ANKYLOSING SPONDYLITIS

Yuliannisa
Faridin HP

Department of Internal Medicine

Medical Faculty of Hasanuddin University
Makassar
2016
VISI
MISI
 INTRODUCTION

Ankylosing spondylitis (AS) is an inflammatory

disorder that extremely can lead to the bony fusion
of vertebral joints, its uncommon but well
established cause of chronic back pain.

AS can reduce the quality of life and increase the

risk of disability and mortality .
 INTRODUCTION
Ankylosing
Spondyliti
s

Reactive Psoriatic
Arthritis Arthritis

Spondyloarthropathy
(SpA)

Enteropat Undifferenti
hy ate
Arthritis SpA
 INTRODUCTION

AS is a chronic inflammation disease that

implicate axial and perifer joints, enthesis and
extra articular manifestation.
Prevalence up to 1-2% from general population
and increase risk 20 fold in HLA-B27 positive
population.
Ratio male and female 3 : 1

Age of onset is < 45 years, a peak in the age of

20-30 years.
 ETIOLOGY

The etiology of AS is still unknown.

Twin-studies suggest that up to 97% of the

susceptibility to AS can be attributed to genetic
factors.
The study showed a strong association with HLA-
B27, which means there are immune factors that
play a role.

The expression of HLA-B27 causes an increase

immunological response.
 ETIOLOGY

Individuals with HLA-B27 positive have a

family history of AS estimated to be 10
times more at risk to develop into AS.

The pathogenetic role of bacteria can be

illustrated by the onset of another subtype
of SpA (reactive arthritis), but their role in
the onset of AS is still under debate.
PATHOLOGY
The primary pathological
location is enthesis
(insertion of ligaments,
capsule and tendon to the
bone). Entesopathy changes
that occur are fibrosis and
ossification of the tissue.

Course of the disease

typically begin from the
sacroiliac joints. Sacroiliitis
characterized by synovitis,
panus formation and
granulation tissue. All these
processes will cause erosion,
destruction and replace
PATHOLOGY
At the vertebrae, chronic
inflammation occur in the
facet join and annulus
fibrosus.

Chronic inflammation cause

bone reabsorption followed
by changes to the vertebral
bodies (squaring). Tissue
granulation will undergo
cartilage metaplasia
followed with calcification
(sclerosis) on the edge of the
vertebra and the outside of
the annulus and cause
syndesmophytes. Thorough
 CLINICAL MANIFESTATION

Inflammatory Back Pain

Age at onset < 45 yo
Duration > 3 mo
Insidious onset
Morning stiffness > 30 min
Improvement with exercise
No improvement with rest
Awaking from pain, especially during second half of night,
with improvement on arising
Alternating buttock pain
The presence of two or more of these features should
arouse suspicion for inflammatory back pain, and the
presence of four or more features can be considered
diagnostic.
 CLINICAL MANIFESTATION

Arthritis of peripheral joints is more common in the

knees, hips, and shoulders. Other peripheral joints
that could be affected are the wrists, elbows and
legs that asymmetrically.

Extra articular bone tenderness caused by local

inflammation, bone involved such as the
intersection costosternal, processus spinosus, iliac
crest, trochanter major, ischial tuberosity, tibial
tubercle or tendon insertions, such as tendons
achilles.
 CLINICAL MANIFESTATION

Extra articular manifestations

Eye : Uveitis (10-30%)

Inflammatory bowel disease (10-60%).
Skin : psoriatic lesion (10-25%).
Heart : Valve insufficiency and conduction
abnormalities (10-30%).
Lung : Rigidity of the chest wall and lung fibrosis
(52%).
Bone : Osteoporosis and vertebral fractures (10-
18%).
 DIAGNOSIS

Physical Examination

Imaging

Laboratory Finding

Criteria Diagnostic
Physical Examination

Modified Schobers
Test (Normal increase in
distance between the two
marks 5 cm)
Physical Examination

Lateral Spinal
Flexion
(Normal change in
fingertip to floor
distance between
standing upright and
laterally flexed 10 cm )
Physical Examination

Occiput to Wall
Distance (Normal occiput to
wall distance 0 cm )
Physical Examination

Chest Expansion Test

(Normal chest expansion
>4 cm )
 Imaging
Plain X-Ray
Progression of x-ray changes in ankylosing
spondylitis.
Grade 1: suspicious
Normal changes in the left
appearing x-ray sacroiliac joint, with
of sacroiliac irregular joint facets
joints. but no sclerosis or
Grade 2: erosions.
minimal Grade 3:
abnormality, unequivocal
small localized abnormality,
areas of erosion moderate to
(black arrow) advanced sacroiliitis,
and sclerosis widespread erosions,
(white arrow), sclerosis,
normal joint pseudowidening of
width. joint space in both
Grade 4: severe
abnormality, complete sacroiliac joints,
ankylosis of both partial ankylosis.
sacroiliac joints.
 Imaging

Squari
ng Bridging
Sclerosis Syndesmophyte
(shiny corners)

Tipical x-ray changes of ankylosing spondylitis in

spine
 Imaging

Recommend for
patients whom
conventional
radiographic findings
were not typical, but
axial spondyloarthritis

MRI
is still suspected.
Finding : Both active
inflammatory lesions
(primarily bone marrow
edema) and structural
lesions (eg, bone
erosion, new bone
formation, sclerosis)
Laboratory
The inflammatory markers C
reactive protein (CRP) and
erythrocyte sedimentation rate
(ESR) should be measured in
patients with possible AS.
However, normal levels of these
markers do not preclude a
diagnosis of AS.

