Sushil Paudel, MS Orthopaedics (AIIMS) TUTH

Types of arthritis

Symptoms of arthritis

Signs of arthritis

Treatment of arthritis

Rheumatoid arthritis (RA) Osteoarthritis (OA)

Sero-negative arthritis Ankylosing spondylitis Psoriatic arthritis Reactive arthritis Enteropathic arthritis

Crystal arthropathies

stands for : A: ALIGNMENT B: BONY MINERALIZATION C: CARTILAGE SPACE D: DISTRIBUTION S: SOFT TISSUE

Normal joint structure

NORMAL SUBCHONDRAL BONE DESTRUCTION

A chronic joint disorder in which there is progressive softening and disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes) and capsular fibrosis

Primary or idiopathic

Secondary Infection Dysplasia Perthes SCFE Trauma AVN

Genetic

Metabolic

Hormonal

Mechanical

Ageing

Disparity between:-

stress applied to articular cartilage and strength of articular cartilage

Increased stress (F/A)

Increased load eg BW or activityDecreased area eg varus knee or dysplastic hip

Weak cartilage

age stiff eg ochronosis soft eg inflammation abnormal bony support eg AVN

Joint space narrowingOsteophytosis Subchondral cysts Subchondral sclerosis

Femoral neck buttressing Tilt deformity ( flattening of head surface

with osteophyte at anteroinferior aspect) Superior >medial migration Secondary OA due to previous trauma or

inflammatory arthritis

Erect weight-bearing AP film Unicompartmental Sharpening of tibial prominence Loose bodies Varus deformity Patellar tooth sign – irregular anterior patellar

surface

OA Affecting Foot

Vacuum Phenomenon Accumulation of Nitrogen Degenarative etiology Better seen in Extension Excludes infective etiology In peripheral joints physiological

SPGR

T1W

SPGR

T2 FATSAT

pain swelling stiffness deformity instability loss of function

Analgesia Oral viscosupplements Intrarticular steroids Intrarticular viscosupplements Altered activity Walking aids Physiotherapy

arthroscopy osteotomy arthrodesis excision arthroplasty replacement arthroplasty

Bilateral symmetry Periarticular soft tissue swelling Uniform joint space loss Marginal erosions Juxta-articular osteoporosis Joint deformity

Inflammation◦ Swollen◦ Stiff◦ Sore◦ Warm

Fatigue Potentially

Reversible

RA

Boutonniere deformity : flexion deformity at PIP jt &

hyperextension at DIP

• Swan neck deformity : combination of flexion at DIP and extension at PIP

B/L KNEE ANKYLOSIS

RA

RA-foot deformity

Atlantodental interspace > 3.0mm Odontoid erosions Subluxation Pseudo basilar invagination Reduced disc space Apophyseal joint: erosion, sclerosis,

ankylosis Sharpened pencil spinous process

ADI > 3.0mm

Soft tissue swellingRotator cuff ruptureHead erosionsTapered distal clavicle due to erosions

Irregular coracoid process

Enlarged Olecranon bursa Fat pad sign Supinator notch sign: erosion at proximal ulna

RA-ELBOW

Uniform bicompartmental joint space loss

Patellofemoral joint also involved

Soft tissue swellingBaker’s cystSubchondral cysts

T1W

T1GRE

◦ Rheumatoid arthritis is a synovial disease

-Osteoarthritis is a disease of the cartilage. -Volar subluxation never in osteoarthritis

Normal joint

Unicompartmental Bicompartmental

Most of the disability in RA is a result of the INITIAL burden of disease

People get disabled because of:◦ Inadequate control◦ Lack of response◦ Compliance

GOAL: control the disease early on!

NSAIDSSteroids

Oral Intra-articularDMARDS

Synthetic Methotrexate Hydroxychloroquine Leflunomide Sulfasalazine

Monoclonal Antibodies to TNF◦ Infliximab ◦ Adalimumab

Soluble Receptor Decoy for TNF◦ Etanercept

Receptor Antagonist to IL-1◦ Anakinra

Monoclonal Antibody to CD-20◦ Rituximab

Cyclo-oxygenase inhibitors

Do not slow the progression of the disease

Provide partial relief of pain and stiffness

Disease Modifying Anti-Rheumatic Drugs

Reduce swelling & inflammation Improve pain Improve function Have been shown to reduce radiographic

progression (erosions)

Dihydrofolate reductase inhibitor

↓ thymidine & purine nucleotide synthesis

“Gold standard” for DMARD therapy

7.5 – 30 mg weekly

Absorption variable Elimination mainly renal

Hepatotoxicity Bone marrow suppression Dyspepsia, oral ulcers Pneumonitis Teratogenicity

Folic acid reduces GI & BM effects Monitoring

◦ FBC, ALT, Creatinine

Sulphapyridine + 5-aminosalicylic acid

Remove toxic free radicals

Remission in 3-6 month

Elimination hepatic

Dyspepsia, rashes, BM suppression

Mechanism unknown◦ Interference with antigen processing ?◦ Anti- inflammatory and immunomodulatory

• For mild disease

Side effects

Irreversible Retinal toxicity, corneal deposits

Ophthalmologic evaluation every 6 months

Competitive inhibitor of dihydroorotate dehydrogenase (rate-limiting enzyme in de novo synthesis of pyrimidines)

Reduce lymphocyte proliferation

Oral T ½ - 4 – 28 days due to EHC Elimination hepatic

Action in one month Avoid pregnancy for 2 years

Hepatotoxicity

BM suppression

Diarrhoea

rashes

Triple Therapy◦ Methotrexate, Sulfasalazine, Hydroxychloroquine

Double Therapy◦ Methotrexate & Leflunomide◦ Methotrexate & Sulfasalazine◦ Methotrexate & Hydroxychloroquine

• Complex protein molecules

• Created using molecular biology methods

• Produced in prokaryotic or eukaryotic cell cultures

TNF is a potent inflammatory cytokine

TNF is produced mainly by macrophages and monocytes

TNF is a major contributor to the inflammatory and destructive changes that occur in RA

Blockade of TNF results in a reduction in a number of other pro-inflammatory cytokines (IL-1, IL-6, & IL-8)

Trans-Membrane Bound TNF

Soluble TNF

Strategies for Reducing Effects of TNF

Macrophage

Monoclonal Antibody (Infliximab & Adalimumab)

Infection◦Common (Bacterial)◦Opportunistic (Tb)

Demyelinating DisordersMalignancyWorsening CHF

Potent anti-inflammatory drugs Serious adverse effects with long-term use To control the diaseas Indications

◦ As a bridge to effective DMARD therapy

◦ Systemic complications (e.g. vasculitis)

Most common childhood chronic disease causing disability.

About 7/100,00 newly diagnosed children with JIA per year.

Prevalence about 1/1,000 children = 1,000 children in BC with JIA.

7 subtypes.

