Joint Pain

Introduction to rheumatology
 Outline
• Introduction to common rheumatological conditions
• Rheumatoid arthritis
• Osteoarthritis
• Crystal arthropathies
• Seronegative spondyloarthropathies
• Autoimmune connective tissue diseases
• Septic arthritis
Introduction

Monoarthritis Oligoarthritis Polyarthritis

(</= 5 joints) (> 5 joints)
Symmetrical Asymmetrical
Septic arthritis Crystal Rheumatoid Reactive
arthropathies arthritis arthritis
Crystal Psoriatic Psoriatic Psoriatic
arthropathies arthritis arthritis arthritis
Osteoarthritis Reactive Jaccoud’s Crystal
arthritis arthropathy arthropathies
(Reiter’s (SLE)
syndrome)
Trauma Ankylosing
(Haemarthrosis) spondylitis
Osteoarthritis
Rheumatoid arthritis
Pathophysiology
Clinical Features
• Bilateral symmetrical swollen, painful, and stiff small joints of the hands
but sparing the DIP joint.
• Morning stiffness > 30 minutes
• May involve large joints
 Five presentations of Rheumatoid Arthritis
- Palindromic: Monoarticular attacks lasting 24–48 hours. The joint becomes acutely painful,
swollen and red, but resolves completely. Further attacks occur in the same or other
joints.

- Transient: A self-limiting disease, lasting less than 12 months and leaving no permanent joint
damage. Usually seronegative for IgM rheumatoid factor and CCP.

- Remitting: There is a period of several years during which the arthritis is active but then
remits, leaving minimal damage.

- Chronic, persistent: The most typical form, it may be seropositive or seronegative for IgM
rheumatoid factor. The disease follows a relapsing and remitting course over many
years. Seropositive (plus anti-CCP) patients tend to develop greater joint damage and
long-term disability. They warrant earlier and more aggressive treatment with disease-modifying
agents.

- Rapidly progressive: The disease progresses remorselessly over a few years and leads
rapidly to severe joint damage and disability. It is usually seropositive (plus anti-CCP), has a
high incidence of systemic complications and is difficult to treat.
Extra-articular manifestations
Investigations
Diagnostic
Criteria
Disease Monitoring – DAS 28
Principles of management – Treat to target
• Non pharmacological – Patient education,
physiotherapy, occupational therapy
• Pharmacological – NSAIDs, Corticosteroids,
conventional DMARDs (methotrexate + folate,
sulfasalazine, hydroxychloroquine, leflunomide),
biologic DMARDs (adalimumab, infliximab, etanercept)
• Surgical intervention may relieve pain, improve function
and prevent deformity
Osteoarthritis
Primary osteoarthritis

• Osteoarthritis is a progressive degenerative joint

disease due to failure in repair of joint damage as a
result of biomechanical, biochemical and/or genetic
factors.
• Joints commonly affected are the knees, hip and
hands.
• Risk factors include advancing age, female gender,
family history, and high body mass index
Secondary osteoarthritis
• Metabolic – Acromegaly, haemochromatosis and
chondrocalcinosis
• Anatomic – Slipped upper femoral epiphysis (SUFE), Legg Perthes
Disease, Congenital dislocation of the hip, and avascular necrosis
• Trauma such as joint injury and fracture
• Inflammatory such as rheumatoid arthritis, psoriatic arthritis, and
septic arthritis.
Clinical Features
• Joint pain and tenderness – Increased
by joint use and relieved by rest
• Stiffness – Lasting < 30 minutes
• Swelling
• Gait disturbance and limited range of
motion
• Muscle wasting – Weakness and loss of
quadriceps muscle bulk
• Limb deformity – Genu valgus or varus
• Instability
• Clicking or grinding and crepitus
Investigations - Imaging
Principles of
Management
Gout
Introduction
• Gout is a disorder of purine metabolism resulting in
hyperuricemia either by overproduction or underexcretion of
uric acid, which in turn deposits as urate crystals in the joints
or bursae.

• This is characterized by attacks of acute inflammatory severe

arthritis, usually involves a single joint. The 1st
metatarsophalangeal joint (Podagra) is typically affected but
can also occur over ankle, foot, knee wrist, elbow and small
joints of hands. Lower limbs are more predominantly affected
than upper limbs.