HLAB27 is also recommended for

all people with suspected AS.
Diagnostic Criteria

Modified New York criteria for AS

 Diagnostic Criteria
ASAS Classification Criteria For Spondiloarthritis
Axial
 MANAGEMENT

The primary goal Management of AS

of treating the consists of
patient with AS is pharmacological
to maximize long and non
term health pharmacological
related quality of treatment
life. modalities
 MANAGEMENT
Non
Pharmacological
Pharmacological
Nonsteroid
Antiinflammatory Surgery
Drugs (NSAIDs)
TNF- Inhibitor Physical Treatments
Disease Modifying
Antirheumatic Drugs
(DMADRs)
Corticosteroids

Interleukin inhibitors
Nonsteroid AntiinflammatoryDrugs
(NSAIDs)

NSAIDs are the first-line drug treatment for pain and

stiffness.

Continuous NSAIDs treatment is recommended for

persistently active and symptomatic disease.

Treatment must be started with the maximum dose

and the dosage should be adjusted based on patient
response and tolerance.
On demand treatment with NSAIDs is acceptable
when continuous treatment causes unacceptable side
effects and is recommended for persons with stable
spondyloarthritis.
 TNF- Inhibitor

For patients whose symptoms are not

controlled by NSAIDs therapy or for
whom NSAIDs have unacceptable side
effects.
TNF inhibitors include
13 infliximab (INF), etanercept
randomize (ETA), adalimumab (ADA), and
d golimumab (GOL) have
controlled produced rapid, profound, and
trials and sustained improvement in
open label both objective and subjective
studies indicators of disease activity
and patient functioning.
 TNF- Inhibitor

Infliximab : 3-5 mg/kg at 0, 2, and 6 weeks

followed by 5 mg/kg every 8 weeks by
intravenously.

Etanercept : 50 mg once weekly by subcutaneous

injection.

Adalimumab : 40 mg weekly by subcutaneous

injection.

Golimumab : 50 or 100 mg every 4 weeks by

subcutaneous injection.
 Disease Modifying Antirheumatic Drugs
(DMADRs)

Sulfasalazine (SSZ) and methotrexate (MTX)

improved severity of pain, duration and
severity of morning stiffness, also ESR and
CRP.

ASAS/EULAR recommendations confirm the

lack of evidence for the efficacy of DMARDs,
including sulfasalazine and methotrexate,
for the treatment of axial disease.
 Corticosteroids

High-dose oral prednisone produces a clinically

meaningful response in patients with active AS.

ASAS/EULAR recommendations advise against the

use of systemic corticosteroids for axial symptoms
of AS because are not effective in low and moderate
dosages.
Local corticosteroid therapy to affected joints or
enthesis can be considered if there are on going
symptoms despite full dose NSAIDs.
 Interleukin inhibitors

Secukinumab
(Cosentyx) Approval of
is a human secukinumab for
IgG1 monoclonal AS was based on
antibody that 2 phase 3 trials.
selectively binds The
to and significant
neutralizes the improvements
pro inflammatory were sustained
cytokine through 52
interleukin 17A weeks.
(IL-17A).
Surgery

Total hip
arthroplasty
Spinal
corrective
osteotomy
Surgical
stabilization
 Physical Treatments

Water therapy
Physiotherapy Aerobic and swimming

Maintaining an Sleeping on a
Deep-breathing erect posture firm mattress
exercises during daily with a thin
activities pillow
MANAGEMENT
MANAGEMENT
 MEASURE OF DISEASE ACTIVITY

In order to evaluate pain, morning stiffness

and functional ability two different
questionnaires have been developed :

BASDAI (Bath Ankylosing Spondylitis Disease

Activity Index).

BASFI (Bath Ankylosing Spondylitis Functional

Index).
 PROGNOSIS

The extent of spinal involvement has a direct

correlation with the patients functional status.

Poor prognostic indicators include peripheral

joint involvement, young age of onset,
elevated inflammatory marker, and poor
response to nonsteroidal anti-inflammatory
drugs (NSAIDs).
 SUMMARY

Ankylosing spondylitis (AS) is a chronic inflammatory disease

that is part of spondyloarthropathy with spinal and
ekstraspinal manifestations.
The etiology of ankylosing spondylitis still unknown but several
studies have shown genetic factor HLA-B27 has a major role in
this disease.
Diagnosis of AS should be considered if the symptoms are
typical with inflammatory back pain accompanied by radiology
finding according to AS.
Diagnostic criteria of AS according to ASAS recommendation.

Management of AS consists of pharmacological and non

pharmacological treatment modalities.
Pharmacological treatment options are limited, but the
discovery of biological agents has reported a significant
improvement in this disease.
Thank You