Joints and joint disease Flashcards
what is connective tissue made up of?
Connective tissue split into:
1) cellular component
2) ECM
ECM further split into:
Fibrous proteins (Elastin and Collagen)
Ground substance
Ground substance made up of proteoglycan, glycoprotein and water.
What are the three types of collagen and where are they found?
What is collagens main property?
Type 1 collagen - think TOUGH, forms tendons, ligaments, bones, dermis and encapsulates organs.
Type 2 collagen - forms HYALINE and ELASTIC cartilage
Type 3 - RETICULAR fibres forms the structural FRAMEWORK of SPLEEN / LIVER / LYMPH / SM/ ADIPOSE tissue
Collagen has TENSILE strength -> resist tensile forces
What is the purpose of elastin?
- Has ELASTIC strength, inherent stretchability and recoil.
- often mixed with collagen to prevent overstretch
- Found in large arteries, lungs, skin
What are the three types of connective tissue?
- Loose irregular -> tends to form underneath structures (e.g lamina propria, under pleural etc.)
- Dense irregular -> forms at regions that need to be tougher, resist forces from all directions. e.g. organ capsules and dermis
- Specialised connective tissue = dense regular -> e.g. tendons/ ligaments/ cartilage
Describe properties of loose irregular CT and where it forms
- High cellular content:
- macrophages
- mast cells
- fibroblasts
- adipose cells
- Loose arrangement of fibres (elastin/ collagen/ reticular fibres).
- abundant ground substance and EC fluid
- has blood vessels and nerves contained within it
- Forms at:
- glands
- underneath skin
- lamina propria of GI/ Resp
- Tunica adventitia
- underneath pleura/ peritoneum/pericardium
Describe the properties of Dense Irregular Connective tissue
where is it found
- Dense irregular made up of:
- low cellular content
- high fibre content, collagen arranged randomly to resist forces from all directions
- elastic fibre network
- Found at:
- Organ capsules
- dermis
- nerve sheaths
describe properties of specialised connective tissue:
dense regular CT
where is it found?
Other types of specialise CT
- Forms ligaments/ tendons/ aponeurosis
- High fibre content, collagen arranged in PARALLEL
- Other tissues:
- Cartilage
- Adipose tissue
- haematopoetic tissue –> lymph glands, blood, bone marrow
Describe structure of cartilage:
ECM
Outer layer
Blood supply
Cartilage formed of ECM and fibrous proteins collagen and elastin.
ECM formed of proteoglycan and GAG’s v hydrated -> resist compressive forces
Covered in outer connective tissue layer called PERICHONDRIUM. Formed of outer FIBROUS layer and inner CELLULAR layer.
Perichondrium absent at articulating surfaces to allow friction free movement.
Cartilage nourished by DIFFUSION assisted by compression, is AVASCULAR therefore slow to heal.
Origin of cartilage cells?
mesenchymal stem cell –> chondroblast (present in periochondrium) –> chondrocyte (mature cell formed after secretion of ECM, sits in own lacuna)
Cartilage growth and repair?
Growth:
1) appositional growth: occurs by chondroblasts in the perichondrium, adds surface layers of cartilage (not at articular surfaces)
2) interstitial growth (at articulating surfaces and endochondral ossification) : chondroblasts grow, divide, secrete ECM, spread out from each other, occupy own lacunae and become chondrocytes.
Repair: poor unless in children
cartilage often replaced by dense regular connective tissue. (ligaments/ tendons/ aponeurosis).
Three types of cartilage?
- Hyaline
- Elastic
- Fibrocartialge
Describe the three types of cartilage
-
Hyaline:
- most common and weakest
- has perichondrium but not at articulating surfaces.
- Formed of short dispersed TYPE 2 collagen fibres plus large amounts of PROTEOGLYCAN
- Present at articulating surfaces, costal cartilage and growth plates.
-
Elastic:
- strong, flexible and resilient
- at regions where deformation and recoil required
- elastic fibres and TYPE 2 collagen
- perichondrium present
- external ear
- epiglottis
- larynx
-
Fibrocartilage:
- strongest form
- thick parallel bundles of TYPE 1 collagen
- alternates with hyaline cartilage matrix
- found in regions of significant forces
- NO PERICHONDRIUM
- insertion points ligaments/ tendons
- IV discs
- joint capsules
- knee menisci
- pubic symphysis
- TMJ
What is a joint?
what different types of joint exist with different movement ability?
