OSTEOARTHRITIS

AND
INFLAMMATORY
ARTHRITIS
PRESENTED BY
NURAFIFAH BINTI SHAMSURI

SUPERVISED BY
DR TEVANTHIRAN A/L GOBAL
Outline
• Osteoarthritis

• Inflammatory rheumatic disorder

1. Rheumatoid arthritis
2. Axial spondyloarthropathies: ankylosing spondylitis
3. Peripheral spondyloarthropathies:
-Reiter’s syndrome & reactive arthritis
-Psoriatic arthritis
-Enteropathic arthritis

• Crystal deposition disorders

1. Gout
2. Calcium pyrophosphate crystal associated arthropathy (CPPD)
OSTEOARTHRITI
S
Introduction
• Chronic disorder of the synovial joint:
o 1. Progressive cartilage destruction
(softening/disintegration)
o 2. Osteophytosis (new bone) at the joint margin
o 3. Subarticular cyst formation

o 4. Sclerosis of the subchondral bone

o 5. Sinovitis (mild)

o 6. Capsular fibrosis
Prevalence and distribution
• Prevalence increase with age
• Affected: knees, hips, hands, feet and spine
• Knee: anteromedial compartment of tibiofemoral joint and lateral
facet of patellofemoral joint
• Hip: superolateral aspect
• Hands and feet: DIP, first MTP and thumb base
Aetiology
• Systemic: Genetics, age, gender, diet and obesity

• Local biomechanical factors:

-Abnormal joint shape and size
-Previous injury
-Neuromuscular problem
-Obesity
-Loading/occupational factors
• Bone mineral density

• Presence of Heberden’s nodes in hand OA (risk of knee OA)

Pathology

Early softening and Intermediate

swelling of articular fragmentation and Late erosion down to
cartilage with increase fissuring of cartilage underlying bone
in its water content surface
Pathology Radiographic correlates
Focal areas of loss of articular cartilage Joint space narrowing (if loss is
extensive)
Bone growth at the joint margins Osteophytes

Sclerosis of underlying bone Sclerosis of subchondral bone

Cyst formation in underlying bone Bone cysts

Loss of bone Bone attrition

Varying degrees of synovial inflammation Effusions may be apparent

Fibrosis and thickening of the joint Not visible on radiographs

capsule
Symptoms and signs
Symptoms
• Joint Pain
• Joint stiffness
• Bony swelling
• Loss of muscle bulk
• Clicking/grinding sensation
• Instability
• Reduced functional ability
Signs
• Altered gait
• Joint tenderness
• Bony swelling
• Reduced range of movement
• Crepitus
• Muscle wasting
• Signs of inflammation
• Deformity and instability
Differential diagnosis & investigation

Ddx
• Inflammatory arthritis
• Avascular necrosis
• Fingers polyarthritis
• Diffuse idiopathic skeletal
hyperostosis (DISH)
Ix
• Blood: Normal
• X-ray (weight bearing)
Kellgren and Lawrence scoring system

0 Normal No features of OA
1 Doubtful Minimal osteophyte, doubtful
significance
2 Minor Definite osteophyte, no loss of joint space
3 Moderate Some diminution of joint space
4 Severe Advanced joint space loss and sclerosis of
bone
Management

The pyramid of treatment for symptomatic osteoarthritis (From Dieppe & Lohmander, 2005.)
Non pharmacological Pharmacological Surgical

