“ANKYLOSING SPONDYLITIS AND ITS PHYSICAL

THERAPY MANAGEMENT”

A project work submitted to the H.N.B. Garhwal University

in partial fulfilment for the award of the degree of

BACHELOR OF PHYSIOTHERAPY

2019-2023

Submitted by

LAXIT CHAUHAN

UNDER THE GUIDANCE OF

DR. PRIYANKA GUSAIN

DEPARTMENT OF PHYSIOTHERAPY

COMBINED (P.G.) INSTITUTE OF MEDICAL SCIENCES & RESEARCH

DEHRADUN UTTARAKHAND

1
 Combined (P.G) Institute of Medical Sciences & Research

DEHRADUN

DECLERATION CERTIFICATE

I hereby declare that the project work entitled “ANKYLOSING SPONDYLITIS AND ITS
PHYSICAL THERAPY MANAGEMENT” embodies the work done by me under the
guidance of DR. PRIYANKA GUSAIN PT, MPT (NEURO) Assistant Professor at
Combined (P.G) Institute of Medical Sciences & Research Dehradun UK. The project work
in part or full has not been submitted to any other University.

Laxit Chauhan

BPT 4th Year

2
 Combined (P.G) Institute of Medical Sciences & Research

DEHRADUN

CERTIFICATE BY THE GUIDE

This is to certify that the project work entitled “ANKYLOSING SPONDYLITIS AND ITS
PT MANAGEMENT” submitted by “LAXIT CHAUHAN” in partial fulfilment of the
requirement for the award of degree of Bachelor of Physiotherapy from HNB Garhwal
University Dehradun Uttarakhand is a bona fide work carried out by him under my
supervision and guidance during the academic year 2023, neither this project nor the part of it
has been submitted for any degree or diploma.

(Signature of Guide)

DR. PRIYANKA GUSAIN PT, MPT (NEURO)

Assistant Professor, Department of Physiotherapy

CIMS&R Dehradun

Place:

Date:

3
 Combined (P.G) Institute of Medical Sciences & Research

DEHRADUN

ENDORSEMENT BY THE HEAD OF THE DEPARTMENT

This is to certify that the dissertation entitled “ANKYLOSING SPONDYLITIS AND ITS
PT MANAGEMENT” is a bona fide dissertation work done by "LAXIT CHAUHAN"
(BPT final year student), under the guidance of DR. PRIYANKA GUSAIN PT, MPT
(NEURO) in partial fulfillment of requirement for the degree of Bachelor of Physiotherapy.

Place:

Date:

(Seal and Signature of HOD)

Dr. PRIYANKA GUSAIN KUMAIN PT,

MPT (Neurology)

Associate Professor, HOD,

Department of Physiotherapy

CIMS&R, Dehradun (U.K)

4
 Combined (P.G) Institute of Medical Sciences & Research

DEHRADUN

CERTIFICATE BY THE EXAMINER

This is to certify that the project work entitled “ANKYLOSING SPONDYLITIS AND ITS
PT MANAGEMENT” submitted by "LAXIT CHAUHAN" under the guidance of DR.
PRIYANKA GUSAIN PT, MPT (NEURO) in partial fulfilment of the award of degree
of Bachelor of Physiotherapy of the HNB Garhwal University, Srinagar Uttarakhand
had been thoroughly delaminated and approved by us.

Accepted /Not Accepted Accepted/Not accepted

………………………………. …………………………….

Signature of Internal Examiner Signature of External Examiner

Name: Name:

Date: Date:

5
 Combined (P.G) Institute of Medical Sciences & Research

DEHRADUN

DECLARATION BY THE CANDIDATE

I hereby declare that the HNB Garhwal University, Srinagar (Uttarakhand) shall have the
right to preserve, use and disseminate this project work in print of electronic format for
academic/research purpose.

LAXIT CHAUHAN

BPT 4TH year

PLACE:

DATE:

6
 Combined (P.G) Institute of Medical Sciences & Research

DEHRADUN

ACKNOWLEDGEMENT

First of all, I would like to thanks Honourable Chairman “ADVOCATE LALIT MOHAN
JOSHI SIR” for providing all the facilities to carry out the work, constant encouragement,
kind suggestion and allowed me to avail the opportunity to work for this prestigious degree.

It gives immense pleasure and satisfaction to place my sincere thanks and appreciation with
the respect and regards for my adorable guide DR. PRIYANKA GUSAIN PT, MPT
(NEURO) Department of Physiotherapy, CIMS&R Dehradun (U.K), it was her blessing
guidance, valuable suggestion and encouragement which helped me to greatly ease the task of
completing this project a reality.

I seek to express my thanks to all the teaching members, Dr. PRIYANKA GUSAIN
KUMAIN PT, MPT(NEUROLOGY) Dr. ANJANA GUSAIN PT, MPT
(ORTHOPAEDIC), Dr. MONIKA BISHT PT, MPT (NEUROLOGY), Dr. BHAWANA
DANI PT, MPT (CARDIOLOGY), & other staff of the Department for the support and
assistant during the work.

Words fall short to express my gratitude to my father and mother whose inspiration,
everlasting moral support and love always elevated my confidence during the work. I humbly
thanks to my friends, colleague for supporting me and helping me in need. Above all I bow
and reference to the god whose blessings have helped me and guide me throughout the
project.

7
SERIAL NO. LIST OF CONTENTS

I DECLARATION CERTIFICATE

II CERTIFICATE BY THE GUIDE

III ENDORSEMENT BY THE HEAD OF DEPARTMENT

IV CERTIFICATE BY THE EXAMINER

V DECLARTATION BY THE CANDIDATE

VI ACKNOWLEDGEMENT

VII FIGURES

VIII CHAPTERS

IX REFERENCES

8
SERIAL NO. LIST OF FIGURES

Fig. 3 Prevalence of male and female

Fig. 4.1 Anatomy of sacroilliac joint

Fig. 4.2 Ligaments of sacroilliac joint

Fig. 5.1 Normal human vertebral column

Fig. 5.2 Motion segments of typical vertebra with surrounding structures

Table 5 Biomechanical comparison of the female and male sacroiliac joint

Fig. 5.3 Pelvis 6 degrees of movement (a) coronal plane, (b) sagittal plane

Fig. 5.4 The force couple

Fig. 6 Stages of inflammation

Fig. 7 Causes of AS

Fig. 8 An illustration showing the difference in anatomy between a normal

spine, and one with ankylosing spondylitis.
Fig. 9 Areas of inflammation

Fig. 11.1 X-ray Ap view of spine showing fusion of the spinous processes of
lumbar vertebrae.
Fig. 11.2 MRI showning romanus lesions on thorax level and inflammatory
changes on anterior maniburosternal joints
Fig. 11.3 Schober test

Fig. 11.4 Chin brow measurement

Fig. 11.5 Chest expanison

9
SERIAL NO. CHAPTERS

1. INTRODUCTION

2. REVIEW OF LITERATURE

3. PREVALENCE

4. ANATOMY

5. BIOMECHANICS

6. PATHOPHYSIOLOGY

7. ETIOLOGY

8. SYMPTOMS

9. CLINICAL FEATURES

10. DIFFERENTIAL DIAGNOSTICS

11. DIAGNOSTIC TEST

12. OUTCOME MEASUREMENT

13. PHYSIOTHERAPY MANAGEMENT

14. REFERENCES

10
 CHAPTER - 1

INTRODUCTION

11
The word is from Greek "Ankylosis" means fused, curved , rounded bones or other hard tissue.
"Spondylitis" means inflammation in your spinal bones, or vertebrae. This condition was
described in the late 1600s by Bernard Connor.[1].