Disease begins at any time during childhood or adolescence.

To be considered JIA, onset must occur before 16 years of age.

JIA is heterogeneous: the presentation of the disease and its natural history vary among individuals and over time.

The disease is typically classified into categories based on the symptoms displayed and their severity. Systemic arthritis Oligoarthritis Rheumatoid-factor positive (RF+) polyarthritis Rheumatoid-factor negative (RF-) polyarthritis Enthesitis-related arthritis Psoriatic arthritis Undifferentiated

G.ahrq.gov/dmardsjia.cfm.

Child under 16 years old

At least one joint with objective signs of arthritis:

› Swelling, or two of the following: pain with movement, warmth of the joint, restricted movement, or tenderness

Duration of more than 6 weeks

Other causes have been excluded (ex. Infections, Lupus and other connective tissue diseases, malignancies)

All kids with JIA have fevers.

All kids with JIA have rashes.

A child with joint pain (but no arthritis) must have JIA.

All arthritis is painful.

If a child has a positive rheumatoid factor, they must have arthritis.

If x-rays are normal, there is no arthritis.

Heterogeneous group of diseases characterized by chronic inflammatory processes involving the synovial

membrane, cartilage, and bone

The classification of JIA subgroups based on clinical and laboratory characteristics including the number of affected joints and the presence of autoimmune markers

Th1 cell-mediated disorder, driven by a population of T cells producing inflammatory cytokines and chemokines

Joint pain, stiffness, and swelling: These are the most common symptoms of JRA, but many children do not recognize, or do not report, pain. Stiffness and swelling are likely to be more severe in the morning.

Loss of joint function: Pain, swelling, and stiffness may impair joint function and reduce range of motion. Some children are able to compensate in other ways and display little, if any, disability. Severe limitations in motion lead to weakness and decreased physical function and sometimes to invalidization.

Limp: A limp may indicate a particularly severe case of JRA, although it also may be due to other problems that have nothing to do with arthritis, such as an injury. In JRA, a limp often signals knee involvement.

Eye irritation, pain, and redness: These symptoms are signs of eye inflammation. The eyes may be sensitive to light. In many cases, however, eye inflammation has no symptoms. If the inflammation is very severe and not reversed, it can cause loss of vision. The most common types of eye inflammation in JRA are uveitis and iritis. The names refer to the part of the eye that is inflamed.

Recurrent fevers: Fever is high and comes and goes with no apparent cause. Fever may “spike” (go high) as often as several times in one day.

Rash: A light rash may come and go without explanation.

Myalgia (muscle aches): This is similar to that achy feeling that comes with the flu. It usually affects muscles throughout the whole body, not just one part.

Lymph node swelling. Swollen lymph nodes are noticed most often in the neck and under the jaw, above the clavicle, in the armpits, or in the inguinal region.

Weight loss. This is common in children with JRA. It may be due to the child’s simply not feeling like eating.

Growth problems: Children with JRA often grow more slowly than average. Growth may be unusually fast or slow in an affected joint, causing one arm or leg to be longer than the other. General growth abnormalities may be related to having a chronic inflammatory condition such as JRA or to the treatment, especially glucocorticoids

ANA (antinuclear antibody) RF (Rheumatoid factor ) CRP (C-reactive protein) ESR (erythrocyte sedimentation

rate) CCP (Cyclic Citrullinated Peptide

Antibody) test

The goals: eliminate active disease, normalize joint function, preserve normal growth, prevent long-term joint damage, and prevent patient disability

The American College of Rheumatology Pediatric 30 criteria (ACR Pedi 30) defines improvement as involving at least 3 of 6 core set variables, with no more than 1 of the remaining variables worsening by > 30%.

The 6 core set includes ◦ Physician global assessment

◦ active joint count

◦ number of joints with limited range of motion

◦ Inflammatory markers

◦ patient or parent assessments

Medications

Doses (mg/kg)

Side effects

Aspirin 50-120 Stomack pain, vomiting, gastrointestinal bleedings, headache, blood in the urine, fluid retention, thinning and scarring of the skin (especially with naproxen), stomach ulcer (aspirin).

Ibuprofen 10-30

Tolmentin 10-15

Naproxen 5-20

Medications Doses (mg/kg)

Side effects

Hydroxychlo-roquine (Plaquenil)

5-7 Upset stomach, skin rash and a eye damage. A child who takes this drug should have his/her eyes examined at least every six months by an ophthalmologist

Sulfasalazine (Azulfadine)

Medications Doses(weekly, depending from body weight )

Side effects

Auranofin, Ridaura, Myochrysine Solganol

20 kg – 10 mg

30 kg – 20 mg

40 kg – 30 mg

50 kg – 40 mg

> 50 kg – 50 mg

Skin rash, mouth sores, kidney problems, a low blood count or anemia

Medications Doses Side effects

Methotrexate (Rbeumatrex)

Azathioprine (Imuran)

Cyclophosphamide (Cytoxan)

Typically 7.5 to 25 mg a week

Loss of appetite, nausea or vomiting, skin rash, unusual bleeding or bruising, tiredness or weakness, sterility.

Biologic Agents, which blocks the protein TNF

Etanercept (Enbrel) Infliximab (Remicade) Glucocorticoid Drugs

(Dexamethasone, Methylprednisolone, Cortef, Prednisolone and Prednisone)

Analgesics (acetaminophen [Tylenol, Panadol], tramadol [Ultram])

Therapeutic exercises Sports and Recreational Activities Splints

Morning Stiffness Relief Diet Eye Care Dental Care Surgery

.

Identify diagnostic criteria for gout

Identify 3 treatment goals for gout

Name the agents used to treat the acute flares of gout and the chronic disease of gout

Prevalence increasing May be signal for

unrecognized comorbidities : ( Not to point of searching)

Obesity (Duh!)Metabolic syndromeDMHTNCV diseaseRenal disease

ORGAN MEATS WILD GAME SEAFOOD LENTILS PEAS ASPARAGUS YEAST BEER

Rich foods have a higher concentration of protein. This could cause major problems for a person afflicted with gout.

Urate: end product of purine metabolism

Hyperuricemia: serum urate > urate solubility (> 6.8 mg/dl)

Gout: deposition of monosodium urate crystals in tissues

Hyperuricemia caused byOverproductionUnderexcretion

No Gout w/o crystal deposition

Urate Oevrproduction Underexcretion

Hyperuricemia

________________________________________

Silent Gout Renal Associated Tissue manifestations CV events & Deposition mortality

Purines are not properly processed in our body

Excreted through kidneys and urine

Hyperuricemia- build-up of uric acid in body and joint fluid

Asymptomatic hyperuricemia

Acute Flares of crystallization

Intervals between flares

Advanced Gout & Complications

Abrupt onset of severe joint inflammation, often nocturnal;Warmth, swelling, erythema, & pain;Possibly fever

Untreated? Resolves in 3-10 days 90% 1st attacks are monoarticular 50% are podagra

90% of gout patients eventually have podagra : 1st MTP joint

Can occur in other joints, bursa & tendons

Asymptomatic

If untreated, may advance

Intervals may shorten Crystals in asx joints Body urate stores increase

Chronic Arthritis

X-ray Changes

Tophi Develop

Acute Flares continue

Chronic Arthritis Polyarticular

acute flares with upper extremities more involved

Solid urate deposits in tissues

Irregular & destructive

Long duration of hyperuricemia

Higher serum urate

Long periods of active, untreated gout

Hx & P.E.

