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cartilage Flashcards

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1
Q

what kind of tissue is the capsule composed of?

A

dense, irregular CT and has a lot of nerves, vessels, and mechanoreceptors here

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2
Q

2 layers of synovium

A

intima and stroma

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3
Q

intima tissue cell type

A

synoviocytes

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4
Q

function of intima

A

to produce synovial fluid (done by synoviocytes) and to phagocytose joint debris

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5
Q

stroma tissue type

A

loose or dense irregular CT

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6
Q

what does stroma tissue blend with?

A

the fibrous joint capsule

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7
Q

specific function of macrophages in the stroma layer

A

to keep the synovial fluid clean of debris

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8
Q

cell population of stroma tissue

A

macrophages, lymphocytes, and mast cells

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9
Q

function of the joint capsule

A

to respond to mechanical loading via mechanoreceptors and stability of the joint (proprioception), as well as stability and vessel/nerve supply

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10
Q

ligaments and capsule relationship

A

capsules blend in with the capsule

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11
Q

free nerve endings

A

are responsible for transmitting messages of temperature, mechanical stimuli, or pain

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12
Q

what do sensory nerves respond to in cartilage?

A

stretch, tension, and pressure

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13
Q

example of sensory nerves in cartilage

A

pacinian corpuscles

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14
Q

tendons vs capsule

A

tendons have more regular tissue (parallel lines) than capsules do to help with force distribution better

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15
Q

main cell type of articular cartilage

A

chondrocytes

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16
Q

chondrocytes function

A

maintain ECM by producing glycosaminoglycan and shock absorption and gliding movement

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17
Q

glycosaminoglycan

A

absorb water and act as shock absorbers in articular cartilage

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18
Q

main collagen type in articular cartilage

A

type II

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19
Q

tide marks

A

represent the point at which calcification in cartilage occurs and is sort of like an insertion point of cartilage to bone (to the end plate)

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20
Q

osteochondral junction

A

is where the collagen fibres from the radial zone insert directly to the bone

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21
Q

OA relationship to osteoporosis

A

osteoporosis is actually protective against OA due to having spongier and less dense bone, thus diffusing the stress distributed to the cartilage (shock absorption)

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22
Q

what part of bone is made of cartilage?

A

the physis

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23
Q

osteochondrosis

A

is when the cartilage of bone can become inflamed due to overuse (is a group of disorders affecting bone)

