OSTEOARTOSTEOARTHHRITISRITIS

FARIDIN HPFARIDIN HPDEPARTMENT OF INTERNAL MEDICINE DEPARTMENT OF INTERNAL MEDICINE UNHAS / DR.WAHIDIN SUDIROHUSODO UNHAS / DR.WAHIDIN SUDIROHUSODO HOSPITAL, MAKASSARHOSPITAL, MAKASSAR

Diagnosis Diagnosis andand

ManagementManagement

Dr. H. Faridin HP, SpPD,KRDr. H. Faridin HP, SpPD,KR

Courses in Rheumatology division :Course Of Osteoporosis in Lido Lake Hotel SukabumiImmuno-Rheumatology in MalangPain in Rheumatic Diseases in Ibis Hotel JakartaOsteoarthritis Course in Lembang, Bandung

Membership organizations IDI, PAPDI, IRA, PEROSI

Education1989: General Practitioner (FKUH)2001: Internist (FKUH)2003: Rheumatologist (FKUI)2004: Rheumatology Consultant (PAPDI)

Occupation: Head of Special Care Sie RSWS Department of Internal Medicine Staff FKUH

ACR Annual Meeting, 1999 :ACR Annual Meeting, 1999 :

Discussion and debate on pathogenesis of Discussion and debate on pathogenesis of OA :OA :

Polling: 52% believe that OA is a process of inflammation 48% believe that OA is a degenerative process Most believe that OA is an inflammatory or degenerative process

LimitationLimitation

OA is a rheumatic disease that affects cartilage OA is a rheumatic disease that affects cartilage where the outcome of pathological processes in where the outcome of pathological processes in the form of joint failure as one organ system.the form of joint failure as one organ system.

Characteristics:Characteristics:focal loss of cartilage with the response of focal loss of cartilage with the response of bone repair / osteofit formationbone repair / osteofit formation

OA is a common rheumatic diseases OA is a common rheumatic diseases found in all parts of the world.found in all parts of the world.

PrevalenPrevalencece::

AmerikaAmerika 12.0 % ( 12.0 % (ttotalotal populationpopulation))Roy D Altman

EpidemiologyEpidemiology1

IndonesiaIndonesiann::

Community-based researchCommunity-based researchCityCity VillageVillage

Malang*Malang* 10.0 % 10.0 % 13.5%13.5%Bandungan**Bandungan** 5.4% 5.4%* * Kalim H, cs 1994,Kalim H, cs 1994, ** ** Darmawan, 1992Darmawan, 1992

Hospital-based researchHospital-based research

RSCMRSCM 43.8% (total43.8% (total of rheumatic patients of rheumatic patients)) 1991-19941991-1994

EpidemiologyEpidemiology2

0

10

20

30

40

50

60

70

30 40 50 60 70

Lutut, Laki-laki

DIP, laki-laki

Lutut, perempuan

DIP, perempuan

Pre

vale

nsi

(%

)

Usia (tahun)

The Prevalence of OA Radiologic The Prevalence of OA Radiologic Imaging in PopulationImaging in Population

Not onlyNot only Wear and TearWear and Tear : :

TherTheree is a difference in the change of cartilage is a difference in the change of cartilage due to aging processdue to aging process ( (aging processaging process))

Can occur in young animals stimulated with Can occur in young animals stimulated with chemicals / traumachemicals / trauma

Pathogenesis of OAPathogenesis of OA

Irregulars subkhondral

bone and thickening,

appeared sklerotic and

cyst formation

Capsules had fibrosis, distortion, thickening

Fibrillation, damage and reduced the volume of cartilage

Chronic sinovitis

Osteofit growth, and thickening of the soft tissue

Normal joints and its changes in OA

Normal texture of subkhondral bone

Normal cartilage, thick and flat

Flat bone edge

Normal sinovium with single cell

layer

Thickening joint capsule

NORMAL OSTEOARTHRITIS

Femoral condyles

Tibial plateausSubchondral bone

Patella

Predileksi Predileksi jointsjointsPredileksi Predileksi jointsjointsMost often : Weight bearing joints - knee - lumbal - cervical

Generalized OA DIP (Heberden’s node)

Thickening capsule

OA kneeNormal knee

Cyst formation

SclerosisSubkhondral bone

Cartilage fibrillation

Hypertrofi synovium

Osteofit formation

Capsule

Cartilage

Synovium

Bone

ACRFP

NORMAL versus OA JOINT

Water 66-78%

Matrix 22-34%

Collagen type II 48-62%

Proteoglycan 22-38%

Hyaluronan <1%

Chondrocytes 0.4-2%

Inorganic 5-6%

Composition of Normal Composition of Normal Articular cartilageArticular cartilage

TThere is degradation and synthesishere is degradation and synthesis imbalanceimbalance

Despite Despite ssyyntnthhesisesis, the , the quality of cartilagequality of cartilage formed poorformed poor

End-stageEnd-stage:: proteoglikanproteoglikan synthesis synthesis is declined is declined, khondrosi, khondrosit t

function function

is decreasedis decreased

OA Cartilage OA Cartilage

Extra Cellular Matrix

Synthesis MMaintainaintain

Chondrocyte functionChondrocyte function

AAnabolinabolicc-kataboli-katabolic factors affectingc factors affecting

khondrosit.khondrosit.