• M:F (4:1)
Classification
• Untreated gout evolves slowly through four clinical phases;

1. Asymptomatic Hyperuricemia
2. Acute gouty arthritis
3. Intercritical gout (Asymptomatic)
4. Chronic tophaceous gout (Polyarticular arthritis with crystal
deposits ‘tophi’)

• +Urate Nephropathy (Acute Urate Nephropathy / Chronic

Urate Nephropathy / Urate Nephrolithiasis)
Risk factors

● Older age
● Consumption of purine rich foods
○ Red meat (Beef, Lamb, Veal)
○ Offal
○ Shellfish
○ Fish (Sardines, Anchovies, Herring)
● Alcohol
● Diuretics (Thiazide and Loop Diuretics)
● Calcineurin Inhibitors (Cyclosporine & Tacrolimus)
● High cell turnover rates (Haematological Malignancies,
Myeloproliferative Disorders, Psoriasis, and Chemotherapy-induced
cell death)
Baseline investigations
Confirmatory Diagnosis

Joint aspiration and urate crystal identification (Gold

Standard)
Strongly negatively birefringent needle-shaped urate crystal
under polarised light microscopy
Send the joint fluid for gram stain or culture to rule out septic
arthritis if in doubt
Imaging

Acute gouty arthritis -

usually normal, may be
reversible soft tissue
swelling around the
involved joint

Chronic tophaceous gout

- soft tissue
abnormalities, erosive
bone lesions (punched-
out lesions), joint space
usually preserved until
the late stages of the
disease
Principles of Management
Non-pharmacological treatment Pharmacological acute attack

1. Patient education 1. NSAIDs (indomethacin, diclofenac, ketoprofen)

2. Lifestyle modification 2. COX-2 inhibitors (etoricoxib)
a. Gradual weight loss 3. Colchicine
b. Reduction in alcohol consumption 4. Intra-articular steroids
c. Restrict consumption of high purine 5. Systemic steroids (if renal insufficiency, hepatic
foods
d. Adequate fluid intake 2 - 3L/day
dysfunction, heart failure and hypersensitivity
3. Physical and occupational therapy to NSAIDs)
4. Manage associated hypertension,
diabetes mellitus and dyslipidemia
Treatment of hyperuricemia
Prophylactic agents against gouty attacks

Allopurinol (xanthine oxidase inhibitor)

Indications of hypouricemic drugs
- Should not be started during an acute attack
- May be started at least 2 weeks after the acute attack 1. Frequent and disabling attacks of gouty arthritis
- Should not be stopped or adjusted during an acute attack (3 or more attacks/year)
- Adverse effects : rash, bone marrow suppression, aplastic 2. Signs of erosive gouty arthritis
anemia, agranulocytosis, life threatening hypersensitivity 3. Presence of tophaceous deposits
syndrome 4. Urate nephropathy
5. Urate nephrolithiasis
Probenecid (uricosuric agent) 6. Impending cytotoxic chemotherapy or
radiotherapy for lymphoma and leukemia
- Should not be used in those with renal impairment
- Assess renal function and 24-hour urinary urate secretion
before initiation of treatment
- Side effects : GI disturbance, hypersensitive rash
Ankylosing spondylitis
Common features of seronegative
spondyloarthropathies
• Seronegative (Rf negative)
• HLA B27 association
• Axial arthritis
• Enthesitis
• Asymmetrical large joint
oligoarthritic
• Dactylitis
• Extra-articular manifestations
Ankylosing spondylitis – Clinical Features
History taking:
-Back pain
-Stiffness that improves with exercise
-Common in young male
-Achilles tendinitis
-Plantar fasciitis

Physical examination:
-General: Question mark posture, protuberant
abdomen (diaphragmatic breathing)
- Schober’s test positive
- Reduced forward and lateral flexion of lumbar
spine
- Reduced intermalleolar distance
- Wall test (occiput to wall distance)
- Chest expansion
Ankylosing spondylitis – Extraarticular manifestations

Extra-articular manifestation:
-Fatigue, anemia
-Acute anterior uveitis; requires slit
lamp (unilateral, *bilateral in
spondyloarthropathy associated
with IBD)
-Apical pulmonary fibrosis
-Cardiac conduction defect
-Aortic incompetence/regurge ->
arrhythmia
-IBD (diarrhea)
-Amyloidosis
-Osteoporosis
-Depression :(
Diagnosis
X- Ray findings of ankylosing
spondylitis
The medial and lateral cortical margins of both sacroiliac joints lose
definition owing to erosions and eventually become sclerotic

The sacroiliac joints are eroded and show marginal sclerosis (white
arrows).