Ankylosing spondylitis (AS) is a chronic, inflammatory disease of the axial spine that can
manifest with various clinical signs and symptoms. Chronic back pain and progressive spinal
stiffness are the most common features of the disease. Involvement of the spine and sacroiliac
(SI) joints, peripheral joints, digits, entheses are characteristic of the disease. Impaired spinal
mobility, postural abnormalities, buttock pain, hip pain, peripheral arthritis, enthesitis, and
dactylitis ("sausage digits") are all associated with AS..[2]

In more advanced cases, this inflammation can lead to fibrosis and calcification, resulting in
the loss of flexibility and the fusion of the spine, resembling “bamboo” with an immobile
position. The main clinical manifestations include back pain and progressive spinal rigidity as
well as inflammation of the hips, shoulders, peripheral joints and fingers/toes. In addition,
there are extra-articular manifestations, such as acute anterior uveitis and inflammatory bowel
disease (IBD). However, these extra-articular manifestations differ between East Asian and
Caucasian populations. In a study involving 988 patients with ankylosing spondylitis in east
Asia, only 0.4% developed inflammatory bowel disease. 1 However, in some analyses
performed in Western countries, ~5%–10% of patients with AS present with inflammatory
bowel disease [3]

The average age at disease onset was 27.7 years in B27(-) and 24.8 years in B27(+) AS (P <
0.01). The average age at diagnosis was 39.1 and 33.2 years and the average diagnosis delay
11.4 and 8.5 years, respectively. The distribution in age at disease onset was significantly
wider in B27(-) (standard deviation 10.0 years) than in B27(+) AS (8.3 years). The
percentages with childhood (age < 16 years) disease onset did not differ significantly (7.6%
vs. 6.2%, respectively), whereas the percentage of late onset (age > 40 years) was
significantly greater among B27(-) (13%) than among B27(+) (5%) patients with AS. There
is a difference in average age at disease onset between male (25.7 years) and female (24.2
years) AS patients, and no difference between patients with primary AS and AS associated

12
with psoriasis, inflammatory bowel disease, or reactive arthritis. Acute anterior uveitis was
significantly less frequent in B27(-) (26%) than in B27(+) (41%) patients with AS.
CONCLUSIONS. This study of a much larger number of B27(-) AS patients than have been
studied previously confirms earlier reports indicating a significantly older average age at
disease onset and a less frequent prevalence of acute anterior uveitis in B27(-) than in B27(+)
AS. The frequency of late disease onset (after 40 years of age) is significantly higher in
B27(-) AS. We provide the first report on significant differences in the distribution curves for
the age at disease onset and for the age at diagnosis between B27(-) and B27(+) patients with
AS. The average delay between the first spondyloarthritic symptoms and the diagnosis is
significantly longer in B27(-) than in B27(+) AS. The frequency of juvenile disease onset
(before age 16 years) is nearly the same, irrespective of the B27 status.[4]

Spondyloarthritis (SpA) represents a group of interrelated diseases with common clinical

features and a close association with HLA-B27. Figures on the incidence and prevalence of
diseases vary highly dependent on methodological differences between studies, the case
definition used to classify disease and on the prevalence of HLA-B27 in the population
studied. When summarizing the available literature, incidence rates of SpA are mainly based
on the ESSG criteria and range between 0.48 and 63/100.000 while prevalence rates vary
between 0.01 and 2.5%. For ankylosing spondylitis (AS), the most widely recognized
representative of the SpA group of diseases, incidence rates of 0.44-7.3/100.000 and
prevalence rates of 0.007-1.7% have been described in studies that were based on the
(modified) New York criteria to classify cases. The incidence of psoriatic arthritis (PsA)
varied from 3.6 up to 23.1/100.000 in different studies and prevalence between <0.1% and
0.4%, using a variety of classification criteria. The incidence of ReA has been estimated
between 0.6 up to 28/100.000 in studies based on different source populations and different
case definitions. The newly proposed criteria for axial SpA and peripheral SpA present an
attractive new approach to facilitate classification of the SpA into two main subtypes and the
axial SpA criteria allow earlier detection of patents with inflammatory back pain. It should be
emphasized that these criteria were developed for use in a (specialized) clinical setting and
not for large epidemiological studies. [5]

Regardless of axial disease, enthesopathy and tarsal disease in children who have arthritis of
the lower, but not of the upper extremities differentiate juvenile onset AS from JRA within 1

13
year of symptoms. The discriminative value of these parameters approaches that of axial
disease (the gold standard) throughout the followup period.[6]

Pulmonary complications are also associated with AS, pulmonary fibrosis in other rheumatic
diseases more frequently involves the lower segments of the lung, those seen in the
spondyloarthropathies involve the upper lobes and may further compromise the patient's
respiratory status, which may be affected by involvement of the costovertebral and
costochondral joints. Lesions of the gastrointestinal tract that are seen with inflammatory
bowel disease and dysentery may also be seen in other spondyloarthropathies without clinical
symptoms. In addition to the urethritis seen in Reiter's subset of the reactive arthritis, there is
an increased occurrence of prostatitis in the spondyloarthropathies.
Immunologically, there is a definite association of the spondyloarthropathies with
the MHC class I molecule HLA-B27, particularly in ankylosing spondylitis, where more than
90% of white patients possess this antigen. Recently, there have been advances which have
better defined the role of HLA-B27 in the pathogenesis of the spondyloarthropathies. For
example, transgenic rat and mice models exist whose cells express human HLA-B27 antigen
with animal/human β2-microglobulin. When these genes are significantly expressed, the
animals develop articular and extraarticular lesions similar to the human diseases. [7]

Ankylosing spondylitis (AS) is a type of arthritis characterized by long-term inflammation of

the joints of the spine, typically where the spine joins the pelvis. Occasionally, areas affected
may include other joints such as the shoulders or hips. Eye and bowel problems may occur as
well as back pain. Joint mobility in the affected areas generally worsens over time.

Although the cause of ankylosing spondylitis is unknown, it is believed to involve a

combination of genetic and environmental factors. More than 85% of those affected in
the UK have a specific human leukocyte antigen known as the HLA-B27 antigen. The
underlying mechanism is believed to be autoimmune or autoinflammatory. Diagnosis is
typically based on the symptoms with support from medical imaging and blood tests. AS is a
type of seronegative spondyloarthropathy, meaning that tests show no presence of rheumatoid
factor (RF) antibodies.

There is no known cure for AS. Treatments may include medication, exercise, physical
therapy, and in rare cases surgery. Medications used
14
include NSAIDs, steroids, DMARDs such as sulfasalazine, and biologic agents such as TNF
inhibitors.

Approximately 0.1% to 0.8% of all humans are affected with onset typically occurring in
young adults. Males and females are equally affected; however, women are more likely than
men to experience inflammation rather than fusion.[8]

Syndesmophytes, which form in the ligaments of the spine, create irreversible spinal damage
and can lead to vertebrae fusing. AS is a type of inflammatory arthritis. Syndesmophytes are
one of the main clinical features of AS, and their formation can cause pain, rigidity in the
spine, and a loss of mobility.

