OSTEOARTHRITISAgus Widiyatmoko
*INTRODUCTIONMostly elderlyAgeing process???Repeated micro trauma to the joint??
OSTEOARTRITIS
*The typical stance of a patient with knee OA: elderly female, often overweight, with genu varum deformity. They usually complain of a mechanical knee pain, characteristically felt on initial standing from a prolonged sitting position. Unlike patients with RA, those with OA do not have any systemic manifestations.
*INTRODUCTIONMany theories of etiology and pathogenesis
Start from breakage of cartilage and pathologic condition of the synovium
Definite treatment ???
Epidemiology
PopulationAge (yrs)Female (%)Male (%)English>357069US Caucasians>404443Alaskan Eskimos>402422Jamaican (rural)35-646254Pima Indians>307456Blackfoot Indians>307461South African Black>355360
Indonesia
Community based
Urban RuralMalang*10.0 % 13.5%Bandungan** 5.4%* Kalim H, cs 1994, ** Darmawan, 1992
Hospital based
RSCM43.8% (total rheumatic patients), 1991-199435.8% (total rheumatic patients), 2000Epidemiology
Prevalence of Radiographic Evidence of OA in the PopulationPrevalence (%)Age (years)
*ETIOLOGY
Knowing a normal tissue around the jointChondrocytesCollagenProteoglycanSynovial fluid
NORMAL versus OACapsul thicknessKnee OANormal KneeBone cystSubchondral schlerosis
Cartilage fibrillationSynovium hypertrophyOsteophyte formationCapsulCartilageSynoviumBone
*OA primarily starts as a cartilage problem, later involving other structures. Once these are affected, the patient starts to develop the pain characteristic of this condition.
*CARTILAGEHyaline cartilageFibro cartilage
*CARTILAGEFibro cartilage : meniscus
1.psd
*The pathologic features readily correlate with the radiographic features of knee OA, i.e. loss of joint space, subchondral cysts, and attempts at repair or regeneration such as sclerosis and osteophytes.
Stresses AbnormalNormal cartilageCartilage abnormalAgingGenetic and metabolic diseaseInflammationAdministration of toxinsImmune responseObesity, Developmental and anatomic abnormalitiesBony remodeling and micro fractureLoss of joint stabilityTraumaTheory A Biomaterial failure collagen networkfractureTheory BCell injuryIncrease of degradative responsesInhibitors reducedProteolytic enzymes increasedDestruction of prteoglycans collagenand other proteinsProteoglycan unravelling
Cartilage breakdown
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Degenerative Joint DiseasePathophysiology
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Degenerative Joint DiseaseClinical ManifestationsPain
Malfunction
Deformity
Elderly,Repetitive Trauma or Major Trauma to Joint
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Assessment of patients with OANature of painMechanical - related to useInflammatory - stiffness, pain aggravated by restNocturnal - suggest intraosseous hypertensionSudden deterioration - consider sepsis, avascular necrosis, fracture, or crystal synovitis
Clinical ExaminationPeriarticular or articular source of painGeneralised pain? - consider fibromyalgiaPresence of deformity?Evidence of muscle wasting?Local inflammation or effusion?Generalised or localised OA?
WeightPotentially modifiable risk factor
Joint lockingOrthopaedic referral probably appropriate
Sleep disturbanceMay be associated with fibromyalgia and depression
Comorbid disease
Assessment of patients with Osteoarthritis
*CLINICALAltman criteria'sAchlback classificationOuterbridege gradingKellgreen
*ALTMANS 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)
*ALTMANS CRITERIASClinical and Radiographic
Knee pain + at least 1 of these 3 : 1. Age > 50 years 2. Stiffness < 30 min 3. Crepitus + osteophytes
*ALTMANS CRITERIASClinical
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
*KELLGREN LAWRENCE GRADINGGRADE 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.
*RADIOLOGYSOFT TISSUE : ATROPHY JOINT SPACE : NARROWINGBONE : OSTEOPHYTE, SCLEROSING, BONE CYST, MALALIGNMENT (VARUS, VALGUS)
KNEE PAIN*
- Synovial fluid (SF) criteria for OA are (1) White blood cell
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*57/F, OA
*64/F, OA
*56/M, OA
presented at National congress of Indonesian Rheumatology Association. 3rd July 2005. Jogyakarta*69/F, OA
presented at National congress of Indonesian Rheumatology Association. 3rd July 2005. Jogyakarta
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2.psd
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*CLINICALAs a wholeHistory.
