Musculoskeletal Pathology & Healing Flashcards
1
Q
Tissue/cells capable of some regeneration
A
- fibroblasts
- chondrocytes
- peripheral nerves
- osteocytes
- endothelial cells
- blood cells
- outer meniscus
2
Q
Tissue not capable of regeneration (scar)
A
- cartilage (micro fracture procedure)
- central nervous system nerves
- disc
- inner meniscus
- cruciate ligament
3
Q
Define acute injury
A
- result of a single trauma
4
Q
Define overuse injury
A
- involves repetitive stresses associated with prolonged activity
- repetitive micro trauma exceeds the healing capacity of the tissue
5
Q
Contributing factors to orthopedic injuries
A
- weakness
- poor endurance
- poor coordination
- poor aerobic capacity
- inadequate nutrition
- insufficient rest/recovery
6
Q
Injuries to muscle can involve
A
- strain (partial or complete tear)
- laceration
- contusion
- post exercise soreness
- compartment syndrome
7
Q
Where is a strain & overuse injury most common
A
- myotendinous joint (MTJ)
8
Q
Characteristics of muscles that are most susceptible to injury
A
- a greater percentage of Type II fibers
- two joint muscles
- muscles subject to high eccentric loading
9
Q
Healing of skeletal muscle occurs via two competing pathways
A
- regeneration of disrupted muscle (myoblasts)
- production of connective tissue scar (fibroblasts)
10
Q
Define regeneration
A
- production of newly synthesized tissue that is structurally & functionally identical to the tissue that was traumatized
11
Q
What can scarring inhibit
A
- it may inhibit the regeneration of muscle fibers if the formation of granulation tissue is excessive
12
Q
What occurs during the first 24 hours of muscle healing
A
- large number of mononuclear cells within damaged muscle cells & in the intercellular connective tissue
- RBCs & fibrin clots at the site of injury
- presence of myoblasts
13
Q
What occurs during 24-48 hours post injury of muscle healing
A
- marked catabolic response with loss of 27% of total protein
- most necrotic muscle fragments have been removed (phagocytosis)
- fibroblasts become prevalent in the connective tissue
- myoblasts begin to orient along the longitudinal axis of the broken ends of the muscle fibers
- a hematoma will be noted in the central portion of the injury
14
Q
What occurs after day 3 of muscle healing
A
- myoblasts show central nuclei & reorganizing sarcomeres, suggesting the early phase of regeneration
- increasing my oblast formation & myotubes begin to form
- muscle protein accumulation begins
- an intact myofiber may be generated within 7 to 14 days following injury
- fibroblasts are activated
- continued phagocytosis (macrophages) of necrotic muscle fibers
- hematoma still visible histologically
15
Q
What occurs during days 5-7 of muscle healing
A
- further progression of regeneration (increased presence of myoblasts & myotubes)
- significant decline in degree of inflammation
- central zone of injury: reduces in size & is filled with granulation tissue
- hematoma small of gone at this point
16
Q
What occurs after day 14 of muscle healing
A
- hematoma has resolved
- young scar tissue
- a few muscle fibers can be seen traversing the scar tissue that separates the torn muscle fibers within this regenerating zone
- collagen continues to be laid down
17
Q
What occurs after the 21 day of muscle healing
A
- complete repletion of the protein loss
- diminished evidence of active muscle tissue regeneration & fibroblast activity
- central zone of the injury all but disappeared, leaving behind a thin connective tissue septum
- regenerating muscle fibers are now extending across the gap (connective tissue septum) & joining surviving muscle stumps
18
Q
Muscle healing limitations
A
- in order to recover normal muscle function following a laceration injury: muscle must regenerate across the repair site & denervated muscle tissue must be reinnervated
- most denervated fragments remain that way
19
Q
Define sarcopenia
A
- age related loss of skeletal muscle mass, function, & ability to regenerate
20
Q
Theoretical causes of muscle mass loss
A
- diet & nutrition
- hormonal change
- loss of ability to innervate myofibers during healing
21
Q
How much muscle mass does an adult lose after the age of 70
A
- 1% of muscle mass per year
22
Q
Effects of sarcopenia
A
- loss of muscle mass changes metabolic rate
- difficulty completing ADLs requiring significant muscle power