AS can also affect other areas of a person’s body, potentially causing:

vision changes and eye pain, shortness of breath, if AS affects the joints connecting the
ribs,skin rashes, abdominal pain and loose bowel movements, loss of appetite and
unexplained weight loss, fatigue.[9]

The pathology of AS include the following process-

Synovitis Initially, the inflammation of the synovium occur, which may be identical
histologically to that in rheumatoid arthritis(RA). Mostly commonly the synovitis starts,
firstly from the sacroiliac joints followed by the other region of the spine.

Enthesopathy This term refers to an inflammatory reaction at the enthesis which is the zone
of ligamentous attachment to the bone, and this is the characteristic feature of AS that occurs
commonly in the spine and near the pelvis.

Capsular Inflammation

Cartilage Destruction and Bony Erosion This occur due to synovitis and the inflammation of
the ligament and the capsules. The cartilage of the joint gets destroyed, and becomes rough
and the bony erosion occurs.

Ossification All the above factors lead to the formation of new bones at these areas, and
bridging takes place between the vertebral bodies, usually from the edge of one body to that

15
of the next, along the outer layer of the disc. This typical phenomenon is known as
the marginal syndesmophyte formation. Ossification also occurs in the anterior and
posterior longitudinal ligament and also in other ligaments of the spine.[10]

Ankylosing spondylitis (AS) is a chronic systemic rheumatic disease that primarily affects the
sacroiliac joints and spine. Even with the development of tumor necrosis factor-alpha
inhibitors, which have revolutionized the treatment of this disease, the combination of
nonsteroidal anti-inflammatory drugs (NSAIDs), physical therapy, and a life-long exercise
program still form the first step in its management. Multiple clinical trials have addressed the
efficacy and safety of both nonselective and selective NSAIDs. Gastrointestinal toxicity
remains their major side effect, with increased concern about the potential of cardiovascular
toxicity, especially with the selective cyclooxygenase-2 inhibitors. A specific set of
recommendations has been proposed for the management of AS.

Ankylosis All the features of the above and most important the ossification part, results into
fusion of all the vertebrae of the spine, and this condition is called bamboo spine. The
formation of the syndesmophytes starts usually from the dorso-lumbar region. After bony
fusion the pain may subside, leaving the spine permanently stiff. [11]

Physiotherapy is an essential part of the treatment of AS. It aims to alleviate pain,

increase spinal mobility and functional capacity, reduce morning stiffness, correct
postural deformities, increase mobility and improve the psychosocial status of the
patients. According to a Cochrane review completed by friends and colleagues, a
supervised or individual home-based exercise program is better than no intervention, The
main aspects of rehabilitation include education, a program of personalised exercises and
outline of physical activities to be completed at home or in a group-based environment.
[12]

Physiotherapy is very effective at relieving the symptoms of ankylosing spondylitis if it is

tailored specifically to your needs. The experienced physiotherapists will provide you with a
full assessment of your symptoms which will help to create a personalised physiotherapy
programme to work towards your goals. Physiotherapy may help in the following ways:

16
  Reduce pain
 Reduce stiffness in your joints.
 Minimise fatigue (tiredness)
 Improve posture.
 Increase strength and range of movement
 Improve cardiovascular fitness.
 Return to normal activities of daily living/sport.

There are a number of different physiotherapy treatments that are useful in managing the
symptoms of ankylosing spondylitis and your physiotherapist at Physio.co.uk will decide the
best treatment options to suit you. Possible physiotherapy includes:

 Hydrotherapy
 Pain control modalities
 Strengthening exercises
 Range of movement exercises
 Cardiovascular activities
 Pacing advice
 Provision of specialist equipment that may help you around the home.
 Gentle mobilisations
 Heat therapy
 Cryotherapy (ice)
 Postural exercises
 Electrotherapy (e.g. mega pulse, ultrasound, TENS)
 Massage
 Splinting of painful joints
 Wax therapy [13]

17
 CHAPTER-2

REVIEW OF LITERATURE

18
1. Wei Zhu, Xuxia He, Kaiyuan Cheng, Linjie Zhang, Di Chen, Xiao
Wang, Guixing Qiu, Xu Cao, and Xisheng Weng (2019 Aug 5) et al conducted a
study on Ankylosing spondylitis: etiology, pathogenesis, and treatments. They
concluded that Ankylosing spondylitis is a painful and debilitating disease, with
considerable socioeconomic burdens. In 2002, the yearly mean total (direct and
productivity) costs of AS were US$6,720 per patient in the USA and Euro 9 462
per patient in Europe. There is no effective disease-modifying treatment largely
due to the unclear pathogenesis. This review focuses on the etiology,
pathogenesis and treatment progress of AS. The etiology of ankylosing
spondylitis may be related to genetic background, immune function, pathogenic
infection, endocrine abnormalities and other factors. HLA-B27 is the gene crucial
to the development of ankylosing spondylitis, while the non-HLA-B27 gene is
also important in its pathogenesis.[3]

2. Ernst Feldtkeller , Muhammad Asim Khan, Désirée van der Heijde, Sjef van der
Linden, Jürgen Braun (2003 Mar 2023) et al conducted a study on Age at disease
onset and diagnosis delay in HLA-B27 negative vs. positive patients with ankylosing
spondylitis. They concluded that this study of a much larger number of B27(-) AS
patients than have been studied previously confirms earlier reports indicating a
significantly older average age at disease onset and a less frequent prevalence of acute
anterior uveitis in B27(-) than in B27(+) AS. The frequency of late disease onset
(after 40 years of age) is significantly higher in B27(-) AS. We provide the first report
on significant differences in the distribution curves for the age at disease onset and for
the age at diagnosis between B27(-)and B27(+) patients with AS. The average delay
between the first spondyloarthritic symptoms and the diagnosis is significantly longer
in B27(-) than in B27(+) AS. The frequency of juvenile disease onset (before age 16
years) is nearly the same, irrespective of the B27 status.[4]

19
3. Carmen Stolwijk, MD, Annelies Boonen, MD, PhD, Associate Professor of
Rheumatology, Astrid van Tubergen, MD, PhD, Rheumatologist, and John D.
Reveille, M.D., Professor and Director (2015 Jun 17) et al conducted a study on
Epidemiology of Spondyloarthritis. They concluded that there was a need for more
reliable tools, reviewed tools to assess the quality and/or risk of bias of prevalence
and incidence studies and reported the absence of agreement on type of items and way
to score items, likely reflecting the need for extensive adaptations depending on the
specific disease and population of interest. In the same paper, they present a new
checklist to assess the methodological and reporting quality of observational studies
of incidence and prevalence that was mainly based on the review of existing
instruments and expert knowledge. Two aspects can be distinguished: external
validity, which is defined as the extent to which the results of a study can be
generalized to the target population, and internal validity, which is the extent to which
the results of a study are correct for the subjects.[5]

4. R Burgos-Vargas , J Vázquez-Mellado (June 1995) et al conducted a study on the

early clinical recognition of juvenile-onset ankylosing spondylitis and its
differentiation from juvenile rheumatoid arthritis. They conducted that Regardless of
axial disease, enthesopathy and tarsal disease in children who have arthritis of the
lower, but not of the upper extremities differentiate juvenile-onset AS from JRA
within 1 year of symptoms. The discriminative value of these parameters approaches
that of axial disease (the gold standard) throughout the followup period.[6]

