Arthritis

Types of Arthritis

Osteoarthritis
Defined as
1. Degenerative bone disease
2. Characterized by
a. Progressive erosion of the
articular surface
3. An intrinsic disease rather than
inflammation due to alteration
in
a. Metabolic
b. Biochemical
i. Leading to breakdown of
articular cartilage
Causes
1. Primary Osteoarthritis
(95%)
a. Idiopathic in nature
b. As part of aging
phenomenom
c. Effects few joints
(OLIGOARTICULAR)
2. Secondary Osteoarthritis
(5%)
a. Predisposing condition like
i. Previous macrotraumatic to
the joint
ii. Repeated microtraumatic
iii. Underlaying disease like
1. Diabetes mellitus
2. Ochronosis
3. Heamochromatosis
Risk Factors
Age
1. in advancing age especially
above 65 years old
Mechanical effects

Pathogenesis

Clinical Features

Morphology

Complication
s

Changes in composition and

mechanical properties of
cartilage
1. breakdown of preexiting
collagen
a. Degenerating cartilage
contains
i. water
ii. proteoglycan
b. apoptosis
i. Leads to functional
chondrocytes
c. Destruction of cartilage
due to level of
i. IL-1
ii. TNF
iii. Nitric Oxide
2. Weakened collagenous
fibers due synthesis of
collagen type II
3. Matrix will be
subsequently getting
a. Vertical and horizontal
fibrillation
b. Cracking

1. Insidous onset
2. Primary osteoarthritis is
often assymptomatic until
the age of 65
a. Younger patient look for
underlying disease
3. Hallmark symptoms
a. Deep aching worsens with
use
b. Morning stiffness
c. Crepitus
d. Limitation of movement
4. Typically oligoarticular;
joints involved are
a. Hips
b. Knees
c. Distal and proximal
interphalangeal join of
finger
d. 1st carpometacarpal joint
e. 1st tarsometatarsal joint
5. Special characteristic in
women
a. HEBERDEN nodes at
finger
i. Represent osteophytes at
the distal interphalangeal
joints

Radiograph
1. Joint space
narrowing
2. Greater lateral
widening at distal
interphalangeal
joints than
proximal

1. Chondrolysis
2. Osteonecrosi
s
3. Stress
fractures
4. Joint
heamorrhag
e
5. Joint
infection

1. Weight bearing joints

2. Obesity
3. Previous bone deformity
Genetic predisposing factors
1. Linkage to chromosome 2 & 11

Types of
Arthritis

Rheumatoi
d Arthritis
Defined as
1. Chronic
systemic
inflammatory
disorder
(autoimmune)
2. Principally
attacks the
joints
3. Producing
a. Nonsuppurative
proliferative
b. Inflammatory
synovitis
4. Progess to
destruction of
the articular
cartilage and
ankylosis of the
joints
5. May also affect
ther tissues and
organs such as
a. Skin
b. Blood vessels

Pathogenesis
1.

Autoimmune disease triggered

by expsure of genetically
susceptible host to an
unknown arthritogenic antigen
2. Activation of CD4+ Tcells by
IL12 due to APC that presents
Arthriogenic antigen in MHC
3. T Cells will secrete cytokines
especially TNF which
subsequently lead to these
events
a. B cell activation which leads
to formation of
i. Autoantibodies
ii. Rheumatoid factor
1. These will lead to
formation and
deposition of immune
complex
2. Subsequently leads to
joint injury
b. Activation of macrophages,
they will then secrete IL-1 to
stimulates
i. Fibrolasts
ii. Chondrocytes
iii. Synovial cells
1. These cells will then
a. Secrete
i. Collagenase
ii. Elastase
b. Proliferate and
increase in numbers
c. Endothelial activation
i. Expression adhesion
molecules leading to
accumulation of

Clinical Features
1.

2.
3.
4.

5.
6.

7.

8.

9.

