Spondyloarthropaties

(Seronegative arthritis)
DR. PRUTHVIRAJ NISTANE
Post-Graduate student
Deptt. Of Orthopaedics,
Govt. Medical College and
Rajindra Hospital, Patiala

Objectives
 Gain a basic understanding of the Spondylo-
Arthritis
 Learn specific Characteristics of SpA
 Differentiate SpA from other chronic Arthritis
( RA, OA )
 Become familiar with articular and extra-articular
manifestations of SpA
 Understand the current treatment paradigm and
medications used

Introduction
 Are a diverse group of chronic, systemic
inflammatory conditions linked by
distinctive clinical, radiographic, and
genetic features
 Refers to inflammatory changes involving
the spine and the spinal joints.
 subtypes often overlap
 may be considered one heterogeneous
and phenotypically diverse disease that
has the potential to evolve into AS.

Introduction
 Absence of Rheumatoid Factor or other
autoantibody serologic abnormalities
 includes
○Ankylosing Spondylitis
○Psoriatic Arthritis
○Reactive Arthritis
○Enteropathic Arthritis-IBD
○Undifferentiated Spondyloarthropathy

ESSG (Europian SpA Study
Group)Criteria for diagnosis of
spondyloarthropathy
 Inflammatory spinal pain or synovitis (asymmetric or
predominantly in lower limbs) plus more than 1 of the
following:
 Positive family history
 Psoriasis
 Inflammatory bowel disease
 Urethritis, cervicitis, or acute diarrhea < 1 mo. before arthritis
 Buttock pain alternating between right and left gluteal areas
 Enthesities
 Sacroiliitis
 Sensitivity 78.4% and specificity 89.6%

RA SpA
• UE>LE
• Often polyarticular
• Sacroiliitis absent
• RF usually pos
• No HLA-B27 assoc
• Sicca, scleritis
• LE>UE
• Oligoarticular
• Sacroiliitis often +
• RF neg
• + HLA-B27 assoc
• Anterior uveitis
• Mucocutaneous

Confusion
Can often see peripheral joint symptoms in
the absence of spinal symptoms

Pathology
 immune
 The pathology of spondyloarthropathies is
very different from that of RA. In RA, it is
the synovitis that plays the major role, and
the synovitis leads to bony erosions.
 In spondyloarthritis there is some synovitis,
but it's the enthesitis that is the major
problem, especially in the axial disease.

Pathology
Osteitis follows
reactive bone sclerosis and
bone absorption, but then
more bone remodeling sets in
and it goes on to result in
new bone formation that can
result in ankylosis

Pathology
 In RA, the cytokines lead to excessive
osteoclastic activity resulting in bone erosions,
 In spondyloarthritis, the cytokines that are
playing a major role result in osteoblastic activity
 Gradual bony bridging follows after being
initiated by the inflammation

Hallmarks
Inflammatory back pain (IBP)
Enthesitis - inflammation at sites where
tendons, ligaments, and joint capsule
fibers attach to bone, with a strong
tendency to produce fibrosis and
calcifications.

Inflammatory Back Pain
 Worse in the late night and early morning
 Pain interferes with sleep to the point that the
patient gets up to walk in the middle of the night
 The discomfort can be characterized by
alternating buttock pain.
 prolonged morning stiffness of greater than 30
minutes.

Inflammatory Back Pain
 Exercise alleviates the pain rest makes it
worse.
 Affects younger patients
 Peaking during the mid-20s
 onset before the age of 40

Spondyloarthropathies
IBP persists for at least 3 months.
detrimental effects on quality of life
 increased disability, and morbidity --
equal, and in some cases
exceeding, that seen in RA

 Also associated with osteoporosis and low bone
mineral density
 Ectopic bone formation occurs within the inflamed
vertebral enthesis
 Bone resorption, (increased osteoclast activity),
occurs at an unregulated rate within the vertebra
and promotes weakening of the spinal column.

