194.27.141.99

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OSTEOARTHRITIS OSTEOARTHROSIS DEGENERATIVE JOINT DISEASE Prof. Dr. Ülkü Akarırmak

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Page 1: 194.27.141.99

OSTEOARTHRITIS

OSTEOARTHROSIS

DEGENERATIVE JOINT DISEASE

Prof. Dr. Ülkü Akarırmak

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DEFINITION

Osteoarthritis OA is a degenerative disease of diarthrodial (synovial) joints, characterized by

Breakdown of articular cartilage

and proliferative changes of surrounding bones

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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

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LIMITED FUNCTION

OA may cause functional loss

Activites of daily living

Most important cause of disability in old age

Major indication for joint replacement surgery

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CHARACTERISTICS OF OA

OA is a chronic disease of the musculoskeletal system, without systemic involvement

OA is mainly a noninflammatory disease of synovial joints

No joint ankylosis is observed in the course of the disease

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CLASSIFICATION OF OA

Primary OA Secondary OA

Etiology is unknown Etiology is known

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AGE

Primary OA > 40 years

Direct correlation

Aging process

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RISK FACTORS FOR PRIMARY OA

Age

Sex

Obesity

Genetics

Trauma (daily)

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SECONDARY OSTOARTHRITISTraumaPrevious joint disorders;Congenital hip dislocationInfection: Septic arthritis, Brucella, TbInflammatory: RA, ASMetabolic: GoutHematologic: HemophiliaEndocrine: DM

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ETIOLOGY OF OA

Cartilage properties

Biomechanical problem

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Morphology of Primary OA

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Primary Generalized OA

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STRUCTURE OF JOINT CARTILAGE

Collagen (Type 2)

Proteoglycan

- Hyaluronic acid

- Glycoseaminoglycan

Water

Condrocyte

Regeneration and Degeneration

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PATHOLOGY OF OA

Fibrillation

Eburnation

Osteophytes

Subcondral cysts

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LABORATORY FINDINGS OF OA

There are no pathognomonic laboratory findings for OA

Laboratory analysis is performed for differential diagnosis

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RADIOLOGIC FINDINGS OF OA

Narrowing of joint space

(due to loss of cartilage)

Osteophytes

Subchondral (paraarticular) sclerosis

Bone cysts

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RADIOLOGIC GRADE OF OA

G1 Normal

G2 Mild

G3 Moderate

G4 Severe

Kellgren Lawrence Classification

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DIAGNOSIS OF OA

CLINICAL FINDINGS

Joint pain

+

RADIOLOGIC FINDINGS

Osteophytes

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CLINIC OF OA SIGNS AND SYMPTOMS

Joint pain - degenerative

Stiffness following inactivity – 30 min

Limitation of ROM – later stages

Deformity – restricition of ADL

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OA OF KNEE JOINT (GONARTHROSIS)

More common in obese females over 50 years of ageJoint stiffness (<30 minutes)Mechanical painPhysical examination findings: CrepitusPain on pressurePainful ROM and functional limitationLimitation of ROM in later stages of OA (first extension)Laboratory analysis within normal limits

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GENU VALGUM - ORTHOSIS

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RADIOLOGIC FINDINGS? GRADE 1 - 4?

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OA OF HIP JOINT

More common in males over 40 years of age

Joint stiffness

Pain of hip, gluteal and groin areas radiating to the knee (N obturatorius)

Mechanical pain

Limited walking function

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COXARTHROSIS

Physical examination:

Antalgic limping

Limitation of ROM (first internal rotation)

Painful ROM

Trendelenburg test positivity

Leg length discrepancy

Laboratory analysis within normal limits

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BIOMECHANICS

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X-RAY OF HIP OA

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Peripheral Joints

Hands

Feet

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ETIOPATHOGENESIS OF OA

Age,gender

Local

Genetic OA biochemical effects

Other factors

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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

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PATHOGENESIS OF OA

Cytokines IL-1, IL-6, TNF-

Cell destruction

Membrane phospholipids

Arachidonic acid

Cox-1, Cox-2

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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

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TREATMENT OF OA

Symptomatic treatment

Structure modifying treatment

Surgical treatment

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STRUCTURE MODIFYING TREATMENT

Hyaluronic acid injection (HA)

Glycose amino glycans (GAG)

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PRIMARY PREVENTION OF OA ??

Regular exercises

Weight control

Prevention of trauma

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AIMS OF OA TREATMENT

Pain relief

Preservation and restoration of joint function

Education

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Non-Pharmacologic Treatment of OA

Patient educationWeight loss (if overweight)Aerobic exercise programsPhysical therapy Range-of-motion exercises Muscle-strengthening exercisesAssistive devices for ambulationPatellar tapingAppropriate footwear Lateral-wedged insoles (for genu varum)BracingOccupational therapyJoint protection and energy conservation

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PHARMACOLOGIC TREATMENT OF OA

Oral Systemic Medical Agents - Analgesics (acetaminophen) - NSAIDs - Opioid analgesics

Intraarticular agents: Hyaluronan Glucocorticoids (effusion)

Topical agents

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HAND OA - RESTING SPLINT

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SYMPTOMATIC TREATMENT OF OA

Decrease of joint loading

- Weight control

- Splinting

- Walking sticks

Exercises

- Swimming

- Walking

- Strengthening

Patient education

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INDICATIONS OF SURGICAL INTERVENTION

Severe joint pain,

resistant to conservative treatment methods

Limitation of daily living activities

Deformity, angular deviations, instability

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INVASIVE METHODS

Joint lavage

Arthroscopy

Cartilage grefting- genetic engineering

Surgery

Osteotomy

Joint replacement

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QUESTIONS?