- slow gait speed
- decreased balance reactions
23
Q
Define myositis ossificans
A
- abnormal formation of bone within a muscle following a muscle contusion injury
24
Q
Symptoms of a myositis ossificans
A
- prolonged disability
- severe pain
- a significant loss of function
25
Signs of a myositis ossificans
- a large, firm/tender mass within a contused muscle in concert with restricted joint motion
- plain radiographs will show a soft tissue density at 3 weeks post-injury
- by 4 to 6 months the bone formation is usually complete
26
Risk factors of myositis ossificans
- hematoma formation
- moderate to severe contusion
- early exercise
- youth
- injury to bone or periosteum
- injury near the musculotendinous junction
- multiple episodes of injury
27
Contraindications for myositis ossificans
- aggressive, early activity
- heat
- ultrasound
- massage
28
Treatment for myositis ossificans
- initial treatment should focus on limiting severity of hemorrhaging
- rest has been the treatment of choice
29
What are the limitations to muscle healing
- it won't get back to 100% but can get close to pre-injury levels, it will take some time
30
What is the primary function of a tendon
- primary function is to transmit muscle force to the skeletal system
31
Describe a tendon
- tendons consist of fibroblasts, collagen, and elastin in a ground substance matrix
- is predominantly type I collagen
- type III and type V collagen make up about 5% of the tendon
32
How do tendons heal
- they heal by repair
- repair is also regeneration
- a healed tendon is not as strong
33
Tendon healing inflammatory phase
- neutrophils are the first inflammatory cells to arrive at injury site
- Day 2 macrophages & lymphocytes are prevalent
- inflammation has ceased by day 14
34
Tendon healing proliferative phase
- Days 5-7 fibroblastic activity increases & inflammation decreases
- developing scar tissue has no significant extracellular matrix for strength & stability (very fragile in this stage)
- extensive collagen synthesis in the healing tendon
- type III collagen is produced 1st
- as healing progresses type III collagen is replaced by type I
- myofibroblasts are most active from days 5-21
- Day 21 bundles of collagen fibrils can be seen
- scar tissue rapidly increases in density up to day 21
35
Tendon healing remodeling phase
- organization of large quantities of collagen fibrils pool into a compact & parallel system
- the tensile strength increases as remodeling progresses
- up through 60 days the scar tissue becomes less cellular & more fibrous
- vascularity starts to diminish while fibroblast activity remains high
- restructuring of the collagen network is very active
- collagen turnover remains high up through day 120
- 85% of the original collagen in the acute wound stage is replaced with new collagen by day 150
36
Tendon properties & aging
- lower metabolic activity
- reduction in tendon stiffness (results in altered force transmission from muscle)
37
Define tendinitis
- involves inflammation
38
Define tendinosis
- degenerative
39
Tendinopathy occurs mostly from overuse
- result from sustained activity
- reparative capacity of tendon is exceeded
- cellular metabolism altered
- damage occurs at cellular level, with subsequent injury to the microvasculature
40
Tendon rehabilitation
- modified tension in the line of stress is the optimal stimulus for tendon regeneration
- wait until 1 week after injury
- progress slowly
- careful & controlled passive motion will increase tendon strength & improve the quality of the repair
- collagen fibers are laid down along lines of mechanical stress
41
What is the effect of mechanical load on the strength of a new scar dependent on
- intensity & duration of the applied load
- time elapsed since injury
42
Describe a ligament
- short, strong bands of fibrous connective tissue that connects bone to bone
- 90% type I collagen & <10% type III collagen
- elastin normally only occupies less than 5% of most skeletal ligaments
43
What is the most common type of ligament injury
- mid-substance tears are more common than avulsion injuries
44
- Ligament sprain classification
- Grade I: mild pain with no increased laxity
- Grade II: moderate pain with slight laxity, partial tear
- Grade III: severe pain with complete disruption of ligament fibers & significant laxity
45
Ligament healing