1. Education 1. Oral treatment: PCM, 1. Arthroscopic

2. Lifestyle
tramal, NSAIDs, COX-2 lavage
inhibitor, glucosamine 2. High tibial
modification
2. Intra-articular osteotomy (HTO)
3. Physiotherapy treatment: Corticosteroids, 3. Total joint
4. Occupational Hyaluronic acid replacement
therapy 3. Topical treatment: 4. Partial joint
5. Orthoses diclofenac replacement
4. Alternative treatment: 5. Arthrodesis
Acupuncture, Avocado
Soybean Unsaponifiables
(ASU), ginger
 OA Variants
• Anatomical • Biochemical • Abnormal • Neuromuscular
and 1. Genetic joint shape and vascular
pathological abnormalities in and stability 1. Neuropathic
1. Atrophic type II collagen 1. Generalized: arthritis
destructive OA’ 2. Alkaptonuria, Skeletal
dysplasia,
2. Spastic cerebral
2. Hypertrophic OA hemochromatos palsy
Mseleni joint
is and other disease
3. Erosive 3. From avascular
metabolic
inflammatory OA of 2. Focal: necrosis
conditions
the interphalangeal
Joints 3. Kashin Beck intraarticular
fractures, DDH, • Chondrocalcinosis,
disease pseudogout and
Perthe’s disease,
SCFE pyrophosphate
arthropathy
 INFLAMMATORY
RHEUMATIC DISORDER
1. Rheumatoid arthritis
2. Axial spondyloarthropathies including ankylosing spondylitis
3. Peripheral spondyloarthropathies
RHEUMATOID ARTHRITIS
• It is a chronic Causes:
inflammatory • Genetic factor
autoimmune disease
• Immunological factor
• Mainly involve joints
but may cause systemic • Environmental factors
manifestation (Eg: infectious agents or
cigarette smoking
• Peak incidence: 3rd – 5th
decades
• Female:male = 3:1
 Stage 1 Stage 2 Stage 3 Stage 4
Pre-clinical Synovitis and joint Early joint Advanced joint
swelling destruction with peri- destruction and
articular erosion deformity
 History
• Onset of the pain is rapid
• Joints symptoms:
• Polysynovitis, swelling and stiffness
• Pain affects joints symmetrically
• Loss of mobility in the proximal joints of fingers (MCP and PIP)
• Generalized stiffness after period of inactivity/rest and improves with activity
• Morning stiffness (> 30 minutes)
• Previous history of muscle pain, fatigue, weakness, loss of weight and low grade fever
• Other joints affected as time passes
• Associated symptoms: rash, dry scaly skin, malar rash, back pain, presence of thophi
 Symmetrically
distributed swelling
and tenderness of
metacarpophalangeal Thickening ,
joints, proximal tenderness and
interphalangeal joints crepitation over back
and the wrist of the wrist or palm
Physical Examination while passively

Early moving the fingers

(tenosynovitis)

stage Local warmth, synovial

Deformity of hypertrophy and intra-
joint (unusual) articular effusion will be
more obvious in larger
joints
Limited joint
movement
 Joint
deformity Restricted and very
become painful joint movement
more Disturbed daily activity
apparent

Later
Physical Examination stage

ulnar deviation of the fingers

Typical radial and volar displacement of
rheumatoid the wrists
deformities valgus knees, valgus feet and
clawed toes

Valgus knee Clawed toes

 Investigation
 Imaging
 Blood  Synovial
investigation • X-ray
biopsy
• Early: synovitis (soft tissue
• FBC: normocytic, • Obtained by swelling and peri-articular
hypochromic needle biopsy, osteoporosis)
anemia via • Later: marginal bony
• Raised ESR and C arthroscope or erosions & narrowing of
reactive protein open articular space
(in active phase) operation • Advance: articular
• Serological test: • Histologically destruction and joint
Rheumatoid non specific deformity
factors and • Ultrasound and MRI
antinuclear • Ultrasound helps in defining
factors presence of synovitis and
early erosions
 Extra-articular Features

• Rheumatoid nodules
• Lymphadenopathy
• Splenomegaly
• Vasculitis
• Muscle weakness
• Visceral disease
 Diagnosis
Typical presentation:
• Presence of bilateral, symmetrical polyathritis
involving the proximal joints of hands or feet
POSITIVE RF + ABSENCE
• Morning stiffness (> 30 minutes)
FEATURES
• Symptoms improve with activity -is not sufficient evidence of RA