Clinical course
 The spine in the patient with AS fuses through:
 ligamentous ossification and
 syndesmophytosis,
 Rigid hyperkyphotic deformity develops.
 Biomechanically, the fused spine acts as a long
bone incapable of appropriately dissipating the
energy of a traumatic event.

 Altered spinal biomechanics
 Combined with the brittle quality of the
osteoporotic bone
 Increase susceptibility to vertebral column
factures, and Spinal Cord injury, even after minor,
often trivial, trauma
 Significantly impaired mobility and peripheral joint
arthritis

Sagittal reformatted CT scan showing a highly displaced
thoracic fracture. Asterisk indicates apposition of the
caudal fracture fragment on the thoracic aorta

Extra-articular
manifestations
 psoriasis,
 anterior uveitis,
 IBD,
 as well as rarer cardiac, renal, and
pulmonary manifestations
 a wide range of clinical manifestations.

Ocular Manifestations
 Uveitis is one of the most common
 occurring in 25% to 40% of patients.
 there appears to be no correlation
between the course of inflammatory
eye disease and that of the arthritis.

Ocular Manifestations
 Presents as acute unilateral pain and photophobia
 Blurring of vision may also occur.
 Cataracts
 Glaucoma
 Increased intraocular pressure
 Posterior synechiae
 Conjuctivities

Cutaneous
Manifestations
 Plaque psoriasis
 Characterized by scaly,
erythematous, hyperkeratotic lesions
 most common form of psoriasis and
is an important component of
diagnosing PsA.

Cutaneous Manifestations
 assessment of less
conspicuous areas
including
 gluteal cleft
 scalp
 scalp line
 groin
 posterior
auricular regions
should be performed.

Nail Changes
 Diffuse and numerous nail pitting (plate
depressions)
 Onicholysis (separation of the nail from
underlying nail bed)
 Crumbling of the nail plate can be observed in
both psoriasis and PsA.
 The extent of nail involvement parallels both
skin and joint disease

Crumbling nail/DIP joint involvement

Other Extra- articular Manifestations
 Apical pulmonary fibrosis : mostly asymptomatic
and typically observed in patients with substantial
disease duration
 Renal disease : beyond analgesic and nonsteroidal
anti-inflammatory drug adverse effects
 IgA nephropathy : proteinuria and hematuria
 secondary amyloidosis : nephrotic syndrome
 renal failure : a poor prognosis.

Gene association
 Up to 70% of individuals suffering from
SpA carry the HLA-B27 gene
 Strength of the association between HLA-
B27 and disease susceptibility varies
among SpA subtypes and ethnic groups

Associations with HLA-B27
Rheumatic diseases
Ankylosing spondylitis
Reiter’s syndrome/reactive
arthritis
IBD related arthritis
Psoriatic arthritis
Normal Associations
Native Americans
Caucasians
Blacks
Degree of
associations
>90%
>80%
~75%
~50%
13%
8%
4%

(MARIE-STRUMPELL DISEASE)
(BECHTEREW DISEASE)

 A chronic, progressively inflammatory
disease of the spine and axial joints leading
to fibrous or bony ankylosis and deformity.
 Systemic disease
 Age – late adolescence or early childhood
(20-40 yrs)
 Sex - 3:1 men: women
 Affects about 6 in 10,000

Etiology
 Not completely understood
 Auto-immune
 HLA-B27 : seen in 90 % patients
 Autosomal inheritance with 70 %
penetration in males
 some family history

Pathology
 Most striking feature - high degree of fibrosis,
bony ankylosis, and inflammation that focus
on bone, cartilage, and tendon-bone
junction.
 Early lesions include subchondral
granulation tissue that erodes the joint and is
replaced gradually by FIBROCARTILAGE
and then OSSIFICATION.
 Occurs in ligaments, fibrocartilage,disc and
capsular attachment sites to bone,called
“enthesitis” )

Gross Pathology
 Start from SI joint
 Destruction of cartilage and articular cortex
 Fibrous or bony bridging
 Para-articular – degeneration and
ossification in spine
ossification of anterior longitudinal ligaments
“bamboo spine”

