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COMSIG REVIEW
64
Volume 2 • Number 3 • November 1993
ANKYLOSING SPONDYLITIS
A SUMMARY AND REVIEW
BRUCE F. WALKER D. C. *
Index Terms: Ankylosing spondylitis (AS), Marie-
Strumpell spondylitis, Von Bechterew's disease,
chiropractic.
Summary: Ankylosing spondylitis is a relatively rare
disease affecting 0.1% to 0.2% of the white population
(1)(2).
It is a disease characterised by inflammatory stiffening
of the spine, affecting in particular the cartilaginous
joints of the spine and the sacro-iliac joints. In the
advanced form there is ossification of ligaments and
spinal fusion with a characteristic stooped posture (3).
Ankylosing spondylitis occurs most commonly in white
men in their twenties with the male:female ratio at 3:1
(2). There is a strong familial occurrence (8), and it is
less common in American Negroes (4).
Ankylosing spondylitis is not a form of rheumatoid
arthritis, although they do have similarities.
Ankylosing spondylitis exists as a spectrum of clinical
presentations both axial and appendicular (3).
Ankylosing spondylitis shares many of its features with
other related seronegative (for rheumatoid factor)
spondyloarthopathies, such as Reiter's Syndrome,
psoriatic arthritis, reactive arthritis, enteropathic
arthropaties (associated with ulcerative colitis, Crohn's
disease and Whipple's disease) and juvenile chronic
arthritis (5).
Approximately 90% of patients with ankylosing
spondylitis have an association with the HLA antigen
with B27 specificity, whereas only 6% - 8% of the
population have the gene (6).
According to Ebringer (7) ankylosing spondylitis is
probably produced by repeated episodes of Klebsiella-
reactive arthritis, usually in HLA-B27 positive
individuals.
He suggests a pathogenetic pathway commencing with
gut wall infection produced by Klebsiella. Followed by
antibody production against Klebsiella produced by
local lymph nodes, related to the gut, sacro-iliac joints
and the lumbar spine.
Then inflammation is produced because anti-Klebsiella
antibodies bind to HLA-B27 positive cells in the spine,
entheses (ligament and tendon attachments to bone)
and lymph nodes thereby activating the so called
"complement cascade".
This is followed by Klebsiella reactive arthritis which is
produced by reoccurent waves of infection due to
commensal Klebsiella, probably evoked by a high
starch diet.
Finally, ankylosing spondylitis appears to be the end
stage of repeated Klebsiella-reactive arthritis, occurring
almost exclusively in HLA-B27 positive individuals (7).
The clinical picture of ankylosing spondylitis
commonly presents as dull pain of insidious onset in
the sacro-iliac region, lumbar region, greater trochanter
region or even down the proximal part of the posterior
thigh. Pain is usually aggravated by sudden
movements and coughing and sneezing.
As the condition worsens back pain and stiffness occur
at rest particularly in the morning. This may last
several hours and is often relieved by heat and exercise
(2.3,6,8).
Enthesitis causing extra-articular bony tenderness can
be a common complaint particularly at the costo-sternal
junctions, spinous processes, iliac crests, greater
trochanters, ischial tubercles or heels (8).
Hip and shoulder joints are involved in one third of
patients. Hip involvement as the presenting
manifestation is more common in childhood or
adolescence (9). Involvement of the peripheral joints is
relatively infrequent (8).
Abstract: A review of the etiology, clinical,
radiological and laboratory presentation, differential
diagnosis and management.
?
PRIVATE PRACTICE
33 WANTIRNA ROAD, RINGWOOD, VICTORIA, 3134. Ph. 879 5555
ANKYLOSING SPONDYLITIS
WALKER
COMSIG REVIEW
Volume 2 • Number 3 • November 1993
65
About 25% of all patients with ankylosing spondylitis
develop at least one episode of acute iritis (3).
Cardiovascular complications such as aortitis, aortic
valve incompetence, pericarditis and cardiomegaly can
occur but are rare. Pulmonary function remains normal
generally due to an increased diaphragmatic
contribution (3,6,8).
As ankylosing spondylitis progresses the patient
becomes stooped into flexion and with cervical
involvement the head is held in an anterior position
and neck movements are restricted. Finally, bony
ankylosis of the entire spine can occur resulting in
profound stiffness and the so-called "bamboo spine"
appearance as seen on radiographs (1,3,10).
Trauma to the ankylosing spondylitis patient may result
in serious fractures and can result in severe
neurological deficits (12). The fractures can occur even
with minimal trauma and are due to spinal immobility
and osteoporosis (12,13).
Differential Diagnosis: A differential diagnosis list
includes rheumatoid arthritis, diffuse idiopathic skeletal
hyperostosis (DISH), psoriatic arthritis, Reiter's
syndrome, enteropathic arthritides, reactive arthritis,
septic sacro-iliitis, Scheuermann's disease, congenital
kyphoscoliosis, osteitis condensans ilii,
hyperparathyroidism, osteoarthritis, gouty arthritis and
infection (1,2,3,5,6,8,11).
