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CNSLF Bone Path 3 - Joint disease/Arthritis (i) (Osteoarthritis (symptoms,…
CNSLF Bone Path 3 - Joint disease/Arthritis (i)
Intro
joints = connections between bones
synovial joints = movable joints of body (e.g. knee)
non-synovial joints = structural integrity, min movement
cartilaginous (e.g. intervertebral joints)
fibrous (e.g. cranial sutures)
synovial joint structures
articular surface covered by hyaline cart (healing is poor)
articular cart acts as a shock absorber between bones
chondrocytes produce matrix, enzymes + cks to degrade it
collagen 2
proteoglycans
H2O
joint capsule (pain sensitive) lined by synovium
ligaments = bands of fibrous connective tissue
bursa = fibrous sac that acts as cushion to ease movement in areas that are subject to friction
synovial membrane
synovial fluid
lubrication + nourishment for cart
colour = colourless to pale yellow
clarity = transparent
WCC < 200 (PMNs < 25%)
glucose nearly equal to blood levels
gram stain -ve - sterile
synovium lacks a BM - quick exchange between blood + synovium
Type A synovial cells are macrophage-like (phagocytic + produce hyaluronic acid)
Type B synovial cells are fibroblast-like (produce protein)
Arthritis types
osteoarthritis
arthritis related to infectious agents
arthritis related to immunological disease
arthritis induced by crystals
arthritis a/w systemic disease
Osteoarthritis
most common type to rheumatic disease
affects 80% of elderly
degenerative disease characterised by progressive erosion of articular cart
non-inflamm process (hence -itis = misnomer, rather osteoarthrosis)
due to wear + tear
can be primary or secondary
primary (idiopathic)
affects elderly
involves weight-bearing joints (e.g. hips, knees)
more common in overweight
also affects interphalangeal joints (flex hand)
some families have Mendelian pattern of inheritance of primary generalised osteoarthritis - mutation in gene for type 2 collagen
secondary
develop @ any age in a damaged joint
i.e. any disease affecting joint can cause osteoarthritis
trauma
RA
gout
TB
acromegaly
HFE
deformity (e.g. hip dislocation)
not caused by regular exercise
pathogenesis
aging + mechanical effects - 'wear + tear'
biomechanics stresses of weight-bearing joints over time
genetic factors
changes in composition + mechanical properties of cart
increased water + decreased conc of proteoglycans
chondrocytes produce IL1, TNFa + NO - stim production of metalloproteinases that degrade matrix
inhibited production of type 2 collagen + proteoglycan
destruction of articular cart
chondromalacia: softening of cart, stains pale
cart fibrillation: fragmentation, cracking appearance
erosion
exposure of subchondral bone plate
constant friction when cart gone
subcentral sclerosis (eburnation - degeneration, ivory)
cyst formation in bone underlying cart, as fluid now has access to bone
small fractures
osteophyte formation (lipping) - outward growth of bone @ the margins of articular surfaces - formed by endochondral ossification
joint mice (detached fragments of bone - osteophytes) - pain + recurrent locking
can be asymp
Heberden's nodes/nodules
osteophytes producing palpable enlargement @ distal interphalangeal joints (distal bony growth) + are often early manifestation of osteoarthritis
Bouchard nodes/nodules are similar but on proximal interphalangeal joints
secondary changes
thickening of synovium with minimal inflamm
atrophy of muscle
deformity of joint - osteophyte formation, subluxation (partial dislocation, slight misalignment)
osteoporosis due to decreased use
symptoms
severe pain
morning stiffness that worsens during day
restricted movement
crepitus - crackling sensation when joint used
compression of N root by osteophytes
deformity
investigations
x-ray
-ve serology
synovial fluid aspiration: clear, viscous, cell count slightly raised/normal
Tx
no cure
glucosamine, chondroitin, s adenomethionine