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A U E R S & T > Chapter 79 - Synovial joint biology > Flashcards

Chapter 79 - Synovial joint biology Flashcards

1
Q

What primary anatomical feature provides frictionless contact surfaces in a synovial joint?

A

Articular cartilage

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2
Q
A
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2
Q
A

Figure 79-1. A normal synovial joint (left), including articular cartilage,
synovial fluid, and synovial membranes, together with changes seen in
a joint with osteoarthritis (right). In an osteoarthritic joint, the following
abnormalities can be present: a, capsular fibrosis; b, synovitis; c, cartilage
failure; d, depolymerized hyaluronic acid; e, osteophytes; f, subchondral
cysts; g, vascular engorgement.

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3
Q
A

Figure 79-4. Synovial and joint capsule laxity or tension based on the anatomic position of the joint. The dorsal aspect of the joint capsule is lax in fetlock extension (A) and under tension in flexion (B). This figure also illustrates the change in joint congruity thought to occur during loading. In an unloaded position (B), it is thought that joints are not completely congruous, but as load is applied, a more congruous joint is formed. (Adapted from McIlwraith CW. Diseases of joints, tendons, ligaments, and related structures.

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4
Q

Name the two layers of the synovial membrane.

A

Intimal and subintimal

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5
Q

How are joints functionally classified based on movement?

A

Synarthroses (immovable), amphiarthroses (slightly movable), diarthroses (movable)

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5
Q

What structure attaches the synovial membrane to bone and stabilizes the joint?

A

Fibrous joint capsule

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6
Q

Which type of joint is most common in the body and facilitates skeleton movement?

A

Diarthrodial joints

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7
Q

What are the three major structural categories of joints?

A

Fibrous, cartilaginous, synovial

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8
Q

Which layer of the synovial membrane is responsible for synovial fluid content?

A

Intimal layer

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9
Q

What distinguishes the intimal layer from other tissues regarding its structure?

A

It lacks a basement membrane.

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9
Q

What cell types are responsible for phagocytosis in the intimal layer?

A

Type A synoviocytes

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10
Q

Which additional synoviocyte type represents a transition between types A and B?

A

Type C synoviocytes

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11
Q

What cell type in the intimal layer is involved in protein secretion?

A

Type B synoviocytes

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12
Q

List two substances secreted by synoviocytes that are found in synovial fluid.

A

Hyaluronan and lubricin

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13
Q

What process allows molecules like glucose and oxygen to enter the synovial fluid from plasma?

A

Ultrafiltration through the subintima

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14
Q

How is hyaluronan clearance achieved in the body?

A

Through the synovium and lymphatics

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15
Q

What is the term for the mechanism that excludes large molecules from the synovial cavity?

A

Steric exclusion (or steric hindrance)

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16
Q

What primary function do hyaluronan and lubricin serve in synovial fluid?

A

Boundary lubrication

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17
Q

How is hyaluronan’s half-life measured in the joint?

A

By tracking radiolabeled hyaluronan degradation and clearance

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18
Q

What cell count in synovial fluid is generally considered normal?

A

Less than 500 cells/μL

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18
Q

Which tissue layer has a strong blood supply and innervation within the synovial membrane?

A

Subintimal layer

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19
Q

What is the role of matrix metalloproteinases (pro-MMPs) secreted by synoviocytes?

A

They contribute to joint metabolism and tissue remodeling

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20
Q

what is the main role of the synovial membrane?

A

The cellular population of the intimal layer is based on two basic functions: phagocytosis and protein secretion
regulate the composition of synovial fluid

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21
Q

Synoviocytes are responsible for the secretion of proteins that compose the synovial fluid, name them

A

hyaluronan,
collagen,
lubricin,
matrix prometalloproteinases (pro-MMPs),
interleukins,
nd eicosanoids (e.g., prostaglandin E2).

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22
Q

The components of the plasma are less than ____ kDa size

A

Components of the plasma, such as glucose, oxygen, carbon dioxide, and proteins, typically less than 10 kDa in size,

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23
Q

Exogenous hyaluronan is cleared within __ hours through the synovium and lymphatics

A

It appears that the majority of exogenous hyaluronan is cleared within 48 hours through the synovium and lymphatics, with degradation occurring in both the synovium and
the liver

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24
Q

What structures primarily provide stability to synovial joints?

A

Periarticular ligaments, fibrous joint capsule, and surrounding muscles.

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25
Q

What effect does suprascapular nerve desensitization have on the shoulder joint?