HistoPathology
Inflammatory cells in
ligamentous and periosteal area
Subchondral marrow oedema
Pannus and new bone formation
Bony erosion
Fibrocartilagenous regeneration
and ossification

Clinical features
 Insidious onset
 Begins in the Sacroiliac Joints –
 backache and morning stiffness
 radiation
 U/L or B/L
 subsides with activity
 returns after sitting in one position for long
period
 Flexor spasm predominateforward
flexion
 Progresses upwards and can involve the entire
spine

Axial joints(a poor prognostic )
 Shoulders
 Hips
 Knees
Painful,swollon,
effusion,
muscle spasms
Flexion,
adduction
deformities

Peripheral joints
 Osteoporosis
 Blurring of margins
 Joint space narrowing
 Bony ankylosis
• Kyphosis
• Loss of spinal mobility
• Decreased chest expansion

Systemic features
 Fatigue
 Weight loss
 Anorexia
 Night sweats
 Anemia

Diagnosis
Modified New York criteria (1984)
1. Limited lumbar motion
2. Low back pain for 3 months improved with exercise
not relieved by rest with morning stiffness
3. Reduced chest expansion
4. Definite radiological sacroilitis
Criteria 4 plus any of 1, 2, or 3.

Juvenile Ankylosing Spondylitis
Onset 8 to 14
Sex Ratio M:F 7 to 1
HLA-B27 91 %
Systemic symptoms rare
Polyarticular 97%
Prognosis good
 Peripheral joint involvement is more to begin
with; later axial symptoms supervene

Physical Examination
 Loss of spinal mobility
 Para spinal spasm

Spinal Involvement
 Tenderness – SI joints
 SI Compression Testing
 Modified Schober Test
 Potentially useful diagnostically
 Limitation of motion

•Occiput to Wall distance
•Chest Expansion
 at the xiphisternum
 Normally > 5 cm
 Measurement is age and sex
dependant
 Useful for following patients over
time

Spinal Involvement
 Finger Tip to Floor Distance
 Measure fingertips to floor
 Useful for following patients over time
Lateral Flexion
 Ask the patient to flex laterally and
mark at the maximal extent of the
fingertips
 Useful for following patients over time
 Cervical Spine
 Can result in Atlanto-Axial Instability

Radiological features
 Within 3 to 6 months
 SI joints – earliest
 Patchy osteoporosis
 Margins ill defined
 Widened
 Later subchondral sclerosis
 Finally bridging and obliteration of joint

Sacroiliitis grading
0-normal
1-possible
2-minimal
3-moderate
4-ankylosing

The Spine
 Sharp squaring of anterior portion of
vertebral body
 Loss of concavity
 Loss of lardosis
 Subluxation of atlanto-axial joint
destruction of transverse
ligament and odontoid

•The reparative process forms
vertical linear bone ossification
along the outer fibers of the
annulus fibrosus of the disc,
called syndesmophyte formation.
•Ossification of anterior longitudinal
ligament and annulus –
“bamboo spine”
•Vertebral bodies tend to become osteoporotic
(dorsal spine appears to become wedge-shaped)

Progression and complications
Early stage(inflammatory)
 Intermittent, low-grade fever
 Fatigue
 Anorexia
 Sacroilitis (inflammation, pain, and
tenderness in the sacroiliac joint)
 Spasm of the vertebral muscles
 Intermittent, low back pain (non-traumatic,
insidious onset)
 Rarely remission within 2 years

Advanced stage(ankylosis)
 Constant low back pain
 Ankylosis , decreased ROM
 Muscle wasting in shoulder and pelvic girdle
 Loss of lumbar lordosis
 Marked dorsocervical kyphosis
 Ultimately in 3 to 5 years – SI joints are
fused, spine , hips ankylosed in forward
flexion, single rounded immobile spinal curve
, residual motion in knees and shoulder.