AAnabolinabolic factorc factor KKataboliatabolic factorc factor

IL-1 / TNF alphaTGF beta / IGF-1

Balance Balance Degradation - SynthesisDegradation - Synthesis

Chondrocyte metabolismChondrocyte metabolism

CatabolismAnabolism

Chondrocyte

Stimulation

IGFs, TGF-beta, PDGF, EGF

Bone morphogenic protein

Cartilage derived morphogenic protein

Growth factor

Stimulation

Gamma- Interferon

TNF-alpha

Prostaglandins

Oxygen radicals, NO

IL-1, TNF-alpha, IL-17, FGFs, gamma interferon

Leukemia inhibitory factor

Glucocorticoid

Pro-collagen fragments

Inhibition

TIMP, Plasminogen activator inhibitor

Calicrein

Inhibition

Non-modifiableNon-modifiable AgeAge RaceRace Genetics (Col 2A1 Genetics (Col 2A1

gene, VDR)gene, VDR) Female sexFemale sex Metabolic and Metabolic and

endocrine diseaseendocrine disease Congenital defectCongenital defect Neurological defectNeurological defect

ModifiableModifiable Major traumaMajor trauma Repetitive stressRepetitive stress Inflammatory joint Inflammatory joint

diseasedisease ObesityObesity Smoking Smoking HormoneHormone Quadriceps muscle Quadriceps muscle

weaknessweakness

Hochberg MC. J Rheumatol 1991; 18: 1438-40.

Risk factors for OARisk factors for OA

Pathology of osteoarthritisPathology of osteoarthritis

SYMPTOMS & SIGNSSYMPTOMS & SIGNS

• Joint pain that increases with activity

• Morning stiffness that is relatively brief and self limited

• Crepitus (a grating sensation with motion)

• Bone enlargement at the joint margin

• Tenderness to palpation over the joint

• Non-inflammatory synovial fluid (<1000 WBC/mm3)

• ESR normal for age

• Radiographic evidence of OA

• ANA (-) and FR (-)

DIAGNOSTIC EXAMINATION

Radiological Examination

It's enough to provide diagnostic valuePreview radiological support an OA:1. Joint space narrowing2. Increased density (sclerosis) of subchondral bone3. Cyst of bone4. Osteofit on the edge of the joints5. Changes joint anatomy

1. Normal

2. JSN, there may osteofit

3. Real osteofit, any JSN or doubtful

4. Moderate osteofit, real JSN, less sclerosis, there may deformity

5. Real deformity

Base on radiological images, The OA-gradation based on the Kellgren-Lawrence :

Conduction

COX-2

v

Clinic : 3/6 criteria - Age > 50 yo - Morning stiffness < 20 minutes - Crepitation - Bone pain - Bone enlargement - Not warm in palpation

The Knee OA The Knee OA 1

Clinic & radiologic- Knee pain

+ 1/3 following criteria :-Age > 50 yo-Morning stiffness < 30 minutes-Crepitation

+ Osteofit

The Knee OAThe Knee OA 2

Clinic & laboratory :

Knee pain

+ 5/9 criteria :-Age > 50 yo -Crepitation-Morn.stiff < 30 mnt -BSR < 40 mm/h-Bone pain -RF (-)-Bone enlargement -SF OA-Not warm in palpation

The Knee OAThe Knee OA 3

Hand pain

+ 3-4 following criteria :-Hard tissue enlargement 2/10 certain joint-Hard tissue enlargement 2 DIP-Swelling < 3 MCP-Minimal deformity 1/10 certain joints

Certain joints : DIP II & III L & R, PIP II & III L & R, MCP I L & R

The hand OAThe hand OA

Coxae pain

+ minimal 2/3 criteria :-BSR < 20 mm/h-Radiographs : osteofit on acetabulum or kaput femoris-Radiographs : joint space narrowing (superior, axial and/or medial)

The Coxae OAThe Coxae OA

Source of painSource of pain::

memechchanianicalcal – – associated with the use of jointassociated with the use of joint

InflamInflammmaattiionon- - stiffnessstiffness, , pain was exacerbated with the restpain was exacerbated with the rest

Night painNight pain – – Intraosseus hyIntraosseus hypertensipertensionon

Pain rapidly deterioratingPain rapidly deteriorating - - ConsiderConsider sepsis, sepsis, avascular necrosisavascular necrosis, fra, fracctur, tur, oror crycrystalstal

synovitissynovitis. .

