[SOLVED] Understanding Joint Health and Mobility

This assignment provides an in-depth analysis of joint health, covering topics such as articular cartilage, rheumatoid arthritis, and gouty arthritis. It also explores the principles of mobility, including functional mobility, balance, and coordination. The assignment aims to educate students on the importance of maintaining healthy joints and mobility, and the consequences of neglecting these aspects.

Musculoskeletal system:
Made up of: tendon, muscle, bone, joint, cartilage
Ligaments: Bands of flexible fibrous connective tissue in one direction to resist force. Limit
normal and prevent abnormal movement. Connects two bones together to stabilize a joint.
Cartilage: a smooth elastic rubber like tissue that acts as padding on the ends of long bones
at the joint
Tendon: strong fibrous collagen tissue that attaches muscle to a bone
Joint: junctions between two or more bones, allow for different types of movement.
Muscle: produce force and motion, maintaining and changing posture, locomotion.
Bone: support the body structurally, protect vital organs, enable movement, house bone
marrow and store minerals (importantly calcium)
Bone marrow: a spongey tissue in the very inner layer of some bones, containing stem cells
that develop into RBC’s, WBC’s and platelets.
Bones form the axial and appendicular skeleton; they articulate at joints and enable skeletal
muscle to provide force for movement at joints under the control of the nervous system
Axial: skull, vertebral column, ribs, sternum and joints between. Function to maintain
upright posture, protect vital organs (brain, spinal cord, heart lungs and thoracic abdominal
organs and reproductive organs) and transfer body weight to the ground through hips.
Appendicular: bones that support appendages and pelvis.
Bone tissue:
- Bone is a connective tissue, formation and remodelling happens continuously.
- Cells are supported by protein fibres; collagen. Hydroxyapatite.
Spongey bone: inner layer = resist forces and protects bone marrow
Compact bone: outer layer = protection and strength of bones
Epiphysis: end of long bones
Osteon: is a cylindrical structure that holds mineral matrix and osteocytes and a central
canal housing blood vessels called the haversian canal, situated in the middle of the osteon.
Lamellae are layers that surround the central canal containing mature bone. The fibres
orientate in different ways = withstand tensile strength and compression
Periosteum: dense layer surrounding bone, where the nerve supply is.
Bone development:
- Has to develop from another tissue
Joints:
Fibrous: bone ends are separated by strong fibrous material preventing movement between
the bones. Found between bones of axial skeleton
Cartilaginous: bone ends separated by flexible cartilage, allowing small amount of
movement. Found between bones of axial skeleton: intervertebral discs, costochondral
joints and public symphysis. Cartilage much more flexible than fibre

Synovial: found between bones of appendicular skeleton, designed for mobility. Much more
common for injury, have a cavity between bone ends lined by synovial capsule = freely
moveable. Mobility is determined by; presence of ligaments, shape of bony surface and
arrangement of muscle around the joints.
Articular capsule: capsule surrounding a synovial joint, containing 2 parts: outer fibrous
membrane and inner synovial layer.
Synovial membrane: connective tissue that lines the inner layer of capsules of synovial joints
Articular cartilage: fluid filled, like kitchen sponge for shock absorption and protection of
bone ends.
Joint cavity: refers to the space between the joints, is filled with synovial fluid that lubricates
joints = reducing friction between bones and allowing for greater movement
Neuromuscular system:
Skeletal muscles are controlled by somatic nervous system
Muscle belly: skeletal muscle portion of all muscle fibres of a given muscle.
Muscle cells exist in groups and separated by connective tissue layers (fascial = a group)
therefore, a muscle is made of many fascicle.
Endomysium: layer surrounding each individual fibre within fascicle.
Perimysium: surrounds the bundles of muscle fibres
Epimysium: connective tissue layered around the whole muscle
Fascia: even stronger connective tissue layered around the epimysium
Skeletal muscle cells:
What allows them to contract/shorten:
Myofibrils: muscle cells are made up of subunits of proteins
Myofilaments: smaller cells in myofibrils, are categorised into
- Myosin: thick
- Actin: thin
These have a regular pattern causing a striped appearance and can overlap on top of
each other to shorten = contraction
Contraction: is controlled by a nerve.
Skeletal muscle is controlled by 2 neuron pathways:
1. UMN: starts in primary motor cortex and travels to the brain stem and spinal cord
2. LMN: travels to skeletal muscle in peripheral nerves
The level of movement in a muscle is determined by the number of muscle cells controlled
by the lower motor neuron (motor unit).
Atrophy: lack of neural stimulation in skeletal muscle causing reduced size.
Control of skeletal muscle/ process of movement:
1. Sensory input: seeing soccer ball moving towards you, sensory signals sent to brain.
2. Integration: brain receives integrates the sensory input and sends the signals for an
appropriate motor response. (message travels from brain down spinal cord)