Synovial fluid analysis

Not Serum Urate

Not reliable

May be normal with flares

May be high with joint Sx from other causes

Male Postmenopausal

female Older Hypertension Pharmaceuticals:

Diuretics, ASA, cyclosporine

Transplant Alcohol intake

Highest with beerNot increased with wine

High BMI (obesity) Diet high in meat & seafood

The Gold standard

Crystals intracellular during attacks

Needle & rod shapes

Strong negative birefringence

Acute Gout: septic arthritis, pseudogout, Reactive arthritis, acute rheumatic fever and other crystalline arthropathies.

Chronic tophaceus gout: Rheumatoid Arthritis, Pseudogout, seronegative spondyloarthropathies and erosive osteoarthritis.

Similar Acute attacks

Different crystals under Micro;Rhomboid, irregular in CPPD

Both have polyarticular, symmetric arthritis

Tophi can be mistaken for RA nodules

Diet is usually impractical, ineffective and rarely adhered to in clinical practice.

Indications for pharmacological therapy includes: inability to reverse secondary causes, tophaceus gout, recurrent acute gout and nephrolithiasis.

139

•Treat acute flare rapidly with anti-inflammatory agent

•Initiate urate-lowering therapy to achieve sUA <6•Use concomitant anti-inflammatory prophylaxis for up to 6 mo to prevent mobilization flares

INITIATE(acute flare)

RESOLVE(urate-lowering therapy)

139

•Continue urate lowering therapy to control flares and avoid crystal deposition•Prophylaxis use for at least 3-6 months until sUA normalizes

MAINTAIN(treatment to control sUA)

Rapidly end acute flaresProtect against future flaresReduce chance of crystal inflammation

Prevent disease progressionLower serum urate to deplete total body urate poolCorrect metabolic cause

Control inflammation & pain & resolve the flare

Not a cure Crystals remain in joints Don’t try to lower serum urate during a flare Choice of med not as critical as alacrity &

duration

NSAIDS

Colchicine

Corticosteroids

Colchicine- reduces pain, swelling, and inflammation; pain subsides within 12 hrs and relief occurs after 48 hrs

Prevent migration of neutrophils to joints

Side effects

Nausea Vomiting Diarrhea Rahes

Colchicine :Not as effective “late” in flareDrug interaction : Statins, Macrolides, CyclosporineContraindicated in dialysis pt.sCautious use in : renal or liver dysfunction; active infection, age > 70

The choice of pharmacologic agent depends on severity of the attack◦ Monotherapy for mild/moderate attack◦ Combination therapy for severe attack or those

refractory to monotherapy Acceptable combination therapy approaches include

◦ Colchicine and NSAIDS◦ Oral steroids and colchicine◦ Intra-articular steroids with all other modalities

Continue current therapy during flare Patient education on signs of flare for self treatment

146Kanna D, et al. Arthritis Care Res (Hoboken). 2012 Oct;64(10):1447-61

Rapidly end acute flaresProtect against future flaresReduce chance of crystal inflammation

Prevent disease progressionLower serum urate to deplete total body urate poolCorrect metabolic cause

Hyperuricemia ≠ Gout Goal sUA < 6 Use prophylaxis for at least 3 months after

initiating gout therapy Do not stop gout medication unless patient

is showing evidence of drug toxicity or adverse reaction

Ask your friendly rheumatologist for help!

148

Colchicine : 0.5-1.0 mg/day Low-dose NSAIDS

Both decrease freq & severity of flares Prevent flares with start of urate-lowering RX

Best with 6 mos of concommitant RX

Won’t stop destructive aspects of gout

Rapidly end acute flaresProtect against future flaresReduce chance of crystal inflammation

Prevent disease progressionLower serum urate to deplete total body urate poolCorrect metabolic cause

Lower urate to < 6 mg/dl : DepletesTotal body urate poolDeposited crystals

RX is lifelong & continuous MED choices :

Uricosuric agentsXanthine oxidase inhibitor

Probenecid, (Losartan & fenofibrate for mild disease)

Increased secretion of urate into urine

Reverses most common physiologic abnormality in gout ( 90% pt.s are underexcretors)

Patients taking uricosuric agents are at risk for urolithiasis. This can be decreased by ensuring high urinary output and by adding sodium bicarbonate 1 gram TID.

The available agents include: probenecid (1-2 g/day) and sulfinpyrazone (50-400 mg BID).

Dose should be increased to decrease uric acid < 6.0 mg/ml

Allopurinol : Blocks conversion of hypoxanthine to uric

acid Effective in overproducers May be effective in underexcretors Can work in pt.s with renal insufficiency

158

hypoxanthine

urate xanthineXO XO

XO=xanthine oxidase

Allopurinol and febuxostat inhibit xanthine oxidase and block uric acid formation

Markel A. IMAJ, 2005.158

Oxypurinol, allopurinol metabolite, cleared by kidney and accumulates in patients with renal failure

Oxypurinol inhibits xanthine oxidase Increased oxypurinol related to risk of allopurinol

hypersensitivity syndrome

allopurinol oxypurinol

Xanthine Oxidase

Stevens-Johnson Syndrome

Allopurinol Hypersensitivity Syndrome

Toxic Epidermal Necrolysis

159

Allopurinol decreases uric acid in overproducers and underexcreters; it is also indicated in patients with a history of urolithiasis, tophaceus gout, renal insufficiency and in prophylaxis of tumor lysis syndrome.

Allopurinol: usual dose is 300 mg/day. Maximal recommended dose is 800 mg/day.

In renal insufficiency dose should be decreased to 200 mg/day for creatinine clearance < 60ml/min and to 100 mg/day if clearance < 30 ml/min).

Start with small doses of allopurinol to reduce the risk of precipitating an acute gout attack.

Most common side effects are rash (2% of patients) but rarely patients can develop exfoliative dermatitis that can be lethal.

Chronic use of colchicine (0.6-1.2 mg/day) is used as prophylaxis for acute attacks.

2% of all allopurinol users develop cutaneous rash

Frequency of hypersensitivity 1 in 260 DRESS syndrome

◦ Drug Reaction, Eosinophilia, Systemic Symptoms

20% mortality rate Life threatening toxicity: vasculitis, rash,

eosinophilia, hepatitis, progressive renal failure Treatment: early recognition, withdrawal of drug,

supportive care◦ Steroids, N-acetyl-cysteine, dialysis prnMarkel A. IMAJ, 2005.

