Osteoarthritis &

Rheumatoid Arthritis
Iwin Soossay Sathianathan
1003C79006

Dr.Alireza
Orthopaedics Posting
Taylors University
Contents
Definition
Epidemiology
Risk factors
Causes
Pathophysiology
Clinical presentation
Complications
Differential diagnosis
Investigation
Management
Definition
Osteoarthritis is 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.
Epidemiology
Most common age group is the elderly.
Females more commonly affected than males
Incidence rates increase with age

Classification of OA
OA
Primary
OA
Secondary
OA
Primary OA
More common than secondary OA
Cause Unknown
Common-in elders where there is no previous pathology.
Its mainly due to wear and tear changes occuring in old
ages mainly in weight bearing joints.

Secondary OA
Due to a predisposing cause such as:
Injury to the joint
Previous infection
Deformity
Obesity
Hyperthyroidism
Risk factors
Modifiable
Obesity
Trauma
Occupation(hard labor)
Non-Modifiable
Gender-females at increased risk
Age
Genetics
Race
Etiology
Disparity between stress applied to articular cartilage
and the ability of the cartilage to withstand that stress.

Weakening of articular cartilage
Possibly due to genetic defects in type II collagen

Increased mechanical stress in some part of the articular
surface
Excessive impact loading
Pathophysiology
In a normal joint, the loading forces are evenly distributed.
Cartilage damage results from increased stress on some part of articular surface.
Cartilage damage occurs & softening (chondromalacia)
Preceding inflammatory disorder
Progressive disintegration of cartilage
Bone is being exposed
Peripheral cartilage (unstressed) proliferate & ossifies
Producing bony growth (osteophyte)
Joint capsule thickening & fibrosis
Cardinal Features of the OA Pathophysiology
Progressive cartilage destruction
Subarticular cyst formation
Sclerosis of the surrounding bone
Osteophyte formation
Capsular fibrosis
Structural changes with Osteoarthritis
Early
Cartilage softens, pits, frays
Progressive
Cartilage thinner, bone ends hypertrophy,
bone spurs develop and fissures form
Advanced
Secondary inflammation of synovial
membrane; tissue and cartilage destruction; late
ankylosis

Normal Knee
structure
Moderately
advanced
osteoarthritis
Advanced
osteoarthritis
Clinical Features of OA
Pain
Stiffness
Muscle
spasm
Restricted
movement
Deformity
Muscle
weakness or
wasting
Joint
enlargement
and
instability
Symptoms
Pain
Starts insidiously & increase slowly over months and years
Continous pain which can be very severe at times
Maybe referred to a distant site
Aggravated: exertion
Relieved: rest
Late stage: pain in bed at night even during rest
Swelling -intermittent: suggest effusion
-continuous: capsular thickening/ large osteophytes
Minimal morning stiffness (<20 min) and after inactivity (gelling)
Loss of function-such as difficult climb stairs, restriction of walking
distance, progressive inability to perform everyday task



Signs(P/E)
Look
Antalgic gait or assumption of a posture that allows minimum weight on a
painful limb or joint
Muscle wasting
Varus deformity
Feel
Palpable bony enlargement
Joint line tenderness
Mild joint effusion
Move
Limited range of motion
Joint tenderness on passive range of motion
Joint crepitus on motion (audible or palpable)
Limb shortening

Varus Deformity
A patient with typical OA
of the knees. In the normal
standing posture there is a
mild varus angulation of
the knee joints due to
symmetrical OA of the
medial tibiofemoral
compartments.


Knee joint effusion
Osteoarthritis of the DIP joints.
This patient has the typical
clinical findings of advanced
OA of the DIP joints, including
large firm swellings
(Heberdens nodes), some of
which are tender and red due
to associated inflammation of
the periarticular tissues as well
as the joint.


Unstable distal
interphalangeal joints in
OA. The examiner is able
to push the joint from side
to side due to gross
instability, a common
finding in late
interphalangeal joint OA.


Differential diagnosis
Avascular necrosis(Osteonecrosis)
Inflammatory arthropathies
Polyarthritis of the finger
Rheumatoid arthritis
Diffuse idiopathic skeletal hyperostosis (DISH)

Complications
Capsular herniation
OA of the knee with a marked effusion and herniation of the
posterior capsule(Bakers cyst)
Loose bodies
Cartilage & bone fragments produce loose bodies, resulting in
episodes of locking.
Rotator cuff dysfunction
OA of acromioclavicular joints may cause rotator cuff
impingement, tendinitis or cuff tears
Investigations
Laboratory
Blood tests: Normal,
WBC increased if infection (secondary OA)
CRP and ESR: indicate any infection (secondary OA)
Renal Profile: Normal


