Bone and cartilage tissues Flashcards
What are some characteristics of bone?
- highly specialized connective tissue
- highly vascular
- can absorb impact
- constant remodeling (Wolf’s Law)
What are some risk factors for fractures?
- history of falling
- advanced age
- female
- BMI <25
- decreased bone mineral density
- nutrition
- neoplasm
- low PA level
- smoking
What are some diseases that can cause bone fractures?
- osteoporosis
- osteomalacia
- rickets
- osteogenesis imperfecta
- paget disease
- ehlers-danos syndrome
What are the phases of healing for bones?
1) Inflammatory (several days)
2) Reparative (3-16wks)
3) Remodeling (months to years)
What are the clinical presentations of a fractures bone?
- pain/ pain w/ WBing and loading
- deformity
- deep, dull ache
- edema/bruising
- could have major loss of function
- pain response w/ ultrasound and/or tuning fork
What are primary and secondary fracture management techniques?
Primary:
- ORIF
- closed reduction internal fixation
- traction for realignment (halo)
- bone lengthening procedures
Secondary:
- no intervention (activity restrictions, brace, crutch, boot, sling)
- closed reduction and casting
What does PT address w/ fractures?
Treat impairments and functional limitations associated with fracture
- impaired ADLs
- ROM
- weakness
How do PTs manage fractures?
Start with mobilization, stretching, joint mobs, and then strengthening with short lever arms first
When appropriate, performing WBing activities to increase bone density
What is the healing prognosis timeline for fractures?
Children: 4-6 wks
Adolescents: 6-8 wks
Adults: 10-18 wks
What are stress fractures?
- creep in bone from repetitive loading over time (bone can’t repair itself fast enough)
most common in LE (tibia, 2nd met, femur neck, pars interarticularis)
What is the clinical presentation of a stress fracture?
- insidious onset with microtrauma
- pain: cortical-local, trabecular-diffuse
- does not improve with activity
- tenderness on palpation
What are some interventions for stress fractures?
- rest/immobilization
- correct muscle imbalances
- graduated return to training
- promote shock absorption
- orthotics prn
- train muscle endurance
What is osteoporosis?
chronic, progressive disease characterized by low bone mass and deterioration of bone tissue
What score is considered an osteoporosis score?
-2.5 SD or less from mean for age and sex
What part of bone has 75% resistance to compression fractures?
cortical bone
When do bone mass changes occur?
- peaks by mid 30s
- bone loss begins several years prior to menopause
genetic factors contribute to 80% of women’s risk of osteoporosis
What are some risk factors of osteoporosis?
Non-modifiable:
- >50 years old
- Caucasian/Asian
- menopausal
- family history
- depression
- lactose intolerance
Modifiable:
- inactivity
- alcohol abuse, tobacco use
- medications
- low BMI
- diet
What are some secondary causes of osteoporosis?
- renal insufficiency
- cushings
- hyperthyroidism
- type II diabetes
- osteomalacia
- pagets disease
- SCI
- stroke
What are some risk factors for osteoporotic falls?
- BMI <21
- corticosteroids
- personal history of fractures
- 1st degree relative with fragility fractures
- smoking
What is the difference between osteomalacia, osteopenia, and osteoporosis?
Osteomalacia:
- softening of bones
Osteopenia:
- decreased bone mass
Osteoporosis:
- low bone strength/density
When should BMD testing occur and how often?
ALL women over 65 and men over 70
- should occur every 2 years
- sooner in those with risk factors
What is some general treatment and prevention dietary advice for those with osteoporosis?
Nutrition:
- calcium
- vitamin D
- reduce caffeine
- vitamin K
- reduce excessive intake of vitamin A
- magnesium
- reduce alcohol consumption
What are some common medications taken for osteoporosis?
Antiresorptives:
- estrogen/HRT (for prevention ONLY)
- selective-estrogen receptor modulators (SERMS) (prevention & treatment)
- calcitonin (treatment)
- bisphosphonates (treatment and most common)
Anabolic PTH: builds up bone mass (treatment w/ daily injections)
What are some non-pharmacological interventions for fractures/osteoporosis?
Exercise:
- strengthening muscles (back and legs)
- WBing exercises
- flexibility
- strengthening exercises
- posture and balance
Orthotics
Gait training
Pain management
What is the major contraindication for exercise and osteoporosis?
spinal FLEXION exercises
- leads to vertebral fractures
What are some educational points for osteoporosis?
- avoid bending forward
- carry loads close to the body
- sleep with back straight
- safe home environment
- never twist with a load
How are vertebral factures managed?