3. Motor output: the muscles needing to be used receive motor signals sent and
contract to move and kick the ball.
The motor unit: the number of muscle cells controlled by a single motor neuron.
- Larger motor unit = less control
- Smaller motor unit = more control
Synapse with effector organ cells:
(synapse = a structure permitting a neuron to pass an electrical or chemical signal to another
neuron or target effector cell)
Lower motor neuron synapses with effector organ (muscle cell) at neuromuscular junction.
Damage to motor pathway:
- can cause paralysis (inability to voluntarily contract muscle)
Types of paralysis: flaccid – LMN damage (floppy) & spastic: UMN damage (caused by
increase in tone)
- paresis: slight ability to voluntarily contract/ weakness
- paraesthesia: abnormal sensation
- anaesthesia: loss of sensation
Neuropathy: atrophy due to nerve damage
Adaptive changes to muscle:
disuse atrophy: causes fewer myofibrils
endurance training: more mitochondria and increased blood supply
resistance training: develops more myofibrils
Changes due to inactivity/ older age causes a decrease in muscle bulk, strength and ROM
due to loss/atrophy of skeletal muscle.
Caused by:
- decreased activity
- decreased nerve supply (dementia)
- nutritional deficiency (not enough protein)
- menopause (drop in bone density due to falling levels of oestrogen which helps
protect bone strength.
Osteoporosis, lecture 1
Metabolic injury to bone
Ossification/ osteogenesis: process of remodelling via laying down of new bone material
Organic component
Cells:
- Osteoblasts: bone forming - deposition
- Osteocytes: maintaining mature bone
- Osteoclasts: remodelling - resorbed

This process happens continuously
Also, - collagen fibres and proteins, help bone resist distortion
Inorganic component:
Calcium (85%) stored in our bone, and prosperous salts
Bone is constantly being remodelled to:
- Restore serum levels
- Ensure if inadequate intake serum calcium is reabsorbed from body stores
- Maintain osteoblastic activity / processes
Hypocalcaemia: low calcium in blood.
Calcium:
- Nerve conduction
- Iron transportation
- Muscle contraction
- Bone deposition
Serum calcium levels:
2.1-2.6 Mmol/L or KG.
- 50% floating free in plasma
- 40% binded to protein like albumin
- 10% bound to other ions
Serum levels affected by:
- Supplementation
- Hormone and renal function
- Diet and absorption
Endocrine control
Parathyroid gland:
- Secreted parathyroid hormone which stimulate increase in serum calcium levels
- GUT, kidney and bones can be used to increase calcium
Thyroid gland:
- Calcitonin – tones down calcium levels
- Does so by inhibiting osteoclasts which break down bones
Vitamin D:
Vitamin d stimulates calcium absorption in the gut
Inhibits parathyroid production
Involved in production of bone
Stimulates immune system – t cells
Inactive d (7-dehydrocholesterol) synthesized in sebatious glands and secreted on the skin
surface and converted by UV like to cholecalciferol vitamin d, goes to liver then kidney and
is now active form calciferol