20
5. Ali Kiapour, Amin Joukar, Hossein Elgafy, Deniz U. Erbulut, Anand K.
Agarwal,And Vijay K. Goel (2020 Feb 10) et al conducted a study on the
Biomechanics of the Sacroiliac Joint: Anatomy, Function, Biomechanics, Sexual
Dimorphism, and Causes of Pain. They concluded that The SIJ lies between the sacrum
and the ilium and connects the spine to the pelvic bones. The SIJ transfers large
bending moments and compression loads to lower extremities. However, the joint
does not have as much stability of its own against the shear loads but resists shear due
the tight wedging of the sacrum between hip bones on either side and the band of
ligaments spanning the sacrum and the hip bones. Due to these, sacrum does not
exhibit much motion with respect to the ilium.[22]

6. Richard L. Dontigny (2011) et al conducted a study on Form and Function – A

Biomechanical Study on sacroiliac joint. He concluded that The sacrum hangs
suspended from the ilia by the dense posterior sacroiliac ligaments and functions as
the reverse of a keystone by hanging more deeply between the ilia with increased
weight loading. Primary loading is on the posterior interosseous ligaments with a
balanced secondary loading on the sacrotuberous ligaments in the opposite direction.
The force of closure at the SIJ is probably essentially nil. The balanced loading
creates a force couple, which serves to decrease loading forces. When the sacrum is
loaded and the pelvis is symmetrical there is essentially no movement in the sacroiliac
joint. Movement occurs during normal ambulation. When the pelvis swings obliquely
into asymmetry the sacrum flexes laterally toward the side of loading to create a
force-dependent oblique axis. It then moves on that oblique axis to drive counter
rotation of the trunk to decrease the forces of loading on that side. At least two
muscles function as prime movers to reposition the sacrum to symmetry at mid-
stance. Repeated sacral flexion during ambulation causes an oscillation of the lumbar
spine, which is diminished as it travels cephalad. The spine functions as a diminishing
waveform to stabilize the visual plane making it more stable for such purposes as
hunting or observing variances in gait patterns in vivo.[23]

7. Luca Pontone Gravaldi, Francesca Bonetti,* Simona Lezzerini, and Fernando De

Maio (2022 Jan 10) et al conducted a study on the efectiveness of Physiotherapy in

21
 Patients with Ankylosing Spondylitis: A Systematic Review and Meta-Analysis. They
concluded that results confirm that a multimodal supervised approach through
exercises, physiotherapy, education, balneotherapy, and other non-pharmacological
interventions helps manage patients with AS. This work shows supervised
physiotherapy is more effective than usual care in improving disease activity,
functional capacity, and pain in patients with ankylosing spondylitis. Further studies
are needed to investigate the main effects of exercises in the medium–long term and
evaluate the effectiveness of mobilisation on the spine. These studies need to be
carried out on larger samples. More incisive conclusions in the literature could
improve AS patients’ everyday lives and reduce the health system’s expenditure.[45]
8.

CHAPTER - 3
22
PREVALENCE

23
Fig. 3 :- Prevalence of male and female

24
 CHAPTER - 4

ANATOMY

Ankylosing spondylitis is an autoimmune disease that is closely related to rheumatoid

arthritis. Alternative names for the condition include rheumatoid spondylitis and Marie-
Strümpell disease, although these are seldom used in the modern medical treatment industry.

Ankylosed sacroiliac joints have become naturally fused and often suffer other related
symptoms, such as stiffness, pain, weakening of the joint, growth of bony outcroppings and
susceptibility to fracture. Ankylosing spondylitis is well known to begin its anatomical
assault on the body in the substance of the sacroiliac joint. This is the location most often
reported as the site of initial symptomatic activity leading to diagnosis of the condition. [14]

The sacroiliac (SI) joint articulates surfaces of the sacrum and the ilium and functions as the
transition between the spine and the pelvis. The main roles of the SI joint are to provide
stability and offset the load of the trunk to the lower limbs. The stability of the joint is
provided by an extensive architecture of ligamentous structures.

25
The SI joint is a diarthrodial synovial joint. It is surrounded by a fibrous capsule containing a
joint space filled with synovial fluid between the articular surfaces. The articular surface is
made up of two, strong, C-shaped layers. It is distinguished from other synovial joints by the
unusual articulation of two different types of cartilage. The sacral capsular surface is
composed of hyaline cartilage while the iliac capsular surface is composed of fibrocartilage.
There are three main types of cartilage found in the body: hyaline, fibrocartilage, and elastic.
Hyaline cartilage is made from type II collagen and is the weakest type of cartilage.
Fibrocartilage is made from type I collagen and is the strongest type of cartilage.

The SI joint is also unique in that its articular surfaces have multiple ridges and depressions
that develop and deepen over one's lifetime. During the natural bone maturation process, the
morphology and characteristics of the sacroiliac joint change. The joint surfaces are relatively
flat in early life and allow for a gliding motion between the sacrum and ilium in all directions.
However beginning in the second and third decades of life, the sacroiliac joint surfaces
develop distinct angulations and lose their flat surface. The joint develops an elevated ridge
along the iliac surface and a depression along the sacral surface. This produces a functional
interlocking between the 2 bones. This interlocking limits the movement at the SI joint which
creates the overall stability of the joint. This increase in the sacroiliac joints’ stability makes
dislocations very rare.[15]

STRUCTURE OF ESTHESIS

Ankylosing spondylitis is a condition that affects mainly the fibrous tissue junctions where
ligaments and tendons attach to bone, called entheses. Entheses are also referred to as
insertion sites, osteotendinous junctions, or osteoligamentous junctions.There are two
types of entheses:

 Fibrous entheses, in which the fibrous tissue of the tendon or ligament attaches to the
bone.
 Fibrocartilaginous entheses, in which the connection between tendon or ligament and
bone is augmented with fibrocartilage. The stiff fibrocartilage helps absorb some of the
physical stress experienced at these connections.[16]
26
 ARTICULAR STRUCTURES

The sacroiliac joint is a synovial-type articulation between the auricular surfaces of

the sacrum and ilium. Even though it is classified as a synovial plane joint, the auricular
surfaces of the sacroiliac joint show marked irregularities in forms of depressions and
elevations. However, these irregularities are reciprocal and congruent in which the central
sacral concavity fits the iliac convexity, therefore interlocking the two auricular surfaces and
providing stability. The auricular surface of the ilium is covered with some type of
fibrocartilage, while the corresponding auricular surface of the sacrum is covered
with hyaline cartilage.

JOINT CAPSULE

The sacroiliac joint is completely encircled by a fibrous capsule that attaches on the articular
margins of the sacrum and ilium. The internal surface of the capsule over the non-articular
surfaces of the joint is lined by synovial membrane.

LIGAMENTS

Due to its position and weight-bearing nature, the sacroiliac joint has to be stabilized with
several strong ligaments. The main ligaments of the joint are anterior and posterior sacroiliac
ligaments, while additional stability is provided with accessory ligaments: sacrotuberous
ligament and sacrospinous ligament.