Usual and Customary Examination Procedures:
1. Physical examination: This reveals loss of
mobility of the lumbar spine. Note here that
flexion may not be a reliable guide to a decreased
lumbar range of motion due to hip movements (8).
A decrease in chest expansion and a stooped
kyphotic posture as the disease progresses are tell-
tale signs(2,8). There is often tenderness over one
or both sacro-iliac joints and the entheses (2).
2. Diagnostic Imaging: Plain radiographs are the
imaging modality of choice although bone scans
may be "hot" in affected joints when the disease is
active (18).
(a) Sacro-iliac joint involvement commences with
pseudo-widening of joint spaces, then erosive and
sclerotic changes particularly on the iliac side, and
finally ankylosis of the joints which narrow and
obliterate. Sclerosis dissipates and is replaced by
generalised osteoporosis (14).
(b) Spine: Syndesmophyte formation, which
represents ligamentous ossification are the spinal
hallmarks of ankylosing spondylitis, often
commencing at the thoraco-lumbar junction but
affecting eventually the entire spine to give the
"Bamboo-spine" appearance (2,8,14).
The apophyseal joints fuse, there is a loss of the
lumbar lordosis and an increase in the thoracic
kyphosis, eventually the spine becomes
osteoporotic (2,3,4,8,13,14).
(c) Peripheral Joints: Initially, the x-ray
appearance of proximal joints in ankylosing
spondylitis may resemble rheumatoid arthritis.
However, there is a greater tendency in ankylosing
spondylitis to central articular erosion's and
proliferative new bone formation at the margins
and whiskery spicules occur due to enthesitis in the
pelvis at the sacrotuberious and sacrospinal
ligament insertions, the greater trochanter of the
femur, plantar fascia and achilles tendon (6).
3. Laboratory Tests:
(a) ESR/CRP is raised in up to 75% of patients
but it is not a reliable indicator of disease activity
(6,8).
(b) Mild normocytic, normochromic anaemia may
be present in 15% of patients (8).
(c) HLA-B27 is positive in over 90% of
ankylosing spondylitis patients (2).
(d) A positive rheumatoid factor is notably absent
(4).
GOALS OF TREATMENT:
1. Control pain and inflammation.
2. Maintain maximum skeletal mobility.
3. Prevent deformities.
4. Maintain or enhance aerobic fitness, muscular
strength and endurance.
5. Educate patients and family about the disease.
CHIROPRACTIC MANAGEMENT:
1. Analgesic and anti-inflammatory physical therapy
modalities can be used for exacerbations.
2. An active exercise programme is the cornerstone of
management (15). Rest should only be prescribed
during acute exacerbations. Exercises should be
aimed at spinal ranges of motion particularly
extension. Swimming is ideal in this regard and it
also is performed without weight bearing and
enhances aerobic capacity.
ANKYLOSING SPONDYLITIS
WALKER
COMSIG REVIEW
66
Volume 2 • Number 3 • November 1993
Cycling and jogging are to be condoned only with
reservation, cycling because of the flexed posture
and jogging because of the jarring effect.
Breathing and chest expansion exercises are also
important (2.3.4.5.6).
Heat applied before and cold applied after exercises
may be useful (3).
3. The use of mobilisation and manipulation in
ankylosing spondylitis is yet to be studied.
However, two factors should be borne in mind:
(a) Ankylosing spondylitis patients like any other
patient may develop mechanical spinal dysfunction
which may respond to mechanical treatment.
(b) The main contraindications to mechanical
treatment are: ankylosing spondylitis in the
actively inflamed stage where treatment might
exacerbate an already inflamed area, joint
immobility or fusion and any attendant
osteoporosis where vigorous treatment could cause
bony damage particularly fracture and atlanto-axial
instability from the disease process itself where
treatment might conceivably result in disastrous
sequelae.
Certainly, gentle techniques in the quiescent phase
of early ankylosing spondylitis would not seem to
be contraindicated where a manipulable lesion
exists.
4. Periodic review is important to gauge the
progression of the disease. In this regard clinical
and x-ray tests are used. Clinical indicators
include measuring pain and inflammation: pain
can be assessed using a visual analogue scale while
inflammation can be gauged by the duration of
morning stiffness (eg. 2 hours) (16).
Mobility of the spinal column should be measured
checking lateral flexions, extension and
rotations. Flexion should be measured using
the Schober method (8). Chest expansion should
also be measure suing reproducible methods (8).
Two other indices of disease progression are the
enthesopathy index proposed by Mander et al (16)
and the articular and functional indices proposed
by Dougados et al (17).
