Inflammatory
Joint Arthritis
Rheumatoid Arthritis and Crystal Arthropathies
Roll no.- 111-125
Rheumatoid Arthritis: Introduction
DEFINITION
A chronic, systemic, inflammatory autoimmune disorder primarily
affecting synovial joints in a symmetrical pattern, leading to progressive
joint destruction, deformity and disability
PATHOPHYSIOLOGY
Antigen presenting cells process and present antigens to T cells,which may
stimulate B cells to produce antibodies and osteoclasts to destroy and remove
bone.
Macrophages stimulated by the immune response can stimulate osteoclasts
to promote inflammation.
They also can stimulate fibroblasts ,which produce matrixmetalloproteinase to
degrade the bone matrix and produce pro inflammatory cytokines.
Activated T cells and macrophages release factors that promote tissue
destruction,increase blood flow, and result in cellular invasion of synovial
tissue and joint fluid.
Major process involved in development of Rheumatoid Arthritis
Clinical Features: Articular
Morning stiffness
> 1 hour, eases with use
Symmetrical pattern
Both sides involved together
Small joints first
MCP, PIP, MTP — DIP spared
Clinical Features: Articular
JOINTS INVOLVED
● Hands: MCP and PIP (DIP characteristically spared)
● Feet: MTP joints — often the earliest site
● Wrists, knees, elbows, ankles, shoulders
● Cervical spine (atlantoaxial subluxation — risk of cord compression)
● TMJ and cricoarytenoid (hoarseness) less commonly
Clinical Features: Articular
CHARACTERISTIC DEFORMITIES
● Ulnar deviation of fingers at MCP joints
● Swan-neck deformity (PIP hyperextension + DIP flexion)
● Boutonnière deformity (PIP flexion + DIP hyperextension)
● Z-deformity of thumb
● Hammer toes, hallux valgus
● Trigger finger from tenosynovitis
Deformities involving the hands
Clinical Features: Extra-articular
EYES BLOOD NERVES
● Keratoconjunctivitis ● Anaemia of chronic ● Carpal tunnel
sicca (Sjögren's) disease syndrome
● Episcleritis, scleritis ● Felty's syndrome: RA ● Peripheral neuropathy
+ splenomegaly + ● Cervical myelopathy
neutropenia (atlantoaxial
subluxation)
Clinical Features: Extra-articular
SKIN LUNGS HEART
● Rheumatoid nodules ● Pleural effusion ● Pericarditis (most
in ~25% (most common) common cardiac)
● Subcutaneous, over ● Pulmonary fibrosis ● Myocarditis, valvular
pressure points ● Caplan's syndrome involvement
(elbows) (RA +
pneumoconiosis)
Investigations
Joint Imaging:
● X-Rays-
-Early - soft tissue swelling and periarticular demineralization.
-Later - include uniform loss of joint space (indicative of diffuse cartilage loss) and
bony erosions (initially along joint margins where intra-articular bone is not covered
by cartilage).
-Advanced - diffuse bony erosions, joint subluxation, and foreshortening of digits.
● Magnetic Resonance Imaging (MRI)
● Ultrasound
Fig.X-ray of feet depicting features of Fig.X-ray of elbow depicting features of
rheumatoid arthritis rheumatoid arthritis
Blood Tests:
Rheumatoid Factor (RF)-
• RF is a specific antibody in the blood.
• A negative RF does not rule out RA. The arthritis is then called seronegative, most
common during the first year of illness and converting to seropositive status over
time.
Anti-citrullinated Protein Antibodies (ACPAs)
• Like RF, this testing is only positive in a proportion of all RA cases.
• Unlike RF, this test is rarely found positive if RA is NOT present, giving it a
specificity of about 95%.
Antinuclear antibodies (ANAs)
Antineutrophil cytoplasmic antibodies (ANCAs)
Other blood tests performed when RA is suspected:
• Erythrocyte Sedimentation Rate (ESR)
• C-Reactive Protein
• Full Blood Count
• Renal Function Test
• Liver Function Test
Synovial Fluid Analysis:
Sterile, turbid synovial fluid with decreased viscosity, and inclusion-bearing
neutrophils.
Treatment
Principles of treatment :
● Induction of remission and its maintenance.
● Preservation of joint function and prevention of deformities .
● Repair of joint damage
Medical treatment :
1. NSAIDS :
● Ibuprofen, indomethacin, COX-2 inhibitors like celecoxib and valdecoxib
(reduce inflammation and relieves pain)
2. Disease Modifying Antirheumatic Drugs (DMARDs)
● There are used with NSAIDs and/or prednisolone to slowdown
destruction caused by RA over time. Examples are
● Methotrexate
● Leflunomide: Immuno suppressant.
● Infliximab/Adalimumab: TNF-d inhibitors.
● Anakinra: IL-I receptor antagonist.
● Rituximab: Anti CDaO antibody.
3. Glucocorticoids or prednisolone
● Prescribed in a small dose to slow joint damage caused by
inflammation.
Physiotherapy
● Splintage of joint in proper position during acute phase
● Heat therapy for symptomatic relief
● Joint mobilisation exercise to maintain joint function
● Muscle building exercise for gain strength
Surgical treatment
1. Synovectomy
● This procedure is used to reduce the amount of inflammatory tissue by
removing the diseased synovium or lining of the joint.