A

It leads to subluxation of the shoulder joint.

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25
Q

How does the contribution of stability structures vary by location in the limb?

A

Higher limb joints rely more on muscles; lower limb joints rely on joint contour and capsule stability..

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26
Q

In the lower limb, which two structures are crucial for joint stability?

A

Joint surface contour and joint capsule stabilit

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27
Q

How does capsular tension in the metacarpophalangeal joint change between extension and flexion?

A

In extension, there is capsular redundancy; in flexion, the capsule is under tension.

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28
Q

What is the primary organizational structure of collagen in ligaments?

A

Parallel fascicles with fibrocytes and blood vessels.

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28
Q

What percentage of organic solids in ligaments and the joint capsule is type I collagen?

A

75%

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29
Q

To what are most joint innervations associated?

A

Sharpey fibers.

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30
Q

What happens to ligament tissues in response to increased activity?

A

They undergo hypertrophy.

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31
Q

What term is used to describe collagen fibers that course through fibrocartilage to the bone?

A

Sharpey fibers.

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32
Q

How does immobilization affect ligaments at a microscopic level?

A

It affects microscopic, enzymatic, and biomechanical properties.

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33
Q

What type of cartilage connects the subchondral bone to articular cartilage?

A

Calcified cartilage.

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34
Q

How does the vascularization of subchondral bone compare to that of articular cartilage?

A

Subchondral bone is abundantly vascularized; articular cartilage is avascular.

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35
Q

How is the Haversian system oriented in subchondral bone relative to the joint surface?

A

Parallel to the joint surface.

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36
Q

What range of thickness was found in the subchondral bone plate of the distal tarsal in horses?

A

2 to 4 mm.

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37
Q

How does the flexibility of the subchondral bone plate in humans compare to the cortical shaft?

A

It is approximately 10 times more deformable than the cortical shaft.

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38
Q

What effect does osteoarthritis have on the subchondral bone plate?

A

It can lead to remodeling or stiffening, which is detrimental to joint function.

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39
Q

What is the main component of articular cartilage’s extracellular matrix?

A

Water.

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40
Q

What is the approximate water content of articular cartilage in adult animals?

A

About 70% in adults.

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41
Q

Which cell type is primarily responsible for creating the extracellular matrix in articular cartilage?

A

Chondrocytes.

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42
Q

What percentage of cartilage volume is typically made up by chondrocytes?

A

1% to 12%.

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43
Q

Name the three main components of the extracellular matrix in cartilage.

A

Collagens, proteoglycans, and water

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44
Q

What structure marks the transition between calcified and noncalcified cartilage?

A

Tidemark.

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45
Q

Which layer of articular cartilage contains the highest density of chondrocytes?

A

The superficial (tangential) zone.

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46
Q

What unique structure has been found in the superficial zone of articular cartilage?

A

The lamina splendens.

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47
Q

How do the chondrocytes in the intermediate zone differ in shape from those in the superficial zone?

A

They are larger and more ovoid to round.

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48
Q

In which direction are collagen fibrils oriented in the deep zone of articular cartilage

A

Perpendicular to the joint surface.

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49
Q

What is the primary function of collagen in articular cartilage?

A

To provide a framework and resist tensile stress.

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50
Q

How does collagen orientation differ between the superficial and deep zones of articular cartilage?

A

Superficial zone collagen is parallel to the surface; deep zone collagen is perpendicular.

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51
Q

How many types of collagen have been identified in mammals?

A

At least 16.

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52
Q

Why is the slow turnover of type II collagen significant in cartilage repair?

A

It limits cartilage’s ability to repair itself.

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53
Q

What is the primary type of collagen in articular cartilage?

A

Type II collagen.

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54
Q

What cell type produces type II collagen in articular cartilage?

A

chondrocytes

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55
Q

What percentage of the total collagen content in articular cartilage does type II collagen constitute?

A

90-95%

56
Q

Which minor collagen types contribute to the stability of the type II collagen network?

A

Types IX and XI.

57
Q

What are two primary differences between type I and type II collagen?

A

Type II has more hydroxylysine molecules and increased glycosylation.

58
Q

How does the structure of type I collagen differ from type II collagen?

A

Type I is a heterotrimer; type II is a homotrimer of three identical alpha-1 chains.

59
Q

What role does type IX collagen play in the structure of articular cartilage?

A

It provides a covalent interface between type II fibrils and proteoglycans, enhancing stability.

60
Q

What happens to type IX collagen content in articular cartilage with age?