Complications
 Fractures - Stiff osteoporotic spine is prone to
fracture and minor trauma. Most common
site of fracture is the lower cervical spine.
 Progressive myelopathy - develops from
cord compression leading to motor/sensory
disturbance.
 Cauda equina syndrome – late complication
Initial deficit is loss of sensation on the
lower extremity

 Spinal stenosis – rare ; Result of bony
overgrowth of the spinal ligament and
facet joint.Symptoms are pain and
numbness of the lower extremities
brought on by walking and relieved by
rest.
 Subluxation of atlanto-axial joint -
chin-on-chest deformity
 Reduced vital capacity

Associated symptoms
 Aortitis
 Aortic dilatation
 Aortic regurgitation – scar tissue in aortic
valves
 Conduction abnormalities
 Apical pulmonary fibrobullous lesion
 Iritis
 Non-granulomatous anterior uveitis
 Colitis

Laboratory Investigations
• Elevated ESR/CRP
 HLA-B27 - found in 90-95% of patients
( 6% of general population)
• Synovial fluid – mononuclear leukocytes
 CBC
 Normochromic normocytic anemia
 Reactive thrombocytosis
• Elevated serum IgA
• Increased ALP
• Decreased vital capacity

Differential diagnosis
 Ankylosing form of RA
 Other spondyloarthropathies
 Other causes of LBA
 Ochronosis
 DISH

Treatment - Goals
 Rehabilitation.
 Initiated before the disease fuses the
vertebrae and involves other organ.
 Directed toward maintaining function
and strength.

Conservative management
 Corticosteroids – reduces inflammation
and relieves pain may overcome
deformity to some extent
 NSAIDS - mainstay of treatment
 Radiation – relieves muscle spasm
given with caution
 Methotrexate
 Sulfasalazine

Latest revolution
 Anti TNF-α therapy
Infliximab
Etanercept
 Rapid, profound and sustained response to
all aspects of disease
 Serious complications
 Very expensive

Posture and exercise
 Recumbence
 Hyperextension , abduction
 Deep breathing exercises
 Traction to lower extremities to overcome
deformity

Surgical management
 To relieve from disabling deformities
Total hip replacement
 Neck osteotomy and head removed
piecemeal
 Accurately identify acetabular margins
 Over come flexion, stooping
 Motion
 Relieve pain
 Restore upright posture
 Prevent spinal osteotomy
 90 % good results

Spinal osteotomy
Done at L2-3 or L3-4 level
Wedge of posterior spinal
column excised and
straightening of spine done.
Multiple complications

(Seronegative arthritis)
II
Moderated by - Dr. K. S. Sandhu
Presented by - Dr. Pruthviraj Nistane

“Recap”
 Are a diverse group of chronic, systemic
inflammatory conditions linked by
distinctive clinical, radiographic, and
genetic features
 Refers to inflammatory changes involving
the spine and the spinal joints.
 subtypes often overlap

Hallmarks
 Immune mediated enthesitis and other
changes
 IBP
 Extra-skeletal manifestations
 Association with HLA – B27

ANKYLOSING
SPONDYLITIS
 PROTOTYPE
 Most common
 Crippling disease affecting young population
 Inflammatory back pain
 From sacro-ilitis to complete fusion on the spine
 Large peripheral joints may be involved
 Anti TNF agents have revolutionised treatment

What is it ???
 Acute non-purulent arthritis complicating
an infection elsewhere in body
 Clinical syndrome triggered by specific
etiological agent in genetically susceptible
host
 Infection – mostly enteric or urogenital

“Reactive”
 viable micro-organisms do not enter the
joints and synovial fluid cultures are thus
negative.
 There is no universal agreement about
the classification and diagnostic criteria
for reactive arthritis.

 Reiter’s syndrome –old aponym for reactive
arthritis
 clinical triad of arthritis, urethritis and
conjunctivitis.
 Reactive arthritis belongs to the family of
spondyloarthropathies because they share
cardinal clinical features together.

Epidemiology
 age - is 18–40 years
 gender ratio in ReA following enteric infection is
nearly 1:1, whereas venereally acquired ReA
occurs mainly in men
 60–85% of patients were found to be B27-
positive - its presence contributes to the
chronicity of the disease.