Terkeltaub RA, in Primer on the Rheumatic Disease, 13th ed. 2008. 16

3

Base choice on above considerations & whether pt is an overproducer or underexcretor : Need to get a 24-hr. urine for urate excretion:

< 700 --- underexcretor (uricosuric)

> 700 --- overproducer (allopurinol/ febuxostat)

Allopurinol UricosuricIssue in renal disease X XDrug interactions X XPotentially fatal hypersen- sitivity syndrome XRisk of nephrolithiasis XMutiple daily dosing X

RX gaps : Can’t always get urate < 6 Allergies Drug interactions Allopurinol intolerance Worse Renal disease

Non-purine selective inhibitor of xanthine oxidase Lowers serum uric acid levels more potently than allopurinol while having

minimal effects on other enzymes associated with purine and pyrimide metabolism

Frequent adverse events reported in clinical trials liver function abnormalities, nausea, arthralgias, and rash

Available as 40- and 80-mg tablets Recommended starting dosage is 40 mg orally once daily. If serum uric acid

concentrations are not less than 6 mg/dL after two weeks, the dosage can be increased to 80 mg orally once daily

Dosage adjustments are not needed in elderly patients or patients with mild or moderate renal or hepatic impairment.

.

Therapeutic goal of urate-lowering therapy is sUA <6.0 mg/dL

Urate lowering therapy indications:◦ Recurrent gout attacks◦ Tophi and/or radiographic changes on initial

presentation Address associated risk factors and

comorbidities – tailor to the individual

168

Zhang W, et al. Ann Rheum Dis. 2006; 65: 1312-1324.168

Lifestyle Modification for all patients with gout

Xanthine Oxidase Inhibitor (XOI) first-line urate-lowering pharmacologic therapy

Target sUA <6 at minimum, sUA <5 better

Starting dose of allopurinol should be 100mg, less in CKD with titration above 300mg prn if needed (even in CKD)

Continue prophylaxis for 3 (no tophi) – 6 months (tophi) after achieving target sUA

169Khanna D, et al. Arthritis Care Res . 2012 Oct;64(10):1431-46

Gout is chronic with 4 stages Uncontrolled gout can lead to severe

disease Separate RX for flares & preventing

advancement Many meds for flares Treating the disease requires lowering

urate Get a 24-hr urine for urate excretion

Calcium pyrophosphate Crystal Deposition Disease (CPPD) is the syndrome secondary to the calcium pyrophosphate in articular tissues.

This includes: Chondrocalcinosis, Chronic CPPD and Pseudogout.

Etiology: It is unknown, but can be secondary to changes in the cartilage matrix or secondary to elevated levels of calcium or inorganic pyrophosphate.

Pathology: CPPD crystals are found in the joint capsule and fibrocartilaginous structures. There is neutrophil infiltration and erosions.

Demographics: It is predominantly a disease of the elderly, peak age 65 to 75 years old. It has female predominance (F:M, 2-7:1).

Prevalence of chondrocalcinosis is 5 to 8% in the general population.

Disease Associations: hyperthyroidsm, hypocalciuria, hypercalcemia, hemochromatosis, hemosiderosis, hypophosphatasia, hypomagnesemia, hypothyroidsm, gout, neuropathic joints, amyloidosis, trauma and OA.

Clinical Manifestations Pseudogout: Usually presents with acute

self-limited attacks resembling acute gout. The knee is involved in 50% of the cases, followed by the wrist, shoulder, ankle, and elbow.

In 5% of patients gout can coexist with pseudogout.

The diagnosis is confirmed with the synovial fluid analysis and/or the presence of chondrocalcinosis in the radiographs.

Acute Pseudogout primarily affects men.

Chondrocalcinosis: Generally is an incidental finding in XRays.

Diagnostic Tests: Inflammatory cell count in the synovial fluid. Rhomboidal or rodlike intracellular crystals. Imaging studies reveal chondrocalcinosis usually in the knee, but can be seen in the radial joint, symphisis pubis and intervertebral discs.

Chronic CPPD: predominately affects women; it is a progressive, often symmetric, polyarthritis.

Usually affects the knees, wrists, 2nd and 3rd MCP’s, hips, spine, shoulders, elbows and ankles.

Chronic CPPD differs from pseudogout in its chronicity, involvement of the spine and MCP’s.

Differential Diagnosis: Includes septic arthritis, gout, inflammatory OA, Rheumatoid Arthritis, neuropathic arthritis and Hypertrofic Osteoarthropathy.

Therapy: It is similar to gout and includes intrarticular corticosteroids. Colchicine can be used in acute attacks and also in prophylaxis. There is no specific treatment for chronic CPPD. It is important to treat secondary causes and colchicine could be helpful.

HLA B-27EnthesitisSynovitisOsteitis

SpondyloarthropathiesAxial and Peripheral AMOR criteria (1990) ESSG criteria (1991)

Axial Spondyloarthritis ASAS classification 2009

Ankylosing spondylitisPrototype of axial spondylitidis Modified New York criteria 1984

Peripheral Spondyloarthritis ASAS classification 2010

Psoriatic arthritis From Moll & Wright 1973 to CASPAR criteria 2006

Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44Taylor et al. Arthritis & Rheum 2006;54:2665-73

Van der Heijde et al. Ann Rheum Dis 2011;70:905-8

ESSG: European Spondyloarthropathy Study GroupASAS: Assessment of Spondyloarthritis International SocietyCASPAR: Classification criteria for psoriatic arthritis

Infliximab (IFX) and Golimumab (GLM)indications

AS is a chronic, progressive immune-mediated inflammatory disorder that results in ankylosis of the vertebral column and sacroiliac joints1

The spine and sacroiliac joints are the common affected sites1

◦ Chronic spinal inflammation (spondylitis) can lead to fusion of vertebrae (ankylosis)1

1 Taurog JD. et al. Harrison‘s Principles of Internal Medicine, 13 th Ed. 1994: 1664-67.

Normal interspace 2-5mm

B/L symmetricLower two thirdRosary bead appearanceReactive sclerosisBony ankylosis osteoporosis

SACROILITIS

Romanus lesion(erosion) Squaring, Osteoporosis Shiny corner sign Marginal Syndesmophytes Bamboo spine Trolley-track sign Dagger sign

SPINE

• Mortality figures parallel RAMortality figures parallel RA6,7,86,7,8

““Rare”Rare”

““Not” a serious disease, functional Not” a serious disease, functional limitation is mildlimitation is mild

““Rarely shortens life”Rarely shortens life”

• Burden of disease significant in pain, sick leave, early retirementBurden of disease significant in pain, sick leave, early retirement3,4,53,4,5

• 0.1-0.9%0.1-0.9%1,21,2

11 Sieper J et al. Sieper J et al. Ann Rheum Dis. Ann Rheum Dis. 2002; 61 (suppl 3);iii8-18. 2002; 61 (suppl 3);iii8-18.2 2 Lawrence RC., Arthritis Rheum 1998; 41:778-99. Lawrence RC., Arthritis Rheum 1998; 41:778-99. 33 Zink A., et al., Zink A., et al., J RheumatolJ Rheumatol 2000; 27:613-22. 2000; 27:613-22.4 4 Boonen A. Boonen A. Clin Exp RheumatolClin Exp Rheumatol. 2002;20(suppl 28):S23-S26.. 2002;20(suppl 28):S23-S26.55 Gran JT, et al. Gran JT, et al. Br J RheumatolBr J Rheumatol. 1997;36:766-771.. 1997;36:766-771.

