MSK Week6 Flashcards
Functions of bone
- Support structures and provide shape to the body
- Protect vital structures
- Allow movement and anchors for muscle
- Provide mineral storage
- Contribute to blood cell formation in the red marrow
True or false: bone is highly specialized connective tissue, highly vascular, most rigid of the connective tissues
True
Risk factors for fracture
- History of fall or trauma
- Advanced age
- Female
- BMI <25
- Decreased BMD
- Nutrition (vitamin D, calcium, caffeine)
- Hormonal factors
- Neoplasm
- Low physical activity level
- Smoking
Phases of Repair for Bone
- Inflammatory - several days (hematoma formation, angiogenesis; fibrous union)
- Reparative - 3-16 weeks (cartilage formation w/ calcification, cartilage removal and bone formation)
- Remodeling - months to years
Primary fracture management
- ORIF
- Closed reduction internal fixation
- External fixator (complicated fx’s)
- Traction for realignment (halo)
- Bone lengthening procedures (ilizarov)
Secondary fracture management
- No intervention: activity restriction, brace, crutch, boot, sling
- Closed reduction and casting: less infection, wait & see
What do healing factors depend on?
The bone involved and type of fracture
General healing time frame - children, adolescents, adults
Children - 4 to 6 weeks
Adolescents - 6 to 8 weeks
Adults - 10 to 18 weeks
Negative predictors for normal healing
- Smoking
- Diabetes
- Corticosteroids
- EtOH
- Renal and vascular insufficiency
Other complications to fracture prognosis
- Poor stabilization
- Damage to blood supply
- Infection
What are stress fractures caused by?
Creep in the bone that results in cyclic or sustained loading 0 repetitive loading over time, which gradually exceeds the bones ability to repair itself
Gold standard diagnostic for stress fractures?
Bone scan
Where are stress fractures most common?
Lower extremities
- Tibia, 2nd met, femoral neck, interarticularis
Interventions for stress fractures
- Rest/immobilization
- Correct muscle imbalances
- Graduated return to training
- Promote shock absorption
- Orthopedics prn
- Train muscle endurance
What is osteoporosis?
- A chronic, progressive disease characterized by low bone mass and microarchitechtural deterioration of bone tissue, leading to decreased bone strength, enhanced bone fragility and a consequent increase in fracture incidence
Primary osteoporosis
- Most common
- Occurs in both genders at all ages
- More often in menopausal women
Secondary osteoporosis
More associated with conditions or medications
Bone strength
Related to bone mass and other factors
- Remodeling frequency (bone turnover)
- Bone size and area
- Bone micro architecture
- Degree of bone mineralization
How much resistance to compression fractures does cortical bone account for?
Up to 75%
Osteoporosis bone pathophysiology
- Imbalance of bone resorption and remodeling
Non modifiable risk factors
- > 50 y.o
- Caucasian/Asian
- Menopausal or post menopausal
- Family history of osteoporosis
- Lactose intolerance
Modifiable risk factors to osteoporosis
- Inactivity, immobilization, sedentary lifestyle
- Excessive EtOH, tobacco, caffeine
- Medications (steroids, immunosuppressants, anticoagulants)
- Low BMI, small body frame
- Diet (deficiency of Ca, Mg, Vit D, Vit C)
- Eating disorders
Osteomalacia
- Softening of the bones
- Disorder of mineralization of newly formed bone - weak and more prone to fracture, vitamin D deficient and low phosphate
Osteopenia
- Low bone mass
- Less bone loss than osteoporosis
Osteoporosis
- Decreased bone density (strength)
- Deterioration of bone tissue and decreased bone strength
- Includes osteopenia
Major risk factors for osteoporotic falls
- Body weight < 70kg or BMI <21
- Corticosteroids
- Personal history of fractures as adult
- First-degree relative with fragility fracture
- Current smoking
Minor risk factors for osteoporotic falls
- Early menopause
- Nutrition
- Decreased activity
- EtOH
- Impaired vision
- Dementia
- Poor health
- Recent falls
Pharmacological management of osteoporosis
- Antiresorptives - estrogens/HRT, selective estrogen receptor modulators, calcitonin, biphosphates
- Anabolic PTH
What do antiresorptives do?