• Persisting for at least 6 weeks

NEGATIVE RF + PRESENCE
FEATURES
-does not exclude diagnosis
Subcutaneous nodules or x-ray of peri-articular
erosion
-diagnosis is certain
 Differential
Diagnosis
• Psoriatic arthritis
• Erosive inflammatory
arthritis
• Polyarticular gout
• Arthritis related to
infection
• SLE
 Management
Medical
Corticosteroids
 Prednisolone
 Methylprednisolone
DMARDs (disease-modifying
antirheumatic drugs)
 Methotrexate
 Combined with sulfasalazine &
hydroxychloroquine
 Leflunomide, if methrotrexate
not tolerated
NSAIDS: control of pain and stiffness
Physiotherapy and Occupational Therapy
• Preventive splinting and orthotic devices
• Encourage activity
• If these fail to restore and maintain function, operative
treatment is indicated
Surgical Management
• Indication: Severe joint destruction, fixed
deformity, and loss of function
• Soft tissue procedures (synovectomy, tendon
repair or replacement and joint stabilization)
• Arthrodesis, osteotomy and arthroplasty
ANKYLOSING SPONDYLITIS
• generalized chronic
inflammatory diseases
• affecting spine and sacroiliac
joints
• characterized by pain and
stiffness of the back
• variable involvement of the
hips and shoulders and
rarely the peripheral joints
• prevalence is 0.1–0.2% in
Western Europe and North
America, much lower in
Japanese and African
peoples
• Males > females (vary from
2:1 to 10:1)
• usual age at onset between
15 and 25 years.
• Associated with HLA-B27
and ERAP1
 Pathology
Synovitis of diarthrodial joints and inflammation at the fibro-osseous
junctions of syndesmotic joints and tendons with enthesopathy

Synovitis of the sacroiliac and vertebral joints causes destruction of

articular cartilage and periarticular bone.

Ossification across the surface of disc gives rise to small bony bridges
(syndesmophytes) linking adjacent vertebral bodies.

If many vertebrae involved, the spine may become rigid

Clinical features
Symptoms:
• backache & stiffness
• Referred pain in the buttocks
and thighs
• Other: fatigue, pain and
swelling of joints, tenderness
at the insertion of the Achilles
tendon, ‘foot strain’, or
intercostal pain and
tenderness
Others:
• reduce chest expansion
• Peripheral joints (1/3): swelling,
tenderness, effusion and loss of
mobility
Extraskeletal :
Fatigue, loss of weight, acute anterior
uveitis (~25% of patients), glaucoma,
aortic valve disease, carditis,
pulmonary fibrosis
Investigation
• Imaging:
1. X ray:
• erosion and fuzziness of sacroiliac joints,
periarticular sclerosis, bony ankylosis
• Early: squaring of vertebral body
• Late: Syndesmophytes
• Bridging at several levels: ‘bamboo spine’
appearance
2. MRI: detail investigation of sacroiliac joints
3. Others:
Raised ESR and CRP (active phase)
HLA-B27 (95% of cases)
Rheumatoid factor usually negative.
 Differential
diagnosis Management
• Mechanical disorders: Complications
muscular strain, facet General:
joint dysfunction, or active lifestyle, spinal • Spinal fractures
spondylolisthesis extension exercise
• Hyperkyphosis
• Diffuse idiopathic Pharmacology:
hyperostosis (Forestier’s • Spinal cord
disease) PCM, NSAIDs, TNF compression
inhibitors for severe
• Other seronegative disease • Lumbosacral nerve
spondyloarthropathies: root compression
Reiter’s disease, psoriatic Operation:
arthritis, ulcerative colitis, Spinal osteotomy
Crohn’s disease,
Whipple’s disease and
Behçet’s syndrome
 PERIPHERAL
SPONDYLOARTHROPA
THIES
-Reiter’s syndrome & reactive arthritis
-Psoriatic arthritis
-Enteropathic arthritis
Reiter’s syndrome & reactive arthritis
Triad of urethritis, arthritis and
conjunctivitis occurring weeks
after dysentery or genitourinary
infection
Pathogens:
Shigella flexneri, Salmonella,
Campylobacter species Yersinia
enterocolitica,
Lymphogranuloma venereum
and Chlamydia trachomatis
Association with HLA-B27 with
bowel or genitourinary
infection as trigger
Pathological changes same as
ankylosing spondylitis,
emphasis on subacute large-
joint synovitis and some with
chronic course tending towards
sacroiliitis and spondylitis
Reiter’s syndrome & reactive arthritis
Acute phase (few weeks to months):
• asymmetrical inflammatory arthritis
of the lower limb joints (knee &
ankle, also tarsal and toe)
• mild conjunctivitis
• urethritis and bowel infections
• cystitis and cervicitis in women
• vesicular or pustular dermatitis of
the feet
• buccal ulceration
Chronic phase (characteristic of
a spondyloarthropathy):
• mild, recurrent episodes of
polyarthritis (including upper
limb joints)
• Sacroiliitis and spondylitis
(resembling ankylosing
spondylitis)
• Uveitis
Reiter’s syndrome & reactive arthritis
• X-rays: Sacroiliac and vertebral changes are similar to ankylosing
spondylitis. Peripheral joints: erosive arthritis.
• HLA-B27 are positive in 75% of patients with sacroiliitis.
• ESR high in the active phase.
• Causative organism can sometimes be isolated from urethral fluids or
faeces.
• Treatment: ensuring the infectious organism responsible has been
cleared, tetracycline (chlamydia). Symptomatic treatment.
 PSORIATIC ARTHRITIS
characterized by
seronegative polysynovitis, prevalence of psoriasis is 1–
erosive arthritis, enthesitis 2%, but only about 5% of
and dactylitis and a significant those affected will develop
incidence of sacroiliitis and psoriatic arthritis
spondylitis