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24
Q

healing capacity of cartilage

A

is very limited due to a lack of vessels

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25
can cartilage fracture?
yes, either in combination with a bone fracture or in isolation
26
what size of cartilage damage never/rarely heals?
anything larger than 2 mm in width
27
how does small cartilage damage heal?
via primary healing which is the local proliferation of chondrocytes and production of new ECM
28
primary cartilage healing
can occur if injury is small and is local proliferation of chondrocytes; production of new ECM not scar tissue
29
secondary cartilage healing
occurs if the injury is larger and extends into the bone; produces scar tissue
30
how many types of chondral injuries are there?
4 types
31
what type of movements often cause chondral injuries?
rotational movements caused by a major shearing force through the cartilage
32
what type of chondral injury mimics a meniscus tear?
type III
33
what type of cartilage injury is similar to osteochondritis dissecans?
type IV
34
what type of chondral tear occurs at the tidemark?
type IV
35
risk factors of chondral injuries
trauma to the joint and advancing age
36
chondral injuries
damage to the articular cartilage and are classified in 4 types; these often can present as asymptomatic
37
pathophysiology of chondral injuries
overload of cartilage leads to disruption of ECM and necrosis of chondrocytes, in which repeated loading predisposes these cells to further injury and can lead to OA
38
prognosis of chondral injuries
not great; after 6-10 months of rehab only 66% returned to sport
39
why are chondral injuries progressive?
lack of healing leads to permanent effects, increased tension at the edges causes risk for more injury, and release of cartilage fragments leads to an abnormal environment
40
signs and symptoms of chondral injuries
often can be asymptomatic, but other symptoms include pain, muscle spasms, swelling, catching, or locking
41
when should you suspect a chondral injury?
when there is a simple joint sprain that is painful and swollen for longer than expected
42
diagnostic tests for chondral injuries
X-ray, MRI, or arthroscopy
43
treatment for chondral injuries
is not clear yet but can include surgery (mosaicplasty, subchondral drilling, and periosteal transplant)
44
PT role in chondral injuries
continuous passive motion, a period of non-weight bearing followed by an increase in ROM and movement, electrical stimulation, and POLICE
45
why is continuous passive motion so important for chondral injuries?
because movement of the joint allows for nutrients to be pumped to the cartilage
46
most important standard in healing to meet before other treatments begin
motor re-education and muscle activation; after this you can move to proprioception, strength, and flexibility, then skill acquisition, then RTS
47
degenerative condition meaning
it gets worse over time
48
osteophyte
normal outgrowth of bone
49
sclerosis
hardening of tissues due to an accumulation of fibrous or scar tissue, causing stiff joints
50
what kind of joints does OA commonly affect?
the weightbearing or heavily used joints; hands, feet, knees, hips, and spine
51
primary OA
is idiopathic and usually involves a combination of factors such as mechanical history, age, and genetic predisposition
52
secondary OA
is another condition that is responsible for OA such as previous trauma, abnormal cartilage structure, or crystal deposition diseases
53
examples of crystal deposition diseases
gout and pseudogout
54
how much of the population has OA?
10%
55
risk factors for OA
physically demanding jobs, textile workers who grip a lot, former elite athletes, age, increased BMI, and varus or valgus knee
56
does exercise increase the risk of OA?
habitual exercise does not but very intense and strenuous exercise can
57
how does the joint change with OA?
reduced joint space, sclerosis, and osteophytes may appear
58
inflammatory response of bone during OA
OA can stimulate an inflammatory response that stimulates healing
59
eburnation
the formation of dense, ivory like bone that is rough and thickened
60
osteonecrosis
is the death of bone due to lack of blood supply and nutrients
61
soft tissue changes during OA
ligaments tend to decrease in laxity then this decreases as joint capsule stiffness/fibrosis develops; muscle weakness can also occur
62
arthrogenic muscle inhibition
is an involuntary protective reflex response that occurs after a joint injury, where altered sensory feedback from the injured joint causes a reduction in muscle activation and weakness
63
nociception and OA
nociception originates from the joint capsule, ligaments, or bone
64
bony changes in OA
subchondral bone thickening, osteophytes, and loose bodies
65
diagnostic tests for OA
pain in joint plus meeting three characteristics off the list (ex. morning stiffness, 50+, tenderness, bony enlargement, etc.)
66
should OA be warm to the touch?
no, if it is it would be something more like RA which includes a systemic response to inflammation
67
what is the grading system used for OA?
kellgren-lawrence system (graded 1-4)
68
GLA:D meaning
good living with arthritis developed in denmark
69
findings of GLA:D program
reduction in pain intensity and increase in PA
70
main focus of GLA:D program
neuromuscular exercises
71
hemophilia
is a group of hereditary or spontaneous disorders in which coagulation in impaired, leading to episodes of uncontrolled bleeding; repetitive bleedings into joint, can cause synovitis and cartilage breakdown
72
what are crystal deposition diseases
are crystals forming in circulation and cause depositions in the joint cartilage, ligaments, or tendons
73
gout
is caused by an excess of uric acid in the circulation, formed deposition of crystals in the synovium, cartilage, and tendons
74
where does gout often show up?
big toe
75
signs of gout
inflammation of joints (often big toe) with cardinal signs
76
most common inflammatory arthropathy
gout (but leads to secondary OA?)
77
treatment for gout
urate lowering treatment, NSAIDs and corticosteroids
78
causes of gout
is often genetic and common in those with renal and excretion issues
79
pseudogout
is caused by calcium pyrophosphate crystals that are deposited in synovium and cartilage, and there is no tophi formation
80
treatment of pseudogout
NSAIDs, corticosteroids, and uric acid lowering treatment, as well as rest
81
what muscle is affected by knee or hip OA the most?
vastus medialis
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