● It may result in less swelling and pain and the slowing or prevention of further
joint damage.
2. Tendon Surgery
● Tendon repair or reconstruction
● Tendon transfer (if rupture occurs)
● Common in hand deformities
3. Arthrodesis (Joint Fusion)
● This procedure fuses two bones together
● Indicated for:
○ Severe pain
○ Unstable joints
● Provides stability but sacrifices movement
● Common joints:
○ Wrist
○ Ankle
○ Cervical spine
4. Joint Replacement Surgery or Arthroplasty
● This is the surgical reconstruction or replacement of a joint.
● Joint replacement surgery involves the removal of the joint, resurfacing and
relining of the ends of bones and replacing the joint with a man-made
component.
● Recommended for severe disease.
● Relieves pain + restores function
● Common joints:
• Hip • Knee • Shoulder • MCP joints
Crystal Arthropathies: Introduction
Definition
Group of joint disorders caused by deposition of crystals in joints and periarticular
tissues, leading to inflammation.
Major Types:
1. Gout - Monosodium urate crystals
2. Pseudogout - Calcium pyrophosphate dihydrate crystals
Gout Pseudogout
● More common in middle - aged man ● More common in elderly
● Risk factors: ● Associated with
- Hyperuricemia - Osteoarthritis
- Alcohol intake - Metabolic disorders
- High purine diet (hyperparathyroidism,
- CKD, Obesity hemochromatosis)
Pathophysiology of Crystal Arthropathy
↑ Uric Acid Solute excess ↑ Ca²⁺ + Pyrophosphate
Causes Causes
● Renal failure ● Osteoarthritis
● Alcohol ● Hyperparathyroidism
● Drugs ● Familial factors
● Cancer chemotherapy ● Haemochromatosis
● Diet ( red meat )
● genetics Supersaturation
Monosodium urate crystals Calcium pyrophosphate crystals
(Gout) (Pseudogout)
Deposition in cartilage or tendon
Shredding into synovial fluid
Inflammation → Arthritis
Clinical Features of Crystal Arthropathies
Typical presentation
● Acute onset joint pain
● Severe pain with swelling, redness, warmth
● usually monoarticular
Systemic features
● may mimic septic arthritis
● Malaise
Clinical features- Gout
● Most common site1st MTP joint
● other joints: ankle,knee,wrist
● Recurrent acute attacks
● In chronic cases, tophi(urate crystal deposits) and joint
deformity also seen
Characteristic:
● Pain is intense, patient cannot tolerate even touch
Clinical features- Pseudogout
● Common joints
-knee(most common)
-wrist, shoulder, ankle
● Acute or subacute arthritis
● Less severe than gout
● May mimic osteoarthritis or RA.
Investigations
1. Synovial Fluid Analysis (GOLD STANDARD)
A. Macroscopy
● Turbid / cloudy fluid in acute attack
● Increased WBCs
B. Microscopy (Polarized light microscopy)
Gout Pseudogout
( urate deposits) ( calcium pyrophosphate)
2. x-ray findings
Gout Pseudogout
● Early: normal ● Chondrocalcinosis (classic)
● Chronic: “Punch-out” erosions with overhanging edges ● Calcification in cartilage
● Soft tissue tophi ● Degenerative changes may be seen
3. Biochemical Investigations
● Serum Uric Acid - ↑ in gout (but can be normal during acute attack)
● Renal function tests - Urea, creatinine
● Calcium, phosphate, magnesium levels
● ESR / CRP- Raised in acute inflammatory attack (non-specific)
Treatment
Acute Management of Gout
● Goal :Rapid suppression of crystal induced inflammation
First line options :
Corticosteroids
NSAIDs Colchicine
Systemic : Prednisolone
High dose 1.2mg Stat, followed (30-40mg) tapered over 7to
Indomethacin or by 0.6mg one 10 days
Naproxen hour later
Intra-articular :
Continue for 48 hours most effective when Triamcinolone injection
after symptoms initiated within (always aspirate joints prior
resolve in 24 hrs to corticosteroids to ensure
not masking a sepsis
arthritis)
Chronic Gout Management
● Goal : achieve Serum Urate target <6 mg/dl to dissolve existing crystals
Xanthine Oxidase Uricosuric Recombinant Uricase
Inhibitor converts purine to more
● Allopurinol : ● Probenecid : soluble allantoin
start low start dosage of
● Pegloticase:
(100mg/day ) and 250 mg twice a day
8mg iv every 2
titrate up and advanced
weeks
slowly up to
● Rasburicase :
● Febuxostat : maximum dose of
nonpegylated
alternative for 3gm a day
recombinant
patients Intolerant uricase
to Allopurinol
Surgical Interventions
● address mechanical complications and joint failure
Tophaceous Gout Surgery End Stage Arthropathy
● Debridement : ● Arthrodesis:
indicated for for small joint instability
infected,ulcerated or painful or severe pain
( especially 1st MTP)
topic
● Total Joint Arthroplasty :
● Tendon decompression :
indicated for significant
removal of deposits causing
joint
nerve compression
destruction(knee/hip) in
syndrome (carpel tunnel
stable ,medically
syndrome)
managed patients
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