Age
a. Any age group, but
mostly 40-70 years old
Gender
a. Female:male (3,2:1)
Begins slowly in most
patients
Starts with
a. Malaise
b. Fatigue
c. Generalized
musculoskeletal pain
Then only joint is clearly
involved
At first small joints are
effected first, include
a. Hands joints
i. Metacophalangeal
joint
ii. Distal
interphalangeal joint
b. Feets joints
i. Metatarsophalangeal
joint
ii. Distal
interphalangeal joint
Followed by systemic
involvement with major
joints such as
a. Wrists
b. Ankles
c. Knees
d. Elbows
Affected joints are
a. Swollen
b. Warm
c. Painful
d. Particularly stiff
following activity
Disease progression vary,
with the greatest damage
happen during the first 4
to 5 years

Morphology
Gross Findings

Histological
Findings

1. Characteristic in
deformities
a. Deformed joints are
i. Unstable
ii. Minimal or no range
of motion
b. Radial deviation of
the wrist
c. Ulnar deviation of
fingers
d. Flexion and
hyperextension of
fingers
i. Swan neck
deformity
ii. Boutonniere
deformity
1. PIP bent toward
the palm
2. DIP bent
backward
2. Become fatal when the
deformity involves
cervical verterbrae
3. Synovial fluid is
a. Turbid
b. Sterile
c. viscosity
d. Poor mucin clot
formation
e. Inclusion-bearing
neutrophils
4. Rheumatoid nodule
(systemic
dissemination)

1. Site of initial
leasion in
synovium
a. Oedematous
b. Thickened
c. Hyperplastic
forming smooth
bulbous fronds
d. Infiltrated by
dense perivascular
lymphocytes
forming lymphoid
follicles
e. vascularity due
to
i. Vasodilation
ii. Angiogenesis
f. Penetration into
bone forming
i. Juxta-articular
erosion
ii. Subchondral
cysts
iii. Osteoporosis
g. Pannus formation
2. Synovial fluid
a. Presence of
neutrophils
b. Rice bodies
i. Floating fibrin
covering portion
of synovium
3. Rheumatoid
nodule (systemic
dissemination)

Complication
s
1.
2.
3.

Osteoporosis
Osteoarthritis
Vasculitic
syndrome
4. Leukocytoclasti
c venulitis
a. Purpura
b. Cutaneous
ulcer
c. Nail bed
infarction

4.

inflammatory cells
All of these subsequent events
will lead to PANNUS formation
a. Destruction of
i. Bone
ii. Cartilage
b. Fibrosis
c. Ankylosis

Types of Arthritis

Gouty Arthritis
1. End point of all
hyperuriceamic
conditions
2. Marked by
a. Transient arthritic
attack due to
deposition of uric acid
crystal with and
about the joints
b. Lead to chronic gouty
arthritis and
deposition of urate in
joints and other sites
(tophi)
Categories

a.
b.
c.

Firm
Non-tender
Round to oval skin
nodule at
subcutaneous level
d. Often happens at
pressure point
i. Elbow
ii. Archiles tendon

a.

Central fibrinoid
necrosis
b. Sorrounded by rim
of inflammatory
cells include
i. Epithelioid
histiocytes
ii. Lymphocytes
iii. Neutrophils
iv. Plasma cells

Pathogenesis

Clinical Features

Morphology

Complication
s

1. Prolonged hyperuriceamia
leads to deposition of urate
crystal (microtophi) in
a. Synovium
b. Joint cartilage
2. These will subsequently
lead to
a. Phagocytosis of urate
crystal by macrophage
i. It will then stimulate
chondrotcytes and
synovial cells by
releasing
1. IL-1
2. IL-6
3. TNF
ii. These 2 cells will then
secrete protease

4 stages
1. Asymptomatic
hyperuriceamia
a. Appears in
i. Male : around puberty
ii. Female : post menopause
2. Acute Gouty Arthritis
a. Sudden onset of severe joint
pain w/o
i. Hypereamia
ii. Warmth
iii. Marked tenderness
b. Majority first attack is
monoarticular
i. 50% metatarsophalangeal
joint
3. Intercritical Gout
a. If remains untreated will
make acute gouty arthritis
lasts for weeks and gradually

Acute Gouty Arthritis

1. Dense neutrophilic infiltrate permeating
the synovium and synovial fluid
2. Long, slender, needle shaped
monosodium urate found in
a. Neutrophil cytoplasm
b. Synovium
3. The synovium is
a. Edematous
b. Congested
c. Contained mononuclear
inflammatory cells
4. Once the crystal resolubilize, symptoms
abate
Chronic Tophaceous Gout
1. Heavily encrusted urates at the
articular surface forming visible
deposits in synovium
2. Synovium becomes
a. Hyperplastic
b. Fibrotic
c. Thickened by inflammatory cells