AtrophyJoint Contracture Activity daily living
ACR 2000 Guidlines-Drug Therapy Options in Osteoarthritis
Baseline program(Weight loss/exercise)
Mild/moderate Moderate/severePain pain/inflammation
AcetaminophenSteroids IA COX-2 specific Inhibitors
NSAIDs Hyaluronans Traditional NSAIDs Tramadol (plus gastroprotection)Propoxyphene OpioidsSurgery
*TREATMENTConservativeOperative.Reduce the symptoms / pain, improve joint function, reduce the progress, and improve quality of life
*CONSERVATIVEPharmacogenic :NSAIDCox 2 inhibitor Intra articular injection: hyaluronic acid, analgesic. steroid
Things to consider when selecting an NSAID Are they different?goodmodbad
Rasio Selektivitas Cox2/Cox1DrugRasio Cox2/Cox1Piroxicam250Acetylsalicylic acid175Indomethacin 60Ibuprofen 15Paracetamol 7.4Sodium salicylate 2.8Carprofen 1Meloxicam 0.8Diclofenac 0.7Naproxen 0.6Nimesulide 0.1ROFECOXIBE 0.02
Selektif Cox 2 Selektif Cox 1Adapted from Vane, J.R. IC50 Value (mol/L) of NSAIDs on COX-2 or COX-1 activity in intact cells
GI Events* Associated With NSAIDsMost Patients AsymptomaticN = 141N = 1,921Armstrong, Blower.Gut. 1987; 28: 527532Singh et al.Arch Intern Med.1996; 156: 15301536
WithoutsymptomsWithsymptoms
42%58%
81%19%*Bleeding, perforation, and gastric outlet obstruction
Mortality Associated With TypicalNSAIDs vs Other Causes in USFries et al. Am J Med. 1991; 91: 213222Wilson, Crouch. Science. 1987; 236: 267270Annual risk of death (%)0.250.200.150.100.050.00
0.400.350.30
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Disease Modifying Osteoarthritis Drugs TetrasiklinGlycosaminoglycan polysulfuric acid (GAPS)Glycosaminoglycan peptide complexesPentosan polysulfateGrowth factors and sitokin (TGF-b)Terapi genetikTransplantasi stem cellOsteochondral GraftAnti TNF Alfa (Etanercept)
Hyaluronic acid Bone Bone Cartilage
OsteoclastOsteoblastChondrocytesHAHASynovial liningCapsuleSynthesis: Synoviocyte, chondrocyte
Reduction of synovial membrane inflammationin the treatment using hyaluronic acid
Before treatmentAfter treatment
*OPERATIVEArthroscopy : lavage, shaving, drilling.OsteotomyArthroplastyMozaic graftStem cell graft
*ARTHROSCOPY
*ARTHROSCOPY
*ARTHROSCOPY
*OSTEOTOMY
*MOSAIC-PLASTY
*MOSAIC-PLASTY
*MOSAIC-PLASTY
*MOSAIC-PLASTY
*ARTHROPLASTY
*ARTHROPLASTY
6.psd
7.psd
8.psd
*STEM CELLS
*STEM CELLS
*STEM CELLS
*STEM CELLS
benefitriskMeasures the risk and benefit for your patients
ALHAMDULILLAHTERIMA KASIH*
*The typical stance of a patient with knee OA: elderly female, often overweight, with genu varum deformity. They usually complain of a mechanical knee pain, characteristically felt on initial standing from a prolonged sitting position. Unlike patients with RA, those with OA do not have any systemic manifestations.*OA primarily starts as a cartilage problem, later involving other structures. Once these are affected, the patient starts to develop the pain characteristic of this condition.*The pathologic features readily correlate with the radiographic features of knee OA, i.e. loss of joint space, subchondral cysts, and attempts at repair or regeneration such as sclerosis and osteophytes.*
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