A

It decreases from about 10% in fetal tissue to about 1% in adults.

61
Q

Where is type XI collagen found in the collagen network, and what is its function?

A

Within the type II triple helix, acting as a core filament for collagen deposition

62
Q

Which collagen type is known for binding hyaluronan and fibronectin in articular cartilage?

A

Type VI collagen.

63
Q

Where in cartilage is type VI collagen typically found?

A

In the perilacunar area.

64
Q

What role does type III collagen play in articular cartilage?

A

It participates in the collagen network, especially at repair sites.

65
Q

In what type of cartilage is type X collagen most commonly found?

A

Juvenile cartilage undergoing endochondral ossification and diseased cartilage.

66
Q

Which major component of articular cartilage makes up about 35% of its dry weight?

A

Proteoglycans.

67
Q

What is the primary proteoglycan in articular cartilage responsible for compressive resistance?

A

Aggrecan.

68
Q

What are the main glycosaminoglycans (GAGs) that make up aggrecan?

A

Chondroitin-4-sulfate, chondroitin-6-sulfate, and keratan sulfate.

69
Q

How does the GAG composition of aggrecan change with age?

A

Chondroitin-6-sulfate increases relative to chondroitin-4-sulfate.

70
Q

What causes cartilage swelling pressure in articular cartilage?

A

Chemical expansive stresses from GAG repulsion and Donnan osmotic pressure.

71
Q

Which domain of aggrecan binds hyaluronan to form large aggregates?

A

The G1 domain.

72
Q

What is the function of the G2 region of the aggrecan core protein?

A

It is a target of aggrecan-degrading enzymes.

73
Q

What percentage of proteoglycans in articular cartilage are small proteoglycans?

A

About 5%.

74
Q

What is one of the earliest detectable changes in osteoarthritis regarding cartilage metabolism?

A

Upregulation of both aggrecan and collagen synthesis.

75
Q

ame two small proteoglycans in articular cartilage that inhibit collagen formation.

A

Decorin and fibromodulin.

76
Q

What role does biglycan play in cartilage healing?

A

It binds TGF-β, affecting its availability for biologic functions.

77
Q

What is the main role of cartilage oligomeric matrix protein (COMP)?

A

It facilitates early matrix assembly and stabilizes the mature matrix.

78
Q
A

Figure 79-12. The three types of joint motion

79
Q
A

Figure 79-13. Models of lubrication: boundary, squeeze film, hydrodynamic, and elastohydrodynamic (a combination of squeeze film and hydrodynamic). (

80
Q
A

Figure 79-14. Schematic representation of time-dependent deformation of cartilage. The steep portion of the curve (A to B) represents initial loading. Subsequently, in the creep phase, there is further deformation of the matrix, which is a result of a slower flow of water through the matrix, until the equilibrium stage (C) is reached.

81
Q

What factors influence the volume of synovial space in a joint?

A

Disease, exercise level, and anatomical location impact synovial space volume.

82
Q

What occurs in a horse’s joints when exercise levels increase?

A

Increased exercise often leads to synovial effusion in joints like the fetlock without necessarily indicating pathology.

83
Q

How is intraarticular pressure in synovial joints typically regulated?

A

he mechanisms remain poorly understood but are influenced by joint position and synovial effusion.

84
Q

At what intraarticular pressure does the human knee reach at extreme flexion and extension?

A

It can increase up to 30 psi.

85
Q

What components are essential in studying joint mechanics?

A

Kinematics, kinetics, and joint lubrication are fundamental.

86
Q

What distinguishes translational motion in joint kinematics?

A

It involves movement without rotation, seen in joints like the spine and shoulder.

87
Q

How does articular cartilage thickness relate to joint congruency?

A

More congruent joints generally have thinner articular cartilage.

88
Q

Define the ‘J-force’ in joint kinetics.

A

The J-force is the force experienced by cartilage in load-bearing situations.

89
Q

What was discovered in research on equine MCP joints during locomotion?

A

The MCP joint bears the highest loads, with peak stress areas linked to common injury sites.

90
Q

What role do hyaluronan and lubricin play in joint lubrication?

A

They serve as boundary lubricants to reduce soft tissue-bone friction.

91
Q

What lubrication model is most accepted for articular cartilage?

A

What lubrication model is most accepted for articular cartilage?
The elastohydrodynamic model, which depends on water attraction by aggrecan molecules.

92
Q

What happens to water in articular cartilage under load??

