSCs in rabbits with induced OA from ACL transection?

A

Reduced osteophyte formation, less cartilage degeneration, and reduced subchondral sclerosis.

101
Q

Why might IA injection of allogeneic MSCs require additional investigation?

A

Studies report a stronger inflammatory response with allogeneic cells compared to autologous cells.

102
Q

What general concern affects medical management in equine joint disease, as mentioned in the text?

A

The reliance on human treatment data and lack of specific equine research challenges therapeutic decision-making.

A U E R S & T (123 decks)

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