Triggering infections
• Reactive arthritis is an arthritis induced by one of
the following bacteria:
 Urogenital:
• Chlamydia trachomatis
 Enteric:
• Shigella (S. flexneri has most often)
• Salmonella
• Yersinia
• Campylobacter
• At least presumptive evidence for a related
antecedent infection is a must

 Form of post infection arthritis that share
same clinical features as SpA.
 Whereas arthritis caused by or related to
other infections is termed “infection-
related/ associated arthritis”

Pathology
• Synovial histology - is similar to that of other SpA
• Enthesitis - increased vascularity
Macrophage infiltration of fibro
cartilage
• Histopathology evidence of
inflammation has occasionally been noted in the colon
and ileum

Pathogenesis
Bacterias
• produce lipopolysaccharide (LPS)
• capacity to attack mucosal surfaces,
• survive intracellularly
HLA-B27 - prolongs the intracellular
survival
Trafficking of infected leukocytes from the
site of primary infection to joints, where an
innate and adaptive immune response to
persistent bacterial antigens promote
arthritis.
synovial T cells that specifically responded to
antigens of the inciting organism were reported
and characterized as predominantly CD4+ with a
TH2 or T regulatory phenotype. More recent work
has documented high levels of IL-17

confusion ????
• Antigens from these bacterias have
been shown to be present in the
synovium and/or synovial fluid
leukocytes
• So atleast in some cases,it may be
chronic form of infection rather than
solely reactive

Clinical picture
 Usually there is a delay of 1-4 wks from
infection till start of arthritis
 ranges from an isolated, transient
monarthritis or enthesitis to severe
multisystem disease
 History suggestive of infection

Musculoskeletal symptoms
Peripheral
• Typically there is asymmetric additive, oligoarthritis,
mainly of Lower limbs.
• Most common are knees, ankles, subtalar , toe IP and
MTP joints.
• Quite painful, and tense joint effusions.
• Dactylitis, or "sausage digit " a diffuse swelling of a
solitary finger or toe, is a distinctive feature of
peripheral SpA

Axial
• Inflammatory low back pain
o Acute sacroiliitis
o insertional inflammation,
o muscle spasm
o arthritis in intervertebral joints.
• Enthesitis
• Plantar fasciitis
• Achilles tendinitis

Extra-articular features in ReA
Mucocutaneous
• Keratoderma Blennorrhagica (20%)
palms and soles
• Circinate balantitis (30%)
• Painless oral ulcers (25%)
• Erythema nodosum
Nail changes
• onycholysis,
• distal yellowish discoloration
• heaped-up hyperkeratosis.

Urogenital lesions
males
• urethritis
• Prostatitis
females
• Cervicitis
• salpingitis
Ocular
• Conjunctivitis (60%)
• Uveitis (unilateral) (20%)
• urethritis• Cervicitis

Constitutional symptoms
 Fatigue
 Malaise
 Fever
 Weight loss
 Cardiac conduction defects
 Aortic insufficiency
 Central or peripheral nervous system lesions
 Pleuropulmonary infiltrates.

Diagnostic Criteria
• Seronegative asymmetric arthropathy
and at least 1 of the following:
• Urethritis or cervicitis
• Diarrhea
• Inflammatory eye disease
• Mucocutaneous disease
• Balanitis, oral ulceration or keratoderma
• Other spondyloarthropathies and rheumatic disease
excluded

Prognosis
 Persists 3–5 months, but courses up to 1 year
can occur.
 Chronic joint symptoms persist in about 15% of
patients.
 Recurrences of the acute syndrome are also
common
 Low-back pain, sacroiliitis, and frank AS are
also common sequelae

