This document summarizes ankylosing spondylitis (AS), a type of spondyloarthritis. It discusses the characteristics, pathogenesis, clinical features, diagnostic criteria, treatment options, and surgical management of AS. Key points include that AS is a seronegative inflammatory disease associated with HLA-B27 antigen that causes inflammation in the axial skeleton. Symptoms include back pain and stiffness that worsens with inactivity and improves with exercise. Treatment involves NSAIDs and TNF-alpha inhibitors. Surgical interventions may include total hip replacement or spinal osteotomies.

2.  AS is a seronegative inflammatory disease of
unknown etiology characterized by inflammation in
the axial skeleton esp; SI joint, principally affecting
young males in the 3rd
decade.
 Course of the disease is said to be one of the
relentless progression with periods of
exacerbation & remission.

3.  Ankylos – bent or fused, spondylos – vetebrae.
 Marie Strumple or Von Bechterew disease
 It belongs to group of spondyloarthritis.
 Share certain C/F & an association with HLA B-27
allele.

4.  M:F 3:1
 2nd
to 4th
decade
 6 per 10,000 of G. population
 Autosomal inheritance, with 70% penetrance in
males, 10% in females.
 90% pts have HLA B- 27 antigen.
 Increased incidence among relatives.

5.  Located in the short arm of chromosome 6
 One of the series of closely linked polymorphic
loci in that region.
 Incidence in N. population – 8% in caucasians, 4%
in blacks.
 Neither necessary nor sufficient to cause AS
 Positive individuals tends to have early onset.
 No correlation with severity.

6.  Carriers of this gene have a 16% to 50%
increased risk of developing AS,
 Virtually absent among the aboriginal populations
of Australia and South America.
 Negative individuals doesn’t have family history.
 Susceptibility to AS almost entirely determined by
genetic factor with HLA constituting about 1/3 of
genetic component.

7.  autoimmune disorder
 subsequent to a Klebsiella pneumoniae infection
in HLA-B27–positive individuals,
 Molecular mimicry,
 incidence of AS in patients with idiopathic bowel
disease is approximately 3.7%.

8.  ENTHESOPATHY , Hall mark of AS.
 combination of inflammation and bony destruction
at the site of tendon insertion
 Ass with prominent edema of the adj bone marrow
& is often characterised by erosive lesions that
eventually undergoes ossification.

9.  Distribution of lesion: in synovium, articular
capsular & ligamentous attachments to bones.
 Articular lesions due to 2 primary mech, synovitis,
enthesitis
 2 subsidary mech, enchondral & trauma.
 In spine: early, there is inflammatory granulation
tissue at the jn of AF of disc cartilage with the
margin of V.B.
 Outer AF is replaced by bone – bony osteophytes,
fusion of adj V.B.

10.  Aches in buttocks.
 Lower lumbar aches
 Bony tenderness.
 Peripheral jt involvement [girdle jts]
 Inflammatory back ache.
1. < 40 yrs onset
2. Insidious onset
3. Duration > 3 months
4. Morning stiffness
5. Improvement with exercise.

11.  Extra articular invoivement
 Most C. anterior uveitis. [30%]
 AR, Third degree heart block.
 Subclinical pulm. Lesion, cardiac dysfn.
 Cauda equina syn & slow progressive upper lobe
fibrosis in long standing cases.
 Progression of the diseaseas monitered by Pt Ht,
chest expansion, scoebers test, occiput to wall
distance.
 Jaw involvement- old pts.
 Thorax involvement.

12.  Loss of lumbar lordosis
 Exaggerated kyphosis
 Head & neck move forwards on the shoulder
 Mister punch posture: rounded dorsal spine,
flattened chest & protrubent abdomen.
 Wide bases stance.

13.  I – phase: Isolated phases characterised by
attacks of pain & stiffness occuring in increasingly
frequent intervals, corresponding to pre-
ankylosing stage.
 II- phase: continuous symptoms & constitutional
upset.
 III- phase: declining disease activity & reduced
symptoms with episodic minor relapses.