A

It exits through surface pores to balance pressure, maintaining joint lubrication and load-bearing.

93
Q

Why is fluid movement in and out of articular cartilage significant?

A

It aids lubrication, load-bearing, and provides nutrients to chondrocytes.

94
Q

What function does the primary cilium have in chondrocytes?

A

It senses flow changes, activating calcium signaling, which may be involved in mechanotransduction.

95
Q

What thickness is considered viable for chondrocyte function in articular cartilage?

A

Up to 6 mm thickness ensures adequate nutrient exchange.

96
Q

How does the avascular nature of articular cartilage affect nutrient supply?

A

Nutrients diffuse from synovial fluid during loading and unloading of the joint.

97
Q

What does the term “viscoelastic” mean regarding articular cartilage?

A

It combines viscous (fluid) and elastic properties in cartilage’s biomechanical response

98
Q

How long might it take for 2-4 mm thick cartilage to reach creep equilibrium?

A

It may take from 4 to 16 hours.

99
Q

Provide an example of a genetic defect associated with osteoarthritis as described in the text.

A

A defect in type II collagen can render the cartilage unable to withstand normal joint loading, leading to osteoarthritis.

100
Q

What is the significance of synoviocytes in osteoarthritis?

A

Synoviocytes produce anabolic and catabolic enzymes, including cytokines, prostaglandins, and MMPs, which affect joint degradation.

101
Q

How does primary synovitis or capsulitis develop?

A

It may result from repetitive trauma, leading to biomechanical damage that affects joint stability.

102
Q

What is the outcome of fibrous tissue repair in the joint capsule after injury?

A

It often results in decreased joint range of motion and altered biomechanics.

103
Q

What is the function of MMPs in articular cartilage?

A

MMPs degrade major components of the cartilage matrix, including collagen and proteoglycans.

104
Q

How are MMPs activated, and what is essential for their function?

A

MMPs are secreted in an inactive form and require zinc at their active site for function.

105
Q

Which MMPs are specifically implicated in collagen degradation?

A

Collagenase MMPs, including MMP-1, MMP-8, and MMP-13, are major contributors.

106
Q

What role do ADAMTS enzymes play in osteoarthritis?

A

ADAMTS enzymes, particularly aggrecanases, degrade aggrecan, leading to proteoglycan loss in diseased cartilage.

107
Q

Which cytokines upregulate MMP-13 in osteoarthritic cartilage?

A

Interleukin-1 (IL-1) and tumor necrosis factor (TNF) increase MMP-13 expression, driving cartilage catabolism.

107
Q

Which enzymes are highly expressed in synovial tissue and cartilage of osteoarthritic equine carpi?

A

ADAMTS-5 and MMP-13 in synovial tissue, and ADAMTS-4 and MMP-13 in osteoarthritic cartilage.

108
Q

What are cytokines and how has their definition expanded over time?

A

Originally, cytokines were thought to be small regulatory proteins associated with catabolic pathways, but now they include catabolic, modulatory, and anabolic proteins produced by one cell that act on another.

108
Q

What are the main catabolic cytokines involved in osteoarthritis, and what is their role?

A

IL-1 and TNF-α are the main catabolic cytokines in osteoarthritis; they promote MMP, nitric oxide, and PGE2 production, while inhibiting aggrecan and type II collagen synthesis.

109
Q

Why is IL-1 considered more critical in cartilage degradation than TNF-α in osteoarthritis?

A

IL-1, particularly IL-1β, is viewed as the principal cytokine responsible for cartilage degradation, whereas TNF-α is more associated with clinical morbidity and pain.

110
Q

How do modulatory cytokines counteract the effects of IL-1 and TNF-α?

A

Modulatory cytokines like IL-4, IL-10, and IL-13 inhibit IL-1 synthesis and promote natural inhibitors such as TIMPs and IL-1Ra, balancing proinflammatory cytokine effects.

111
Q

What is the mixed mode of action of IL-6, and how does it influence osteoarthritis?

A

IL-6 amplifies IL-1’s effects but also promotes TIMP synthesis, thus both supporting and moderating cartilage degradation pathways.

112
Q

Describe the role of anabolic cytokines in osteoarthritis and give examples.

A

Anabolic cytokines, such as IGF and TGF, stimulate matrix production and inhibit degradation, aiding cartilage repair. IGF-1, for example, promotes proteoglycan and type II collagen production.

113
Q

What is the significance of BMPs in cartilage metabolism, and which BMPs are of particular interest?

