OSTEOARTHRITIS

DEFINITION

• Osteoarthritis OA is a degenerative disease

of diarthrodial (synovial) joints,
characterized by Breakdown of articular
cartilage and proliferative changes of
surrounding bones
 EPIDEMIOLOGY
• Osteoarthritis(OA) is the most common joint
disease
• OA of the knee joint is found in 70% of the
population over 60 years of age
• Radiological evidence of OA can be found in
over 90 % of the population
 CLASSIFICATION OF OA
• Primary OA Secondary OA

Etiology is unknown Etiology is known

 AGE
• Primary OA > 40 years

• Direct correlation

• Aging process
 RISK FACTORS FOR PRIMARY OA
• Age
• Sex
• Obesity
• Genetics
• Trauma (daily)
 SECONDARY OSTOARTHRITIS
• Trauma
• Previous joint disorders;
• Congenital hip dislocation
• Infection: Septic arthritis, Brucella, Tb
• Inflammatory: RA, AS
• Metabolic: Gout
• Hematologic: Hemophilia
• Endocrine: DM
 ETIOLOGY OF OA

• Cartilage properties

• Biomechanical problem
Primary Generalized OA
 PATHOLOGY OF OA
• Fibrillation

• Eburnation

• Osteophytes

• Subcondral cysts
 LABORATORY FINDINGS OF OA

• There are no pathognomonic laboratory

findings for OA

• Laboratory analysis is performed for

differential diagnosis
 RADIOLOGIC FINDINGS OF OA
• Narrowing of joint space
(due to loss of cartilage)

• Osteophytes

• Subchondral (paraarticular) sclerosis

• Bone cysts
 RADIOLOGIC GRADE OF OA

• G1 Normal
• G2 Mild
• G3 Moderate
• G4 Severe

• Kellgren Lawrence Classification

 DIAGNOSIS OF OA

CLINICAL FINDINGS
Joint pain
+
RADIOLOGIC FINDINGS
Osteophytes
 CLINIC OF OA
SIGNS AND SYMPTOMS

• Joint pain - degenerative

• Stiffness following inactivity – 30 min
• Limitation of ROM – later stages
• Deformity – restricition of ADL
 Peripheral Joints
• Hands
• Feet
 ETIOPATHOGENESIS OF OA
• Age,gender
Local
• Genetic OA biochemical
effects

• Other factors
 ETIOPATHOGENESIS OF OA

• Dysfunction of joint cartilage

• Condrocyte function: 1- Degredative enzymes
(metalloproteases)
2- Inhibitors
Degeneration and regeneration functions are
balanced
• IL-1  , degredative enzymes + synovial
inflammation results: Breakdown of cartilage
 PATHOGENESIS OF OA

• Cytokines IL-1, IL-6, TNF-

• Cell destruction

• Membrane phospholipids

• Arachidonic acid

• Cox-1, Cox-2
• IL-1 and metalloproteases have been found
to play an important role in cartilage
destruction.

• Local growth factors, especially

transforming growth factor (TGF) are
involved in the formation of osteophytes
 TREATMENT OF OA

• Symptomatic treatment

• Structure modifying treatment

• Surgical treatment
 STRUCTURE MODIFYING TREATMENT

• Hyaluronic acid injection (HA)

• Glycose amino glycans (GAG)

 AIMS OF OA TREATMENT

• Pain relief

• Preservation and restoration of joint

function

• Education
 PHARMACOLOGIC TREATMENT OF OA

• Oral Systemic Medical Agents

- Analgesics (acetaminophen)
- NSAIDs
- Opioid analgesics

• Intraarticular agents:
Hyaluronan
Glucocorticoids (effusion)

• Topical agents
HAND OA - RESTING SPLINT
 SYMPTOMATIC TREATMENT OF OA

• Decrease of joint loading

- Weight control
- Splinting
- Walking sticks
• Exercises
- Swimming
- Walking
- Strengthening
• Patient education
 INDICATIONS OF SURGICAL
INTERVENTION

• Severe joint pain,

resistant to conservative treatment
methods
• Limitation of daily living activities
• Deformity, angular deviations, instability
 INVASIVE METHODS

• Joint lavage
• Arthroscopy
• Cartilage grefting- genetic engineering
• Surgery
Osteotomy
Joint replacement