OSTEOART H RIT

IS Diagnosis
and
Management

FARIDIN HP
DEPARTMENT OF INTERNAL MEDICINE
UNHAS / DR.WAHIDIN SUDIROHUSODO
HOSPITAL, MAKASSAR
 Dr. H. Faridin HP, SpPD,KR
Education
1989: 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
Courses in Rheumatology division :
Course Of Osteoporosis in Lido Lake Hotel Sukabumi
Immuno-Rheumatology in Malang
Pain in Rheumatic Diseases in Ibis Hotel Jakarta
Osteoarthritis Course in Lembang, Bandung
Membership organizations
IDI, PAPDI, IRA, PEROSI
ACR Annual Meeting, 1999 :
Discussion and debate on pathogenesis of
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
Limitation
OA is a rheumatic disease that affects cartilage
where the outcome of pathological processes in
the form of joint failure as one organ system.

Characteristics:
focal loss of cartilage with the response of
bone repair / osteofit formation
Epidemiology 1

 OA is a common rheumatic diseases

found in all parts of the world.

 Prevalence:
Amerika 12.0 % (total population)
Roy D Altman
Epidemiology 2

Indonesian:
 Community-based research
City Village
Malang* 10.0 % 13.5%
Bandungan** 5.4%
* Kalim H, cs 1994, ** Darmawan, 1992

 Hospital-based research

RSCM 43.8% (total of rheumatic patients)

1991-1994
The Prevalence of OA
Radiologic Imaging in
Population

70
60
50
Prevalensi (%)

40
30
20
Lutut, Laki-laki
10 DIP, laki-laki

0 Lutut, perempuan
30 40 50 60 70 DIP, perempuan
Usia (tahun)
Pathogenesis of OA

Not only Wear and Tear :

 There is a difference in the change of cartilage

due to aging process (aging process)

 Can occur in young animals stimulated with

chemicals / trauma
 Normal joints and its changes in OA

Irregulars subkhondral
Normal texture of bone and thickening,
subkhondral bone
appeared sklerotic and
cyst formation
Normal cartilage, Capsules had fibrosis,
thick and flat distortion, thickening

Flat bone edge Fibrillation, damage and

reduced the volume of
cartilage
Normal sinovium
with single cell Chronic sinovitis
layer

Osteofit growth, and

Thickening joint thickening of the soft
capsule tissue
NORMAL OSTEOARTHRITIS

Patella

Femoral condyles
Tibial plateaus
Subchondral
bone
Predileksi
joints
Most often : Weight bearing joints
- knee
- lumbal
- cervical

Generalized OA ⇒ DIP
(Heberden’s node)
 NORMAL versus OA JOINT

Normal knee OA knee

Thickening capsule
Capsule
Cyst formation
Cartilage Sclerosis
Subkhondral bone
Synovium
Cartilage fibrillation

Bone Hypertrofi synovium

Osteofit formation

ACRFP
Composition of Normal
Articular cartilage

Water 66-78%
Matrix 22-34%
Collagen type II 48-62%
Proteoglycan 22-38%
Hyaluronan <1%
Chondrocytes 0.4-2%
Inorganic 5-6%
OA Cartilage
 There is degradation and synthesis imbalance

 Despite synthesis, the quality of cartilage

formed poor

 End-stage: proteoglikan synthesis

is declined, khondrosit function
is decreased
Chondrocyte
function

Synthesis Maintain

Extra Cellular Matrix

Balance
Degradation - Synthesis

Anabolic-katabolic factors affecting

khondrosit.

Anabolic factor Katabolic factor

TGF beta / IL-1 / TNF

IGF-1 alpha
 Chondrocyte metabolism
Stimulation Stimulation
IGFs, TGF-beta, PDGF, EGF Gamma- Interferon
Bone morphogenic protein TNF-alpha
Cartilage derived morphogenic Prostaglandins
protein
Oxygen radicals, NO
Growth factor

Chondrocyte
Anabolism Catabolism

IL-1, TNF-alpha, IL-17, FGFs, TIMP, Plasminogen activator

gamma interferon inhibitor
Leukemia inhibitory factor Calicrein
Glucocorticoid Inhibition
Pro-collagen fragments
Inhibition
Risk factors for OA

Non-modifiable Modifiable
 Age  Major trauma
 Race  Repetitive stress
 Genetics (Col 2A1  Inflammatory joint
disease
gene, VDR)
 Obesity
 Female sex  Smoking
 Metabolic and  Hormone
endocrine disease  Quadriceps muscle
 Congenital defect weakness
 Neurological defect
Hochberg MC. J Rheumatol 1991; 18: 1438-40.
Pathology of osteoarthritis
 SYMPTOMS &
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 value
Preview radiological support an OA:
1. Joint space narrowing
2. Increased density (sclerosis) of subchondral bone
3. Cyst of bone
4. Osteofit on the edge of the joints
5. Changes joint anatomy
 Base on radiological images, The OA-
gradation based on the Kellgren-Lawrence :

