OSTEOARTHRITIS (OA)

Prakash Thakulla
Intern
• Joint Capsule:
– Inner: synovial
membrane
– Outer: fibrous
membrane
• Articular cartilage:
– Proteoglycanelasticity
– Collagen fiberstensile
strength
– Chondrocytes and water
 Introduction
• Most common form of arthritis in the world.
• It is a chronic disorder of synovial joints in which
there is progressive softening and disintegration
of articular cartilage.
• It is accompanied by:
– Osteophyte formation
– Cyst formation
– Subchondral sclerosis
– Mild synovitis
– Joint fibrosis
• 2 categories: Primary and Secondary
 Etiology
• Multifactorial
• Risk Factors
– Age
– Female gender
– Obesity
– Anatomical factors
– Muscle weakness
– Joint injury (occupation/sports activities)
• Predisposing conditions in secondary OA:
– Trauma or injury, congenital joint disorders, inflammatory
arthritis, AVN, infectious arthritis, Paget disease, osteopetrosis,
osteochondritis dissecans, metabolic disorders,
hemoglobinopathy, Ehlers-Danlos syndrome, or Marfan
syndrome
 Pathophysiology
Risk Factors + Mechanical stress + Abnormal
joint mechanic

Pro-inflammatory markers and proteases

Increase in water content and depletion of the

proteoglycans
Repeated weight-bearing leads to fibrillation and
cracking of matrix

Cartilage gets abraded by the grinding

mechanism

Further 'rubbing', the subchondral bone

becomes hard and glossy (eburnation)

Underlying cancellous bone becomes sclerotic

and thickened
• Small fracture through articulating bone
synovial fluid seeps into subchondral
regionloculated fluid collectionfibrous walled
cysts (subchondral cysts).
• After cartilage injury, the collagen matrix is
damaged causing chondrocytes to proliferate and
form clusters. A phenotypic change to
hypertrophic chondrocyte occurs causing cartilage
outgrowths that ossify and form osteophytes.
• The loose flakes of cartilage incite synovial
inflammation and thickening of the capsule,
leading to deformity and stiffness of the joint.
 Cardinal features
• Progressive cartilage destruction
• Subarticular cyst formation
• Sclerosis of the surrounding bone
• Osteophyte formation
• Capsular fibrosis.
 Clinical Features
• TRIAD: joint pain, stiffness, and locomotor
restriction.
• Joints primarily involved: PIP and DIP, first
CMC, hips, knees, first MTP joints, and joints
of the lower cervical and lumbar spine
• Clinical presentation: monoarticular or
polyarticular
 Examination findings
• Bony enlargement
• Crepitus
• Effusions (non-inflammatory)
• Limited range of motions.
• Tenderness may be present at joint lines, and there may
be pain upon passive motion.
• Classic physical exam findings in hand OA
– Heberden’s nodes (posterolateral swellings of DIP joints)
– Bouchard’s nodes (posterolateral swellings of PIP joints)
– Squaring at the base of the thumb (first CMC joints)
 Evaluation
• It is a clinical diagnosis and can be diagnosed with
confidence if the following are present:
– Pain worse with activity and better with rest
– Age > 45 years
– Morning stiffness lasting less than 30 minutes
– Bony joint enlargement
– Limitation in range of motion
• X-ray of affected joint:
– Marginal osteophytes
– Joint space narrowing
– Subchondral sclerosis
– Cysts
 Contd…
• Blood tests
– CBC, ESR, RF, ANA, uric acid: usually normal in OA
– If the synovial fluid is obtained, the WBC count
should be <2000/uL, predominantly mononuclear
cells (non-inflammatory) to be consistent with a
diagnosis of OA
• Differential Dx:
– RA, psoriatic arthritis, crystalline arthritis,
hemochromatosis, bursitis, AVN, tendinitis,
radiculopathy
 Management
• Pharmacological:
– Oral/ topical NSAIDs
– Intra-articular
glucocorticoids
– Intra-articular hyaluronic
acid injection
– Chondroprotective agents:
Glucosamine and
Chondroitin sulphate
– Duloxetine
– Opoids
• Non-pharmacological:
– Avoidance of activities
exacerbating pain or
overloading joint
– Exercise to improve strength
– Local heat
– Weight loss
– Occupational therapy for
unloading of joint via brace,
splint, cane, or crutch 
– Surgical: osteotomy, joint
replacement, joint
debridement, arthroscopic
procedure
 Complications
• Pain
• Falls
• Difficulty ambulation
• Joint malalignment
• Decreased range of motion of the joint
• Radiculopathies
RHEUMATOID ARTHRITIS (RA)
 Introduction
• Chronic non-suppurative inflammation of synovial joint
• Systemic disease, changes can be seen in number of
tissues of body
• Women affected 3-4 times more than man
• It occurs between the age of 20-50 years
• Typical features-
– Symmetrical polyarthritis & tenosynovitis
– Morning stiffness
– Elevation in ESR
– Presence of RF in serum
 Criteria for Diagnosis
• Given by American Rheumatism Association (1987)
• FOR MORE THAN 6 WEEKS
– Morning Stiffness
– Swelling of three or more specified joints
– Swelling of joints in hands and wrist
– Symmetrical swellings
– Rheumatoid nodule
– Rheumatoid factor positive
– X-ray changes- erosion or peri-articular osteopenia
• If at least four of them is presentRA
• Sensitivity: 93 % , Specificity: 90 %
 Aetiology
• The exact aetiology is not known
• It is thought to have association with following factors:
 Genetic susceptibility:
 More common in first degree relative of patient
 Association with HLA-DR4 in chromosome 6
 Inflammatory reaction:
 Initiation of APC/T cell interaction by various local factors
such as cytokines: TNF,IL-1& IL-6
 Progressive enhancement of immune system=> synovitis
Chronic synovitis and joint destruction
Biological agents- mycoplasma, clostridium and some
viruses (EB virus)
 Pathogenesis
Immune reaction