- hematoma formation & inflammation are followed by relatively slow repair & remodeling phase
- collateral ligaments are well vascularized & follow classic wound healing
- final outcome may take over a year
- pre-injury strength typically not fully recovered (reduced by 30%-50%)
- ACL heals poorly & without surgery, it will regress or disappear completely (gets most of its nutrition from synovial fluid)
46
What does the quality of ligament healing vary by
- the location of the injury
- location of the ligament
- amount of exposure to synovial fluid
47
What are the parts of the joint capsule
- outer layer: stratum fibrosum
- inner layer: synovial membrane
48
Describe the stratum fibrosum
- dense, rough, fibrous connective tissue with specific areas of thickening (collateral ligaments)
- helps maintain the joint's mechanical integrity by securely joining the bones that form the articulation
49
Describe a joint capsule
- menisci, fascia, & other periarticular connective tissues attach themselves to the joint capsule
- relatively poor blood supply, but a rich supply of nerve fibers
50
Joint capsule sprain classification
- basically the same as ligaments
51
Describe joint capsule injury
- it reacts to trauma with increases in vascularity & fibrous tissue
- can eventually result in capsular thickening
52
In what ways does joint capsule healing occur
- regeneration of the stratum fibrosum
- formation of scar tissue (more likely)
53
What are the major functions of the synovium
- lubrication
- nourishment to avascular articular cartilage
54
Describe the synovium
- covers the inner surface of the fibrous joint capsule & forms a sac enclosing the synovial cavity
- composed of richly vascularized fibrous connective tissue with lymphatic & nerve supply
- capable of full regeneration
55
What happens to the synovium following trauma
- increase in synovial fluid volume by 10-20 times the normal
- increased production of exudate (cells, protein, solid material, & fluid)
- viscosity (thickness) decreases due to decrease in hyaluronic acid concentration
- synovium will thicken & synovial fluid will be altered
56
Absorption of fluid & cells from the joint cavity is facilitated by
- active or passive ROM
- massage
- intra-articular hydrocortisone
57
The basic inflammatory response in the synovial membrane is
- proliferation of surface cells
- increase vascularity
- gradual fibrosis of subsynovial tissue
58
Healing complications of the synovium
- laxity & instability
- damage to intra-articular inclusions (menisci)
- the formation of loose bodies in the joint
59
What joints can menisci be found
- radiohumeral
- acromioclavicular
- sternoclavicular
- knee
- first carpal metacarpal
- spinal facets
60
Describe knee menisci
- 90% type I collagen
- blood supply only reaches the outer 25-33%
- lesions/injuries in avascular regions of meniscus do not regenerate or repair
61
What population do traumatic meniscus tears typically occur in
- usually occur in relatively young athletes or active persons
- often involve other ligaments
62
What population do degenerative meniscus tears occur in
- degenerative tears are more common in persons 40 years of age or older
- often associated with degenerative articular cartilage
63
Knee meniscus healing
- healing occurs through repair of the defect with a combination of scar tissue & hyaline like cartilaginous tissue
- lesion may be filled with dense scar tissue by 10 weeks
- remodeling of the fibre/vascular scar into hyaline like cartilaginous tissue can take several months
64
Describe articular cartilage
- avascular
- aneural
- alymphatic
- mainly composed of chondrocytes embedded in a matrix of type II collagen, proteoglycans, & non-collagenous protein
65
What kills chondrocytes & disrupts the matrix
- blunt trauma
- penetrating injuries
- frictional abrasion
- sharp concentration of weight bearing forces (contact pressure)
66
What does the healing response of articular cartilage to penetrating injury depend on
- depends on whether the defect lies entirely within the substance of the articular cartilage or extends into subchondral bone
67
What happens during a partially penetrating injury to articular cartilage
- chondrocytes at the site of trauma are killed
- no inflammation, bleeding, hematoma formation, fibrin clots, or formation of granulation tissue if injury does not penetrate subchondral bone
68