Anterior sacroiliac ligament

The anterior sacroiliac ligament is composed of many thin strands that form
a strong, broad and flat band. It lies on the pelvic surface of the joint, forming the
anteroinferior component of the joint capsule. The anterior sacroiliac ligament extends from
the ala of the ilium, just anterior to the auricular surface, to the pelvic surface of the sacrum.

27
 The part of the pelvic surface that lies between the auricular surface and the upper rim of the
greater sciatic notch often shows a rough preauricular sulcus that provides an attachment site
(origin) for the lower fibers of the anterior sacroiliac ligament that then insert onto the third
sacral segment. This part of the ligament is particularly well developed, whereas the rest of
the ligament is rather thin.

Posterior sacroiliac ligament

The posterior sacroiliac ligament is a compound ligament composed of three distinct bands. It
lies posterior and superior to the joint, filling the space between the corresponding
tuberosities of the ilium and the sacrum. The posterior sacroiliac ligament is much thicker
and stronger than its anterior counterpart. The bands that compose this ligament are as
follows:

 Interosseous sacroiliac ligament: a short but very strong band that spans the gap between
the sacrum and ilium on the posterior side of the joint by attaching on their tuberosities, just
behind the auricular surfaces. Occasionally, one or two accessory joint cavities can be
identified within the ligament.

 Short posterior sacroiliac ligament: a short ligament found superficial to the interosseous
sacroiliac ligament. It fills the upper part of the gap between the ilium and sacrum. The short
posterior sacroiliac ligament originates on the first and second transverse tubercles of the
sacrum and extends horizontally to attach on the tuberosity of the ilium.

 Long posterior sacroiliac ligament: a long band that is the most superficial of the posterior
sacroiliac ligaments. It extends from the posterior superior iliac spine to the third and fourth
transverse tubercles of the sacrum.

Accessory ligaments

The accessory ligaments aid the main ligaments and contribute to the stability of the
sacroiliac joint. The main function of these ligaments is to prevent forward tilting of the
sacral promontory.

28
 Sacrotuberous ligament: a flat, triangular ligament that has several superior attachments;
one band of the ligament arises on the gap between the posterior superior and posterior
inferior iliac spines, where it is partially blended with the posterior sacroiliac ligaments. A
second band arises on the lateral side of the sacrum below the auricular surface, and the third
on the lateral side of the upper part of the coccyx. The three bands converge and extend
inferiorly, forming a triangular shape before inserting on the lower margin of the ischial
ramus. Right before the insertion occurs, the bands diverge again, thereby prolonging the
inferior attachment point. This prolonged attachment is called the falciform process and is
situated just below the pudendal canal, where it blends with the fascial sheath of the internal
pudendal vessels and pudendal nerve. The posterior surface of the ligament is blended with
the gluteus maximus, whereas the inferior fibers of the ligament continue into the tendon of
biceps femoris.

 Sacrospinous ligament: a thin, triangular band found deep to the sacrotuberous ligament. It
originates from the border of the lower sacral and upper coccygeal segments, anterior to the
sacrotuberous ligament. The ligament is broad in its origin, but narrows as it extends laterally
to insert onto the ischial spine. The sacrospinous ligament is thought to be a fibrous part of
the coccygeus muscle, as it is largely blended with it.

Besides their main function, the sacrotuberous and sacrospinous ligaments also transform the
greater and lesser sciatic notches into the greater and lesser sciatic foramina, respectively.

 Greater sciatic foramen: an opening bounded by the posterior border of the iliac bone
anterosuperiorly, the sacrotuberous ligament posteromedially, and the sacrospinous ligament
and ischial spine inferiorly. The contents of this foramen are the piriformis muscle, gluteal
vessels and nerves, internal pudendal vessels, pudendal nerve, sciatic and posterior femoral
cutaneous nerves and the nerves to obturator internus and quadratus femoris.

 Lesser sciatic foramen: an opening bounded by the ischial body anteriorly, spine of
the ischium and sacrospinous ligament superiorly, and the sacrotuberous ligament posteriorly.
Its contents include the tendon of obturator internus, the nerve to obturator internus, and the
internal pudendal vessels and pudendal nerve.

INNERVATION

29
 The sacroiliac joint receives innervation primarily from branches of the anterior and posterior
rami S1-S2 spinal nerves and the superior gluteal nerve. Additionally, the joint receives
contributions from the obturator nerve and lumbosacral trunk.

BLOOD SUPPLY

The sacroiliac joint receives arterial blood supply from branches of the iliolumbar, superior
gluteal and lateral sacral arteries. The venous blood is drained from the corresponding veins
into the internal iliac vein.

MOVEMENTS

Due to its arrangement and strong ligaments, the sacroiliac joint allows little to no movement.
Like other plane-type synovial joints, the sacroiliac ligament only allows for some amount
of gliding and rotatory movements. The rotatory movements of the sacroiliac joint are
described as nutation and counternutation.

 Nutation: occurs as the superior segment of the sacrum tilts downwards and anteriorly, while
the inferior portion of the sacrum and the coccyx tilt posteriorly in the opposite direction. This
movement is also referred to as sacral flexion, and occurs only in conjunction with trunk
flexion or hip extension.

 Counternutation: occurs as the superior segment of the sacrum tilts upwards and posteriorly,
while the inferior portion of the sacrum and the coccyx tilt anteriorly in the opposite direction.
This movement is also referred to as sacral extension and occurs only in conjunction with trunk
extension or hip flexion.

The main function of the sacroiliac joint lies in the fact that it comprises one of the pillars of the
pelvic mechanism for transmitting the weight of the head, trunk and upper limbs to the lower
limbs. The lack of mobility in the sacroiliac joint favors strength and stability to maximize
weight bearing capabilities. These characteristics are especially important in order to maintain
stability in the erect position during standing or walking. Interestingly, during childbirth, this
changes due to the hormone relaxin, which loosens the joint and its ligaments to allow for more

30
 mobility. This puts the sacroiliac joints in counternutation, which is important to increase the
pelvic inlet and outlet diameters to allow for the passage of the fetus.[17]

LOCATION

The SI joints are located between the iliac bones and the sacrum, connecting the spine to the
hips. The two joints provide support and stability, and play a major role in absorbing impact
when walking and lifting. From the back, the SI joints are located below the waist where two
dimples are visible.[18]

MUSCLES

Anatomically, the SI joint is surrounded by over 40 muscles. The main muscle groups that
affect the SI joint are the:

 Back muscles, such as the erector spinae, quadratus lumborum, and multifidus lumborum.

 Hip muscles, such as the iliopsoas.

 Core muscles, such as the rectus abdominis.

 Buttock muscles, such as the gluteus maximus and piriformis.

 Thigh muscles, such as the biceps femoris from the hamstring group.[19]

31
 Fig. 4.1:- Anatomy of sacroilliac joint

UILI

32
Fig. 4.2:- Ligaments of sacroilliac joint

33
 CHAPTER - 5

BIOMECHANICS

34
The spine is a complex and functionally significant segment of the human body. Providing
the mechanical linkage between the upper and lower extremities, the spine enables motion in
all three planes, yet still functions as a bony protector of the delicate spinal cord. To many
researchers and clinicians, the lumbar region of the spine is of particular interest because low
back pain is a major medical and socioeconomic problem in modern times.