Joint = where two or more bones articulate
- synarthroidal -> no movement
- amphiarthroidal -> slightly moveable
- diarthroidal -> freely movable
Breakdown the different types of joint
1) synovial
2) fibrous joint -> sutures and syndesmoses
3) cartilaginous joint –> primary cartilaginous joint (growth plates, costal cartilage) and secondary cartilaginous joint (symphysis, IV discs, manubriosternal joint )
What fibrous joints are there?
sutures -> between flat bones of skull, immovable (synarthroidal)
syndesmoses -> interosseous membrane between tibia and fibula/ radius and ulna, slightly moveable (amphiarthroidal)
Joint mainly collagen no cartilage.
What cartilaginous joints are there?
Cartilaginous joints formed entirely by cartilage either hylaine or with/without fibrocartilage
Primary cartilaginous joint = SYNCHONDROSES
HYALINE cartilage ONLY
at GROWTH PLATES and COSTAL CARTILAGE.
Secondary cartilaginous joint = SYMPHYSIS
HYALINE cartilage sandwiching FIBROCARTILAGE (H-FC-H)
E.g PUBIC SYMPHYSIS, IV DISCS, MANUBRIOSTERNAL JOINT.
Describe synovial joint
what is it reinforced by?
what is a bursa?
Articulating surfaces covered with hyaline cartilage
Enclosed in a fibrous joint capsule on the outside with inner synovial membrane (synovium) that secretes synovial fluid.
Nourishes and lubricates the joint.
often reinforced by fibroelastic ligaments that cross the joint preventing excessive movement.
e.g. MENISCI in the knee = FIBROCARTILAGE.
Bursa = sac made of synovial membrane contains synovial fluid decreases the friction of structures moving over one another.
Describe the different types of joint that occur at different regions of the body
how can joints be classified based on movements in planes?
Hinge joint -> flexion and extension i.e elbow
Ball and socket -> glenohumeral and hip joint (several axes movement)
Plane joint -> permits gliding/ sliding e.g. acromioclavicular joint
Saddle joint -> metatarsophalangeal (convex and concave surfaces)
condylar -> metacarphophalangeal (extension/ flexion/ ab and adduction/ circumduction)
pivot joint -> atlantoxial joint (between C1 and C2 permits rotational movements).
Planes: 1) uniaxial 1 plane 2) Biaxial 2 planes 3) multiaxial movement in 3 planes
What is osteoarthritis?
what are the risk factors?
Risk factors for OA
O- obesity and A- age
Think FAT SOB G
Female
Age
Trauma
Stress (Mechanical) on joint
Obesity
Bone density: either increase and risk of development or decreased and risk of progression
Genetics
Bold= non modifiable RF’s
What two forms of OA are there?
Where does OA primarily affect?
Primary -> genetic, occurs in absence of insult
Secondary -> as a sequelae of multiple factors e.g. trauma/ inflammatory disease/ infection
OA primarily affects:
HIPS
KNEES
SMALL JOINTS OF HANDS
How does OA begin?
Normally begins with some form of insult to the joint, damages the cartilage leading to a chondrocyte response –> secretion of inflammatory cytokines and mediators.
Describe the pathophysiology/ pathogenesis of OA
- Stimulus/ insult causing cartilage damage –> chondrocyte response to release INFLAMMATORY CYTOKINES
- Macrophages invade joint to phagocytose the cartilage debris, release PROTEASES
- PROTEASES –> CARTILAGE DESTRUCTION, FIBRILLATION (Surface cracks in cartilage)
- Chondrocytes respond by releasing GF and more INFLAMMATORY CYTOKINE
- further invasion by inflammatory cells, protease release —> cycle of joint destruction –> eventually loss of cartilage, decrease of COLLAGEN/ PROTEOGLYCAN, reduced SHOCK ABSORBTION and exposure of subchondral bone.
- bone rubbing on bone = EBURNATION –> SUBCHONDRAL CYSTS and MICROFRACTURES
- disorganised attempt to heal itself –> SUBCHONDRAL SCLEROSIS and OSTEOPHYTES
- SYNOVIAL inflammation = SYNOVITUS and HYPERPLASIA
- REDUCED/ RESTRICTED JOINT –> STIFFNESS
Describe the radiological features of OA
OA Joints Suck Major
Osteophytes
Asymmetrical Joint space narrowing
Subchondral sclerosis/ cysts
Malalignment
Describe the SX of OA
Morning stiffness (short lived)
Post inactivity stiffness
Pain worsens throughout the day, joint pain is worse on movement
Night/ rest pain
Functional limitation
Examination findings in OA
Reduced range of movement
Crepitus
Bone SWELLING –> Heberdens DISTAL IP, Bouchards PROXIMAL IP (B before H in alphabet, therefore proximal)
Joint effusion/ deformity/ instability
muscle wasting
Management of OA
advice and education
Non pharma: physiotherapy, exercise to increase muscle strength, weight loss, aids and devices
Pharma: Pain management via NSAID/ PARACETAMOL/ CAPSAICIN, STEROID INJECTION
Surgical Management: Joint replacement (arthroplasty), joint realignment, joint fusion or excision
Types of inflammatory arthritis? (3 plus breakdown of one form).