What happens if injury to articular cartilage reaches the subchondral bone
- shows repair by hematoma formation, growth of vascular tissue, migration & proliferation of osteogenic cells, & formation of fibrous tissue or fibrocartilage
69
Articular cartilage injury classification
- Blunt trauma: can penetrate into the subchondral bone
- Type I defect: superficial laceration does not penetrate into subchondral bone (does not involve injury to blood vessels) & does not involve normal inflammatory & repair components
- Type II defect: deep, full thickness injury penetrating to the subchondral bone & its blood vessels which elicits an inflammatory response
70
What will a blunt trauma injury result in
- surface loss of proteoglycans
- cellular degeneration
- fibrillation (splitting)
- penetration of the subchondral capillaries into the calcified layer of cartilage
71
Type I articular cartilage injury healing
- necrosis occurs at wound margins together with signs of increased metabolic activity
- response does not repair the defect & the laceration persists unaltered
72
Type II articular cartilage injury healing
- initial response is formation of a fibrin clot within 48 hours of injury
- after 1 week fibroblasts & collagen fibers will have replaced the clot
- after 2 weeks cartilage develops within the fibroblastic tissue as chondrocytes begin to appear in the defect
- after 1 month most of the fibroblast type cells will differentiate into chondrocytes
- after 6 months defects still present on cartilage surface
- after 12 months a majority of the defects initially repaired have degenerated into erosive lesions resembling early osteoarthritis (OA)
- the defect fills in with weak scar tissue
73
Describe a disc
- the annulus fibrosus (outer layer) consists of alternating oblique layers of collagen fibrils
- the nucleus pulpous (inner layer) consists of a proteoglycan gel with a water content as high as 88%
- only the outer portion of the annulus fibrosus has a direct blood supply & has a poor capacity to heal with no regeneration of annular fibers
- internal disc injuries & internal ruptures of inner annulus fibrosus do not heal
74
Disc injury healing
- a tear in the annulus fibrosus facilitates degeneration of the disc internally
- may take up to 8 months for granulation tissue to mature, scar, & bridge a defect in the outer annulus fibrosus
75
What are the 4 stages to a disc herniation
1) degeneration
2) prolapse
3) extrusion
4) sequestration
76
Effects of prolonged immobilization of muscle
- atrophy
- decreased strength
- contracture
- reduced capillary to muscle fiber ratio
- reduced mitochondrial density
- reduced endurance
77
Effects of prolonged immobilization of bone
- generalized osteopenia of cancellous & cortical bone
78
Effects of prolonged immobilization of tendons & ligaments
- disorganization of parallel arrays of fibrils & cells
- increased deformation with a standard load or compressive force
79
Effects of prolonged immobilization of ligament insertion site
- destruction of ligament fibers attaching to bone
- reduced load to failure
80
Effects of prolonged immobilization of cartilage
- adherence of fibrofatty connective tissue to cartilage surface
- loss of cartilage thickness
- pressure necrosis at points of contact where compression has been applied
81
Effects of prolonged immobilization of synovium
- proliferation of fibrofatty connective tissue into joint space
82
Effects of prolonged immobilization of menisci
- adhesions of synovium villi
- decreased synovial intima length
- decreased synovial fluid hyaluronan concentrations
- decreased synovial intima macrophages
83
Effects of prolonged immobilization of joint
- 0-12: weeks impaired ROM, increased intraarticular pressure during movements, decreased filling volume of joint cavity
- after 12 weeks: force required for the first flexion-extension cycle is increased more than 12-fold
84
Effects of prolonged immobilization on the heart
- reduced strength of contraction (SV)
- reduced maximal cardiac output
- reduced endurance
- increased work of the heart for a sub maximal load
85
Effects of prolonged immobilization on the lungs
- reduced airway clearance of mucous
- increased likelihood of pneumonia
- reduced maximal ventilatory volume
86
Effects of prolonged immobilization on blood
- reduced hematocrit & plasma volume
- reduced endurance & temperature regulation
