Chapter 89 - OCD Flashcards

1
Q

What does “osteochondritis dissecans” mean?

A

Inflammation of bone and cartilage resulting in loose fragments.

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2
Q

What condition is most commonly associated with osteochondrosis in horses?

A

Developmental orthopedic disease (DOD).

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3
Q

What does the term “osteochondrosis” refer to?

A

A disorder of bone development in growing horses.

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4
Q

What is the primary characteristic of “osteochondritis dissecans”?

A

Cartilaginous or osteochondral separation.

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5
Q

What does “OC latens” represent?

A

Focal chondronecrosis in the growth cartilage.

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6
Q

What does “OC manifesta” indicate?

A

Impaired endochondral ossification and cartilage retention.

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7
Q

What does “OC dissecans” describe?

A

Cleft formation in necrotic cartilage.

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8
Q

What are examples of JOCC?

A

OCD, cuboidal bone disease, and other immature skeletal failures.

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9
Q

What term includes disorders related to immature joints or growth plates?

A

Juvenile osteochondral conditions (JOCC).

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10
Q

What is “endochondral ossification”?

A

The process of bone development from cartilage.

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11
Q

At what stage does endochondral ossification begin?

A

Fetal stage.

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12
Q

What is Wolff’s law?

A

Bone remodels in response to biomechanical load.

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12
Q

Where does longitudinal growth of long bones occur?

A

At growth plates or physe

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13
Q

What is the typical presentation of an OC patient?

A

A yearling with joint effusion, usually without lameness.

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14
Q

Which breed shows a high prevalence of OC in the tarsocrural joint?

A

Warmbloods and Standardbreds.

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14
Q

Which advanced imaging modalities outperform radiography?

A

Computed tomography (CT) and magnetic resonance imaging (MRI).

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14
Q

What is the role of radiography in diagnosing OC?

A

It’s the gold standard for detecting OC lesions.

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14
Q

Which joint commonly shows evidence of OC on radiographs?

A

The tarsocrural or femoropatellar joint.

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15
Q

What joints are most affected by OC in horses?

A

Tarsocrural, femoropatellar, and MCP/MTP joints.

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15
Q

What is a limitation of radiography for OC?

A

It may miss lesions limited to cartilage or subtle bone changes.

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16
Q

What joints are most often affected bilaterally by OC?

A

Tarsocrural and femoropatellar joints.

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17
Q

What is a predilection site for OC in the tarsocrural joint?

A

Distal intermediate ridge of the tibia.

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18
Q

What is the common location of OC in the shoulder joint?

A

The glenoid and humeral head.

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19
Q

Where are OC lesions commonly found in the femoropatellar joint?

A

Lateral trochlear ridge of the femur.

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20
Q

Are POFs part of OC?

A

No, they are traumatic in origin.

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21
Q

What do POFs indicate histologically?

A

More osteoarthritis than osteochondrosis.

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22
Q

What biomarker profile difference exists between OC and traumatic joint injuries?

A

OC has an increase in C2C, while traumatic injuries have increased CPII.

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22
Q

Can young foals show lameness with OC?

A

Yes, especially with large lesions in the femoropatellar joints.

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23
Q

What role does genetic predisposition play in OC?

A

Racing Thoroughbreds.

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24
Q

What makes diagnosing OC in very young animals challenging?

A

The lack of mineralization in subchondral bone.

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25
Q
A
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26
Q

Can OC lesions regress in young animals?

A

Yes, they can regress during early juvenile phases.

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27
Q

What is the primary period for the development of OC?

A

During active endochondral ossification in growing animals.

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28
Q

At what age do tarsocrural lesions typically resolve?

A

By 5 months, though some persist.

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29
Q

When do femoropatellar lesions commonly stabilize?

A

Around 8 months of age.

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30
Q

What was a unique finding in Lusitano foals regarding OC?

A

More lesions at 1 month of age in the femoropatellar joint.

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31
Q

Can minor OC lesions resolve after 12 months?

A

Yes, up to 24 months in some cases.

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32
Q

What is the “age of no return” for lesion resolution in most joints?

A

Generally set at 12 months.

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33
Q

What enzyme’s level change reflects cartilage metabolism in young animals?

A

Matrix metalloproteinase-3 (MMP-3).

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34
Q

Why does the healing of cartilage lesions decrease with age?