A

MPs, particularly BMP-2 and BMP-7, are signaling proteins involved in chondrocyte development and physiology; BMP-7 has shown strong antidegradative effects.

114
Q

How do FGF-2 and FGF-18 differ in their effects on osteoarthritis?

A

FGF-18 has anabolic effects on extracellular matrix synthesis, while FGF-2 has mixed effects, with its function potentially regulated by antagonist suppression.

115
Q

Explain the role of nitric oxide in osteoarthritis and its controversial aspects.

A

Nitric oxide, produced in response to IL-1, contributes to chondrocyte apoptosis and matrix degradation, but its precise role in osteoarthritis remains debated.

116
Q

What are prostaglandins’ roles in osteoarthritis, particularly PGE2?

A

PGE2 levels increase in osteoarthritic joints and are linked to synovitis, lameness, and are produced after IL-1 and TNF-α stimulation.

117
Q

How do natural inhibitors like IL-1Ra and solubilized TNF receptors inhibit cytokine activity?

A

IL-1Ra binds to IL-1 receptors without triggering a response, blocking IL-1 activity, while solubilized TNF receptors bind TNF-α, preventing its interaction with membrane receptors.

118
Q

What are TIMPs, and how do they regulate MMP activity?

A

TIMPs (TIMP-1, TIMP-2, TIMP-3) are inhibitors of MMPs, forming inactive complexes with MMPs and helping regulate joint degradation processes.

119
Q

Which newly identified members of the IL-1 superfamily may influence osteoarthritis?

A

ILF-5, ILF-10, and TNFα-6, though their roles in osteoarthritis are not fully defined.

120
Q

How might IGF-1 and growth hormone deficiencies lead to osteoarthritis?

A

Deficiencies in these anabolic cytokines have led to osteoarthritis-like lesions in experimental models due to reduced matrix production.

121
Q

How might selective MMP inhibition be beneficial in osteoarthritis treatment?

A

Targeting specific MMPs can prevent excessive degradation without entirely blocking necessary MMP functions in cartilage health.

122
Q
A
123
Q
A
124
Q
A
125
Q

What type of fibers innervate the tissues surrounding articular cartilage?

A

Unmyelinated C fibers and small myelinated Aδ fibers.

126
Q

Which receptor type is responsible for proprioceptive functions in joint capsules?

A

Type 1 receptors.

127
Q

What is the role of Type 4 receptors in articular tissues?

A

They respond to thermal, chemical, and mechanical stimuli.

128
Q

Name two chemical mediators that directly stimulate pain fibers in osteoarthritis.

A

Kinins and substance P.

129
Q

How does substance P contribute to osteoarthritis inflammation?

A

It stimulates monocytes to release cytokines like IL-1 and TNF-α.

130
Q

Which mediator is considered highly potent in producing osteoarthritic pain?

A

Bradykinin.

131
Q

What effect does morphine have on osteoarthritic synovitis in horses?

A

It reduces synovial WBC count, prostaglandin E2, and bradykinin levels.

132
Q

What was found to be associated with joint hypernociception in murine studies?

A

Leukotriene B4 (LTltB4).

132
Q

In osteoarthritis, why may pain levels not correlate with structural joint damage?

A

Radiographs lack sensitivity for detecting soft tissue structures causing pain.

133
Q

What term describes repair involving cells from outside the cartilage?

A

Extrinsic repair.

134
Q

What is a common method for enhancing articular cartilage repair?

A

Subchondral bone microfracture.

135
Q

What is the purpose of matrix-assisted autologous chondrocyte implantation (MACacI)?

A

It introduces chondrocytes to the defect for cartilage repair.

136
Q

How might mesenchymal stem cells (MSCs) aid in cartilage regeneration?

A

By being injected intraarticularly or held in a defect with a matrix

137
Q

Why are full-thickness defects over 3-5 mm² challenging to repair?

A

They typically exhibit poor healing potential.

138
Q

What are two main types of collagen found in cartilage repair tissue?

A

Type II collagen and, initially, type I and III in granulation tissue.

139
Q

Why are outcome parameters like radiographs often unreliable for pain assessment?

A

They do not correlate well with soft tissue damage and associated pain.

139
Q

What are the main components required for optimal cartilage repair?

A

Aggrecan and type II collagen content.

140
Q

How does computed tomographic arthrography (CTA) compare with radiography for diagnosing joint injuries?

A

CTA detects more lesions in cruciate ligaments and femoral condyles.

A U E R S & T (123 decks)

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