Lecture Oa
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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
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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
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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
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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
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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
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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
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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
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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
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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
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NORMAL OSTEOARTHRITIS
Femoral condyles
Tibial plateausSubchondral bone
Patella
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Predileksi Predileksi jointsjointsPredileksi Predileksi jointsjointsMost often : Weight bearing joints - knee - lumbal - cervical
Generalized OA DIP (Heberden’s node)
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Thickening capsule
OA kneeNormal knee
Cyst formation
SclerosisSubkhondral bone
Cartilage fibrillation
Hypertrofi synovium
Osteofit formation
Capsule
Cartilage
Synovium
Bone
ACRFP
NORMAL versus OA JOINT
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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
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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
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Extra Cellular Matrix
Synthesis MMaintainaintain
Chondrocyte functionChondrocyte function
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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
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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
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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
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Pathology of osteoarthritisPathology of osteoarthritis
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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 (-)
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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
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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 :
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Conduction
COX-2
v
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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
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Clinic & radiologic- Knee pain
+ 1/3 following criteria :-Age > 50 yo-Morning stiffness < 30 minutes-Crepitation
+ Osteofit
The Knee OAThe Knee OA 2
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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
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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
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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
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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
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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
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DIAGNOSIS BANDINGDIAGNOSIS BANDING
Septic ArthritisSeptic Arthritis Rheumatoid ArthritisRheumatoid Arthritis Gout ArthritisGout Arthritis Pes anserinePes anserine
Differential DiagnosisDifferential Diagnosis
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Management ofManagement of OA OA
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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
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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
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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
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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)
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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
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Free Radical & NSAIDFree Radical & NSAIDFree Radical & NSAIDFree Radical & NSAID
Free Radical (DVD Movie), Naito Y, et al. 2006
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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
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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)
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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
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DIAGNOSIS AND MANAGEMENT GUIDELINES OADIAGNOSIS AND MANAGEMENT GUIDELINES OA IRAIRA
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SEMOGA BERMANFAAT