Decrease amount of bone lost
What does anabolic PTH do?
Build up bone mass
Nutrition general treatment and prevention recommendations of osteoporosis
- Calcium - decrease bone loss
- Vitamin D - reduced risk of hip and non-vertebral fx
- Calcium AND Vitamin D
- Caffeine - may reduce calcium absorption
- Vitamin K - may help with bone metabolism and reducing urinary calcium excretion
- Vitamin A - high levels = increased risk of hip fx
- Magnesium
- ETOH - can suppress osteoblasts; mod intake = decreased risk of hip fx
Non-pharmacological interventions for osteoporosis
- Rehabilitation
- Avoiding substances
Rehabilitation interventions for osteoporosis
- Exercise —> strengthen muscles: back and legs
- Orthotics
- Gait training
- Pain management
What types of exercises can be done to help osteoporosis?
- Weight bearing - walking.hopping, light jog; maintain BMD
- Flexibility
- Strength - weights, resistance bands, water resistance
- Postural and balance
** Best is combo of all **
Patient education for osteoporosis
- Body mechanics - help prevent falls and fxs
- Make the home environment safe
Management of vertebral fractures
- Conservative - oral pain management, PT
- Surgical - kyphoplasty, vertebroplasty (inject cement to help restore vertebral body height; last resort)
What is the tidemark line of articular cartilage?
Where articular cartilage affixes to the subchondral bone
What are the two main components of articular cartilage?
- Extracellular matrix
- Cells (chondrocytes)
What are chondrocytes responsible for?
- Making all the extracellular matrix components
- Produce matrix, maintain matrix surrounding it, break down any waste products within the matrix
Qualities of articular cartilage
- A few mm thick
- No blood or nerve supply
- No pericondrium
How does articular cartilage get their nutrient supply and get rid of waste?
Through synovial fluid, which is facilitated by the loading and unloading of the tissue
Qualities of deeper chondrocytes
- Produce higher volumes of proteoglycans
- Rate of turnover is slow
What makes up the extracellular matrix?
- Fibrous proteins
- Ground substance
Qualities of superficial chondrocytes
More elongated and will lay parallel to the surface
What are the four zones of articular cartilage fibers?
- Superficial/tangential zone
- Middle/transitional zone
- Deep zone
- Calcified cartilage zone
Superficial or tangential zone
- Highest concentration of fibrils
- Aligned parallel to the surface
Middle or transitional zone
Fibers appear disorganized
Deep zone
Fibers perpendicular to surface
Calcified cartilage zone
- Fibers perpendicular to the surface
- Deeper zones better fiber orientation to resist secondary tensile loads
Ground substance
- Proteoglycan chains
- Negatively charged hydrophilic molecules
- Water
- Highest concentration of PGs in middle zones
- Fluid concentration lowest in deepest regions
What does water do for cartilage?
Gives cartilage the ability to absorb compressive loads
Proteoglycan chains
- Glycosaminoglycan (GAG) chains
- Core protein
- Hyaluronan
Negatively charged hydrophilic molecules
- Repel each other
- Draw water in (swelling pressure) - resisted by collagen fibril network
Biphasic material
- Solid phase
- Fluid phase
Solid phase
Fatigue resistant, sustains high stress and strains of loading
Fluid phase
- Compliant, able to diffuse load over increased surface area
- Where the load is being accepted and being managed by the movement of fluid within the cartilage
Viscoelastic material
- Time-dependent behavior (creep)
- Initial loading, fluid phase supports 90% of load (15 min)
- Transfer to solid phase over 2.5-6 hours
- Fluid flow reversed when load removed
Combination of lubrication for articular cartilage
- Fluid film between articulating surfaces
- Boundary lubricant bound to/absorbed on articular surface
Fluid film condition
In fast low load
Boundary condition
In slow severe load
Nutrition of articular cartilage
- Avascular and alymphatic
- Synovial fluid exchange
- Passive diffusion
- Compression - induced convection
- Reciprocal loading essential for tissue health
Compression-induced convection
Reciprocal loading and unloading is constantly squeezing fluid in and out, like a sponge
Synovial fluid exchange
- Nutritional products
- Respiratory gasses
- Systemic signaling molecules - hormones and inflammatory molecules
- Waste products
What is activity regulated by?