14.  Early stage of the disease with typical symptoms
od spondylitis in absence of definite radiological
changes in the SI jt.
 Associated with systemic symptoms include
anorexia, Wt loss, fatique, low grade quotidion
fever.

15.  Iridocyclitis
 Cardiovascular complications
 Lung changes
 Neurological changes
 Amyloidosis
 Complication of treatment.

16.  ESR, CRP
 HLA B-27
 Raised globulin fraction
 Alkaline phosphatase.
 RA factor negative
 Rise in CSF protein level
 Urinary 17- ketosteroid levels increase,

17.  ASCA IgA levels are significantly high in AS &
other SpA than in healthy controls & Pt with RA
 I Serological marker ass. With SpA
 Can be marker of radiological damage & more
severe course in A.S

18.  Blurring of cortical margins of subchondral bone
 sclerosis & erosion  pseudowidening of jt
space  fibrous & bony ankylosis
 Shiny corner sign- vetebral squarring
 Star sign- SI jt.
 Rail road track lines – zygoapophyseal jts
 Marginal syndesmophytes
 Bambo spine

19.  Bone scan
 MRI – si jt in early stages, more sensitive &
specific
 DEXA- reduced BMD
 Falsely elevated reading related to spinal
ossification can be avoided by using lateral
projection of L3 vetebrae.

21.  graded 0 (normal),
 1suspicious,
 2 minimal sacroiliitis
 3 moderate sacroiliitis
 4 ankylosis

22.  NSAIDS
 Indomethacin
 Phenyl butazone
 Sulphasalazine
 Anti TNF -alpha

23.  definitive diagnosis of AS;
 presence of the disease for at least 4 weeks;
 presence of refractory disease(defined by the
failure of two types of NSAIDs during a single 3-
month period);
 failure of local corticosteroid injection into inflamed
sacroiliac joints;
 failure of sulfasalazine in patients with peripheral
disease;
 no medical contraindications to the initiation of
treatment.

24.  Infliximab: anti TNF – alpha monoclonal Ab
 5 mg /kg body wt repeated 2 wks later, again 6
wks later, then at every 8 wks interval.
 Etanercept: 25 mg by S.C inj twice weekly

25.  Bisphosphate Pamidronate at a dose of 60 mg
monthly IV
 Thalidomide 200 mg / day [inhibit TNF]
 Alpha emitting isotope 224 Ra at a dose of 1 MBq.

26.  Thirty percent to 50% of patients with AS exhibit
involvement of the hips; of those, 90% present
bilaterally.
 THR is the most common surgery done in AS.
 Mobilising the hip by THR before spinal
osteotomy makes easier to determine desired
degree of correction in spine.

27.  AS patients are more prone to anterior dislocation
when acetabular components are placed in their
normal position relative to the pelvis.
 When positioning the acetabular component in a
patient with AS, one must account for the
relationship of the pelvis to the lumbar spine in the
sagittal plane in order to avoid an excessively
hyperextended hip once the patient resumes an
upright position.

28.  GT – not to be osteotomised
 Due to osteoporosis & extensive capsular &
pericapsular fibrosis  during dislocation of the
hip, increased chance of fracture.
 Osteotomy of the neck & head can be removed as
piecemeal.
 Capsulectomy should be adequate.
 Precautions to avoid postop dislocation.

29.  The level of risk for heterotopic bone formation
after THA in patients with AS remains
controversial.
 The proportion of AS patients with functional
ankylosis secondary to HO following THA is
likely substantially lower than previously
thought.
 High-risk
 patients with preoperative ankylosis, with
previous hip surgery, with previous infection,
and/or in whom a transtrochanteric approach to
the hip was used should be considered for HO
prophylaxis

30.  To improve the erect position there by to balance
the effect of gravity
 To increase the respiratory function
 To increase the GI fn.
 Smith Peterson O.
 Confined to the laminae & articular facets.
 Ideally done at L2 & L3 levels.

31.  Surgical intervention also may be indicated for
management of deformity, pseudarthrosis,
fracture, and spondylodiscitis.