Serial radiographs are useful to monitor the disease
progression but may not correlate to any favourable
effect of treatment (8).
5. Anti-inflammatory drugs are the most useful
medical therapy. They suppress the pain and
stiffness and facilitate exercise programmes (3).
However, drug therapy does not alter the
progression of the disease (6). The aim of
prescription is to find the smallest dose necessary
for repeated symptomatic relief (5).
6. Counselling and education for patients and family
regarding ankylosing spondylitis should be an
integral part of management (3.15).
PROGNOSIS:
Although not curable, ankylosing spondylitis is one of
the most rehabilitable of all the chronic rheumatic
diseases (3). Less then 10% develop relentlessly
crippling disease. Most longitudinal studies of
ankylosing spondylitis survival curves approximate that
of the general population (6). Death if it occurs is
usually attributable to cardiac involvement, cervical
spine fractures or rarely secondary amyloidosis (2).
REFERENCES
1. Rodnan G.P. (Ed). Primer on the rheumatic
Diseases. Edition 7. 1973. Arthritis Foundation,
Atlanta GA. p.67.
2. Lisse J.R. Ankylosing Spondylitis. An Optimistic
Outlook. Postgraduate Medicine. Vol. 86. No. 1.
July, 1989. P. 147-53.
3. Bluestone R. Ankylosing Spondylitis. In:Arthritis
and Allied Conditions. A Textbook of
Rheumatology. Lea and Febiger. Ed:McCarty D.J.
1985. Edition 10. P. 189-840.
4. Moll J.M.H. Rheumatology-Colour Aids.
Churchill Livingsone. 1984. p.10-23.
5. Dudley Hart F. (Ed). clinical Rheumatology
Illustrated - Ankylosing Spondylitis and other
Seronegative Arthropathies. Williams and
Wilkins. Chapter 3. p. 27-76.
6. Schned E.S. Ankylosing Spondylitis. In:Manual of
Rheumatology and Outpatient Orthopaedic
Disorders. Editors: Beary J.J., Christian C.L.,
Johnason N.A. Publisher: Little Brown and Co.
Boston/Toronto. 1987. p. 133-40.
7. Ebringer A. The Relationship between Klebsiella
Infection and Ankylosing Spondylitis. In Balliere's
Clinical Rheumatology. Vol 3. No. 2. Aus, 1989.
p. 321-38.
8. Khan M.A., van der Linden S.M. Ankylosing
Spondylitis. Clinical Aspects. In:Spine, State of the
Art Reviews. Ankylosing Spondylitis and Related
Spondyloarthopathies. Vol 4. No.3. 1990. p. 529-
51.
9. Garcia-Morteo O., Maldonado-Cocco J.A., Suarez-
Almazor M.D. et al. Ankylosing Spondylitis of
Juvenile Onset: Comparison with Adult Onset
Disease. Scand. J. Rheumatol. 12:246,1983.
ANKYLOSING SPONDYLITIS
WALKER
COMSIG REVIEW
Volume 2 • Number 3 • November 1993
67
10. Aegerter E., Kirkpatrick J.A. (Eds). Orthopaedic
Diseases. Edition 4. W.B. Saunders Co. 1975. p.
671-3.
11. Dixon A. St.J. Diagnosis of Low Back Pain.
In:The Lumbar Spine and Back Pain. Edition 2.
Ed:M.I.V.Jayson. 1980. p. 135-55.
12. Graham B., Van Peteghen P.K. Fractures of the
Spine in Ankylosing Spondylitis. Spine:Vol. 14,
No. 8. 1989. p. 803-7.
13. Will R., Palmer R., Bhalla A.K. et al.
Osteoporosis in early Ankylosing Spondylitis. A
primary pathological event? The Lancet. Dec.
23/30. 1989. p. 1483-5.
14. Yochum T.R.Y., Rowe L.J. Essentials of Skeletal
Radiology. Vol. 2. Williams and Wilkins., 1987.
p. 614-28.
15. Kraag G., Stoker B., Groh J. et al. The Effects of
Comprehensive Home Physiotherapy and
Supervision on Patients with Ankylosing
Spondylitis - A Randomised Controlled Trial. The
Journal of Rheumatology. 1990. 17:2 p. 228-33.
16. Mander M., Simpson J.M., McLellan A., et al.
Studies with an Enthesis Index as a Method of
Clinical Assessment of Ankylosing Spondylitis.
Ann. Rheum. Dis. 46:197-202, 1987.
17. Dougados M., Gueguen A., Nakache J.P. et al.
Evaluation of a Functional Index and an Articular
Index in Ankylosing Spondylitis. J. Rheumatol.
15:302-7. 1988.
18. Sandman K.B. Ankylosing Spondylitis: A Review
and Clinical Update. J.Manip. and Physiol. Ther.
Vol. 5. No. 4. Dec, 1982. p. 183-5.