Radiological
X-Ray

X-Ray

X-rays illustrating the
Cardinal Signs
Narrowing of the joint space
Sclerosis of the subchondral
bone
Cysts close to the articular
surface
Osteophytes at the margins of
the joint
Remodelling of bone ends on
either side of the joint
Late features: joint
displacement and bone
destruction
*Important criteria of taking a
X-Ray of an OA patient is???
Kellgren & Lawrence System
The Kellgren & Lawrence system is method of
classifying the severity of knee osteoarthritis. This is
classified into five grades:
grade 0 - no radiographic features of OA are present
grade 1 - doubtful joint space narrowing (JSN) & possible osteophytic lipping
grade 2 - the presence of definite osteophytes and possible JSN on
anteroposterior weight-bearing radiograph.
grade 3 - multiple osteophytes, definite JSN, sclerosis, possible bony deformity
grade 4 - large osteophytes, marked JSN, severe sclerosis & definitely bony
deformity

Management
Depends on the joint involved, the stage of disorder, the
severity of the symptoms, the age of the patient and
his/her functional needs.
There are two branch
-Conservative
-Operative
Conservative emphasis on 1.Relieving pain
2.Reducing load
3.Improving mobility

Early
Analgesic medication (PCM, NSAIDS)
Load reduction
protecting the joint from excessive load may slow down the rate of cartilage loss
effective in relieving pain
Physical therapy
Maintaining joint mobility
Improving muscle strength
Intermediate
Joint debridement(removing osteophytes, cartilage tags & loose bodies)
May be done either by arthroscopy or by open operation
Late
Three basic operations:
Realignment osteotomy
Arthroplasty (total joint replacement)
Arthrodesis

Definition
A chronic disease characterized by the inflammation of the lining of
the joints, which is called the synovium.
Known as an autoimmune disease because the bodys immune
system attacks the joint lining.
Epidemiology
Affects about 3% of the population
Women is more at risk than men, 3:1

Etiology
The exact cause of RA is unknown.
Suspected causes are:
Bacterial Infection
Genetic Marker
Stress
Viral Infection
Pathophysiology
All tissues throughout the body is affected, brunt attack falls on synovium.
3 stages of progression of the disease.
Stage 1: Synovitis (Synovial membrane becomes inflamed and thickened,
giving rise to a cell rich effusion. Although painful and swollen, the joints and
tendons are still intact an dthe disorder is reversible)
Stage 2: Destruction(Persistent inflammation causes tissue destruction.
Articular cartilage is eroded and tendon fibres may rupture)
Stage 3: Deformity(The combination of articular destruction, capsular
strecthing and tendon rupture leads to progressive instability and deformity)

Diagnostic Criteria
Morning stiffness
Arthritis of 3 or more joints
Arthritis of hand joints
Symmetric arthritis
Rheumatoid nodules
Serum rheumatoid factor
Radiographic changes

*A person shall be said to have rheumatoid arthritis if he or she
has satisfied 4 of 7 criteria, with criteria 1-4 present for at least
6 weeks

Clinical Features of RA
Symptoms
Fatigue
Swelling on proximal finger joints and wrist
Stiffness, especially in early morning and after sitting
a long period of time
Low grade fever
Weakness
Muscle pain and pain with prolonged sitting
Symetrical, affects joints on both sides of the body
Limited joints movements

Signs
Rheumatoid nodules
Deformity of joints over time
Hallux valgus
Hammer toe
Bouttoinniere thumb


Subcutaneous nodules (disappear
and appear without warning)
Rheumatoid Arthritis: PIP Swelling
Swelling is confined to the area
of the joint capsule
Synovial thickening feels like a
firm sponge


Rheumatoid Arthritis:
Ulnar Deviation and MCP Swelling
Prominent ulnar deviation in the
right hand
MCP and PIP swelling in both
hands
Synovitis of left wrist
Differential diagnosis
Reiters Disease
Polyarticular gout
Polyarticular osteoarthritis
Polymyalgia rheumatica
Seronegative polyarthritis

Complications
Infection
At risk for septic arthritis
Tendon Rupture
Nodular infiltration may cause this
Joint Rupture
Joint lining ruptures and synovial contents spill into soft tissues
Secondary Osteoarthritis
Articular cartligae erosion may leave joint so damaged, end
stage of disease will be similar to advanced osteoarthritis


Investigations
Laboratory
Blood tests: Normal,
WBC increased if infection
CRP and ESR: indicate any infection
Renal Profile: Normal
Serological Test: Rheumatoid Factor (+)

Radiological
X-Ray

X-Ray

Features of X-Ray
Stage 1 - Only soft tissue swelling and periarticular
osteoporosis
Stage 2 - Narrowing of joint space and marginal bony
erosion, especially around wrists and proximal joints of
hands and feets
Stage 3 Articular destruction and joint deformity
Management
There is no cure for RA.
Patient needs reassurance and management can be
done by alleviating symptoms and delay progression.
Principles of treatment is to:
1. Stop the synovitis
2. Keep the joints moving
3. Prevent deformity
4. Reconstruct
5. Rehabilitate



X-ray Features of Osteoarthritis (LOSS)
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

X-ray Features of Rheumatoid Arthritis (LESS)
Loss of joint space
Erosions
Soft tissue Swelling
Soft bones (osteopenia)
References
Apleys Concise System of Orthopaedics and Fractures.
3
rd
ed.
Apleys System of Orthopaedics and Fractures. 9
th
ed.
Ortho Bullets
Joint Protection: Dos and Donts
Thank You