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Ankylosing Spondylitis (2023!12!06 18-21-52 Utc)

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ANKYLOSING

SPONDYLITIS

BY
DR IMRAN KHAN MAHER
SENIOR REGISTRAR
Department of Orthopedic surgery and traumatology
LUMHS Jamshoro
Ankylosing spondylitis.
 This is a generalized chronic inflammatory disease
 its effects are seen mainly in the spine and sacroiliac joints.
 It is characterized by pain and stiffness of the back, with
variable involvement of the hips and shoulders and (more
rarely) the peripheral joints.
 Complete fusion results in a complete rigidity of the spine, a
condition known as BAMBOO SPINE
 AS is a systemic rheumatic disease and is one of the
SERONEGATIVE SPONDYLOARTHROPATHIES
 the usual age at onset is between 15 and 25 years.
 Males are affected more frequently than females (estimates
vary from 2:1 to 10:1)
 There is a strong tendency to familial aggregation
 association with the genetic marker HLA-B27.
There is considerable evidence regarding ankylosing
spondylitis (AS) as a genetically determined
Immunopathological disorder.
There are various theories about the ‘triggering factor’
that initiates the abnormal immune response.
CAUSES
 may be a bacterial antigen, which closely resembles
HLA-B27 that induces an antibody response, which
also targets the HLA-B27 positive cells; or, as in the
in the presentation of a specific antigen to the T cells
 HLA-B27
 Human leukocyte antigen B27 is a class I surface antigen
encoded by the B locus in the major histocompatibility
complex on chromosome 6 and presents antigenic peptides
to T cells.
Pathology
Synovitis of the sacroiliac and vertebral facet joints
causes destruction of articular cartilage and peri-
articular bone
.
Pathological changes proceed in three stages:
 (1) an inflammatory reaction with cell infiltration, granulation
tissue formation and erosion of adjacent bone;
 (2) replacement of the granulation tissue by fibrous tissue; and
 (3) ossification of the fibrous tissue, leading
to ankyloses of the joint.
 If many vertebrae are involved the spine
may become absolutely rigid.
 Formation of syndesmophytes
Clinical features
 The disease starts insidiously: a teenager or young
adult complains of backache and stiffness.
 the symptoms are worse in the early morning and after
inactivity.
 Referred pain in the buttocks and thighs may appear as
‘sciatica’
 Gradually pain and stiffness become
continuous.
 General fatigue, pain and swelling of joints.
 Pain in ankle, or pain and stiffness of the hip.
slight flattening of the lower back and
limitation of extension in
the lumbar spine.
 Tenderness over the spine and sacroiliac
joints
 loss of extension of spine earliest and the
most severe disability
 Unable to perform ‘wall test’.
 Generalized fatigue and loss of weight.
 As spine fusses or stiffens their neck and low
back lose their normal curve
 The mid back curves outward(kyphosis) and
a fixed bent forward position can result
leading to significant disability

 Inflammation of the small joints joining the


ribs and collarbone to the breastbone
 Cause less expansion of the chest wall with
breathing
 DIAGNOSIS
 Blood test for the HLA B27 gene….95% cases
 ESR and CRP mostly elevated
 Schobers test a useful clinical measure of flexion of the
lumbar spine performed during examination
X ray
show characteristic spinal changes and sacroilitis.
 Erosion and fuzziness of sacroiliac joint later on peri
articular sclerosis and bony ankyloses.
 Syndesmophytes and bridging of vertebrae's.
X-RAYS (A)
AN EARLY SIGN IS ‘SQUARING’ OF THE LUMBAR
VERTEBRAE.
(B,C) Bony bridges
(syndesmophytes) between
the vertebral bodies convert
the spine into a rigid column.
MRI
 MRI sacroiliac joints may show typical erosions and
features of inflammation such as bone edema.
TREATMENT

 General measures to maintain satisfactory posture and preserve


movement;
 Anti-inflammatory drugs to counteract pain and stiffness;
 The use of TNF inhibitors for severe disease;
 Operations to correct deformity or restore mobility.
NSAIDS
such as ibuprofen, naproxen, and aspirin are a
frequently effective and inexpensive option for treating the
pain and stiffness of AS.
 Another class of NSAID known as COX-2 inhibitors, which
includes the prescription medication Celebrex (Celecoxib),
may reduce the risk of these GI side effects.
Exercise
 exercise is a first-line treatment for AS. That’s
because physical activity is key to loosening up
the joints, relieving pain, and keeping your spine
flexible.
Biological treatment
 When NSAIDs and exercise are not effective enough at controlling
your symptoms, or the side effects of NSAIDs become too severe

The first choice is usually a tumor-necrosis factor inhibitor (TNFi).


TNFi biologics approved to treat AS include:
 Cimzia (certolizumab)
 Enbrel (etanercept)
 Humira (adalimumab)
 Remicade (infliximab)
 Simponi (golimumab)
Corticosteroids

 they’re more likely to be given as an injection directly into


inflamed joints for temporary pain relief during flares. Steroid
injections are only used for peripheral joints such as the knees
or the pelvis and generally aren't used in the spine
disease-modifying anti-rheumatic drugs (DMARDs)
 work to limit tissue damage from inflammation.
 Azulfidine (sulfasalazine)
 Rheumatrex (methotrexate), a chemotherapy drug
Surgery for AS
Only in rare cases, surgery may be done to straighten a spine
that has fused into a curved forward position because breathing is
restricted.

 Some AS patients may eventually need joint replacement


therapy—usually in the knees or hips—for severe damage that
makes daily activities difficult.
Complications
 Spinal fractures
 The spine is often both rigid and osteoporotic;
 The commonest site is C5–7.
 Hyper kyphosis
 Spinal cord compression
 Lumbosacral nerve root compression

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