There is bridging syndesmophyte formation at the thoracolumbar

junction (black arrows).
In advanced disease, there is
calcification of the
interspinous ligaments and
fusion of the facet joints, as
well as syndesmophytes at
all levels. The sacroiliac
joints fuse.
Progression of the disease can lead to loss
of lordosis, and osteitis of the anterior
corners of the vertebral bodies with
subsequent erosion, leading to “squaring”
or even “barreling” of one or more vertebral
bodies.

Progressive ossification leads to eventual

formation of marginal syndesmophytes,
visible on plain films as bony bridges
connecting successive vertebral bodies
anteriorly and laterally.
Romanus lesion and shiny
corner sign
The Romanus lesion represents an early finding in
inflammatory spondyloarthropathies, such as ankylosing
spondylitis and enteropathic arthritis, and appears as
irregularity and erosion involving the anterior and
posterior edges of the vertebral endplates

Healing response to these inflammatory erosions

appears radiographically as reactive sclerosis, which is
known as the shiny corner sign.
Dagger sign
The dagger sign is a
radiographic feature seen in
ankylosing spondylitis as a single
central radiodense line on frontal
radiographs related to ossification
of the supraspinous and
interspinous ligaments secondary
to enthesitis.
Investigations for extra articular manifestations

Echocardiogra
m, ECG, renal
function test,
chest X-ray, CT
thorax
 MANAGEMENT OF ANKYLOSING SPONDYLITIS
Management

Non-pharmacological Pharmacological

Physiotherapy/
Surgery First line: NSAIDS Second line: Immunosuppressive
Exercise programs
● Infliximab (IV 5mg/kg, repeat at 2
● Maintain Total hip arthroplasty:
Indicated for severe hip Reduce pain and slow weeks, 6 weeks and 8 weeks
range of
joint pain, arthritis and down radiographic interval)
movement
● Adalimumab (S/C 40mg biweekly)
● Improve stiffness progression
● Etanercept (S/C 50mg once weekly)
posture
● Secukimumab (S/C 150 mg weekly
● Reduce pain
x 4 weeks, and every month)
Monitor: BASDAI
Reactive arthritis
 Clinical Features
• Can't see, can’t pee, can’t climb a tree..
• Swelling, tenderness and hot joint
(lower limb more common)

• Reiter’s syndrome (anterior uveitis,

urethritis, arthritis)
• After GI or urogenital infection (4
weeks)
• Microorganism:
• GI (Salmonella, Shigella, Yersinia,
Campylobacter)
• STD (Chlamydia ureaplasma,
Urealiticum)

• Additional features:
• Keratoderma blennorrhagica (vesico-
pustular waxy lesion with a yellow
brown colour. These lesions may join
together to form larger crusty plaques
with desquamating edges)
• Enthesitis
• Sacroiliitis
• Spondylitis
• Nail dystrophy
• Symmetrical acute redness,
Clinical Features
 Investigations
• Routine laboratory testing – We
obtain a complete blood
count and differential, acute
phase reactants, renal and
liver chemistries, and
urinalysis to obtain supportive
evidence of acute inflammation
and to exclude other systemic
disorders.

• Radiographic changes may be

absent or confined to juxta
articular osteoporosis. With
long-standing disease,
radiographic features share
those of PsA; marginal
erosions and loss of joint
space can be seen in
affected joints.

