SPONDYLOARTHROPATHY(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.

IntroductionAbsence 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 historyPsoriasisInflammatory bowel diseaseUrethritis, cervicitis, or acute diarrhea < 1 mo. before

arthritisButtock pain alternating between right and left gluteal areasEnthesitiesSacroiliitis

Sensitivity 78.4% and specificity 89.6%

RA SpA

• UE>LE

• Often polyarticular

• Sacroiliitis absent

• RF usually pos

• No HLA-B27 assoc

• Sicca, scleritis

• Nodules

• 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

Spondyloarthropathies

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.

Spondyloarthropathies 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

Nail Pitting

Onicholysis toe nails

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 spondylitisReiter’s syndrome/reactive arthritisIBD related arthritisPsoriatic arthritis

Normal AssociationsNative AmericansCaucasiansBlacks

Degree of associations>90%>80%

~75%~50%

13%8%4%

ANKYLOSING SPONDYLITIS

(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”

HistoPathologySubchondral 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 predominateforward 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

DiagnosisModified 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 mobilityPara spinal spasm

Spinal Involvement Tenderness – SI joints SI Compression Testing Modified Schober Test

Potentially useful diagnosticallyLimitation of motion

• Occiput to Wall distance

• Chest Expansion at the xiphisternumNormally > 5 cmMeasurement is age and sex

dependantUseful for following patients

over time

Spinal Involvement Finger Tip to Floor Distance

Measure fingertips to floor

Useful for following patients over time

Lateral FlexionAsk the patient to flex laterally and

mark at the maximal extent of the

fingertips

Useful for following patients over time

Cervical SpineCan 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 grading0-normal 1-possible2-minimal3-moderate4-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)

MRI – Early changes

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 anemiaReactive 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 replacementNeck osteotomy and head removed

piecemealAccurately identify acetabular marginsOver come flexion, stoopingMotionRelieve painRestore upright posturePrevent spinal osteotomy90 % 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

Thank you

SPONDYLOARTHROPATHY

(Seronegative arthritis)

II

Moderated by - Dr. K. S. SandhuPresented 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

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 historyPsoriasisInflammatory bowel diseaseUrethritis, cervicitis, or acute diarrhea < 1 mo. before

arthritisButtock pain alternating between right and left gluteal areasEnthesitiesSacroiliitis

Sensitivity 78.4% and specificity 89.6%

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

REACTIVE ARTHRITIS(Reiter’s syndrome)

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• p

roduce 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

oAcute sacroiliitis

oinsertional inflammation,

omuscle spasm

oarthritis 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.

Pustules KB

Keratoderma Blenorrhagicum

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

Laboratory investigations

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:

PSORIATIC 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 %

Arthritis of the DIP joints

Arthritis of the DIP joints

Asymmetric oligoarthritis

Asymmetric oligoarthritis

Symmetric polyarthritis

Axial involvement

Arthritis Mutilans

Arthritis Mutilans

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 lesionsPsoriatic 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

Dactylitis

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

Laboratory investigations

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 featuresSmall 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.

Radiology

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:

oHLA-B27 correlates with spondylitic involvement

oHLA-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

How to Tell the Difference

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

ENTEROPATHIC ARTHRITIS

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.

UNDIFFERENTIATED AND JUVENILE-ONSET

SPONDYLOARTHRITIS

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

SAPHO SYNDROME

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

WHIPPLE'S DISEASE

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

SPONDYLOARTHOPATHIESA 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 !