- oral pain management
- PT
- kyphoplasty & vertebroplasty
What is the tidemark of articular cartilage and what are the 2 main components of articular cartilage?
Tidemark: edge of calcified zone that is before the deep zone
Extracellular matrix: has fibrous proteins and ground substance
Cells: chondrocytes
What are some properties of articular cartilage?
- avascular & aneural
- gains nutrients through synovial fluid
- superficial cells lay more flat than deeper cells
- absorbs compression
- resists tensile load
- mainly type II cartilage
What are the 4 zones of fibers in articular cartilage?
- superficial: increased concentrations of fibrils; lays parallel
- middle: fibers disorganized
- deep: perpendicular to better resist secondary tensile loads
- calcified: same as deep
What is in ground substance?
Proteoglycan chains:
- glycosaminoglycan chains that are attached to core proteins that are attached to hyaluronan
- negatively charged hydrophilic molecules that repel each other and draw water in
60% water
What are some biomechanics of articular cartilage?
Biphasic material that includes:
- solid phase: fatigue resistant & sustains high stress & strains of loading
- fluid phase: compliant & diffuses load over increased surface areas
Viscoelastic material:
- creep
- initial loading = fluid phase
- moves to solid phase after about 2.5-6 hours
EXTREMELY slick to help with movement of joints
How does articular cartilage get its nutrients?
- through passive diffusion in the synovial fluid and compression-induced convection
- basically squeezing in/out nutrients w/ load
What do chondrocytes do?
Synthesize, repair, remodel the extracellular matrix
Activity is regulated by:
- chemical factors
- mechanotransduction
- electrical fields w/in cartilage
How does immobilization affect articular cartilage?
- greater degeneration with longer, rigid periods of immobilization
- cartilage does not completely recover after longer periods of immobilization
What are some aging affects in articular cartilage?
- chondral cell proliferation ceases at skeletal maturity
- rate of synthetic activity is decreased
- total number of chondrocytes is reduced
- progressive decrease in tensile properties
How do OA and articular cartilage degeneration relate to one another?
- with mechanical OA, there is a decrease in tensile stiffness and diminished compressive properties with articular cartilage
What is the degree of cartilage repair dependent upon?
- extent of damage
- nature of activity following damage
What does a lack of repair of articular cartilage result from?
- lack of blood flow
- lack of inflammatory process
- lack of chondrocyte mobility
- ineffective matrix formation across lesion
How good is the repair of articular cartilage?
NOT good as new
- only temporary
- fibrocartilage characteristics
- leads to eventual breakdown
What is the medical treatment of articular cartilage injury?
- NSAIDs
- corticosteroid injections
- viscosupplementation
- regenerative medicines
- total joint replacement
What is the rehabilitation process of articular cartilage injury?
After prolonged immobilization:
- there is greater risk of injury during early phase (2-4 wks)
- graded joint loading program
- motion is lotion (AROM/PROM, unloaded, cyclic)
What is OA in a nutshell?
- articular cartilage failure with secondary components of inflammation
- most common arthritis type
- knees, hips, and hands most common places
- multifactorial: genetic, metabolic, biochemical, and biomechanical
What is the pathology and disease process of OA?
- chondrocytes fail to repair damaged articular cartilage which leads to an unstable matrix
- decreased water content makes the matrix stiff and brittle
What are some macro changes of OA?
- progressive cartilage loss
- subchondral bone reaction/remodeling
- osteophyte formation
- synovial inflammation
What are the two different types of osteoarthritis?
Primary: Idiopathic
- localized or generalized forms
- localized OA most commonly affects the hands/hips/spine/knees/feet
- generalized OA is three or more sites
Secondary:
- post-traumatic
- congenital or development disorders
- calcium pyrophosphate dihydrate deposition disease (CPPD)
- others (paget disease, RA, gouty arthritis)
What is the etiology of OA?
Multifactorial:
- aging
- obesity
- joint injury (trauma or repetitive microtrauma)
- chronic low-grade inflammation
- heredity/genetics
What are some risk factors of OA?
- age (50+)
- sex (male <45, female >45)
- family history
- occupation/hobbies
- past injuries
- obesity
What are some clinical signs of OA?
- crepitus
- bony enlargement
- decreased ROM
- malalignment or deformity
- TTP
- mild, localized joint effusion
- impaired muscle performance
- Gelling (morning stiffness for 5-10 minutes)
- stiff after still, improved with movement
- locking or giving way
What are some clinical symptoms of RA vs OA?