- Chemical factors
- Mechanotransduction
- Electrical fields within cartilage
Metabolism of articular cartilage
- Chondrocytes are main source —> synthesize, repair, remodel extracellular matrix
- PGs are broken down/synthesized at higher rate than collagen
Skeletal maturity and aging
- Chondral cell proliferation ceases
- Rate of synthetic activity decreased
- Total number of chondrocytes reduced
Osteoarthritis
- Collection of pathologies
- Impacts articular cartilage, subchondral bone, joint capsule, synovial membrane, ligaments and periarticular muscles
Mechanically - OA cartilage
- Decreased tensile stiffness
- Diminished compressive properties
Early phase of OA
Increase synthesis/turn over of matrix to keep up with ongoing damage
Advanced disease - OA
- Altered distribution of cells, eventual cell die off
- More of the load on solid phase —> more damage
- Subchondral bone may become exposed as cartilage layer completely wears away
Cartilage repair - Chondrocytes
- They’re metabolically active
- Maintaining matrix
- Respond to changes in mechanical stimuli
- Often not able to prevent cartilage matrix loss
What does the degree of repair success of cartilage depend on?
- Extent of damage
- Nature of activity following damage
What would cause lack of repair for cartilage?
- Lack of blood flow
- Lack of inflammatory process
- Isolated from sources of stem cells
- Lack of chondrocytes mobility
- Ineffective matrix formation across lesion
When is there a greater risk of injury for cartilage?
- During early phase of healing (2 to 4 weeks)
Treatment for OA
- Medical (medications and such)
- Rehabilitation
- Surgical/procedural
What happens after prolonged immobilization (about 6 weeks +) or known cartilage injury?
- Mindful of degradation of connective tissue
- Greater risk of injury during early phase
- Graded joint loading program (acceleration loading can be damaging)
- Motion is lotion —> A/Prom, unloaded, cyclic
Post surgical/post procedural treatment for OA
- Protocol driven
- Surgical repairs typically have WB restriction period
- Injections will have minimal restrictions
What type of exercises give more shear forces?
Closed kinetic chain exercises
Arthrocentesis
Flushing the joint with saline - bad long term outcomes
Arthroscopy
- Flush joint
- Clear debris, loose bodies
- Shave down raggedy cartilage - smooth things out
- A clean up
Arthrodesis
Fuse the joint - more common in small joints where total joint replacement can’t be done
Clinical presentation of stress fractures
- History —> insidious onset w/ microtrauma
- Pain —> Cortical-local; trabecular - diffuse
- Does not improve w/ activity
- Tenderness on palpation
- (+) hop or percussion test
- (+) tuning fork
PT interventions for fractures - immobilization phase
- Transfer training
- ADL’s
- Gait
- Per MD order
PT interventions for fractures - If ORIF
- Watch for screws, wires, refracture and infection
What will most fractures have associated with them?
- Soft tissue injuries —> examine the soft tissue upon cast removal or when appropriate
What impairment and functional limitations are associated with fractures?
- Impaired ADLs
- Decreased ROM
- Weakness
How should you begin with mobility after immobilization?
Begin stretch/mobilize with short lever ROM and joint mobilization
What is weight bearing and resumption of activity based on?
Communication with the ortho MD