• Patients with concurrent or past

heel pain may show calcaneal
spurs
Management of reactive arthritis
Psoriatic arthritis
Clinical Manifestations:
Joint manifestations

Pattern of arthritis:

- Polyarthritis
- Distal arthritis (Involvement of DIP joints)
- Asymmetric oligoarthritis ( <5 small/large joints affected asymmetrically)
- Symmetric polyarthritis - sometimes indistinguishable from RA

- Arthritis mutilans, deforming

destructive arthritis
- Spondyloarthritis (sacroiliatis and
spondylitis)
Diagnostic Criteria
 Investigations
Laboratory testing is done to determine evidence of systemic
inflammation and to exclude other conditions
Full Blood Count :
➔ May reveal which can be either due to anaemia
of chronic disease or by iron deficiency resulting
from prolonged used of NSAIDS
➔ Leukocytosis can be seen in patients with 1/3rd
of patients
ESR and CRP
➔ Acute phase reactants are elevated in about
40% of patients only
ANA
Rheumatoid Factor, Anti-CPP - To rule out Rheumatoid Radiographs :
Arthritis but it can also be positive in minority of patients ➔Characteristically there is presence of
with psoriasis both erosive changes and new bone
formation
HLA - B27 Testing - Should be obtained in patients ➔Joint Destruction and Ankylosis
presenting with arthritis in whom psoriatic arthritis is ➔Fingers - Pencil in Cup Deformity
suspected despite the absence of psoriasiform skin lesions
Management
NSAIDS :
➔ Patients with mild peripheral arthritis can be effectively treated using NSAIDS
➔ Choice of NSAIDS : Naproxen, Celecoxib, Ibuprofen and Diclofenac
Non-Biologic DMARDS :
➔ In patients whose peripheral arthritis remains active despite using NSAIDS, we
can start conventional DMARDS
➔ Conventional DMARDS can also indicated in patients with moderate to severe
arthritis who lack erosive bone changes and substantial functional limitations
➔ Choice of conventional DMARDS : Methotrexate, Leflunomide, Azathioprine
Tissue Necrosis Factor Inhibitor :
➔ Indicated in patients presenting with moderate to severe disease who already
have erosive changes and functional limitation
➔ Also indicated in patients who do not improve substantially after 3 months of
treatment with a conventional non biologic DMARDS
➔ Choice of TNF Inhibitor : Etanercept, Infliximab, Adalimumab and
Golimumab
SLE
An inflammatory multisystem
autoimmune disease of
unknown aetiology.
SLE
An inflammatory multisystem
autoimmune disease of
unknown aetiology.
Pathogenesis
Clinical Features
Diagnostic Criteria
Management - Pharmacological
Management – Non -Pharmacological
• Sun protection
• Diet and nutrition
• Exercise
• Smoking cessation
• Immunizations
• Treating comorbid conditions
• Issues with specific medications and
therapies [30% have sulfa allergy]
• Pregnancy and contraception (active
disease especially with organ
impairment- high risk of miscarriage and
exacerbation of SLE. Recommended at
least 6 months quiescence before getting
pregnant)
Systemic Sclerosis
Systemic sclerosis vs scleroderma
Pathogenesis

3 main abnormalities observed:

1. Vasculopathy
- Extensive endothelial injury &
vasomotor dysfunction
- Raynaud’s phenomenon

1. Inflammation
2. Fibrosis
- Hallmark feature, excess deposition of
collagen and extracellular material in
vessels/organs
Clinical Features
Investigation
Complete blood count Anemia

Serum muscle enzyme levels Creatine kinase increased if myopathy or myositis

Erythrocyte sedimentation rate Almost always normal; if elevated = poor prognosis

Urine UFEME Proteinuria

Autoantibody assays Antinuclear antibody (ANA)

-Positive in 95% cases

Topoisomerase I antibodies (SCL-70)

- positive in diffuse type and higher risk of ILD
- absent in limited type

Anti centromere
-For limited

RNA Polymerase I and III

-For diffuse
Systemic Assessments
Management
Dermatological Cardiac Gastrointestinal Musculoskeletal
(Morphea)
Topical Diuretics High dose PPI NSAIDS
-Topical ACEI (eg (arthralgia)
Tacrolimus Omeprazole,
0.1% ointment - Pantoprazole) Inflammatory
active and arthritis
inflammatory -Low dose
morphea glucocorticoids
-Corticosteroid -
-Topical vitamin Hydroxychloroq
D uine
-Methotrexate