66 Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94. Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94. 77 Myllykangas-Luosujarvi R, et al. Myllykangas-Luosujarvi R, et al. Br J Rheumatol.Br J Rheumatol. 1998;37:688-690. 1998;37:688-690.

88 Khan MA, et al. Khan MA, et al. J Rheumatol.J Rheumatol. 1981;8:86-90. 1981;8:86-90.99 Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22. Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22.

The incidence of AS may be underestimated due to unreported cases1

HLA-B27 gene is associated with AS6

Age of onset typically between 15 and 35 years1,2,3

2-3 times more frequent in men than in women6

1The Spondylitis Association of America. Available at: www.spondylitis.org. Accessed December 2,2004. 61(suppl 3);iii8–18. 6Khan MA. Ann Intern Med. 2002;136:896–907.

Axial manifestations:• Chronic low back pain

• With or without buttock pain

• Inflammatory characteristics:

– Occurs at night (second part)

– Sleep disturbance

– Morning stiffness

• Limited lumbar motion

• Onset before age of 40 years

Sengupta R & Stone MA.

Inflammatory back pain (IBP) = Characteristic symptom

MRI sacro-iliac joint

AS: Characteristic Pathologic FeaturesAS: Characteristic Pathologic Features

Sieper J. Arthritis Res Ther 2009;11:208Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035

• Chronic inflammation in:

– Axial structures (sacroiliac joint, spine, anterior chest wall, shoulder and hip)

– Possibly large peripheral joints, mainly at the lower limbs (oligoarthritis)

– Entheses (enthesitis)

• Bone formation particularly in the axial joints

Most striking feature of AS = New bone formation in the spine with:

Spinal syndesmophytes

Ankylosis

Both can be seen on conventional radiography

Bamboo spine and bilateral sacroiliitis

X-ray showing syndesmophytes

Even in patients with longer-standing disease, syndesmophytes are present in ～ 50% patients and a smaller percentage will develop ankylosis

Sieper J. Arthritis Res Ther 2009;11:208

Marginal erosions and new bone formation

Unilateral sacroiliitis

Peripheral manifestations

Enthesitis Peripheral arthritis Dactylitis

1Cruyssen BV et al. Ann Rheum Dis 2007;66:1072-10772Sidiropoulos PI et al. Rheumatology 2008;47:355-361

2

The first abnormality to appear in swollen joints associated with spondyloarthropathies is an

enthesitis2

Likelihood of erosions is higher for digits with dactylitis than

those without1

1Brockbank. Ann Rheum Dis 2005;62:188-90; 2McGonagle et al. The Lancet 1998;352.

EAM Prevalence in AS Patients (%)

Anterior uveitis 30-50

IBD 5-10

Subclinical inflammation of the gut 25-49

Cardiac abnormalitiesConduction disturbancesAortic insufficiency

1-33 1-10

Psoriasis 10-20

Renal abnormalities 10-35

Lung abnormalitiesAirways diseaseInterstitial abnormalitiesEmphysema

40-88 82

47-65 9-35

Bone abnormalitiesOsteoporosisOsteopenia

11-18 39-59

Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035

Terminal ileitis

Anterior uveitis

Cardiac abnormalities

Bad QoL1

◦ Pain◦ Sleep problems◦ Fatigue◦ Loss of mobility and

dependency◦ Loss of social life

Effect employability1

Higher rate of mortality2

High socio-economic consequences

AS=23.7 years

90.283.1

62.454.1

0

20

40

60

80

100

Stiffness Pain Fatigue PoorSleepN=175

AS mean duration: 23.7 yr

Per

cen

tag

e o

f P

atie

nts

(%

)

1

Adapted from Feldtkeller E et al. Rheumatol Int 2003;23:61–66Sengupta R & Stone MA. Nat Clin Pract Rheumatol 2007;3:496-503

First symptoms

First diagnosis

Age in years

Males (n=920)Females (n=476)

00 10 20 30 40 50 60 70

20

40

80

60

100P

erce

nta

ge

of

Pat

ien

ts (

%)

Average delay in diagnosis: 8.8 years B27(+) 8.5 vs B27(-) 11.4

Delay Worse clinical outcomes contributing to both physical and work-related disability

Modified New York Criteria for AS1

◦ Low back pain > 3 months (improved by exercise and not relieved by rest)

◦ Limitation of lumbar spinal motion in sagittal and frontal planes◦ Chest expansion decreased relative to normal◦ Bilateral sacroilitis grade 2-4 or unilateral sacroilitis grade 3 or 4

Detection of sacroilitis via X-ray or MRI1

◦ MRI can be used for earlier detection of inflammation (enthesitis) at other sites.

There is no specific laboratory test for AS1

◦ ESR and CRP can indicate inflammation 50-70% of active AS patients will have increased ESR and CRP2

◦ Rheumatoid factor is not associated with AS◦ HLA-B27

1Khan M, Ankylosing Spondylitis-the facts; 2002:Oxford University Press:94-98.2Sieper J, et al. Ann Rheum Dis. 2002;61(Suppl 8).

Diagnostic Standard for AS: Modified NY Diagnostic Standard for AS: Modified NY Classification Criteria (1984)Classification Criteria (1984)11

• Clinical components:

– Low back pain and stiffness for more than 3 months which improves with exercise, but is not relieved by rest

– Limitation of motion of the lumbar spine in both the sagittal and frontal planes

– Limitation of chest expansion relative to normal values correlated for age and sex

• Radiological component:

– Sacroiliitis Grade >2 bilaterally or Grade 3-4 unilaterally

Definite AS if the radiological criterion is associated with at least one clinical criterion2

Probable AS if three clinical criteria present or radiologic criteria present without clinical criteria2

1Linden VD et al. Arthritis Rheum 1984;27:361-3682Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008

• Old criteria

• Defined before TNF blockers

• Sacroiliitis detectable by X-ray occurs lately

• No magnetic resonance imaging (MRI)

• Used for clinical trial

Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008Brandt HC et al. Ann Rheum Dis 2007;66:1479-84

Time (years)

Back PainSyndesmophytes

Radiographic stage

(Ankylosing Spondylitis)

Back PainRadiographic

sacroiliitis

Modified NY criteria (1984)

Diagnostic Standard for AS: Modified NY Diagnostic Standard for AS: Modified NY Classification Criteria (1984) (Cont’d)Classification Criteria (1984) (Cont’d)

The greatest problem in the management of AS was the lack of effective treatments. In recent years, NSAIDs and TNF-blockers have been shown to have good efficacy in the treatment of AS.

Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008

Time (years)

Back PainIBP

MRI active sacroiliitis

Back PainSyndesmophytes

Radiographic stage(Ankylosing Spondylitis)

Pre-radiographic stage(Axial undifferentiated SpA)

Back PainRadiographic

sacroiliitis

Modified NY criteria (1984)

Diagnostic Standard for AS: Modified NY Diagnostic Standard for AS: Modified NY Classification Criteria (1984) (Cont’d)Classification Criteria (1984) (Cont’d)

• Recent application of MRI techniques has demonstrated (and confirmed) that ongoing active (“acute”) inflammation in fact does occur in the sacroiliac joints and/or spine prior to the appearance of changes detectable radiographically

• The presence and absence of radiographic sacroiliitis in patients with SpA represent different stages of a single disease continuum

In patients with back pain ≥3 months and age at onset <45 years

Sacroiliitis* on imaging

plus

≥1SpA feature**

HLA-B27

plus

≥2 other SpA features****SpA features:•Inflammatory back pain•Arthritis•Enthesitis (heel)•Uveitis•Dactylitis•Psoriasis•Crohn’s disease/ulcerative colitis•Good response to NSAIDs•Family history for SpA•HLA-B27•Elevated CRP

*Sacroiliitis on imaging:

•Active (acute) inflammation on MRI highly suggestive of sacroiliitis associated with SpA

or

•Definite radiographic sacroiliitis according to modified New York criteria

Rudwaleit M et al. Ann Rheum Dis 2009;68(6):770-6

OR

Patients will be categorized as an ASAS 20 responder if the patient achieves the following:◦ >20% improvement from baseline and absolute baseline

improvement of >10 (on a 0-100mm scale) in at least 3 of the following 4 domains: Patient global assessment Spinal pain Function (BASFI) Inflammation

Average of the last 2 BASDAI questions concerning level and duration of morning stiffness

◦ No deterioration from baseline (>20% and absolute change of at least 10 on a 0-100 mm scale) in the potential remaining domain

Anderson JJ, et al. Arthritis Rheum. 2001;44(8):1876–1886.

Chronic progressive, inflammatory disorder of the joints and skin1

◦ Characterized by osteolysis and bony proliferation1

◦ Clinical manifestations include dactylitis, enthesitis, osteoperiostitis, large joint oligoarthritis, arthritis mutilans, sacroiliitis, spondylitis, and distal interphalangeal arthritis1

PsA is one of a group of disorders known as the spondyloarthropathies2

Males and females are equally affected3

PsA can range from mild nondestructive disease to a severely rapid and destructive arthropathy3

◦ Usually Rheumatoid Factor negative3

Radiographic damage can be noted in up to 47% of patients at a median interval of two years despite clinical improvement with standard DMARD therapy41Taylor WJ. Curr Opin Rheumatol. 2002;14:98–103.

2Mease P. Curr Opin Rheumatol. 2004;16:366–370.3Brockbank J, et al. Exp Opin Invest Drugs. 2000;9:1511–1522.

4Kane D, et al. Rheumatology. 2003;42:1460–1468.

Spondyloarthritis (SpA) The prevalence of SpA is comparable to that of RA (0.5–1.9%)1,2

Psoriasis (Pso) Psoriasis affects 2% of population 7% to 42% of patients with Pso will develop arthritis3

Psoriatic Arthritis A chronic and inflammatory arthritis in association with skin psoriasis4

Usually rheumatoid factor (RF) negative and ACPA negative5

◦ Distinct from RA Psoriatic Arthritis is classified as one of the subtypes of

spondyloarthropathies◦ Characterized by synovitis, enthesitis, dactylitis, spondylitis, skin and nail

psoriasis4

1Rudwaleit M et al. Ann Rheum Dis 2004;63:535-543; 2Braun J et al. Scand J Rheumatol 2005;34:178-90;3 Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009;

4Mease et al. Ann Rheum Dis 2011;70(Suppl 1):i77–i84. doi:10.1136/ard.2010.140582;5Pasquetti et al. Rheumatology 2009;48:315–325

Juvenile SpA

Reactivearthritis

Arthritis associated with

IBD

PsA

UndifferentiatedSpA (uSpA)

Ankylosingspondylitis (AS)

RA: Rheumatoid arthritis

Affects men & women equally Occurs in 4-6% up to 30% of patients with

known psoriasis◦ 60 – 70%: Skin psoriasis first◦ 15%: Psoriatic arthritis first◦ 15%: Skin and arthritis diagnosed at same time

Prevalence of psoriasis in the general population: 0.1-2.8%.

Prevalence of psoriasis in arthritis patients: 2.6-7.0%.

Prevalence of arthritis in the general population: 2-3%.

Prevalence of arthritis in psoriatic patients: 6-42%.

Epidemiological Evidence

Morning stiffness lasting >30 min in 50% of patients1

Ridging, pitting of nails, onycholysis – up 90% of patients vs nail changes in only 40% of psoriasis cases2,3

Patients may present with less joint tenderness than is usually seen in RA1

Dactylitis may be noted in >40% of patients2,4

Eye inflammation (conjunctivitis, iritis, or uveitis) — 7–33% of cases; uveitis shows a greater tendency to be bilateral and chronic when compared to AS2

Distal extremity swelling with pitting edema has been reported in 20% of patients as the first isolated manifestation of PsA5

1Gladman DD. In: Up To Date. Available at: www.uptodate.com. Accessed December 3, 2004. 2Taurog JD. In: Harrison's Online McGrawHill. Available at: http://www3.accessmedicine.com/popup.aspx?

aID=94996&print=yes. Accessed January 2,2005.3Gladman DD. Rheum Dis Clin N Amer. 1998;24:829–844.

4Veale D, et al. Br J Rheumatol. 1994;33:133–38.5Cantini F, et al. Clin Exp Rheumatol. 2001;19:291–296.

