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OSTEOARTHRITISAgus Widiyatmoko

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INTRODUCTION

• Mostly elderly

• Ageing process???

• Repeated micro trauma to the joint??

ACRFPACRFP

OSTEOARTRITISOSTEOARTRITIS

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INTRODUCTION

Many theories of etiology and pathogenesis

Start from breakage of cartilage and pathologic condition of the synovium

Definite treatment ???

Epidemiology

Population Age (yrs) Female (%) Male (%)

English >35 70 69

US Caucasians >40 44 43

Alaskan Eskimos >40 24 22

Jamaican (rural) 35-64 62 54

Pima Indians >30 74 56

Blackfoot Indians

>30 74 61

South African Black

>35 53 60

Indonesia

• Community basedUrban Rural

Malang* 10.0 % 13.5%

Bandungan** 5.4%

* Kalim H, cs 1994, ** Darmawan, 1992

• Hospital based

RSCM 43.8% (total rheumatic patients), 1991-1994

35.8% (total rheumatic patients), 2000

Epidemiology

Prevalence of Radiographic Evidence of OA in the Population

Pre

vale

nce

(%

)

Age (years)

0

10

20

30

40

50

60

70

30 40 50 60 70

Knee, man

DIP, man

Knee, women

DIP, women

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ETIOLOGY

Knowing a normal tissue around the joint

1. Chondrocytes

2. Collagen

3. Proteoglycan

4. Synovial fluid

NORMAL versus OA

Capsul thickness

Knee OANormal Knee

Bone cystSubchondral

schlerosis

Cartilage fibrillation

Synovium hypertrophy

Osteophyte formation

Capsul

Cartilage

Synovium

Bone

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CARTILAGE

1. Hyaline cartilage

2. Fibro cartilage

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CARTILAGEFibro cartilage : meniscus

ACRFPACRFP

Stresses Abnormal

Normal cartilage

Cartilage abnormal

Aging

Genetic and metabolic disease

Inflammation

Administration of toxins

Immune response

Obesity, Developmental

and anatomic abnormalities

Bony remodeling and micro

fracture

Loss of joint stability

Trauma

Theory A Biomaterial failure

collagen networkfracture

Theory BCell injuryIncrease of degradative responsesInhibitors reducedProteolytic enzymes increasedDestruction of prteoglycans collagenand other proteins

Proteoglycan unravelling

Cartilage breakdown

Degenerative Joint DiseaseDegenerative Joint Disease

Pathophysiology

Degenerative Joint DiseaseDegenerative Joint Disease

Clinical Manifestations◦Pain

◦Malfunction

◦Deformity

Elderly,Repetitive Trauma or Major Trauma to Joint

Assessment of patients with OA

Nature of pain• Mechanical - related to use• Inflammatory - stiffness, pain aggravated by rest• Nocturnal - suggest intraosseous hypertension• Sudden deterioration - consider sepsis, avascular necrosis,

fracture, or crystal synovitis

Clinical Examination• Periarticular or articular source of pain• Generalised pain? - consider fibromyalgia• Presence of deformity?• Evidence of muscle wasting?• Local inflammation or effusion?• Generalised or localised OA?

Weight• Potentially modifiable risk factor

Joint locking• Orthopaedic referral probably appropriate

Sleep disturbance• May be associated with fibromyalgia and depression

Comorbid disease

Assessment of patients with Osteoarthritis

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CLINICAL

1. Altman criteria's

2. Achlback classification

3. Outerbridege grading

4. Kellgreen

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ALTMAN’S CRITERIAS • CLINICAL and LABORATORY Knee pain plus at least 5 of these 9 : 1. Age > 50 years 2. Stiffness < 30 min 3. Crepitus 4. Bony tenderness 5. Bony enlargement 6. No palpable warmth 7. ESR < 40 mm/h 8. RF < 1: 40 ( Rheumatoid Factor ) 9. SF OA ( Synovial Fluid Sign of Osteoarthritis)

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ALTMAN’S CRITERIAS

• Clinical and Radiographic Knee pain + at least 1 of these 3 :

1. Age > 50 years

2. Stiffness < 30 min

3. Crepitus + osteophytes

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ALTMAN’S CRITERIAS

• Clinical Knee pain + at least 3 of these 6 : 1. Age > 50 years 2. Stiffness < 30 min 3. Crepitus 4. Bony tenderness 5. Bony enlargement 6. No palpable warmth

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KELLGREN LAWRENCE GRADING

• GRADE CRITERIA 0 Normal 1 Doubtful narrowing of joint space, possible osteophytes 2 Definite osteophytes, absent or questionable narrowing of joint space 3 Moderate osteophytes, definitive narrowing, some sclerosis, possible deformity 4 Large osteophytes, marked narrowing, severe sclerosis, definite deformity.

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RADIOLOGY

• SOFT TISSUE : ATROPHY

• JOINT SPACE : NARROWING

• BONE : OSTEOPHYTE, SCLEROSING, BONE CYST, MALALIGNMENT (VARUS, VALGUS)

KNEE PAIN

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Synovial fluid (SF) criteria for OA are (1)

White blood cell <2,000/mm3; (2) Clear color; (3)

Viscous

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27

28

29

30

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57/F, OA

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64/F, OA

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56/M, OA

presented at National congress of Indonesian Rheumatology Association. 3rd July 2005.

