Inflammatory Joint Disease

Question 1

osteonecrosis

Answer 1

death of bone in the absence of infection

characterised by loss of osteocytes from lacunae, necrotic marrow

Question 2

osteonecrosis usually occurs due to

Answer 2

vascular compromise - avascular necrosis

Question 3

avascular necrosis

Answer 3

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

Question 4

anatomically valnerable sites

Answer 4

head oof femur, tibia and scaphoid are more anatomically vulnerable to avascular necrosis

Question 5

traumatic avascular necrosis

Answer 5

eg. displaced fracture or fracture with non-union, complication of surgery, sometimes in athletes

Question 6

non-traumatic AVN

Answer 6

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

Question 7

AVN leads to

Answer 7

jooint pain and instability

Question 8

AVN presents as

Answer 8

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

Question 9

necrotic bone healing in trabecular bone

Answer 9

heals by creeping substitution

necrotic marrow is replaced by invading neovascular tissue, bone remodelling and intramembranous ossification

Question 10

necrotic bone healing in cortical bone

Answer 10

heals by cutting cones

osteoclast bore holes into the necrotic cortex via vascular channels with osteoblasts trailing forming new lamellar bone

Question 11

osteonecrosis of the mandible

Answer 11

post dental extraction
spontaneous
biphosphate associated osteonecrosis (bisphosphate treatment for osteoporosis)

Question 12

osteoradionecrosis

Answer 12

following radiotherapy
difficult to heal
combination of vascular damage, direct and indirect of radiation on cells, often complicated by infection (bacterial/fungal)

Question 13

arthritis overveiw

Answer 13

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

Question 14

symptoms of arthritis

Answer 14

pain, stiffness, deformity, loss of function

some systemic disease have arthritis as part of a spectrum of systemic findings (predominantly immunologically mediated/autoimmune diseases)

Question 15

signs of arthritis

Answer 15

heat, redness, swelling, reduced range of movement, deformity, tenderness, crepitus, joint effusion

Question 16

degenerative joint disease (osteoarthritis)

Answer 16

most common joint disorder in the developed world
predominantly degenerative, inflammatory component is secondary or absent
altered joint anatomy

Question 17

altered joint anatomy in degenerative joint disease

Answer 17

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

Question 18

degenerative joint disease predominantly occurs in which anatomical lcations

Answer 18

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

Question 19

primary DJD

Answer 19

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

Question 20

secondary DJD

Answer 20

occurs in context of underlying disease, including diabetes, haemochromatosis, severe obesity

Question 21

pathophysiology of DJD

Answer 21

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

Question 22

other non-nflammatory processes that causes arthritiis

Answer 22

• haemochromoss
• onchronosis
• hypertrophic pulmonary osteoarthropathy
• acromegaly
• tendonitis/tendinosis
• bone tumours

Question 23

automimmune arthritis

Answer 23

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

Question 24

rheumatoid arthritis

Answer 24

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

Question 25

rueumatoid arthritis occurs in

Answer 25

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

Question 26

immunology of rueumatoid arthritis

Answer 26

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

Question 27

rheumatoid factor

Answer 27

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

Question 28

pathogenesis of rhuematoid arthritis

Answer 28

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

Question 29

important cytokines released by CD4+ T cells

Answer 29

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

Question 30

4 stages of rheumatoid arthritis

Answer 30

1. triggering
2. maturation
3. targeting
4. fulminant

Question 31

triggering stage

Answer 31

anti-citrullinated peptide antibodies (ACPA) production
triggered by something in the environment eg. smoke, silica
or infectious agents eg. EBV

Question 32

maturstion stage

Answer 32

initiated at the site of secondary lymphoid tissue or bone marrow
citrullination of proteins active T-cells and B-cells = more ACPA production

Question 33

targeting stage

Answer 33

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

Question 34

fulminant stage

Answer 34

synovial hyperplasia, pannus, encroaches on articular cartilage
bone and cartilage destruction, joint capsule and ligaments
fibrous fusion = ankylosis

Question 35

rhuematoid arthritis clinically

Answer 35

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

Question 36

systemic symptoms of rheumatoid arthritis

Answer 36

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