Helliwell PS & Taylor WJ. Ann Rheum Dis 2005;64(2:ii)3-8Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009

*Low levels of RF and ACPA can be found in 5-16% of patients; **To a lesser degree than in RA ***Spinal disease occurs in 40-70% of PsA patients

1Gladman D et al. Arth & Rheum 2007;56:840; 2 Kane. D et al. Rheum 2003;42:1460-1468 3 Gladman D et al. Ann Rheum Dis 2005;64:188–190; 4Lawry M. Dermatol Ther

2007;20:60-675Jiaravuthisan MM et al. JAAD 2007;57:1-27; 6Yamamoto Eur J Dermatol 2011;21:660-6

Enthesopathy (38%)2

Dactyilitis (48%)3

DIP involvement (39%)2

Back involvement (50%)1

Nail psoriasis (80%)4, 5

Skin

Invo

lvemen

t

In nearly 70% of patients, cutaneous lesions precede the onset of joint pain, in 20% arthropathy starts before skin manifestations, and in 10% both are concurrent. 6

DIP: Distal interphalangeal

Pso patients6-8

• Psychosocial burden• Reactive depression • Higher suicidal ideation• Alcoholism

Metabolic Syndrome3-5

• Hyperlipidemia• Hypertension• Insulin resistent • Diabetes • Obesity Higher risk of Cardiovascular disease (CVD)

Ocular inflammation1

(Iritis/Uveitis/ Episcleritis)

IBD2

1Qieiro et al. Semin Arth Rheum 2002;31:264; 2Scarpa et al. J Rheum 2000;27:1241; 3Mallbris et al. Curr Rheum Rep 2006;8:355; 4Neimann et al. J Am Acad Derm 2006;55:829; 5Tam et al. 2008;47:718; 6Kimball et al. Am J Clin Dermatol 2005;6:383-392;

7Naldi et al. Br J Dermatol 1992;127:212-217; 8Mrowietz U et al. Arch Dermatol Res 2006;298(7):309-319

D a c ty lit is E n th e s it is

P so ria tic A rth rit is

Ritchlin C. J Rheumatol. 2006;33:1435–1438.Helliwell PS. J Rheumatol. 2006;33:1439–1441.

ACR Slide Collection on the Rheumatic Diseases; 3rd edition. 1994.1Brockbank J, et al. Ann Rheum Dis. 2005;64:188–190.

2Veale D, et al. Br J Rheumatol. 1994;33:133–38.

• Diffuse swelling of a digit may be acute, with painful inflammatory changes, or chronic wherein the digit remains swollen despite the disappearance of acute inflammation1

• Also referred to as “sausage digit”1

• Recognized as one of the cardinal features of PsA, occurring in up to 40% of patients1,2

• Feet most commonly affected1

• Dactylitis involved digits show more radiographic damage1

Entheses are the regions at which a tendon, ligament, or joint capsule attaches to bone1

Inflammation at the entheses is called enthesitis and is a hallmark feature of PsA1,2

Pathogenesis of enthesitis has yet to be fully elucidated2

Isolated peripheral enthesitis may be the only rheumatologic sign of PsA in a subset of patients3

1McGonagle D. Ann Rheum Dis. 2005;64(Suppl II):ii58–ii60.

2Anandarajah AP, et al. Curr Opin Rheumatol. 2004;16:338–343.3Salvarani C. J Rheumatol. 1997;24:1106–1140.

Achilles Tendon Insertion ErosionPlantar Spur

Achilles Tendon Spur

ACR Slide Collection on the Rheumatic Diseases; 3rd edition. 1994.Data on file, Centocor, Inc.

Oligoarthritis Distal Arthritis

Polyarticular Pattern

Arthritis Mutilans

Tuft resorption

Periostitis

Distal asymmetric distribution Ray pattern Soft tissue swelling( sausage/spindle) Preserved bone density Marginal erosions Fluffy periosteitis

Pencil in cup deformity Mouse ear sign Arthritis mutilans Nonmarginal syndesmophytes Bilateral asymmetric involvenent of SI joint

Including 5 clinical patterns:◦ Asymmetric mono-/oligoarthritis (~30% [range 12-70%])1-4

◦ Symmetric polyarthritis (~45% [range 15-65%])1-4

◦ Distal interphalangeal (DIP) joint involvement (~5%)1

◦ Axial (spondylitis and Sacroiliitis) (HLA-B27) (~5%)1,3

◦ Arthritis Mutilans (<5%)1,3

References see notes

• However patterns may change over time and are therefore not useful for

classification 5

HLA: Human leucocytes antigen

McHugh et al. Rheum 2003;42:778-783

Clinical subgroups at baseline and follow-up:

Monoarthritis Monoarthritis

Oligoarthritis Oligoarthritis

DIP DIP

Polyarthritis Polyarthritis

Spondyloarthritis Spondyloarthritis

Mutilans Mutilans

No clinical evidence ofjoint disease

Inflammatory articular disease (joint, spine, or entheseal)

With 3 points from following categories:− Psoriasis: current (2), history (1), family history (1) − Nail dystrophy (1)− Negative rheumatoid factor (1)− Dactylitis: current (1), history (1) recorded by a

rheumatologist− Radiographs: (hand/foot) evidence of juxta-articular

new bone formation Specificity 98.7%, Sensitivity 91.4%

Taylor et al. Arthritis & Rheum 2006;54: 2665-73

SpondyloarthropathiesAxial and Peripheral AMOR criteria (1990) ESSG criteria (1991)

Axial Spondyloarthritis ASAS classification 2009

Ankylosing spondylitisPrototype of axial spondylitidis Modified New York criteria 1984

Peripheral Spondyloarthritis ASAS classification 2010

Psoriatic arthritis From Moll & Wright 1973 to CASPAR criteria 2006

Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44Taylor et al. Arthritis & Rheum 2006;54:2665-73

Van der Heijde et al. Ann Rheum Dis 2011;70:905-8

ESSG: European Spondyloarthropathy Study GroupASAS: Assessment of Spondyloarthritis International SocietyCASPAR: Classification criteria for psoriatic arthritis

Infliximab (IFX) and Golimumab (GLM)indications

Rheumatoid Arthritis◦Symmetric◦PIP, MCP, not

distal◦Ulnar deviation,

swan neck deformities

◦Rheumatoid nodules

Ankylosing Spondylitis◦Strong HLA B27

association◦Male predominance◦Axial skeletal

involvement – sacroilitis

◦Bamboo spine◦Schober test

demonstrating limited flexion

Uptodate.com

Reactive Arthritis◦ LE arthritis◦ 1-4 weeks after an

infection◦ Infectious agents:

Shigella Salmonella Yersinia Campylobacter Chlamydia

◦ Triad: urethritis, conjunctivitis, arthritis

◦ Keratoderma Blennorhagicum

Inflammatory Bowel Disease Associated◦ Crohn’s◦ LE distribution

AAFP

Bare area erosions Terminal tuft erosions Ray pattern Irregular periosteal bone apposition Feet more severely affected than hands’ Severe bone destruction without regional osteoporosis Subluxations

1 – NSAIDS 2 – DMARDS

◦ MTX◦ Leflunomide◦ Sulfasalazine◦ Cyclosporine◦ TNF α inhibitor

Coordinate b/w Rheumatology and Dermatology

Psoriatic Arthritis Response Criteria (PsARC)Psoriatic Arthritis Response Criteria (PsARC)

Clegg D.O. et al. Arthritis Rheum 1996;39:2013.