A

Due to reduced metabolic and repair capacity.

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35
Q

What is the prevalence of OC in Dutch Warmblood yearlings?

A

Around 67.5%.

36
Q

hat prevalence rate is typical in Dutch Warmbloods at age 3?

A

Approximately 30%.

37
Q

What was OC prevalence in South German Coldbloods?

A

61.7%.

38
Q

What is the OC prevalence in Thoroughbred yearlings?

A

23%.

39
Q

How does OC prevalence vary in Thoroughbred studies using repository radiographs?

A

Lower than in clinical records, likely due to preselection.

40
Q

Are Warmblood horses more susceptible to OC than Thoroughbreds?

A

Yes, they generally have a higher prevalence of OC.

41
Q

How often is OC found in ponies?

A

Rarely, with low prevalence.zad

42
Q

What is a potential primary cause in OC pathogenesis?

A

Damage to cartilage canal vessels.

42
Q

How might feral horses’ OC prevalence differ from that in managed horses?

A

Lower, possibly due to different management and breeding.

43
Q

What does OC latens refer to?

A

Clinically silent, early lesions in OC development.

44
Q

How might genetics play a role in OC pathogenesis?

A

Certain genes related to vascularization are linked to OC susceptibility.

45
Q

How does chondrocyte activity change in long-existing OC lesions?

A

Metabolic rate decreases, indicating possible exhaustion.

46
Q

How does collagen VI distribution differ in OC lesions compared to normal tissue?

A

Collagen VI distribution is different in OC lesions compared to normal tissue.

47
Q

What post-translational modifications were observed in early OC lesions?

A

Differences in post-translational modifications of collagen type II were demonstrated in samples from early lesions.

48
Q

What gene showed strong mRNA expression near OC lesions?

A

TGF-ß mRNA showed strong expression in chondrocyte clusters surrounding OC lesions.

49
Q

What were the changes in collagen expression in osteochondrotic cartilage?

A

OC cartilage showed increased expression of collagen types I, II, III, and X, and MMP-13, ADAMTS-4, and TIMP-1, while TIMP-2 and TIMP-3 decreased.

50
Q

Was MMP-16 significantly altered in osteochondrotic cartilage?

A
51
Q

What was demonstrated regarding cathepsin B activity in OC?

A

A strong increase in cathepsin B activity was observed in chondrocyte clonal clusters in OC.

52
Q

What was the effect of copper supplementation on cathepsin B?

A

Copper supplementation confirmed the increase in cathepsin B activity in OC

53
Q

How did OC tissues differ in proteoglycan content?

A

OC tissues produced significantly less GAGs, and there was increased activity of gelatinases (MMP-2 and MMP-9).

54
Q

What role did IGF-1 play in osteochondrotic tissue?

A

IGF-1 was upregulated in osteochondrotic tissue, likely related to the repair response.

55
Q

How did OC severity correlate with biomarkers at 11 months of age?

A

OC severity correlated negatively with osteocalcin and collagen degradation markers and positively with anabolic markers.

55
Q

What correlation was found in biomarker research regarding osteocalcin?

A

A strong correlation was found between serum osteocalcin levels and OC severity in foals.

56
Q

What signaling pathways are known to regulate cartilage differentiation?

A

Wnt/β-catenin, Ihh/PTHrP, and retinoid signaling pathways.

57
Q

What evidence supports the role of the Wnt/β-catenin pathway in OC?

A

Significant changes in expression of Wnt signaling components were found in OC cartilage.

58
Q

What inhibitors were upregulated in OC lesions?

A

A Wnt signaling inhibitor, sclerostin, was strongly upregulated in OC lesions.

59
Q

How does diet influence OC according to the text?

A

High-energy diets characterized by easily digestible carbohydrates influence OC significantly.

60
Q

What mitochondrial changes have been observed in OC cartilage?

A

Abnormal mitochondria have been observed in the deep zone of OC cartilage.

61
Q

What factors determine the osteochondrotic phenotype?

A

Genetic components and environmental factors.

62
Q

What is heritability in the context of OC?

A

Heritability estimates how much variation in a trait is due to genetic variation.

63
Q

Which joint showed the highest heritability for OC?

A

The tarsocrural joint, with an average heritability of around 0.30.

64
Q

How does breed affect OC susceptibility?