Jogyakarta

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69/F, OA

35

36

37

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CLINICAL

As a whole

• History.

• Atrophy

• Joint Contracture

• Activity daily living

ACR 2000 Guidlines-Drug Therapy Options in Osteoarthritis

Baseline program(Weight loss/exercise)

Mild/moderate Moderate/severePain pain/inflammation

Acetaminophen Steroids IA COX-2 specific Inhibitors

NSAIDs Hyaluronans Traditional NSAIDs Tramadol (plus gastroprotection)

Propoxyphene Opioids

Surgery

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TREATMENT

1. Conservative

2. Operative.

Reduce the symptoms / pain, improve joint function, reduce the progress, and improve quality of life

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CONSERVATIVE

Pharmacogenic :

1. NSAID

2. Cox 2 inhibitor

3. Intra articular injection: hyaluronic acid, analgesic. steroid

Things to consider when selecting an NSAID

PO

PO,TOP

PO

PO

PO,SUP

PO,SUP

PO

PO

PO

PO,INJ, SUP,TOP

PO

Formula

+

+

+

+

+

+

+

+

+

+

?

Eff.

$15-20M?++?+Celecoxib

$7-12S++++Diclofenac

$20-25L( -- )++?+Rofecoxib

$3L?-?+Piroxicam

?S?+?+Nimesulide

$35-45M?-?+Naproxen

?L?+?+Meloxicam

$8-10S?-++Ketoprofen

$9S+-++Indomethacin

$7S+-?+Ibuprofen

$11-18M?+++Etodolac

CostT1/2Cod.COX-2BKPGNSAID

Are they different?goodgood modmod badbad

Rasio Selektivitas Rasio Selektivitas Cox2/Cox1Cox2/Cox1DrugDrug Rasio Cox2/Cox1Rasio Cox2/Cox1

PiroxicamPiroxicam 250250 Acetylsalicylic acidAcetylsalicylic acid 175175 IndomethacinIndomethacin 60 60 IbuprofenIbuprofen 15 15 ParacetamolParacetamol 7.4 7.4 Sodium salicylateSodium salicylate 2.8 2.8 CarprofenCarprofen 1 1 MeloxicamMeloxicam 0.8 0.8 DiclofenacDiclofenac 0.70.7 NaproxenNaproxen 0.6 0.6 NimesulideNimesulide 0.1 0.1 ROFECOXIBE ROFECOXIBE 0.020.02

Se

lek

tif

Co

x 2

Se

lek

tif

Co

x 1

Adapted from Vane, J.R.Adapted from Vane, J.R. ICIC5050 Value ( Value (mol/L) of NSAIDs on COX-2 or COX-1 activity in intact cellsmol/L) of NSAIDs on COX-2 or COX-1 activity in intact cells

GI Events* Associated With NSAIDs

Most Patients Asymptomatic

N = 141 N = 1,921

Armstrong, Blower.Gut. 1987; 28: 527–532

Singh et al.Arch Intern Med.

1996; 156: 1530–1536

Withoutsymptoms

Withsymptoms

42%58% 81%

19%

*Bleeding, perforation, and gastric outlet obstruction

Mortality Associated With TypicalNSAIDs vs Other Causes in US

Fries et al. Am J Med. 1991; 91: 213–222Wilson, Crouch. Science. 1987; 236: 267–270

Annual risk of death (%)0.250.200.150.100.050.00 0.400.350.30

Cigarette smoking

Cancer

NSAID use

Motor vehicle accident

Home accident

Airplane crash (frequent flyer)

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Disease Modifying Osteoarthritis Drugs

• Tetrasiklin

• Glycosaminoglycan polysulfuric acid (GAPS)

• Glycosaminoglycan peptide complexes

• Pentosan polysulfate

• Growth factors and sitokin (TGF-b)

• Terapi genetik

• Transplantasi stem cell

• Osteochondral Graft

• Anti TNF Alfa (Etanercept)

Hyaluronic acid Hyaluronic acid

Bone

Bone

•• • •• •

Cartilage

OsteoclastOsteoblast

Chondrocytes

HA

HA

Synovial lining

Capsule

Synthesis: Synoviocyte, chondrocyte

Reduction of synovial membrane inflammationReduction of synovial membrane inflammationin the treatment using hyaluronic acidin the treatment using hyaluronic acid

Before treatment

After treatment

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OPERATIVE

1. Arthroscopy : lavage, shaving, drilling.

2. Osteotomy

3. Arthroplasty

4. Mozaic graft

5. Stem cell graft

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ARTHROSCOPY

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ARTHROSCOPY

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ARTHROSCOPY

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OSTEOTOMY

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MOSAIC-PLASTY

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MOSAIC-PLASTY

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MOSAIC-PLASTY

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MOSAIC-PLASTY

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ARTHROPLASTY

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ARTHROPLASTY

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STEM CELLS

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STEM CELLS

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STEM CELLS

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STEM CELLS

benefitbenefitriskrisk

Measures the risk and benefit for your patients

ALHAMDULILLAH

TERIMA KASIH

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