Study patients with OAStudy patients with OA

WeightWeight Risk factor interventionRisk factor intervention

Joint lockingJoint locking Consider referral to an orthopedic surgeonConsider referral to an orthopedic surgeon

Sleep disturbanceSleep disturbance MMay be related to fibromyalgia and depressionay be related to fibromyalgia and depression

CComorbid diseasesomorbid diseases

Study patients with OAStudy patients with OA

DIAGNOSIS BANDINGDIAGNOSIS BANDING

Septic ArthritisSeptic Arthritis Rheumatoid ArthritisRheumatoid Arthritis Gout ArthritisGout Arthritis Pes anserinePes anserine

Differential DiagnosisDifferential Diagnosis

Management ofManagement of OA OA

IdentifiIdentificcaation tion of risk factors for the of risk factors for the

occurrence of occurrence of OA.OA.

ModifiModificationcation of risk factors such as body of risk factors such as body

weight (obesity) and repeated minor weight (obesity) and repeated minor

traumatrauma

PreventionPrevention

GeneralGeneral Maintain optimal weight / idealMaintain optimal weight / ideal Maintain activity and regular exerciseMaintain activity and regular exercise Maintain a positive approachMaintain a positive approach

SpecificSpecific Strengthening the musclesStrengthening the muscles Pay attention to the specific Pay attention to the specific

disability(shopping, work at home, work)disability(shopping, work at home, work)

Lifestyle changesLifestyle changes

Short termShort term

Non Steroid Anti Inflammation Drugs Non Steroid Anti Inflammation Drugs (NSAIDs)(NSAIDs)

Analgetic (Opioid, non-opioid)Analgetic (Opioid, non-opioid) Antispasmodik Antispasmodik

Symptomatic treatmentSymptomatic treatment

Outbreaking mechanism of the damage Outbreaking mechanism of the damage of Gastric Mucous Membrane (Direct of Gastric Mucous Membrane (Direct Action) by Acid NSAIDSAction) by Acid NSAIDS

Gastric epithelium(pH7 - 7.4)

Stomach lumen(pH1 - 2)

Non-ion Type (lipophilic)

Ion Type (hydrophilic)

NSAIDs accumulatedDestruction of the gatewayof the gastric mucous membrane

Back diffusion of H+

Damage of the gastricmucous membrane

Lipid cell membrane

Lipid cell membrane

Capillary vessel (pH7.4)

LTC4

LTD4

LTB4

Free radicals play an important role in NSAIDs-induced gastric mucosal injuries

NSAID

Decrease of PGs

Decrease mucus productionDecrease bicarbonat secretionDecrease of microcirculation

Decrease of mucosal defense

Increase of LTs

Vasospasm

Neutrophil activation

Release of FREE RADICALS

H+dependent pathway

Accumulation in cells

Direct damage on cells

Ischemia-Reperfusion

Cyclo-oxygenase Lipooxygenase

Phospolipid

Phospolipase

Arachnidonic acid

GASTRIC MUCOSAL INJURY

Hiraishi H et al., Mebio 1994;11(19):86 (Japanese)

Lypo-oxygenase

Free Radical & NSAIDFree Radical & NSAIDFree Radical & NSAIDFree Radical & NSAID

Free Radical (DVD Movie), Naito Y, et al. 2006

Long termLong term

Depokortikosteroid intra-artikulerDepokortikosteroid intra-artikuler

Asam hialuronat intra-artikuler*Asam hialuronat intra-artikuler*

S-adenosilmetionin (SAM)*S-adenosilmetionin (SAM)*

Nutraceutical:Nutraceutical:

Kondroitin-sulfat oral *(SYSADOA)Kondroitin-sulfat oral *(SYSADOA)

Glukosamin-sulfat (Dona) *Glukosamin-sulfat (Dona) *

Ginger-based products?Ginger-based products?

cat’s claw?cat’s claw?

shark cartilage?shark cartilage?

Orgotein intra-artikuler *Orgotein intra-artikuler *

Diacerhein*Diacerhein*

Avocado/soy nonsaponifiables *Avocado/soy nonsaponifiables *

Symptomatic treatmentSymptomatic treatment

TetrasiklinTetrasiklin Glycosaminoglycan polysulfuric acid (GAPS)Glycosaminoglycan polysulfuric acid (GAPS) Glycosaminoglycan peptide complexesGlycosaminoglycan peptide complexes Pentosan polysulfatePentosan polysulfate Growth factors and sitokin (TGF-b)Growth factors and sitokin (TGF-b) Gene therapyGene therapy SStem celltem cell transplantation transplantation Osteochondral GraftOsteochondral Graft Anti TNF Alfa (Etanercept)Anti TNF Alfa (Etanercept)

Disease Modifying OA DrugsDisease Modifying OA Drugs(DMOAD)(DMOAD)

OA characterized by cartilage destruction and OA characterized by cartilage destruction and

osteofit formation.osteofit formation.

OA is not just the OA is not just the wear and tearwear and tear..

Prevention of risk factors that can be changedPrevention of risk factors that can be changed

Farmakologic symptomatic therapy and Farmakologic symptomatic therapy and

rehabilitatif (combination)rehabilitatif (combination)

Have not found a DMOADHave not found a DMOAD

ConclusionConclusion

DIAGNOSIS AND MANAGEMENT GUIDELINES OADIAGNOSIS AND MANAGEMENT GUIDELINES OA IRAIRA

SEMOGA BERMANFAAT