1. Joint
deformities
and motion
incapabalities
2. Kidney stones
formation
3. Heart disease
a. Due to
deposition
of urate
crystal in
major
arteries

1. Primary Gout (90%)

a. Basic metabolic
defect is unknown
b. Gout is the main
manifestation of the
disease
i. Hypoxanthine
Guanine
Phosphoribosyltransf
erase (HGPT)
enzyme defficiency
2. Secondary Gout
a. Known causes of
hyperuriceamia
b. Gout is not the main
manifestation of the
disease
i. production
1. Leukaemia nucleic acid
turnover
ii. excretion
1. Chronic renal
failure

b. Complement pathway
activation
i. Complement
chemotactic protein
initiates neutrophil
movements to synovium
ii. Neutrophil will engulf the
urate crystals, then this
event leads to
1. Lysis of neutrophils
bursting the engulfed
crystals and other
neutrophil will continue
to engulf
2. Neutrophil will release
a. LTB4
b. Prostaglandins
c. Free radicals
d. Lysosomal enzymes
3. All of these events will lead
to massive destruction of
tissue and inflammation

gains complete resolution

4. Chronic Tophaceous Gout
a. After years when symptoms
failed to resolved completely
b. Progress to severe crippling
disease
Factors Contribute to
Symptomatic Hyperuriceamia
1. Age
a. Rare before 20-30 years old
2. Genetic predisposition
a. X linked HGPT deficiency
b. Maltifactorial inheritance
3. Heavy alcoholism
4. Obesity
5. Theraputic drug
a. Diuretics
i. Frusemide
ii. Hydrochlorothiazide
b. Anti-TB
i. Pyrazinamide
6. Lead toxicity

d.

Forming a pannus destroying the

underlying structures
i. Leads to JUXTAARTICULAR bone
erosion
e. Severe cases, ankylosis might
happen
3. Gouty Tophi
a. Formed by
i. Large aggregation f urate
crystals
ii. Surrounded by intense
inflammatory reactions of
1. Lymphocytes
2. Macrophages
3. Foreign body giant cells
a. Attempting to engulf
the urate crystal
b. Can appear at
i. Articular cartilage of joint
ii. Periarticular ligaments and
tendons
iii. Soft tissues
1. Ear lobes
2. Nasal cartilages
3. Skin of the fingertips
a. Superficial tophi can
lead to massive skin
ulceration

Septic Arthritis
Infection to articular structure via
1. Heamatogenous spread
2. Direct innoculation
3. Contiguous spread from
a. Soft tissue abscess
b. Focus of osteomyelitis

Types of Arthritis

Suppurative
Arthritis

Pathogenesis
1. Bacteria seed at the articular
joint episodes of bacterimia
2. In neonates, it is due to
contiguous spread from
underlying epiphyseal
osteomyelitis

Clinical Features
1. Sudden painful, hot and
swollen joint
2. Restricted movement
3. Fever
4. Leukocytosis
5. ESR

Morphology
1. Fluid exudate
a. protein content
b. specific gravity
2. Large number of
neutrophils
3. Culture positive for

Complication
s
1. Permanent
joint
destruction
2. Septiceamia
3. Osteomyeliti
s

Tuberculous
Arthtritis

3. Most common organism

a. Gonococcus
b. Staphylococcus
c. Streptococcus
d. Heamophilus influenza
e. Gram ve bacteria
i. Salmonella spp
ii. E. coli
iii. Pseudomonas
1. Mode of spread
a. Complication of osteomyelitis
b. Hematogenous spread from
visceral infection (usually
lungs)
2. Mycobacterial seeding leads to
granulomatous reaction
forming caseating granuloma
with central necrosis
3. Affected area may grow pannus
over articular cartilage
a. Erode bone along the joint
margin
b. Severe destruction with
ankylosis

bacteria

1. Insiduous onset
2. Gradual progressive pain
3. W/o systemic symptoms

1. Fluid exudate
a. protein content
b. specific gravity
2. Presence of
a. Mononuclear
inflammatory cells
b. Macrophages
3. Culture +ve for
Mycobacterium