Clinical assessment of joint improvement, no skin assessment

Improvement in at least 2 of 4 criteria, one of which must be tender or swollen-joint score◦ Physician global assessment (> 1 unit)◦ Patient global assessment (> 1 unit)◦ Tender-joint score (> 30%)◦ Swollen-joint score (> 30%)

No worsening in any criterion

Urethritis, conjunctivitis, arthritis Lower extremity Osteoporosis/soft tissue swelling Uniform joint space loss Marginal erosion/periosteitis Asymmetric broad based nonmarginal

syndesmophytes Bilateral asymmetric involvenent of SI

joint

Reiter’s Disease

Wave like hyperostosis Flowing ossification >4 contiguous vertebras Thoracic spine ossified anterior longitudinal ligament Normal SI joint Normal disc space

Calcification of cartilage, synovium, capsule, tendon or ligaments

More than one joint exclusive of the intervertebral disks.

Crystals aspirated from joints showing absent or weakly positive birefringence

Joint-space narrowing, sclerosis, cyst formation

Bony fragmentation, and osteophytosis

Cartilage calcification Degenarative Gout, Pseudogout Hemochromatosis Wilson disease ochronosis

Hypertrophic- weight bearing joints Disorganization Bone destruction Dislocation Debris Preserved bone density Atrophic- non weight bearing joints Amputated/lick candy stick

Syringomyelia Syphilis Diabetes Leprosy Alcoholism Multiple sclerosis Trauma

Neuropathic joint

Neuropathic

Disc calcification Vaccum phenomenon Osteophytes Ankylosis Osteoporosis Key is disc changes with advanced degenarative changes in unexpected locations

Childbearing female Hands affected predominantly Bilateral symmetry Osteoporosis Normal joint spaces calcification Ulnar drifting/deformities Hitch-hiker’s deformity Soft tissue atrophy

SLE

Recurrent attacks of rheumatic fever Deforning nonerosive peripheral

arthropathy Normal joint space Juxta articular osteoporosis Soft tissue swelling Ulnar drifting Flexion at MCP

Joint pain, swelling, and limitation of motion

3-5 th decade male Knee> hip Multiple intraarticular calcified nodules,

uniform in size Laminated to stippled appearance Promote early degenarative disease Chondrosarcoma in 5%

Synovial Osteochondromatosis

PD

PD

Benign proliferative disorder of the synovium

May affect the joints, bursae, or tendon sheaths

Preserved joint space No osteoporosis

PVNS

Haemophilic Arthropathy

Resorption of distal tuftRetraction of fingertips <20%Soft tissue calcificationDisuse osteoporosis Joints may be normal or erosive arthropathy

SCLERODERMA

Usually monoarticular Cartilage destruction Subchondral bone erosion Osteoporosis Effusion More aggressive course & bone destruction in pyogenic Bony ankylosis

Monoarticular involvement Soft-tissue swelling Joint effusions Periarticular osteopenia Marginal erosions. Joint space narrowing is unusual

TIW

T2W

POSTGAD

Bone erosion Marrow signal abnormalities Extra-articular extension Soft tissue abscess

Postgad

Chronic hemodialysis Plasma cell dyscrasia Bilateral Juxtaarticular soft-tissue masses Periarticular osteopenia Subchondral cysts Joint effusions, erosions Preserved joint spaces

Synovitis Acne Pustulosis Hyperostosis Osteitis Sternoclavicular joint>Flat bones Recurent osteomyelitis Hot on bone scan

Gout Neuropathic CPPD PVNS Synovial Chondronatosis Postel’s arthritis

JRAPsoriaticReiter’sHemophiliaHPA

Osteoarthritis Gout CPPD Psoriatic Anktlosing Spondylitis Neuropathic Reiter-chronic case

Rheumatoid arthritis JRA Infective Haemophilia Scleroderma SLE

CPPD GOUT Alkaptonuria Haemochromatosis Wilson Acromegaly

Acromegaly

Increased joint spaceIncreased joint space

DEGENRATIVE RA CPPD AVN

Ankylosing Spondylitis Psoriasis Inflammatory Bowel Disease

Primary OA Rheumatoid arthritis

DISTAL : Psoriasis Reiter’s syndrome Osteoarthritis

PROXIMAL : RA CPPD

OA RA CPPD Ankylosing spondylitis Pigmented villonodular synovotis Synovial osteochondromatosis

AS IBD PSORIASIS REITER’S SYNDROME OA INFECTION

Certain questions to be answered 1). It is a monoarticular / pauci/

polyarticular involvement 2). It is synovial or chondropathic 3).if polyarticular, specific distribution

and pattern 4). Sacroiliac and CVJ etc. 5). Clinical presentation (history)

Any monoarticular synovial jt. Involvement is assumed to be infective unless proved otherwise.

Any monoarticular chondropathic jt. is considered as degenerative.

Polyarticular jt. Involvement s/o inflammatory noninfective etiology.

Synovial arthropathy:

1). Periarticular osteopenia

2). Jt. Space effusion (soft tissue)

3). Erosions

4). Loss of jt. space (late feature)

D/D of synovial arthritis

Infection- >3month---tuberculous acute onset— pyogenic RA Seronegative spondyloarthritis GOUT

CHONDROPATHIC ARTHROPATHY:

Loss of jt. Space Sclerosis Osteophytes Subchondral cyst.

D/D of chondropathic arthritis

OA GOUT CPPD HEMOCHROMATOSIS.

If Polyarticular

Distribution Ass. Findings Chondrocalcinosis.

P S O R IA S ISR E ITE R 'SR A ; S L E

N E U R O P A TH IC

A L IG N M E N T

O AC P P DG O U T

P R E S E R V E D

S U B C H O N D R A L P yog en ic

G E N E R A L IZ E DC T d iso rd ers

J U X TA A R TIC U L A RR A

L O S T

B O N YM IN E R A L IS A TIO N

O A

C P P DH E M O C H R O .

C A R TIL A G ES P A C E L O S S

P IP

R AC P P D

D IP

O A ; R E ITE R 'SP S O R IA S IS

D IS TR IB U TIO N

IN C R E A S E D

P S O R IA S ISR E ITE R 'S

D E C R E A S E D

S C L E R O D E R M AD E R M A TO M Y O

G E N E R A L IS E D L O C A L IS E D

R AG O U T

S O F T TIS S U E

A R TH R ITIS

RAJRANFECTIVEHEMOPHILIASLE

RAJRAHEMOPHILIAINFECTIVESLE

ARTHRITS

Erosive Erosive+ Productive NO Erosion/

Productive Productive

RA Psoriasis OA SLE Gout Reiter, AS DISH

Dermatomyositis Erosive OA JRA, Neuropathic