The spine consists of a curved stack of 33 vertebrae divided structurally into five regions.
Proceeding from superior to inferior, there are 7 cervical vertebrae, 12 thoracic vertebrae, 5
lumbar vertebrae, 5 fused sacral vertebrae, and 4 small, fused coccygeal vertebrae. There may
be one extra vertebra or one less, particularly in the lumbar region.

35
 FIG. 5.1 NORMAL HUMAN VERTEBRAL COLUMN

A. Left lateral and B. posterior views of the major regions of the spine.

Because of structural differences and the ribs, varying amounts of movement are permitted between
adjacent vertebrae in the cervical, thoracic, and lumbar portions of the spine. Within these regions,
two adjacent vertebrae and the soft tissues between them are known as a motion segment. The motion

segment is considered the functional unit of the spine

36
 Fig. 5.2:- MOTION SEGMENTS OF TYPICAL VERTEBRA WITH SURROUNDING
STRUCTURES

The motion segment, composed of two adjacent vertebrae and the associated soft tissues, is
the functional unit of the spine. Each motion segment contains three joints. The vertebral
bodies separated by the intervertebral discs form a symphysis type of amphiarthrosis. The
right and left facet joints between the superior and inferior articular processes are diarthroses
of the gliding type that are lined with articular cartilage.[20]

37
 Biomechanical Aspects Female Male

SIJ motions More rotational More translational

Angular range of motions Higher (Up to 2.8°) Lower (Up to 1.2°)

Sacral cartilage Thicker Thinner

Iliac bone cortical layer Thinner Thicker

SIJ surface area Lesser Greater

Pelvis Wider, shorter Narrower, taller

Sciatic notch Wider Narrower

Acetabula Wider Narrower

Pubic angle Larger (90° to Smaller (50° to 80°)

100°)

Interosseous sacroiliac Larger Smaller

ligament

Anterior sacroiliac ligaments Smaller Larger

Posterior sacroiliac ligaments Smaller Larger

TABLE A BIOMECHANICAL COMPARISON OF THE FEMALE AND MALE SACROILIAC JOINT (SIJ).[21]

TABLE 5

38
The sacrum can move with respect to the ilium in 6 degrees of freedom, although this motion
is minimal. It is shown that the SIJ ROM is greatest in flexion-extension (about 3°), followed
by axial rotation (about 1.5°), and lateral bendings (about 0.8°). The male and female SIJ
ROM values are also different with the maximum ROM of 1.2° degrees (men) and 2.8°
(women). Moreover, the average translation of the joint is about 0.7 mm and seldom exceeds
2 mm. In addition, the motion of the SIJ while standing on one leg is higher than when
standing on both legs.[22]

Fig. 5.3:- Pelvis 6 degrees of movement (a) coronal plane, (b) sagittal plane.

THE FORCE COUPLE

The balanced ligaments create force couples on each side. (See Figure 3.3) These balanced
tensile forces result in a tendency to rotate around a transverse axis created by and
perpendicular to the force couples. Force couples absorb, balance and redirect various forces
such as linear velocity, linear acceleration, angular velocity, angular acceleration, linear
momentum, angular momentum, the rate of change of momentum, force and moment of
force.[23]

39
Fig 5.4:- The force couple

40
 CHAPTER - 6

PATHOPHYSIOLOGY

41
The primary pathology of spondyloarthropathies, including AS, involves enthesitis. This
chronic inflammation involves infiltrating immune cells such as CD4 and CD8 T
lymphocytes and macrophages. Cytokines, particularly tumor necrosis factor-α (TNF-α) and
transforming growth factor-β (TGF-β), are also important in the inflammatory process. They
contribute to inflammation, fibrosis, and ossification at sites affected by enthesitis.[24]

The pathological changes of enthesitis, especially in the early stages, have been difficult to
study for technical and ethical reasons. The importance of enthesitis relative to synovitis,
subchondral marrow inflammation, and osteitis in AS is under debate. However, more recent
work suggests that the entheseal fibrocartilage is the major target of the immune response and
the primary site of the immunopathology. Theoretically, immunocompetent cells could get
access to fibrocartilage derived antigens from bone marrow derived blood vessels. It has been
suggested that not only fibrocartilage but also cartilage in general at the interphase with bone
should be regarded as the primary site.

Enthesitis was originally considered as the hallmark of AS on the basis of findings from two
cases of advanced AS in the 1970s. A more recent study evaluated changes in the sacroiliac
joints (SIJs) of 12 patients with AS, including five biopsies, and compared them with 22
control necropsy cases. Mild but destructive synovitis and myxoid subchondral bone marrow
were the earliest changes identified in SIJs from patients with AS. The adjacent articular
tissues were destroyed by these lesions and were followed by varying degrees of fibrous
scarring, woven bone, and new cartilage formation. Both original and new cartilages were
replaced by bone through fusion; the predominant mode of ankylosis was chondral fusion.[25]

42
 Fig. 6 :- Stages of inflammation

The association of AS with HLA-B27 suggests the condition involves CD8 T cells, which
interact with HLA-B. This interaction is not proven to involve a self-antigen, and at least in
the related reactive arthritis, which follows infections, the antigens involved are likely to be
derived from intracellular microorganisms. There is, however, a possibility that CD4+ T
lymphocytes are involved in an aberrant way, since HLA-B27 appears to have a number of
unusual properties, including possibly an ability to interact with T cell receptors in
association with CD4.[26]

Bacterial infections are suggested to be triggering events , as documented in ReA. Because

bacterial DNA, RNA, and proteins can be detected in affected joints, it is believed that the

43
subsequent immune response triggers the arthritis. T cells with specificity for these bacteria
have been isolated in synovial fluid and peripheral blood of patients with ReA. The close
relationship between AS and inflammation of the gut mucosa, associated with clinical or
subclinical forms of IBD, suggests that normal gut bacteria and, subsequently, immune
reaction directed against gut bacteria, may also participate in the pathogenesis of AS. [27]

44
 CHAPTER - 7

ETIOLOGY

As an autoimmune disease, AS develops through complex interactions between genetic

background and environmental factors. Although significant progress has been achieved in
the past decades, the etiology of AS remains unclear to some extent. To date, studies have
revealed some factors that may be related to the occurrence of AS, including genetic
background, immune reaction, microbial infection, and endocrinal abnormity.[28]

Ankylosing spondylitis has no known specific cause, though genetic factors seem to be
involved. In particular, people who have a gene called HLA-B27 are at a greatly increased
risk of developing ankylosing spondylitis. However, only some people with the gene develop
the condition.[39]

45
 Fig.7 :- causes of AS[40]

Having one of these conditions may also increase your risk:

 Non-radiographic axial spondyloarthritis – the main symptoms are similar to ankylosing

spondylitis – pain and stiffness around the spine. But there won’t be physical changes to
the back that can be seen on an x-ray. Some people with this condition are later
diagnosed with ankylosing spondylitis.

 Psoriatic spondyloarthritis is a form of psoriatic arthritis that can occur alongside the skin
condition psoriasis. People with psoriasis can get red, scaly patches of skin.

 Spondyloarthritis associated with inflammatory bowel disease, which is also called

enteropathic arthritis. This is related to bowel conditions such as Crohn’s disease or
ulcerative colitis. The bowel is part of the digestive system that helps to break down the
food we eat.

 Reactive arthritis is diagnosed when your arthritis is a reaction to an infection.

