Osteo-Arthritis and Rheumatoid Arthritis

Question 1

Roughly compare OA and RA

Answer 1

Both are disorders of joints (chronic inflam) but differ in their pathogenesis, presentation and complcations
. OA: result in subchondral cysts/sclerosis
. RA: result in panus and have ankylosis

Question 2

What is OA?

Answer 2

. AKA ‘Wear and tear’ disease
. Degenerative joint disease
. Erosion and disordered repair of articular cartilage that result in subchondral bone damage
. affect LARGE joints

Question 3

Etiology (causes) of OA?

Answer 3

. physical stress - affects weight bearing joints
. wear and tear disease (age)
. genetic predispose to chondrocyte injury

Question 4

What altered chondrocytes homeostasis (making it proliferate)?

Answer 4

. decrease proteoglycan conc
. decrease collagen type II fibres
=> result in hyperplasia of chondrocytes

Question 5

List the main pathological changes of OA

Answer 5

1. Fibrillation of cartilage
2. Eburnation
3. Sclerosis
4. Subchondral cysts
5. Osteophytes

Question 6

Pathological changes of OA (1)

Fibrillation of cartilage

Answer 6

. loose cartilage

. cartilage break down and become dehydrated until it’s completely lost

Question 7

Pathological changes of OA (2)

Eburnation

Answer 7

. Bone grinding bone - ‘shiny’ due to devoid of cartilage

Question 8

Pathological changes of OA (3)

Sclerosis

Answer 8

. Hardening of bone

. may contribute to the weight distribution

Question 9

Pathological changes of OA (4)

Subchondral Cysts

Answer 9

. Joint’s fluid (synovial) creep into the eburnated articulating bone forming cysts surrounded by fibrosis

Question 10

Difference between cyst and abscess

Answer 10

Cyst = cavity filled with fluid (synovial)
Abscess = cavity filled with pus

Question 11

Pathological changes of OA (5)

Osteophytes

Answer 11

. Narrowing of joint space due to mushroom-shaped bony outgrowths

note: osteophytes of the distal interphalangeal joints in women called ‘Herberden nodes’

Question 12

What’s special about OA?

Answer 12

NO ankylosis
NO inflam at synovial
NO swollen joints
NO treatment or prevention yet

Question 13

What is RA?

Answer 13

. Systemic autoimmune disease chracterized by inflam polyarthritis
. have RF and ACPAs
RF= rheumatoid factor which is aB against IgG
APACs = anti-citrullinated peptide aB
. affects SMALL joints (hand and feet)

Question 14

In RA, what makes T and B cells response to self antigens, including antigens in joint tissue?

Answer 14

1. Susceptibility genes (HLA) leads to failure of tolerance and unregulated lymphocyte activation
2. Environmental factors (infection, smoking) leads to enzymatic modification of self protein (citrullination)

Question 15

In RA, what cytokines create joint inflammation, triggering activation and proliferation of synovial cells, chondrocytes and fibroblasts?

Answer 15

IFN-g : Th1 cells
IL-17 : Th17 cells
TNF : Mø (main)

Question 16

What are clinical features of RA?

Answer 16

Female bias
Pain in hand joints, morning stiffness
Swelling wrist, metacarpal phalangral and proximal of interphalangeal (not distal)

Question 17

What diseases associated with RA?

Answer 17

Diabetes Type 1
SLE (Systemic lupus erythematosis)
Graves Disease
Hashimoto Thyroiditis

Question 18

What does joint changes in RA? What is the name of change?

Answer 18

. Proliferated synovial lining cells, inflammatory cells, granulation tissue and fibrous tissue
. they release proteases to damage cartilage
. called PANNUS

Question 19

What can we see in synovial histology in RA patients?

Answer 19

. synovial cell thickening with formation of villi + multiple layers of synovium –> HYPERPLASIA
. Lots infiltration of synovium by inflammatory cells (p/m B cell and lymphocyte)

Question 20

What are local complication of RA?

Answer 20

Joint instability
Eroding cartilage
Bony and fibrous ankylosis

Question 21

What are systemic complications of RA?

Answer 21

Hallmarks of chronic disease:

• anaemia
• fatigue
• loss of appetite
• high CRP and acute phase proteins
• intermittent fever, weight loss

Subcutaneous rheumatoid nodules develop along extensor of skin and may involve viscera

Question 22

4 features of hand deformities in RA

Answer 22

1. Radius deviation = wrist
2. Ulnar deviation = finger (metacarps)
3. Boutonnière = flexion of proximal interphalangeal + hyperextension of distal
4. Swanneck = opposite

Question 23

Aim of treatment for RA

Answer 23

. Control pain
. Early treatment to prevent joint destruction and consequent deformity and disability
. Active monitoring
. Improving patient’s quality of life

Question 24

Treatment available for RA

Answer 24

. pain relief
. physiotherapy
. immunosuppression (steroids, Disease-modifying Anti-Rheumatic drugs) like TNF antagonists
. methotrexate

Question 25

What is osteomyelitis?

Answer 25

Inflammation of Bone MARROW caused by infection of bacteria (S.aureus)

Question 26

In osteomyelitis, how does bacteria gain entry into the bone?

Answer 26

Haematogenous dissemination, spread of infection from adjacent side, trauma, iatrogenic

Question 27

What happens if not treating osteomyelitis?

Answer 27

. becomes CHRONIC:

• increase P leads to dead medullary bone which forced pus to arrive to under periosteum
• Lifting periosteum stops supply of blood to cortical bone, lead to necrotic bone - sequestrum
• Periosteum lays down new bone on surface that entraps the sequestrum - involucrum
• Pus ooze out into soft tissues - sinuses

note: sequestrum may extrude through a sinuse

Question 28

Treatment of osteomyelitis

Answer 28

. Antibiotics

. Surgical debridement (if no clinical improvement in 24-48h)