strong genetic component:

history of psoriasis; increased usual age at onset is 30–50
incidence of other years (often later than skin
spondyloarthropathies in lesions)
close relatives; HLA-B27.
 Psoriatic arthritis

Features:
asymmetrical joint distribution,
involvement of distal finger joints,
the presence of sacroiliitis or
spondylitis and the absence of
rheumatoid nodules
X-ray may show severe destruction of
the interphalangeal joints of the hands
and feet.
Treatment
Topical preparations, NSAIDs,
immunosuppressive agents
(methotrexate) and TNF inhibitors.
Arthrodesis of the distal
interphalangeal joints for unstable
joints.

HLA-B27 occurs in 50–60%

RF negative
 Enteropathic arthritis
Peripheral arthritis (15%):
Both Crohn’s disease and pain and swelling may appear quite
ulcerative colitis may be suddenly and last for 2–3 months before
associated with either subsiding involving larger joints. Synovitis,
peripheral arthritis or joint erosion may occur
sacroiliitis and spondylitis
Treatment is directed at the underlying
disorder.
Sacroiliitis and spondylitis (10%):
Other complications of IBD:
Septic arthritis of the hip, HLA-B27 positive in 60%.
psoas abscess, osteopenia No temporal relationship to gastrointestinal
inflammation and its course is unaffected by treatment
of the bowel disease.
Management is the same as that of ankylosing
spondylitis.
 Crystal Deposition
Disorders

Calcium
Basic calcium
pyrophosphate
Gout phosphate crystal
dihydrate (CPPD)
deposition disease
deposition disease
 GOUT
DEFINITION
A crystal deposition disease
caused by deposition of
monosodium urate crystals in
joints and other tissues,
secondary to hyperuricemia
EPIDEMIOLOGY
oCommon arthritis seen in general
practice in Malaysia
oHigher prevalence in developed
countries (purine rich food, high
saturated fat, alcohol)
oAffects 1-2.5% of adults in
developed countries
omen > women
 CLASSIFICATION OF GOUT
Primary Secondary
• 95% occur in absence of • 5%
any obvious cause • prolonged hyperuricaemia
• Due to acquired disorders:
• under excretion of urate • Myeloproliferative disease
• Diuretics usage
• overproduction of urate • Renal failure
 PATHOPHYSIOLOGY
Urate crystals deposited in in articular cartilage
Purine
Remain inert for months or years
Xanthine
oxidase
Trauma - the needle-like crystals are dispersed
into the joint and surrounding tissues where it Uric acid
triggers acute inflammatory reaction

Urate deposits (tophi) may accumulate in joints,

periarticular tissues, tendons and bursae. Renal excretion
CLINICAL FEATURES
ACUTE GOUT
– Sudden onset of severe joint
pains which lasts for a week or
2 before resolving completely.
– May be precipitated by:
– Minor local trauma
– Operation
– Intercurrent illnesses
– Alcohol consumption
– Exercise
Site :
- joints of lower extremities >
upper extremities
(MONOARTICULAR)
– eg; 1st MTP joint (podagra),
ankle, knee, forefoot, wrist,
elbow, finger
- extra-articular ; olecranon
bursa and Achilles tendon
PHYSICAL EXAMINATION
Unilateral/bilateral
Red and shiny
Warm
Painful swelling
Skin desquamation overlying affected joint
 CLINICAL FEATURES
CHRONIC GOUT
• progressive accumulation of
urate & recurrent attack of
inflammation
• polyarticular gout & chronic
destructive arthritis
• joints erosion can cause:
chronic pain, stiffiness, and
deformity
• tophi appear around the joints
and it can ulcerate
DIAGNOSTIC CRITERIA FOR GOUT
Clinical diagnosis (2 out of following)
1. Presence of clear history of at least 2 attacks of painful joint swelling with complete
resolution within 2 weeks
2. A clear history or observation of podagra (painful big toe)
3. Presence of tophus
4. Rapid response to colchicine within 48 hours of starting treatment