Laboratory investigations
Demonsration of the urogenital tract or bowel
infections
 During the acute phase:
• urine culture,
• genital swabs,
• stool culture
 After arthritis developed:
• Serodiagnosis to detect antibodies
• PCR

 inflammatory arthritis:
• ↑ESR, CRP
• leucocytosis
• Synovial fluid analysis and culture
 HLA B27 (especially in chronic arthritis)-85 %
 Imaging :
MRI, CT, Plane x-ray for detection of
• Sacroilitis – asymmetrical
• Enthesopathy
• Juxtaarticular osteoporosis
• Marginal erosions
• Loss of joint space
• Spondylitis – can begin anywhere in lumbar spine
• Reactive new bone formation

Differintial diagnosis
 Disseminated gonococcal
disease
 psoriatic arthropathy
 Other spondyloarthropathies

Treatment
 Eradicate triggering infection (antibiotics)
 Treat extra-articular manifestations:
Topical steroid
Uveitis - topical steroids, mydriatics
 Skin lesions ordinarily require only
symptomatic treatment

1. NSAIDs: in full doses
Indomethacin, 75–150 mg/d in divided doses is the initial
treatment of choice
2. Local steroids injections
in mono/oligo arthritis, enthesopathy
3.Immuno-suppresants
• Sulfasalazine
• Azathioprine
• methotrexate
4. Biologics: anti-TNF- α
in resistant disease
Treatment of arthritis:

What is it ???
 Psoriatic arthritis (PsA) refers to an
inflammatory arthritis that
characteristically occurs in individuals with
psoriasis.

Who Gets Psoriatic
Arthritis?
 Age of onset - 30-50 years
 1-3% of the population has psoriasis
 5 – 10 % of people with psoriasis get psoriatic
arthritis
 Family studies suggest a 50-fold increase in the risk
of psoriatic arthritis in 1st degree relatives
 HLA-Cw6 gene is directly associated with psoriasis
 HLA-B27 is associated with psoriatic spondylitis

Pathology
 shares pathogenic mechanisms with psoriasis
 immune-mediated
 Infiltration with T cells, B cells, macrophages,
and NK receptor–expressing cells
 Resembles that of RA - less hyperplasia and
cellularity than in RA, & greater vascularity

Pathology
 synovial overexpression of proinflammatory
cytokines
• Interleukin 2
• Interferon
• TNF
 marked increase in osteoclastic precursors in
peripheral blood and upregulation of receptor
activator of nuclear factor ligand (RANKL) in the
synovial lining layer.

Clinical Features
 Psoriasis present before the onset of joint disease
(70%)
 Psoriasis comes with the arthritis (15%)
 Psoriasis comes after the arthritis (15%)

Confusion
Psoriatic Arthritis is a heterogenous disease
which can present in a multitude of ways

Wright and Moll Classification
(1) Arthritis of the DIP joints; 15 %
(2) Asymmetric oligoarthritis; 30 %
(3) Symmetric polyarthritis similar to RA; 40 %
(4) Axial involvement (spine and sacroiliac joints);5%
(5) Arthritis mutilans, a highly destructive form of
disease5 %

Presentation
 Typical presentation is a peripheral inflammatory joint
disease – usually a mono or oligo arthritis
 Knees
 Wrists
 May occasionally present with polyarthritis
 Initial presentation of inflammatory spinal disease is
rare

Progression -- later stages
 Sacroiliac Involvement
 Sacroiliitis in 1/3 of patients
 Usually asymmetric (unilateral)
 May be asymptomatic
 Spinal Involvement
 May affect any part of the spine in a random fashion
 Different from ankylosing spondylitis

Other features
 Mucocutaneous Involvement
 Psoriatic skin lesions
 Psoriatic Nail lesions
 Entheseal Involvement
 Tenosynovities
 Dactylitis ->30 %
• Shortening of digits because of underlying osteolysis
• Both fibrous and bony ankylosis of small joints
• Ankylosis of one or more PIP joint
 Ocular Involvement - uveitis - bilateral, chronic,
and/or posterior,
- conjuctivitis
 Aortic valve insufficiency

Nail changes
Occur in 90% of patients with PsA
 Pitting
 Horizontal ridging
 Onycholysis
 Yellowish discoloration of the nail margins
 Dystrophic hyperkeratosis
 Combinations