Rheumatoid
Crystal arthritis -> GOUT
Spondyloarthritis -> HLA B27 associated. Umbrella term for inflammatory diseases invoving both joints and entheses (where ligaments and tendons insert).
Three forms:
Psoriatic spondyloarthritis (rashes)
Anklyosing spondyloarthritis (spine and sacroiliac joints)
Enteropathic arthritis (ass. w IBS).
Main features of Rheumatoid A?
- Autoimmune disease, destruction of synovial membrane and articulare surfaces leading to inflammation of the joint and joint destruction
- Often positive for Rheumatoid Factor and inflammatory markers
- Joints appear symmetrically : hot, swollen, tender, deformed
- Main characteristics:
- morning stiffness lasts > 1 hr
- systemic inflammatory Sx –> skin/ eyes/ heart (IHD) (peridcardium)/ lungs (pleura).
Contrast main features of OA vs RA
OA:
- Develops later than 40 yrs
- Slowly over years
- Biomechanical loss of cartilage matrix
- Asymmetrical affecting weight bearing joint (knees and hips) and hands
- Pain on use of joint, inflammatory signs less common
- No systemic signs of illness
- morning stiffness last less than 20 mins
- Rheumatoid factor absent
- Osteophytes present
- Common both M and F
RA:
- Develops between 25-50 yrs
- Develops over weeks to months
- Autoimmune destruction of synovium and articulating surface, joint inflammation
- symmetrical, affects smaller joints and some large (elbow)
- inflammatory markers present, signs of inflammation (heat, swelling, tenderness)
- systemic signs of illness –> fatigue/ weight loss/ anaemia
- morning stiffness > 1 hr
- Rheumatoid factor present
- osteophytes absent
- More common females
Define gout
general cause
types
Purine metabolism pw?
Gout is an inflammatory response to the deposition of URATE crystals deposited in and around joints and synovial fluid.
General cause: hyperuricaemia (uric acid)
leads to synovitis, joint and cartilage destruction.
acute and chronic (tophic) forms
primary (genetic) and secondary (induced)
Purine metabolism : Purine –> xanthine –> Uric acid
Uric acid excreted via kidney and GI tract
If insufficient get uric acid circulation in excess and TOPHI formation.
Primary vs secondary gout
Primary (95%) cases –> genetic reason for either overproduction or underexcretion of urate crystals
Secondary (5%) –> overproduction: 1) increased purine intake 2) increased nucleotide turnover (lymphoma/ preeclampsia) 3) drugs
–> under excretion: 1) kidney failure, 2) alcohol 3) drugs
Urate crystals get deposited in renal parenchyma –> can itself result in renal failure and urate calculi.
Acute vs chronic gout SX
Acute: sudden onset, often precipitated by alcohol/ dehydration/ diuretics, tender, swollen and red and often 1st metatarsophalangeal joint.
Chronic (Tophaceous) : often associated with chronic renal failure and long term diuretics.
Tophi formation in bursae/ tendons/ cartilage/ periarticular bone.
may ulcerate or discharge
chronic joint pain
may have superimposed acute gout attacks.
Chronic Gout :
Radiographic changes
GOUT –> No POUT
Narrow joint space (late stage)
“Punched out” bony lesions w sclerotic margins/ overhang
Opacities or TOPHI in soft tissue
(Uric acid)
Tissue swelling (soft tissue)
Management of gout
- decrease alc intake
- avoid purine rich food
- lose weight
- medication review (diuretics)
Acute attack: NSAID and COLCHINE (unknown MOA interrupt monosodium urate cycle and decrease inflamm).
Chronic:
ALLOPURINOL –> xanthine oxidase inhibitor –> decrease synthesis of uric acid
URICOSURIC DRUGS –> increase urinary excretion of uric acid –> be aware of urate caliculi.