Definitive diagnosis: monosodium urate crystal in synovial fluid or tissue

 INVESTIGATIONS
Joint aspirations and crystal identification(definitive)

(CPG, 2008)
Blood and urine test
RADIOLOGIC FINDINGS IN GOUT
 MANAGEMENT
Acute attack Long term therapy Surgical
• Non-pharmacology • Non-pharmacology patient • Ulcerating tophi that
bed rest education: fail to heal with
• Pharmacologic • Losing weight conservative
• NSAID, COX-2 • Reduce alcohol intake treatments can be
inhibitor, Colchicine • Diet control (avoid foods that evacuated by
contain high level of purine ) curratage.
• If tense joint effusion- • Eliminating diuretics (thiazide, • The wound is left
Aspiration and loop) open and dressing
intrarticular injection • Pharmacologic applied until it heals
of corticosteroids • Allopurinol – drugs of choice
(produce rapid (started 3 weeks after attack)
dramatic relief) • Uricosuric drugs (probenecid)
 Calcium pyrophosphate crystal
associated arthropathy (CPPD)
• Metabolic disorder due to deposition of Epidemiology
calcium pyrophosphate dihydrate (CPPD)
within the joint space. • Commonly affects the
• It consists of 3 overlapping conditions :
elderly (age >60 years)
• Chondrocalcinosis – appearance of • Female and Male are
the calcific material in cartilage equally affected
• Pseudogout - a crystal induced • Rarely affects younger
synovitis
patient, unless it occur
• Chronic pyrophosphate arthropathy –
a type of degenerative disease
in conjunction with
other disease.
 CLINICAL FEATURES
• Calcification of menisci is common in
elderly patient and usually asymptomatic
Asymptomatic • However, In patient with ,<50 years of age
Chondrocalcinosis – suggest the probability of underlying
metabolic disease or familial disorder.

• Acute pain and inflammation in one of the

larger joints - knee
Acute synovitis • Untreated conditions last for a few weeks
and then subsides spontaneously

Chronic • Presents with polyarticular ‘osteoarthritis’

affecting larger joints (hip, knee) and
phyrophospate unusual joints where OA is seldom seen
arthropathy (eg: ankle, shoulder, elbow)
CLINICAL FEATURES

Symptoms Physical examination

• Acute onset joint • Erythematous,
tenderness monoarticular arthritis
• Warm and redness of • Palpation : tenderness
the joints of the joint
• Commonly on knee • May observe superficial
and wrist joints mineral deposits under
the skin at the affected
joints
INVESTIGATION
• X-rays
Intra-articular and peri-articular Degenerative arthritis
calcification
non-weightbearing
Seen in/around knee, wrist, joints, isolated
shoulder, hip, pubic patellofemoral
symphysis and compartment in knee
intervertebral discs and talonavicular joint in
foot
Often bilateral and
symmetrical Advanced cases: joint
destruction, formation
- In articular cartilage = a thin line of lose bodies
parallel to the joint
• Synovial fluid
- In fibrocartilaginous menisci and analysis - positively
discs = cloudy, irregular opacities birefringent crystals
 MANAGEMENTS
ACUTE ATTACK CHRONIC CPPD ARTHROPATHY

• Must be • Usually affects multiple joints

distinguished from and it has to be distinguish from
other acute other polyarticular arthritis
inflammatory • No treatment available to
disorders dissolve the crystal deposits.
• To relieve the pain : • Can give
• NSAID • Colchicine (prophylactic help to
• Splint prevent recurrence)
Reference
• Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley &
solomon's system of orthopaedics and trauma. CRC Press.
• Malaysian Clinical Practice Guidelines : Management of Osteoarthritis
(Second Edition, 2013)
• Malaysian Clinical Practice Guidelines : Management of Rheumatoid
Arthritis, 2019
• Malaysian Clinical Practice Guidelines : Management of Gout, 2008