 Enthesitis -related juvenile idiopathic arthritis is the name used when children and
teenagers develop inflammation in entheses, the sites where tendons and ligaments attach
to bones.[29]

46
47
 CHAPTER - 8

SYMPTOMS

In the early stages, ankylosing spondylitis is likely to cause::

 stiffness and pain in your lower back in the early morning that lasts at least 30 minutes and

then eases through the day or with activity

 pain that wakes you in the night

 pain in one or both buttocks and sometimes the backs of the thighs.

The condition can sometimes be mistaken for common backache.

Common backache often comes in short and painful spells. But the pain from ankylosing

spondylitis is likely to be long lasting.

48
 You may also have neck, shoulder, hip or thigh pain, which is worse when you’ve not been

active for a time, for example if you sit for long periods working at a desk. Some people have

pain, stiffness and swelling in their knees or ankles.

The pain and stiffness can vary over time. If most of the spine is affected, it can cause

difficulty with activities that involve bending, twisting or turning.

Other possible symptoms include:

 soreness at the heel or in the arch of your foot

 pain and swelling in a finger or toe

 tenderness at the base of your pelvis, which can make sitting on a hard chair uncomfortable

 chest pain or a tightness around the chest that comes on gradually. This can make it difficult

to take deep breaths. Your ribs may feel very tender, and you may find that you’re short of

breath after even gentle activity. Coughing or sneezing may cause discomfort or pain.

 inflammation of the bowel. People with ankylosing spondylitis can develop bowel problems

known as inflammatory bowel disease (IBD) or colitis. It’s a good idea to see your doctor if

you have diarrhoea for more than two weeks or have bloody or slimy poos.

 fatigue, which is severe tiredness that doesn’t improve with sleep or rest. This can be caused

by the condition itself, as well as by anaemia. This is when people have a lack of red blood

cells, which carry oxygen around the body.

 depression and anxiety.

 inflammation of the eye, called either uveitis or iritis. The first signs are usually a painful and

sometimes red eye. It may become uncomfortable to look at bright lights.[30]

In the later stages, ankylosing spondylitis is likely to cause:

• Lower back pain and stiffness.

• Hip pain.

49
 • Joint pain.

• Neck pain.

• Difficulty breathing.

• Fatigue.

• Loss of appetite and unexplained weight loss.

• Abdominal pain and diarrhea.

• Skin rash.

• Vision problems.[41]

The symptoms of ankylosing spondylitis tend to come and go. The symptoms can also vary in
severity between people.

The more common symptoms involve pain and stiffness in your spine. The
inflammation usually starts in the sacroiliac joints (where your pelvis meets your
spine).

Symptoms may include:

 stiffness in your back, neck or buttocks, which may be worse in bed at night
 other joint pain
 pain in tendons and ligaments, such as in your chest wall, soles of your feet, or heels

Typically, ankylosing spondylitis symptoms:

 last for longer than 3 months

 include morning stiffness and night pain
 improve with physical activity — and don’t improve with rest.[31]

50
Fig. 8:- An illustration showing the difference in anatomy between a normal spine, and one with
ankylosing spondylitis.

CHAPTER - 9

CLINICAL FEATURE

51
Skeletal Chronic low back pain and stiffness, which typically worsens
following a period of prolonged inactivity (e.g., morning
stiffness/stiffness after rest)

Alternating buttock pain

Night pain: Patients often woken up in the second half of the night
with pain and often need to get up and move around before going
back to sleep

↓ lumbar spine mobility in all planes especially trunk lateral

flexion and rotation

Abnormal posture: ↑ thoracic kyphosis and ↓ lumbar lordosis

Arthritis of ‘girdle joints’ (hips and shoulders)

Improvement of pain on exercise

Muscle Spasm

Enthesitis
Radiographic Radiographic findings in advanced disease include erosions,
features sclerosis of adjacent bones, pseudo-widening of the sacroiliac joint
space, and fibrosis, calcification, interosseous bridging, and
ossification of the sacroiliac joints

52
Extra-skeletal Uveitis

Fatigue

Cardiovascular involvement

Pulmonary involvement

53
 Fig. 9:- Areas of inflammation

CHAPTER - 10

DIFFRENTIAL DIAGNOSIS

54
Condition Diffrentiating sign and symptom
Rheumatoid arthritis Affects smaller joints, hands and feets
Common in females
Morning stiffness

Increased eye sensitivity and dryness

Reiter’s syndrome Urethral inflammation

Inflammation triggered by infection

Psoriatic Arthritis Dactylitis (severe swelling of finger and toe joints)

Skin rash

Anemia
Osteoarthritis Common over 40 years
Wear and tear of cartilage

Limited range of movement

Paget’s disease Disorder of bone metabolism

Broken bones.

Damaged cartilage in joints

Thoracic spinal Intermittent aching pain

stenosis
Radiates to the lower back and legs

Difficulty moving side to side

55
 CHAPTER - 11

DIAGNOSTIC TESTS

56
A diagnosis of AS can usually be confirmed if an X-ray shows inflammation of the sacroiliac
joints (sacroiliitis) and you have at least 1 of the following:

•at least 3 months of lower back pain that gets better with exercise and doesn't improve with
rest

•limited movement in your lower back (lumbar spine)

•limited chest expansion compared with what is expected for your age and sex

If an X-ray cannot confirm AS, you'll usually be offered an MRI scan.[32]

Physical examination

A physical exam may include:

 Examining your joints, including your spine, pelvis, heels, and chest.
 Watching how you move and bend in different directions, checking for flexibility.
 Asking you to breathe deeply to check for rib stiffness and inflammation.[33]

Appearance of the Patient

 Patients with ankylosing spondylitis usually appear normal.

Vital Signs

 Vital signs are within normal limits in patients with AS.

Cervical spine

 Forward stooping of the thoracic and cervical spine.

 The degree of flexion deformity is measured by asking the patient to stand erect with
heels and buttocks against a wall and to extend the neck while keeping the mandible in
the horizontal position and ask the patient to touch the wall.

57
 The degree of flexion deformity is measured by the distance between the occiput and the
wall.

Thoracic spine

 The degree of chest expansion is measured by the range of motion of

the costovertebral joints and is measured at the level of the xiphoid process.
 The physician must ask the patient to raise their arms beyond their heads and then ask the
patient to maximal forced expiration how much they can and that is followed by a
maximal inspiration.
 In normal individuals the expansion is usually >2 cm.
 In normal individuals it is greater than 10 cm.

Lateral spinal flexion

 Physician must ask the patient with AS to standing erect with heel and back against a
wall and knees and hands extended and measure the distance between the tip of the
middle finger and the floor.
 Then ask the patient to bend sideways without bending the knees.

Sacroiliac joint tenderness

 In AS patients to bring out sacroiliac pain apply direct pressure over the sacroiliac joint.
 Sacroiliac joint tenderness is also elicit by the following
o Ask the patient to be supine position, then apply direct pressure on
the anterior superior iliac spine and, at the same time physician must apply force on
iliac spine laterally.
o Ask the patient to be on the side, then physician must apply pressure to compress
the pelvis.

58
 o Ask the patient to be supine position, physician must ask the patient to flex one of the
knees and then to abduct as well as externally rotate the corresponding hip, then
apply pressure on the knee which is flexed and this elicit pain on the sacroiliac joint.