85-100 mmol/L optimal range for optimal bone mass
Sun is required more than dietary intake
Can be indirectly tested through serum 25-hyrdoxvitamin D
Bone mass density
- increases in childhood and peaks in young adulthood
- Mass of mineral per volume of bone
- Peak bone mass occurs when you have the most bone you will ever have
Peak mass affected by:
- Genetics
- Hormones
- Exercise
- Calcium intake and absorption
- Environmental factors
Bone mineral densitometry tests:
- Used to diagnose osteoporosis
- Determine bone density (thickness) by examining the minerals (calcium and
phosphorus)
- Via dual x-ray in hip or lumbar spine as it’s a common site for fracture
- It compares your results to a normal one of the same age
Osteopenia:
- Lower density than expected with age
can be caused by:
- Imbalance between bone formation and destruction
- Inadequate mineralisation
- Excessive bone ossification
Not a diagnosis but describes the loss of bone density
Osteoporosis:
- A metabolic bone disorder = decrease in density, decrease in mineralisation, increase
in porosity.
Pathology:
DBD – impaired osteoblastic activity, enhanced osteoclast activity.
Risk factors:
- Age, osteoblast have reduced replication and less growth hormone stimulation
- Ethnicity, white and Asian women have higher stats
- Low body weight
- Postmenopausal
- Celiac disease
- Inflammatory diseases
- Lack of physical activity – weight bearing
- Smoking
- Calcium/ vitamin D deficiency

- Excessive alcohol intake
- Hyperthyroidism
Pharmacological risk factors:
- Corticosteroids – decrease collagen formation, decrease calcium reabsorption in gut,
increase secretion of PTH – increase of calcium secretion
- Heparin
- Chemotherapy – reducing androgen production, decreasing oestrogen and
testosterone
- Anticonvulsants
Prevention and treatment:
- Weight bearing exercise – increase osteoblast activity
- Smoking cessation
- Increased UV exposure
- Vitamin D3 supplementation -25microgram per day
- Adequate calcium intake
- Treating underlying conditions – CD, celiac
- Bisphosphonate therapy – fosemax
Bisphosphonate therapy:
- Work against bone demineralisation
- Used a lot in aged care
- Can be weekly, monthly oral or iv yearly
Oral administration –
- GIT upset
- Poor bioavailability only 50% reaches target tissue
- No food 2 hr prior and 30 min post, remain upright 30min post – difficult for elderly
to adhere to – affects effectiveness
- Increase apoptosis - cell death (osteoclasts) = decreases break down of bones, aim
to reduce fracture incident rather than rebuild bones in elderly
- Infusions come with post op side effects, fever.

Fractures: lecture 2
Traumatic injury to bone
Traumatic:
- direct or indirect force – most common cause of fracture
Pathological:
- osteoporosis
- osteogenesis imperfect
- infections – osteomyelitis

- tumours - osteosarcoma
Common fractures:
- NOF – major cause of nursing home admission and death in women, healing is
difficult due to disruption of blood supply and potential necrosis of head and neck of
femur.
- Colle’s fracture – distal radius, often following a fall to an outstretched forearm.
- Pott’s fracture – malleoli of tibia, fibula. Medial or lateral bone of ankle, common in
menopausal women
- Scaphoid fracture – base of thumb, often in fighting or boxing, has dual blood supply
and can sometimes cause non-union to blood supply
Diagnosis of fracture
- History/ what happened
- Observation of physical manifestations: deformity – bone coming through skin =
open/ compound fracture, swelling, temporary shock = loss of movement/ nerve
function – paralysis and numbness (nerves effected)
- X-ray imaging to confirm
Treatment:
- Reduce = bone ends are properly aligned
- Immobilise to give time to heal
External: splints, casts
Internal fixation: plates, rods, screws to hold in place enables weight bearing sooner
= encourages bone deposition
- Preservation of musculoskeletal function – cast to protect/ immobilize joint below
and above fracture. Maintain mobility for the rest of joints, rehab for atrophy
Observation and monitoring: to ensure perfusion is adequate
Observation: skin colour, deformity
Palpation: skin temp, peripheral pulse, perfusion (cap refill)
- Blood supply can be compromised – fracture bone is sharp and can compromise
blood vessels – skin colour will change and skin will become cool – immediate
management required
- Plaster, cast or bandage may be too tight if swelling occurs after the time of
application – skin colour will change and skin will become cool – immediate
management required
4 stages of fracture healing:
1. hematoma formation:
- produces a clot
- establishes a fibrous network – fibres in blood from clot
- influx of inflammatory cells
- new capillary beds
- bone cells in area die
2. formation of fibrocartilaginous callus
- soft callus forms on the break to stabilize:

- fibroblast cells produce new connective tissue, fibres and collagen where the blood
clot was – forms scaffold, connects to bone ends
- not strong enough for weight bearing
3. bony callus (soft bone) formation:
- osteoblasts convert cartilage callus into spongy bone
- begins 3-4 weeks after injury and lasts up to 4 months
4. bone remodelling:
- Remodelling of spongy bone callus to compact bone structure on the edge
- Removal of bony collar from outside of bone
Factors that affect healing:
- Age: bioactivity (age of cells) – elderly, decreased osteoblastic activity.
- Type of injury: long bone fractures and displaced fractures take longer (severity)
- Medications: corticosteroids, anticonvulsants, heparin etc - slower osteoblastic
activity.
- Local stress/movement around fracture site – splinting to limit this
- Circulation problems – new osteoblasts and fibroblasts brought via circulation =
diminished capacity to form clots and bring required cells
- Coagulation disorders – affected ability to form hematoma initially in healing steps
- Poor nutrition – protein required to build, calcium and vitamin D.
Complications of fracture healing:
- Delayed union – failure to heal in predicted time
- Malunion - deformity at fracture site/ bone doesn’t heal properly (twisted, shorter,
bent). Can occur if improper alignment occurs during mobilization, cast removal
prematurely.
- Non-union - failure of bone to heal before the repair stops: infection, movement,
poor blood supply. Normal healing process is impaired, stem cells used sometimes
to aid this recently.
Sprains and strains: lecture 3
Altered joint structure: traumatic injury
Trauma – acute disruption due to damaging forces across the joint
- Children – falls, bicycle injury and sporting accidents.
- Young adults – MVC
- Over 65: falls
- Sport injuries: acute, repetitive use
Strain: stretching causing partial or complete tear of a tendon or muscle.
Caused by – excessive sudden stretch of contracting muscle. Commonly affects 2 muscle
groups including: hamstrings, quads, gastrocnemius. Sporting injury and in middle to old age
people as muscle is less elastic.
Grades -
Type 1: only a few muscle fibres affected, localised pain, no loss of strength or function
Type2: significant fibres affect, loss of strength, pain on contraction

Type 3: complete tear, often where muscle joins to tendon, surgery required.
Sprain: stretch or rupture of ligament or the fibrous capsule of synovial joints
Caused by: excessive normal or abnormal movement. Common sites: weight bearing joints;
ankle, knee
Both cause an inflammatory response: Pain, swelling, stiffness
Repair of fibrous connective tissue:
- Process of inflammation
- Influx of inflammatory chemicals – macrophages – function to rid dead cells,
fibroblasts – function to make new connective tissue fibres
- Capillaries infiltrate area to bring new fibroblasts and nutrients
- Fibroblasts from the tendon sheath also build new fibres
- Normal tensile (stretching) strength only achieved after 6-8 weeks making
immobilization important.
Treatment: goal is to minimize inflammation (reduce bleeding, swelling)
Rice: 48-72 hours
R: rest – crutches, taping or sling
I: ice - every 20 minutes for 2 hours
C: compression – minimize swelling, vasc obs important too
E: elevation – injured area above heart level as long as possible to minimize swelling and
bleeding
No harm should also be applied immediately
H: heat
A: alcohol
R: running/activity/
M: massage
A synovial sheath is one of the two membranes of a tendon sheath which covers a tendon.
Tendonitis/ tendons: a connective tissue connecting bone and muscle, capable of resisting
high tensile forces while transmitting forces from muscle to bone. Collagenous tissue made
up of fibers. Tendonitis is inflammation of a tendon, RSI can cause.
Bursitis/ bursa: bursa is a small fluid filled sac and are located where muscles and tendons
move over bony/ hard fibrous areas to reduce friction and facilitate movement. Bursitis:
inflamed due to overuse sometimes.
Capsulitis/ capsule: tough connective tissue membrane that is attached to bone and
encloses the joint cavity to hold bones and other parts of the joint together. Capsulitis =
inflammation within/ of the capsule.
Rotator cuff / injury: small muscles to help keep the head of the humerus aligned and in the
shoulder socket. Also helps rotation and raise movement of the arm. Tendonitis, bursitis and
supraspinatus tendon rupture or injury can all contribute to Rotator cuff injury. Symptoms
include: pain, tenderness over area, possibly atrophy, reduced ROM.