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
COX-2

v
The Knee OA 1

Clinic : 3/6 criteria

- Age > 50 yo
- Morning stiffness < 20 minutes
- Crepitation
- Bone pain
- Bone enlargement
- Not warm in palpation
The Knee OA 2

Clinic & radiologic

- Knee pain

+ 1/3 following criteria :

-Age > 50 yo
-Morning stiffness < 30 minutes
-Crepitation

+ Osteofit
The Knee OA 3

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 hand OA

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 Coxae 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)
Study patients with OA

Source of pain:

 mechanical – associated with the use of joint

 Inflammation- stiffness, pain was exacerbated with the rest

 Night pain – Intraosseus hypertension

 Pain rapidly deteriorating - Consider sepsis, avascular necrosis, fractur, or crystal synovitis.
Study patients with OA

Weight
 Risk factor intervention

Joint locking
 Consider referral to an orthopedic surgeon

Sleep disturbance
 May be related to fibromyalgia and depression

Comorbid diseases
Differential Diagnosis
DIAGNOSIS BANDING
DIAGNOSIS BANDING
 Septic Arthritis
 Rheumatoid Arthritis
 Gout Arthritis
 Pes anserine
Management of OA
Prevention

 Identification of risk factors for the

occurrence of OA.
 Modification of risk factors such as body
weight (obesity) and repeated minor trauma
Lifestyle changes

General
 Maintain optimal weight / ideal
 Maintain activity and regular exercise
 Maintain a positive approach

Specific
 Strengthening the muscles
 Pay attention to the specific
disability(shopping, work at home, work)
Drugs of OA

 Optimum dose of a simple analgesic

 Topical preparations(NSAIDs, liniment or
capcaisin)
 NSAIDs
 IA steroid injection
 IA hyaluronan injection
 Disease modifying osteoarthritis drugs
(DMOAD)
Symptomatic treatment

Short term

 Non Steroid Anti Inflammation Drugs

(NSAIDs)
 Analgetic (Opioid, non-opioid)
 Antispasmodik
Outbreaking mechanism of the
damage of Gastric Mucous
Membrane (Direct Action) by Acid
NSAIDS
Non-ion Type (lipophilic)
Stomach lumen Ion Type (hydrophilic)
(pH1 - 2)

Lipid cell membrane

NSAIDs accumulated
Destruction of the gateway
Gastric epithelium of the gastric mucous membrane
(pH7 - 7.4)
Back diffusion of H+
Damage of the gastric
mucous membrane
Lipid cell membrane
Capillary vessel (pH7.4)
 Free radicals play an important role in
NSAIDs-induced gastric mucosal injuries
NSAID
Phospolipid
Phospolipas
e
Arachnidonic
Cyclo-oxygenase acid Lypo-oxygenase
Lipooxygenase

Decrease of PGs Increase of LTs H+dependent

pathway
LTC4 LTB4
Decrease mucus LTD4 Accumulation in
production
Decrease bicarbonat cells
secretion Vasospas Neutrophil
Decrease of m activation
microcirculation
Ischemia-
Reperfusion
Decrease of Direct damage
mucosal Release of FREE RADICALS on cells
defense

GASTRIC MUCOSAL INJURY

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

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

Symptomatic treatment

Long term
Depokortikosteroid intra-artikuler
Asam hialuronat intra-artikuler*
S-adenosilmetionin (SAM)*
Nutraceutical:
Kondroitin-sulfat oral *(SYSADOA)
Glukosamin-sulfat (Dona) *
Ginger-based products?
cat’s claw?
shark cartilage?
Orgotein intra-artikuler *
Diacerhein*
Avocado/soy nonsaponifiables *
Disease Modifying OA Drugs
(DMOAD)

 Tetrasiklin
 Glycosaminoglycan polysulfuric acid (GAPS)
 Glycosaminoglycan peptide complexes
 Pentosan polysulfate
 Growth factors and sitokin (TGF-b)
 Gene therapy
 Stem cell transplantation
 Osteochondral Graft
 Anti TNF Alfa (Etanercept)
Conclusion

 OA characterized by cartilage destruction and osteofit

formation.
 OA is not just the wear and tear.
 Prevention of risk factors that can be changed
 Farmakologic symptomatic therapy and rehabilitatif
(combination)
 Have not found a DMOAD
DIAGNOSIS AND MANAGEMENT GUIDELINES OA
IRA
SEMOGA BERMANFAAT