Systemic
-Methotrexate
-Glucorticoids
 Management
Pharmacotherapy Non
pharmacotherapy
Pulmonary Renal Raynaud’s Phototherapy - UV
phenomenon light therapy
(localized
Interstitial Lung Disease ACEI CCB (Amlodipine scleroderma or
-Mycophenolate mofetil CCB 5-20mg OD, relieving skin
-Cyclophosphamide Nifedipine 30- thickening)
-Low dose 120mg OD)
glucocorticoids -to make skin
-Azathioprine softer
-not for
hypertension

PDE-5 inhibitors
(Sildenafil 20mg
OD)

Topical nitrate
 Patient education
● Physical and occupational therapy
● Rest if joints become inflamed
● Skin care is very important to keep a good supply of blood flowing to the skin
● Cosmetic makeup may be used to cover up lesions
● Avoid high doses of vitamin C (>1000 mg) as it promotes collagen formation
● Avoid emotional stress as it reduces blood flow
● Quit smoking
● Avoid cold temperature
● Minimize caffeine intake
● Avoid sympathomimetic decongestant medications (eg Pseudoephedrine)
● Avoid high-dose corticosteroid use (>15 mg of Prednisone daily) if possible
● Check blood pressure regularly to monitor for possible complications
Osteoporosis
 Definition
• Osteoporosis is defined as
Bone Mass Density (BMD) more
than 2.5 standard deviation
below the young adult value (T-
score < -2.5)
• Osteoporsis results in an
increased risk for fracture from
bone fragility due to the
reduction in bone mass and
micro-architectural deterioration
of the bone.
• Related to ongoing bone loss
OR inadequate peak bone mass
Classification of
osteoporosis
Risk factors
Clinical Features
1. Osteoporosis have no clinical
presentation until there is a fracture
2. Vertebral collapse are the most
common clinical manifestation of
osteoporosis.
3. Hip Fractures are relatively common
as well.
4. Another common fracture would be
colles’ fracture (Distal radius)
 Investigations
• Dexa Scan is the gold standard. (Osteoporosis is diagnosed when
the BMD T-score is < -2.5) - Screen all women above 65 and men
above 70)
Other investigations
• Initial investigations are done to exclude causes of low bone mass
other than age and oestrogen deficiency. (osteomalacia,
hyperthyroidism and hyperparathyroidism)

1. Full Blood Count and ESR

2. Serum Calcium, Phosphate, Albumin
3. Alkaline Phosphatase
4. Renal Function
5. Plain x-rays - osteoporosis is apparent only after 30% of bone loss
has occurred
5. Thyroid Function
Management
Osteoporosis - Principles of Management
Prevention is better than cure!

- Nutrition - Calcium 300-400 mg daily; Vitamin D (Daily Supplementation of 800 IU)

- Maintaining a Body Weight not less than 19 kg/m2

- Lifestyle changes such as stopping smoking, reducing alcohol intake, adequate intake of
calcium (700-1000 mg/day, 1500 mg postmenopausally) and Vitamin D (400-800 IU/day)

- Regular weight bearing exercises

Osteoporosis - Management
Hormone Replacement Therapy (HRT): Beneficial in
prevention and treatment of postmenopausal
Osteoporosis

Bisphosphonates (Inhibits osteoclasts and therefore

bone resorption) [Alendronate, Risedronate]

Calcitonin ( Anti-resorptive agent and have an

analgesic effect for acute pain)

Activated Vitamin D (Calcitriol, Alfacalcidol - should

avoid excessive Calcium in order to prevent
Hypercalcemia and renal stone disease)
Septic Arthritis
Aetiology and pathogenesis
• Most commonly caused by
Staphylococcus aureus. Other
organisms include Neisseria
gonorrhoea and Haemophilus
influenzae
• Salmonella is the most common in
people with sickle cell disease
Clinical Features
• Septic arthritis is a medical emergency.
• Symptoms include redness, warmth, swelling,
and agonising pain.
• In elderly or immunocompromised patients,
there may be lack of systemic symptoms.
Investigations
• Joint aspiration and
send for Gram
staining, culture, and
biochemical analysis.
The fluid is usually
purulent.
• Full blood count –
Leucocytosis
• Skin, sputum, throat
swabs and urine
cultures may indicate
source of infection
• ESR/CRP raised
Management
Thank you 