Diagnosis done via arthroscopy. First line management cortisone injection and rest, often
surgery and rehab after.
Carpal tunnel: overuse of flexor tendons in hand that run over synovial sheath can inflame
the synovial sheath. Inflammation of the sheath compresses the median nerve.
Symptoms: pain, typical inflammatory symptoms, tingling in the distribution of the median
nerve = supplies palmar surface of the first 3 and ½ fingers and the muscles used to move
those fingers including the thumb, muscle weakness in those fingers and prolonged use,
atrophy.
Dislocation: surfaces of bones not in contact
Subluxation: surfaces of bones in partial contact
Abnormal displacement of bones at a joint
Most often associated with traumatic injury, fracture. Can also be caused by congenital
disorder which cause muscle imbalance, i.e. hip dysplasia and aged population with torn
supraspinatus.
Common sites:
- knee joints and hip/femur dislocating head of femur joint in MVCs
- Head of radius/elbow in small children due to ossification of bones not complete yet
- Shoulder/acromioclavicular joint in sport injury, recurring common
Diagnosis: H/O, Imaging, physical exam.
Treatment: depends on which joint, whether its complete or partial and mechanism of
injury (method damage occurs). I.e. manipulation (relocation) and immobilizing.
Spondylolishthesis:
Forward slipping from one vertebra on another due to abnormality in shape or orientation
of the vertebra, trauma, degenerative fracture of vertebrae arch or joints can allow them to
slip.
Commonly found in lumbar spine due to curvature of that area, the pressure from above
the vertebral column accepts and transfers the weight of the upper body through to the
pelvis and then ground. Meaning the force is on the front of the vertebra causing forward
slipping.
Symptoms: inflammation, nerve involvement, reduced movement, abnormal gait, abnormal
posture to alleviate pain and pain due to muscle spasm happening to try and protect the
joint.
Disc Herniation/slipped disc:
Intervertebral discs are found between each vertebral body and function is to allow each
vertebrae to move on one another and absorb shock (able to be compressed). Function is to
weight bear through jelly like centre to evenly distribute forces around outer/anulus.
Made up of 2 parts, outer ring: anulus fibrosis and inner: nucleus pulposus.
Disc herniation occurs when rupture occurs in the anulus fibrosis allowing the jelly like
nucleus pulposus to move through the anulus and compress the spinal nerves.

Traumatic or degenerative changes to the nucleus pulposus or anulus fibrosis can lead to
uneven distribution of load than ruptures the anulus causing the inner jelly to ooze through.
Usually a posterior ooze as injurious occurs during flexion = increased weight on anterior
surface of disk. Compresses spinal nerves causing neurological symptoms.
Arthritis: lecture 4
Causes: inflammation, congenital and degenerative.
Localised examples: osteoarthritis
Systemic examples:
- Collagen disorders: osteogenesis imperfecta
- Rheumatoid arthritis – destruction of multiple joint components
- Gout – uric acid crystal deposition in joint
- SLE systemic lupus erythematosus – damage to synovial membrane
Osteoarthritis: degenerative joint disease, most common type of joint disease
Caused by: wear and tear to articular cartilage
Risk factors:
- Age – accumulative exposure to other risk factors
- Gender – more women than men
- Bone mass
- Obesity – greater force on articular cartilage
- Repetitive injury/use
Primary: unknown cause, more likely to be generalised
Secondary: trauma, wear and tear
1. Risk factor/cause
2. Chondrocyte response
3. Release inflammatory chemicals
4. Production, release protease enzymes (break down proteins) – (leads to): loss of
cartilage surface, development of surface cracks, destruction of subchondral
bone (underneath cartilage)
5. Destruction of joint structure
6. Osteophyte formation
7. Inflammation of synovial membrane = swelling
Presentation:
Pain, general ache caused by use and relieved by rest
Stiffness – difficulty starting movement after inactivity
Joint enlargement/ swelling
Loss of ROM
Grinding sound in joint = crepitus
Usually affects larger weight bearing joints: knees, lumbar vertebra. Due biomechanical
wear and tear. Can be big toe, cervical spine and fingers.
Treatment: aim to relieve pain and maintain, improve ability