Deposition of immune complex in synovium

Synovium becomes edematous and filled with fibrin

exudates and cellular infiltrates

Gets hypertrophied & surrounds the periphery of

articular cartilage

Pannus formation
 Cartilage loses smooth shiny appearance
Pannus extends over the cartilage & burrows
into the subchondral bone

Cartilage become worn off and bone surface

becomes raw

Fibrosis of capsule and other soft tissues

Joint deformity
 Pathological stages

Stage 1 : pre-clinical
 Beginning of immune
pathology
 Before RA becomes
clinically apparent
 Raised ESR, CRP and RF
may be detectable
 Stage 2: Synovitis
 Vascular congestion with
new blood vessel formation
 Proliferation of synoviocytes
and cellular infiltration of
the subsynovial layers
 Thickening of the capsular
structures & villous
formation of the synovium
 Disorder is potentially
reversible
 Stage 3: Destruction
 Persistent inflammation causing joint
and tendon destruction
 Articular cartilage is eroded by:
- proteolytic enzyme
- direct invasion by a pannus of granulation tissue
 Subchondral bone is eroded by granulation
tissue invasion and osteoclastic resorption
 Swelling of the joints, tendons and bursae
due to synovial effusion of fibrinoid
material
 Stage 4: Deformity
• Instability and deformity of joint due to
– Articular destruction,
– Capsular stretching and
– Tendon rupture
 Extra-articular Involvement
1. Rheumatoid nodules: small granulomatous
lesion
2. Lymphadenopathy
– nodes draining inflamed joints & distant nodes can
also be affected
3. Vasculitis: can be life threatening condition
4. Muscle weakness
5. Visceral disease: lungs, heart, kidneys, GIT, brain
etc.
6. Anemia
• Atlanto-axial joint Uncommon
• Facet joints of cervical spine
• Hip joint Less common
• Temporalo-mandibular joint
• MP joints of hand
• PIP joints of fingers
Common
• Wrists, knees, elbows, ankles
Affected Joints
 Clinical Features
• Insidious onset, rarely may start quite suddenly
• Most commonly affected MCP joints, particularly that of
the index finger

• The presentations in acute stage are:

Polysynovitis with soft tissue swelling
 Morning stiffness for >30 min.
 Pain, loss of mobility & inflammation in at least 3 joints,
particularly in the morning
 May have previous hx of myalgia, tiredness, wt. loss
 Contd…
• Examination finding:
– Symmetrical swelling and tenderness of MCP, PIP
and wrist joints
– Tenosynovitis in extensor compartment of wrist
and flexor sheath of fingers
– Joint movement limited
– If larger joint involved,
• Local warmth, synovial hypertrophy & effusion
 Contd…
Later Stage
• Acute pain of synovitis replaced by constant pain
• Joint instability & tendon rupture produces typical
rheumatoid deformities
• Joint movement restricted and very painful
• Pt. may need help on dressing, eating etc.
• May be fever, rash and signs of vasculitis
• Subcutaneous nodule- elbow, finger, viscera, eye
• Less specific features:
– Muscle wasting, skin atrophy
– lymphadenopathy
– peripheral neuropathy, nerve entrapment syndrome etc.
 Deformities
Hand
–Ulnar drift of the hand
–Boutonniere deformity
–Swan-neck deformity
–Elbow: Flexion deformity
Knee
–Early - flexion deformity
–Late - triple* subluxation
Ankle: Equinus deformity
Foot
–Hallux valgus, Hammer toe
* Flexion, posterior subluxation and external rotation.
 Blood Investigations
• Hb: anemia
• Elevated ESR, CRP
• Serology: ACPA, ANA, RF
• ACPA: most specific
• Presence of ACPA established RA is associated with
disease severity
• Generation of ACPA in early stage of disease is strongly
predictive of progression of full blown disease
• Anti CCP antibodies
 X-ray
Early stage: features of synovitis- soft tissue
swelling & periarticular osteoporosis
Later stage:
 Erosion of articular margin of bone
 Reduced joint space
Advanced cases:
 Articular distruction and joint deformity
Others
 Subchondral cysts, Juxta-articular rarefaction
Synovial fluid examination
 Other Investigations
• Synovial biopsy

• USG: presence of synovitis & early erosion

• Doppler USG

• MRI
 Differential Diagnosis
• Sero negative inflammatory poly arthritis- SLE,
Psoriatic arthropathy
• Osteoarthritis
– Older patients, DIP joint involvement
– Lack of features like fever, weight loss, morning stiffness,
joint swelling
• Reiter’s disease
• Polyarticular gout
• Calcium pyrophosphate deposition disease
• Ankylosing spondylitis
• Sarcoidosis
 Method of Treatment
A) Medical

B) Orthopaedic
1. Non-operative
2. Operative
 Medical Management
I. Non-steroidal anti-inflammatory drugs
(NSAIDs)
II. Disease modifying anti - rheumatic
drugs(DMARDs) and
III. Steroids
 DMARDs
1. Conventional Synthetic DMARDs (csDMARDs)
– MTX, Azathioprine, Chloroquine, HCQ, Cyclophosphamide,
Cyclosporine, Leflunomide, MMF, Sulfasalazine
2. Targeted Synthetic DMARDs (tsDMARDs)
– Tofacitinib
3. Biologic DMARDs: Biologic original (boDMARDs) and
biosimilar DMARDs (bsDMARDs)
– T-cell modulating agent: Abatacept
– B-cell cytotoxic agent: Rituximab
– Anti-IL-6 agent: Tocilizumab
– IL-1 inhibiting agent: Anakinra, Rilonacept, Kanakinumab
– TNF-α blocking agent: Adalimumab, Infliximab, Etanarcept,
Golimumab, Cetrolizumab
 Non-Operative Methods
Physiotherapy
 Splintage of joints in proper positions, heat therapy
 Joint mobilization exercises
 Muscle building exercises

Occupational therapy
 To help patient with his occupational requirement in
comfortable way

Rehabilitaion
 Braces
 Walking aids
 Operative Method
• Preventive surgery
– To prevent damage to joint and nearby tendons by inflamed
synovium
– Synovectomy

• Palliative surgery
– Done when general condition of patient doesn’t permit
corrective surgery
– Relief can be provided by bone block operations, tendon
lengthening etc

• Reconstructive surgery
– Tendon transfer, total joint replacement
How to Monitor Disease Activity??
• CF • To monitor damage
– Pain (VAS) – X-ray
– Early morning stiffness – Functional assessment
(min) • To monitor drug safety
– Joint tenderness – Urinalysis
– Joint Swelling – CBC
– ESR and CRP – RFT
– USG – LFT
– DAS 28 score
 Complications
• Fixed deformities
• Muscle weakness
• Joint rupture
• Infection
• Spinal cord compression
• Systemic vasculitis
• Amyloidosis
 References
• Apley’s System of Orthopaedics and Fractures,
9th Edition
• Essential Orthopaedics, J. Maheshwari, 4th
Edition
THANK YOU !!!