Hip joint

 When a patient with AS is exhibiting abnormal gait hip involvement should be suspected.
 In AS patients hip involvement lead to flexion deformities and can be assessed
by internal and external rotation of the hip.

Dactylitis

 Dactylitis also called as sausage digits.In AS patients the fingers looks like in appearance.

Lungs

 Restrictive lung disease

 Upper lobe fibrosis

Cardiovascular

 Patients with AS present with following cardiovascular features

o Valvular heart disease
o Aortitis
o Conduction disturbance[34]

Imaging Tests

X- Ray

 A standard anteroposterior (AP) plain x-ray of the pelvis helps in recognizing the AS.
 Findings on an x-ray suggestive of/diagnostic of ankylosing spondylitis(AS) include

59
 o Erosions
o Ankylosis
o Changes in joint width
o Sclerosis
o Bamboo like appearance of vertebral column
 Fusion and large erosions more obvious as the disease becomes more advanced.
 With the severity in x-ray hip involvement we can correlates the severity of
the spinal disease.[35]

60
 Fig. 11.1:- X-ray Ap view of spine showing fusion of the spinous processes of
lumbar vertebrae.

CT SCAN

Computed tomography (CT) scanning is useful in selected situations (eg, in equivocal cases
of sacroiliitis and in cases in which subtle radiographic changes are present) and in the
evaluation of complications. Although CT scanning is useful in evaluating sacroiliitis, normal
variations of the sacroiliac joints may simulate the findings of inflammation. Because of its
high radiation dose, CT scanning is not ideal for imaging long segments of the spine. In
patients with advanced ankylosing spondylitis, multidetector CT (MDCT) scanning is the
imaging modality of choice for the evaluation of fractures of the cervical spine.

MRI
Magnetic resonance imaging (MRI) is useful in assessing early cartilage abnormalities and
bone marrow edema. MRI has revealed a very early clinical phase of the disease in which
there is symptomatic axial involvement but no structural changes. [36]

Fig. 11.2:- MRI showning romanus lesions on thorax level and inflammatory changes on
anterior maniburosternal joints

61
 HLA B27 GENE
A genetic blood test may sometimes be carried out to see if you carry the HLA-B27 gene
variant, which is found in most people with AS. This can contribute towards a diagnosis of
AS, but it's not entirely reliable as not everyone with the condition has this gene variant and
some people have the gene variant without ever developing AS [37].

C - Reactive protein
C-reactive protein (CRP) is a marker of inflammation. Ankylosing spondylitis
(AS) is one of several health conditions that may cause elevated CRP. Other
autoimmune conditions, infections, or lifestyle factors may also increase CRP
levels.[37]

SPECIAL TESTS

A physical examination for ankylosing spondylitis often also includes the following:

 Schober Test: Limited motion in the lumbar spine is an AS symptom. The Schober test
measures the degree of lumbar forward flexion as you bend over as though touching your
toes. Limited motion usually warrants an X-ray.

 Gaenslen Test: Sacroiliac (SI) joint pain—pain where the “wings” of your pelvis (iliac
crests) meet the lower part of your spine (the sacrum)—is often an early sign of ankylosing
spondylitis. Gaenslen's maneuver, another name for the Gaenslen test, stresses the sacroiliac
joints. You’ll lay down on an exam table, pull one knee up to your chest and dangle the other
leg off the side of the table. Your doctor will press on both knees. Increased pain in the
dangling leg during this exam could mean AS.

62
 Chin-Brow Measurement:(normal angle −1.5° to 5.8°) This method measures the spine's
curve in the neck. Picture a straight line running from the middle of your forehead to the end
of your chin. In people with healthy spines, that imaginary line will be vertical, or close to
it. People with AS often have necks that angle forward sharply as the spine stiffens, so your
doctor will measure the angle your chin-brow line makes and how far from vertical it is. If
the doctor is going to use the chin-brow measurement to monitor your angle, the first time he
or she takes the measurement will be called your "baseline." After that, the doctor will
compare each successive chin-brow measurement to the baseline to see if the angle is getting
worse.

 Chest Expansion: When ankylosing spondylitis affects the mid-back region (thoracic spine),
you may not be able to expand your chest normally. The amount of chest expansion is
measured with a tape measure from a deep exhale to a full inhale. Measurements significantly
less than one inch, which is normal chest expansion, could indicate AS.

 Range of Motion: To test how well and far your joints allow you to move, the doctor
measures the degree to which you can perform movements of flexion, extension, lateral
bending, and spinal rotation.[38]

Fig. 11.3:- Schober test

63
 Fig:- Gaenslen maneuver

Fig. 11.4:- Chin brow measurement

64
Fig. 11.5:- Chest expanison

65
 CHAPTER - 12

OUTCOME MEASUREMENT

66
Objective. There is currently no universally accepted measure of quality of life in ankylosing
spondylitis (AS). Our objective was to develop and evaluate a patient-reported outcome
measure of quality of life in AS, EASi-QoL.

Methods. We used patient interviews, a literature review, and completion of an

individualized measure of AS quality of life during clinic-based and pilot surveys to derive
questionnaire content. Classical and modern psychometrics were then used to evaluate the
questionnaire using data from a large UK-based postal survey of 1000 patients with AS.

Results. Data analysis from the interviews and clinic-based and postal surveys produced a
57-item self-completed questionnaire. Fifteen items were removed as a result of patient
interviews and the pilot survey. In total, 612 (64.0%) patients responded to the main postal
survey. After assessment of data quality, confirmatory factor analysis, and Rasch analysis, 20
items were found to contribute to 4 domains of AS-related quality of life: physical function,
disease activity, emotional well-being, and social participation. Item-total correlations ranged
from 0.66 to 0.84. Cronbach’s alpha and test-retest reliability estimates were 0.88–0.92 and
0.88–0.93, respectively. Confirmed hypothesized correlations with the AS Quality of Life
questionnaire, the Bath AS Disease Activity Index, Bath AS Functional Index, SF-36, EQ-
5D, and the Hospital Anxiety and Depression Scale were evidence for the construct validity
of the EASi-QoL.

Conclusion. The EASi-QoL has good evidence of data quality, internal reliability, test-retest
reliability, and content and construct validity, and should be considered for use with patients
in routine practice settings and in evaluative studies including clinical trials. Measurement
responsiveness and minimal important change are currently being assessed.

67
 CHAPTER – 13
PHYSIOTHERAPY MANAGEMENT

68
The management of AS aims to improve and maintain spinal flexibility and normal posture,
relieve symptoms, decrease functional limitations, and reduce complications.

The main clinical manifestations of AS are back pain and progressive spinal rigidity, as well
as inflammation of the hips, shoulders, peripheral joints, and fingers/toes. Furthermore,
inflammatory skin conditions, inflammatory bowel disease, enthesitis, and anterior uveitis
can also be present.

The effectiveness of exercise might depend on the individual’s adherence to the prescribed
programme, considering the dose–response relationship between exercise and health effects.
Therefore, physiotherapy plays a crucial role in the management of AS. Patient training and
exercise programmes supervised by a physiotherapist may improve symptoms and teach
patients how to independently and adequately handle AS throughout life, thereby reducing
the cost impact of physiotherapy. To date, a specific non-pharmacological protocol is not yet
available, and the effect of different types of exercise programmes remains unclear [45].

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