Inflammatory Joint Disease Flashcards
osteonecrosis
death of bone in the absence of infection
characterised by loss of osteocytes from lacunae, necrotic marrow
osteonecrosis usually occurs due to
vascular compromise - avascular necrosis
avascular necrosis
loss of blood from to area of bone, usually at one end, most often due to loss of perforating artery
may be traumatic or non-traumatic
anatomically valnerable sites
head oof femur, tibia and scaphoid are more anatomically vulnerable to avascular necrosis
traumatic avascular necrosis
eg. displaced fracture or fracture with non-union, complication of surgery, sometimes in athletes
non-traumatic AVN
occurss predominantly in younger adults and is often bilateral
alcohol, corticosteroids, other drugs that affect bone, emboli, systemic infection, haemotological disorders, gout, idiopathic, legg-calve-pethes disease
AVN leads to
jooint pain and instability
AVN presents as
similar to osteoarthritis but more sudden and acute onset, imaging findings different
results in collapse of subchondral bone, disruption of articular surface and accelerated degeneration
necrotic bone healing in trabecular bone
heals by creeping substitution
necrotic marrow is replaced by invading neovascular tissue, bone remodelling and intramembranous ossification
necrotic bone healing in cortical bone
heals by cutting cones
osteoclast bore holes into the necrotic cortex via vascular channels with osteoblasts trailing forming new lamellar bone
osteonecrosis of the mandible
post dental extraction
spontaneous
biphosphate associated osteonecrosis (bisphosphate treatment for osteoporosis)
osteoradionecrosis
following radiotherapy
difficult to heal
combination of vascular damage, direct and indirect of radiation on cells, often complicated by infection (bacterial/fungal)
arthritis overveiw
a general term referring to joint pain leading to loss of function and disability
inflammation is usually but not always part of the disease process - not always the underlying cause of the disease
symptoms of arthritis
pain, stiffness, deformity, loss of function
some systemic disease have arthritis as part of a spectrum of systemic findings (predominantly immunologically mediated/autoimmune diseases)
signs of arthritis
heat, redness, swelling, reduced range of movement, deformity, tenderness, crepitus, joint effusion
degenerative joint disease (osteoarthritis)
most common joint disorder in the developed world
predominantly degenerative, inflammatory component is secondary or absent
altered joint anatomy
altered joint anatomy in degenerative joint disease
joint space narrowing, formation of osteophytes (bone spurs/outgrowths), cortical irregularity of sclerosis, formation of subcortical and subchondral cysts
damage (fibrillation) and loss of articular cartilage and wear and wear of underlying bone (eburnation), microfractures, osteosclerosis
degenerative joint disease predominantly occurs in which anatomical lcations
weight bearing synovial joints (hip, knee) and fingers, more common in bones and joints that have been previously injured or damaged due to other bone disease
primary DJD
idiopathic
occurs insidiously over time, more common in hips in men, knees and hands in women
more common in over 50s and about half of people over 70 have some symptoms
secondary DJD
occurs in context of underlying disease, including diabetes, haemochromatosis, severe obesity
pathophysiology of DJD
interplay of genetics and environment
biomechanical cartlage injuery, leads to chondrocyte prolferation and upregulation of MMPs, cytokines, but side effect is degradation of collagen and proteoglycans
other non-nflammatory processes that causes arthritiis
- haemochromoss
- onchronosis
- hypertrophic pulmonary osteoarthropathy
- acromegaly
- tendonitis/tendinosis
- bone tumours
automimmune arthritis
inflammatory and autoimmune process commonly affect the joints as part of a systemic involvement
eg.
- rheumatoid arthritis
- systemic lupus arythematosus
- psoriatic arthritis
- behcet disease
- ankylosing spondylitis
rheumatoid arthritis
chronic, common, multisystem, progressive autoimmune disorder that primarily involves the joints but most patients have at least one other site of involvement
other sites of involvement may include skin, lung, heart, pericardium, subcutis, vessels, salivary and lacrimal glands - rheumatoid nodules, vasculitis
rueumatoid arthritis occurs in
3x more common in women
varies with ethnicity, slight familial tendency but also associated with other autoimmune diseases
onset occurs in all age groups - 30s and 40s are most common
disease follows a progressive and relapsing remitting course
nothing to do with rheumatic fever or rhuematic heart disease
immunology of rueumatoid arthritis
raised serum Ig - usually have characteristic antibody against Ig called Rhuematoid factor
evidence tends to suggest that disease is diver by cellular immune mechanisms more than humoral
rheumatoid factor
not everyone who is RF positive has RA and vice verse
so called ‘seronegative’ arthritis is RF negative, at least initially, and RF levels tend to correlate with severity
pathogenesis of rhuematoid arthritis
initiated by CD4+ helper T cells
exact triggers are unknown for most patients - interplay between suscepetibility genes and environment
pathological changes are mediated by cytokines release by CD4+ T cells
important cytokines released by CD4+ T cells
IFN-y from Th1 cells - activated macrophages and resident synovial cells
IL-17 from Th17 cells - recruits neutrophils and monocytes
RANKL expressed on activated T cells - stimulated bone resorption
TNF and IL-1 from macrophages - stimulate resident synovial cells to secrete proteases that destroy hyaline cartilage
4 stages of rheumatoid arthritis
- triggering
- maturation
- targeting
- fulminant
triggering stage
anti-citrullinated peptide antibodies (ACPA) production
triggered by something in the environment eg. smoke, silica
or infectious agents eg. EBV
maturstion stage
initiated at the site of secondary lymphoid tissue or bone marrow
citrullination of proteins active T-cells and B-cells = more ACPA production
targeting stage
involvement of joints - synovitis and joint swelling
ACPA leads to elevation in cytokines eg. TNF alpha, IL-17A etc.
infiltration of monocytes, macrophages, mast cells, DC cells, T and B cells
fulminant stage
synovial hyperplasia, pannus, encroaches on articular cartilage
bone and cartilage destruction, joint capsule and ligaments
fibrous fusion = ankylosis
rhuematoid arthritis clinically
fatigue, lamaise, musculoskeletal pain
localised joint symptoms after weeks-months, persisting and progressing
generally symmetrical and smalljoints>large joints - usually distal-proximal progression and frequency
in hands and feet tends to be MCP and PIP joints of all digits
leads to redial deviation of the wrist, ulnar deviation of the fingers and flexion-hyperextension of the fingers
systemic symptoms of rheumatoid arthritis
vary
pulmonary fibrosis from lung lesions, skin and subcutaneous nodules and purpura or range of other symptoms
sequelae include joint fusion, deformity of joints and disability, side effects of immunosupresion