Exercise to decrease load on joint
NSAIDs
Intra-articular therapy: corticosteroids, hyaluronic acid
Glucosamine, chondroitin
Tens (transcutaneous electrical nerve stimulation) machine = analgesia short term
Acupuncture
Joint replacement, surgery, prosthesis
Articular cartilage:
- Covers bone ends in synovial joints
- Provides smooth frictionless joint surface
- Absorbs weight transferred during weight bearing and spreads evenly across surface
of joint
- Composed of collagen fibres (proteins) and cartilage cells (chondrocytes) cells and
fibres are in a thick jelly substance rich in proteoglycans, cartilage is high in water.
Underload the water is squeezed out and reabsorbed when the joint is reloaded
(pumping action important in spreading synovial fluid over joint surface).
Rheumatoid arthritis:
- Autoimmune inflammatory joint disease
- genetic predisposition present, family H/O
- Women more affected than men
- Remission and flare
- An abnormal immune response causing synovial membrane inflammation and
overtime destruction of joint architecture.
Immune response:
1. Immune cells release enzymes that destroy articular cartilage = inflammatory
response in synovial membrane
2. Inflammatory response = increased vascularisation (growth in capillaries) = increase
blood flow, permeability and synovial fluid = joint swelling
3. Formation of pannus overtime (network of destructive blood vessels in synovial
membrane) = irreversible, destructive effect on cartilage and bone = reduced joint
movement
Symptoms:
- Fatigue
- Pain
- Weakness
- Aching
- Stiffness
- Polyarticular: both side of body and multiple joints.
Early: wrist and hand affected – ADL affected: hand crafts
Swelling can alter direction of muscles, causing joint deformities i.e. swan neck deformities
Management: limit inflammation
- Corticosteroids – short acting
- NSAIDS – short onset
- Immunosuppressants/ DMARDs – long acting to demonstrate clinical affect

Gout/ gouty arthritis: Caused by hyperuricaemia – urid acid is produced during
breakdown of purines are compounds found in food or produced in the body, its then
carried in the blood and filtered out by the kidneys. In gouty arthritis there is a build-up
= hyperuricaemia.
Asymptomatic hyperuricaemia
Acute gouty arthritis,
- Acute high levels of urate concentration
- Results in formation of crystals and inflammation in usually a joint (big toe 50%)
Tophaceous Gout
- Chronic stage - less ability to clear uric acid or overproduction of purines or both
- Tophi form in cartilage
Symptoms:
Pain, redness, swollen
Episodic flare ups
Monoarticular
Hyperuricaemia not always present at time of flare
Causes: metabolic disorders, dietary intake
Treatment:
Pain relief: NSAIDs, hydrocortisone injections
Diet modification – alcohol intake, low purine
Review of current medications, i.e. diuretics
Urosuric drugs to prevent urate reabsorption in renal tubules
Alopurinol reduces serum urate production
Can contribute to renal disease
Principles and practices of mobility:
Falls related to mobility leading cause of mortality and morbidity in population over 65 in
AUS
NOF:
- Most common
- 25% mortality
- Significant loss of mobility
- Burden and cost on health care
- 30% falls occur in hospital
Functional mobility: requires
- Coordination of musculoskeletal and nervous system -functional mobility affected by
damage to nervous system. I.e. stroke, dementia
- Muscle strength and joint range
- Absence of pain
- Good posture – alignment of body parts promotes optimal position for joints,
muscles, tendons, ligaments

- balance – state of equilibrium the forces around the joints counteract each other
and is the result of proper body alignment. Line of gravity, centre of gravity within
the base of support.
- Patient cooperation and confidence
- Awareness of surroundings