Psoriasis/Nail changes/arthritis DIPs
and Sausage deformity

Classification of Psoriatic
Arthritis (CASPAR) criteria; 2006
A patient must have inflammatory articular disease (joint,
spine, or entheseal) with 3 points from any of the following
five categories:
1) Evidence of current psoriasis,or history of it
2) Typical psoriatic nail dystrophy
3) A negative test result for rheumatoid factor
4) Either current dactylitisf or a history of it
5) Radiographic evidence of juxtaarticular new bone formation in
the hand or foot

Physical Examination
 Skin and Nail Involvement
 Peripheral Joint Involvement
 Peripheral Entheseal Involvement
 Spinal Involvement
 Schober Test
 Occiput to Wall Distance
 Spine ROM
 Finger tip to floor distance
 Lateral flexion

 assessment of less
conspicuous areas
including
 gluteal cleft
 scalp
 scalp line
 groin
 posterior
auricular regions
should be performed.

Peripheral Joint Involvement
 Inflammatory Joint Count
 Number of Joints Involved
○ Prognostic Importance
○ Therapeutic Importance
 Pattern of Joints Involved
○ Diagnostic Importance
 Evidence of Damage
 Dactylitis

 ESR and CRP elevated
 Uric acid may be elevated in the
presence of extensive psoriasis
 HLA-B27 is found in 50–70% of patients
with axial disease, but 20% in patients
with only peripheral joint involvement.

Radiographic features
Small joints involvement
 classic "pencil-in-cup" deformity
 marginal erosions
 adjacent bony proliferation(whiskering)
 small-joint ankylosis
 osteolysis of phalangeal and metacarpal bone
 telescoping of digits
 Periostitis
 proliferative new bone at sites of enthesitis.

Fusion
Pencil in Cup
deformity
•Subchondral bone resorption of
the distal interphalangeal joint of
the thumb and middle fingers
has resulted in the "pencil-in-
cup" appearance.
•A flexion deformity of the distal
interphalangeal joint of the small
finger is present
•corresponding joint of the ring
finger has fused.

Axial involvement
 Asymmetric sacroiliitis
 Syndesmophytes
 Fluffy hyperperiostosis on anterior vertebral bodies
 Severe cervical spine involvement, with a
tendency to atlantoaxial subluxation
 Sparing of the thoracolumbar spine
 paravertebral ossification

Prognosis
 Erosive disease develops in the majority
 Progressive disease with deformity and disability
is common
 Mortality was found to be significantly increased
compared with the general population
 The psoriasis and associated arthropathy seen
with HIV infection both tend to be severe and can
occur in populations with very little psoriasis

Indicators of Bad
Prognosis
 Younger age at onset
 Presence of certain HLA antigens:
o HLA-B27 correlates with spondylitic involvement
o HLA-DR3, DR4 correlates with erosive disease
 Extensive skin involvement
 Polyarticular involvement
 Lack of clinical response to NSAIDs
 Association with HIV infection

Differntial diagnosis
 Gout
 Inflammatory Osteoarthritis
 Multicentric reticulohistiocutosis
 Other forms of SpA

Treatment
 coordinated therapy is directed at both the skin and
joints
 anti-TNFagents - revolution
• Etanercept
• Infliximab
• Adalimumab
• Golimumab.
 Methotrexate
 Sulfasalazine
 leflunomide
 PUVA
 7 % of patients with PsA required musculoskeletal
surgery

 A relationship between arthritis and IBD
 Ulcerative colitis (UC) as well as
Crohn's disease (CD)
 prevalence of IBD is 0.05–0.1%,
 AS was diagnosed in 1–10%, and peripheral
arthritis in 10–50% of patients with IBD
 one-third to two-thirds of patients with AS have
subclinical intestinal inflammation

 tendency to familial aggregation, more so for
CD
 HLA-B27 - 70% of patients with IBD and AS
-15% of patients with IBD and
peripheral arthritis
 alleles of the NOD2/CARD15 gene in SpA
patients with chronic inflammatory gut lesions