A

Many identified quantitative trait loci (QTL) for OC are breed-specific.

65
Q

What two major environmental influences affect OC?

A

Loading (biomechanical factors) and nutritional factors.

66
Q

How does biomechanical loading influence OC?

A

It plays a crucial role in conditioning the musculoskeletal system during early juvenile development.

67
Q

What is the relationship between energy intake and OC?

A

High energy intake, particularly from carbohydrates, is associated with increased OC risk.

68
Q

What hormonal response is triggered by high energy intake?

A

Postprandial hyperinsulinemia, which varies between horses and may affect OC susceptibility.

69
Q

How do thyroid hormones relate to OC?

A

Thyroid hormones are involved in chondrocyte differentiation and blood vessel invasion during ossification.

70
Q

How did copper levels relate to OC incidence in early studies?

A

Low copper levels in feed were associated with OC, but further studies showed that extremes in copper intake could provoke lesions.

71
Q

What is the importance of the calcium/phosphorus ratio in bone metabolism?

A

Severe aberrations in this ratio can lead to various bone disorders, including OC.

72
Q

What has been concluded about loading as a cause of OC?

A

Loading is considered an additive factor rather than a sole cause of OC.

73
Q

How did pasture access affect OC prevalence?

A

Foals with irregular pasture access or those kept in large plots showed a higher prevalence of OC.

74
Q

What has been observed in horses on normal diets regarding OC?

A

OC lesions can also develop in horses on normal diets without insulin metabolism abnormalities.

75
Q

What are the two main treatment options for OC?

A

The two main treatment options are conservative management and surgical management.

76
Q

What does conservative treatment primarily involve?

A

Conservative treatment mainly consists of rest and controlled exercise.

77
Q

What medications may be used in conservative treatment?

A

Systemic NSAIDs and intraarticular medications such as corticosteroids and disease-modifying osteoarthritic drugs may be administered.

78
Q

In what cases is nonsurgical management theoretically successful?

A

It can be successful in very young animals or very mild cases of OC.

79
Q

What size and depth of lesions are likely to heal with conservative treatment?

A

Lesions less than 2 cm long and less than 5 mm deep without fragmentation are likely to heal.

80
Q

what recent data suggests about conservative treatment in scapulohumeral joint OC?

A

Recent data suggests it may be a viable option in mild cases involving the glenoid cavity.

81
Q

What is the preferred treatment for tarsocrural OC in athletic horses?

A

Many authors recommend surgical intervention for tarsocrural OC in athletic horses.

82
Q

What happens during the surgical management of OC?

A

Loose fragments and cartilage flaps are removed, and the surrounding tissue is débrided.

83
Q

What is crucial when débriding subchondral bone in young animals?

A
84
Q

What percentage of success was found in horses with reattached cartilage flaps?

A

A 95% success rate was reported in horses with reattached cartilage flaps.

85
Q

What innovative technique was used in a Thoroughbred filly for osteochondrotic defects?

A

A sponge impregnated with growth factors and stem cells was used for healing.

86
Q

What was the outcome of using a multilayered osteochondral scaffold?

A

The filly showed good performance and improvement in bone contour at follow-up.

87
Q

What factors influence the prognosis after surgical intervention?

A

The prognosis varies based on joint involvement, lesion extent, and definition of “favorable outcome.”

88
Q

What success rate was reported for the femoropatellar joint?

A

A 64% success rate was reported for this joint in mixed populations.

89
Q

What percentage of horses treated for tarsocrural OC perform as intended?

A

About 76% of horses treated for tarsocrural OC were able to perform as intended.

90
Q

What is the prognosis for shoulder OC?

A

The prognosis is less favorable, with a reported success rate of only 15% in racehorses.

91
Q

What types of lesions in the MCP and MTP joints require immediate surgical intervention?

A

Lesions with fragmentation or loose bodies should be treated surgically to prevent osteoarthritis.

92
Q

What is the percentage of return to athletic activity reported for proximal sagittal ridge lesions?

A

A 90% return to athletic activity has been reported for proximal sagittal ridge lesions.

93
Q

What common surgical treatment method is used for OC?

A

Arthroscopy is the common surgical treatment method used for OC cases.

94
Q

What limitations exist in eliminating OC from the equine population?

A

Current management practices and breeding goals complicate efforts to eliminate OC.