RA:
- systemic autoimmune
- symmetrical
- morning pain/stiffness >30 minutes
- small joints of hand (MCPs and PIPs)
- boutonniere, swan-neck, and ulnar drift
OA:
- local joint disease
- unilateral/asymmetrical
- morning stillness <30 minutes
- hand joints (PIPs and DIPs, thumb CMC)
What are some self-efficacy and self-management techniques for OA?
- stress reduction and coping strategies
- weight loss
- joint protection and energy conservation
- maintain ROM and strength
- use stronger and larger muscles when possible
What is the best exercise for OA?
NO BEST EXERCISE - is what pt will adhere to
- mobility: ROM and stretching
- strengthening: avoid pain and w/in pt tolerance (low intensity more reps)
- neuromuscular training
- aerobic conditioning: aquatic exercise
What is RA in a nutshell?
- progressive, systemic, autoimmune inflammation
- often aggressive, devastating consequences
- unknown etiology (auto immune, infection, smoking)
What are some characteristics of RA?
- symmetric synovitis
- joint erosions, cartilage and bone destruction
- multisystem extra-articular manifestations
- onset usually slow & insidious over months
- aggressive management leads to good control
What is the main cause of RA as an autoimmune disease?
- imbalance b/w pro/anti-inflammatory mediators
- leads to chronic inflammation
What are the mediators of joint destruction in RA?
- cytokines (TNF)
- chemokines (IL-1, IL-6)
- MMP (VEGF)
What is the natural course of RA?
- undifferentiated polyarthritis
- early RA - Mild disease
- severe RA w/ deformities
25% require surgical treatment
What are the diagnosis criteria for RA?
Four or more of the following must be present:
- morning stiffness > 1 hour
- arthritis of >3 joint areas of the 28 possible joints
- arthritis of hand joints (MCPs, PIPs, wrists)
- symmetric swelling
- serum rheumatoid factor (antibody to IgG)
- rheumatoid nodules
- radiographic changes
first 4 have to be present for 6 weeks or more
What are some of the typical joints involved in RA?
- wrist and MCP joints
- index/middle MCP joints
- PIP, MCP, MTP
- elbows, shoulders
- knees, ankles, hips lumbosacral NOT involved
- atlanto-axial joint (C1-2), subluxation
Why is the atlanto-axial joint involved or affected with RA?
Only purely synovial joint in spine
- could lead to spinal cord involvements
What are some extra-articular systemic manifestations of RA?
- MSK wasting
- tenosynovitis, bursitis
- osteoporosis, Rh nodules
- vasculitis
- pericarditis, myocarditis
What are the main deformities involved with RA in the hands?
- Swan-neck: DIPs
- Boutonniere
- Ulnar drift
What are some predictors of a poor prognosis in those w/ RA?
- presence of >20 inflamed joints
- radiographic evidence of bone erosion
- Rh nodules
- high titers of RA factor and anti CCP
- higher class of functional disability
- persistent inflammation
- advanced age of onset
40-85% of RA pts unable to work in 8-10 years
What are some complications of RA?
- carpal tunnel
- Baker’s cyst
- systemic vasculitis
- peripheral neuropathy
- cardiac and pulmonary involvement
- risk of lymphomas is 3x greater
- risk of infection due to disease and treatment
What is the main pharmacological treatment of RA?
DMARDs:
- inhibit autoimmune response underlying RA
- inhibits production of cytokines and cellular activation
Main DMARD is Methotrexate (Rheumatrex)
What do some of the newer DMARDs do?
- inhibit key inflammatory mediators (TNF-alpha)
- relatively selective
What is the new treatment paradigm for RA?
Patient education -> PT -> OT -> Orthopedic surgery
What are the main goals of PT in those w/ RA?
- decrease pain, inflammation
- maintain functional ability and increase QoL
- control systemic involvement
- slow progression of disease
- protect articular structures
How does PT manage RA?
- weight management
- education on joint protection/energy conservation
- avoid deforming positions and prolonged static positions
- assistive devices
- superficial heat
- aquatic therapy
How does PT differ with acute vs subacute/chronic exacerbations of RA?
Acute:
- respect pain & fatigue
- Grade I-II joint mobs
- active ROM through available ROM NO stretching
- joint protection & energy conservation
- modify ADLs prn
Subacute/Chronic:
- joint protection/energy conservation
- flexibility and strength w/in joint tolerance
- low load resistive training
- low impact aerobic activity to tolerance
Vigorous stretching or manipulations contraindicated