Pathology
Similar to other spondyloarthritides
1. Enthesiopathy (7%)
2. Spondylitis (2%)
3. Peripheral arthritis (10%)

Pathogenesis
 The specific pathogenic mechanisms are
poorly understood
 Immune-mediated
 Trafficking of leukocytes between the gut and
the joint
 Mucosal leukocytes from IBD patients have
been shown to bind avidly to synovial
vasculature

Clinical Features
 AS - clinically indistinguishable from idiopathic AS
course independent of the bowel disease
 peripheral arthritis - includes acute self-limited
attacks of oligoarthritis (4-6 weeks) of LL
chronic and symmetric polyarticular arthritis
course parallel to disease
 Enthesitis , arthralgias or fibromyalgia symptoms.

Extraintestinal
manifestations
Uveitis
Pyoderma gangrenosum
Erythema nodosum
Finger clubbing

In IBD-associated SpA, erythema nodosum can be
observed in Crohn's disease

Laboratory Findings
 inflammatory and metabolic
manifestations of IBD
 Joint fluid is usually at least mildly
inflammatory
 30–70% carry the HLA-B27 gene,

Radiographic
Findings
 axial skeleton are the same as in
uncomplicated AS.
 Erosions are uncommon in peripheral
arthritis but may occur, particularly in the
metatarsophalangeal joints.
 Isolated destructive hip disease has
been described.

Differential diagnosis
(Diarrhea and arthritis)
Reactive arthritis
Celiac disease
Blind loop syndromes
Whipple's disease

Treatment
anti-TNF agents
• Infliximab
• adalimumab
Other treatment for IBD
 sulfasalazine and related drugs,
 systemic glucocorticoids
 immunosuppressive drugs
usually of benefit for associated peripheral
arthritis.

 Approximately one-half of the patients with
undifferentiated SpA are HLA-B27-positive
 often eventual progression to classical AS

 In juvenile-onset SpA - begins between ages 7 and 16
o most commonly in boys (60–80%)
o an asymmetric, predominantly lower-extremity
oligoarthritis and enthesitis without extraarticular
Features
 The prevalence of B27 in this condition, which has
been termed the seronegative enthesopathy and
arthropathy (SEA) syndrome, is approximately 80%.

management
 anti-TNF- therapy
 Newer - doxycycline and rifampin

SYNOVITIS
ACNE -CONGLOBATA,
FULMINANS,
HIDRAENITIS SUPURATIVA
PUSTULOSIS -PALMO PLANTAR
HYPEROSTOSIS - STERNO-CLAVICULAR
SPINAL
OSTEOMIELITIS - STERIL MULTIFOCAL
RECURRENT

 In some cases, bacteria, most often
Propionibacterium acnes, have been cultured
 ESR is usually elevated, sometimes
dramatically
 Inflammatory bowel disease was coexistent in
8%
 B27 is not associated

Management
 High-dose NSAIDs
 Pamidronate or other
bisphosphonates
 Anti-TNF therapy

 Rare chronic bacterial infection, mostly
of middle-aged white men, caused by
Tropheryma whipplei
 75% of affected individuals develop an
oligo- or polyarthritis.
 Joint manifestations usually precede
other symptoms of the disease by 5
years or more
 Large and small peripheral joints and
sacroiliac joints may be involved.
 abrupt in onset, migratory, usually lasts
hours to a few days

 systemic disease
 PCR amplification
 penicillin (or ceftriaxone) and Streptomycin for
2 weeks
followed by
 trimethoprim-sulfamethoxazole for 1–2 years

SPONDYLOARTHOPATHIES
A summary
 Absence of rheumatoid factor
 Involvement of sacroiliac and spinal joints
 Peripheral arthritis (predominantly lower limb)
 Enthesopathy
 Familial clustering
 Increased incidence of HLA-B27
 Common spectrum of extra-articular features
(predominantly muco-cultaneous)
 Anti TNF agents are the latest revolution !

Spondyloarthropaties

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