Inflammmation on Rheumatic

Disease and relationship with its

management
Focus on
OSTEOARTHRITIS

Hendrata Erry Andisari

Div of Rheumatology-Allergy, Dept of Internal Medicine
Medical Faculty Hang Tuah University/ Ramelan Naval Hospital, Surabaya.
2017
Inflammation
The development of inflammatory respon is an important
mechanism by which an organism defenst itsaelf against
pathogenic agents and initiates both structural ang
functional repair of damage tissue.

It represent a complex interaction of phatogenic agents,

parenchymal cell ang tissue components, the vasculature,
and both plasma and cellular component of blood.

Inflammation is characterized by the movement of fluid,

plasma proteins, and leukocytes into tissues in response
to injury, microbial invasion, foreign material, or antigens.
Walker BAM and Fantone JC, 1994. The inflammatory responses. In (LH Sigal & Y Ron), Immunology and
Inflamation, Basic and Clinical Consequences. New York : McGraw-Hill.359-386.
 Possible consequences of inflammation

Exogen causes Endogen causes

Tissue injury

Chemical reaction vascular reaction cellular reaction

Release of: Vasoconstriction Acute : Neutrophil

Histamine Vasodilatation Lining
Metabolites of AA Emigration
ROP Phagocytosis
Other enzymes Chronic: Macrophage &
lymphocytes
Cyokines

Inflammation

Recovery Granulomatous inflammation Scar

(Chronic) and tissue disfunction

Note: AA = Arachidonic Acid, ROP Reactive oxygen product

 Acute inflammation mediators

Stimulus IL-12

TNF IL-1

IL-6 Vascular IL-8 Low Collagenase

Endothelium molecular Proteoglicanase
Mediators Proteoglican synthesis

(PGE,POR,NO)

Acute Selectins Leucocyte Blood

Phase HEV chemotaxis flow
Protein,
fever

Systemic response Local Inflamation Tissue destruction

Rheumatic Ds
• Arthriti is an abnormality of joint and its
• Inflammation is the central point of the pathogenesis
• Osteoarthritis is the most common rheumatic ds

OSTEOARTHRITIS (OA) :
a condition that represents a complex of interactive
degradative and reparative processes
in cartilage and bone
with secondary inflammatory changes.

Poole AR and Howell DS, Etiopathogenesis of OA. Osteoarthritis. 3d Edt. Diagnosis and Medical/Surgical Management.
Structure of Cartilago

1. Chondrocyte
2 % of total volume
Produce a matrix
2. Matrix
Hydrated extracellular matrix
2.1 collagen ( type II and IX,XI)
2.2 Proteoglican
Negative charge (absorbant)
A complex macromollecules with a protein
core to which are attaced glycosaminoglycan
chains.
Glycoaminoglycan chains : chondroitin sulfate
and keratan sulfate
Risk Factors of OA

1. Quality of cartilago
Genetics
such as disturbance of collagen formation (mutation of
gen COL 2A1, formation of type 2 collagen)
Abnormal structure and quality of cartilago
2. Burden of the joint
Trauma
Excessive joint burden
Excessive destruction of cartilago
Aging proccess
Causing changing of composition, structure, and
the ability of cartilago( tissue)
Etiologies of OA

Multifactors:
1. Primary OA
1.1 Hereditary
1.2 Age (elderly)
1.3 Mechanical (microtrauma)
1.4 Biochemical disorder of chondral bone
2. Secondary OA
2.1 caused by other diseases
Degradation and synthesis of matrix cartilago
The evolution of cartilago in OA

Degradasi TR
Degradation of Cartilage

Sintesis
Sintesis TR
of cartilage
(decrease of quality)
(kwalitas kurang)

Bulla
Edema
Edema

Bulla
Bulla

Erosi
Fibrillation
Fibrilasi

Erosion of cartilage
Erosi
 Primary destruction of cartilago

Stimulate cytokines ( TNF α, IL-1) and

hystamine formation
Release of metalloprotease enzyme

Damage of cartilago joint and synovium

Secondary synovitis
Mediators of inflammation in pathologic change of OA
Phatologic change of joint in OA
Erosion
Erosionof
ofcatiliage
catiliagesurface
surface
Pathological Abnormality
in knee OA

Abnormalities of cartilago
edema, cleft, fibrillation,
erosion, thinning
Subchondral bone
sclerosis, cyst, eburnation,
osteophyte
Chronis synovitis (secondary)
Joint effusion
Surrounding tissue:
thickening of joint capsule,
muscle weakness, tendon
weakness
 Circuluc Vicious of OA

Efussion pain inflammation

Reduced
integrity of decreased
biomechanical of joint space
factors

muscle atrophy reduced muscle efussion

contraction
Supporting diagnosis of OA

• Radiology study :
- plain photo
- Others :MRI. Scintigrapphy
• Arthroscopy
• Laboratorium : normal
Diagnosis of Knee OA

Clinical assesment
Criterias for genu OA
(Subcommittee ACR)
1. Paint on genu
2. Ro : osteophyte with
3. One of following :
a. Age > 50 years
b. joint stiffness< 30
minutes
c. Crepitation
 Management of OA

Objective :
1. Reduced symptoms
2. Prevent further damage
Modalities for management of OA
- Education
- Physical treatment / non medicinal
- Medicinal
- Phsycologycal
- Operatif
 Ethiologyc factors
1.primary
2.secondary

Alteration of biomechanical &

biochemistry of cartilago

Fracture of
--cell proliferation
subchondral Chondrocyte response - Increased matrix
bone
synthesis

Collagen
alteration
DMOADs ?

Release of degradative enzymes

Matrix alteration Inflammation

Osteophyte formation Structural destruction ( immunological reaction)

Simple analgetic, NSAID Corticosteroids

OSTEOARTHRITIS

Pysical Therapy Surgical treatment

Education

Etiopathogenesis and Treatment of OA

Principals in management of rheumatic diseases

Etiological factors Disease procces

- Exogen (inflammation) Symptoms
- Genetic

Eleminate corticosteroid Analgetic

etiologic DMOADS NSAID
factors Biological therapy

Gene therapy
Medicinal
- As a primary therapy??
- Mild OA :
- Systemic therapy is not necessary
- Topical medicine

- Analgetic
1. simple analgetics : paracetamol
2. NSAID ( selective non selective)
3. Narcoties analgetic
- Local Corticosteroid ( not systemic)
- Other drugs
DMOADS ?
Chondroprotective drug ?
Biological drug IL-1 Ra
Pharmacological treatment prescribe (n = 2430)
Drug treatment
• Paracetamol 95.8%
• NSAID 34.2%
• Other analgesic 28.0%

Treatment prescribe as first time

• Paracetamol only 60.6%
• NSAID only 1.8%
• Other analgesic only 1.0%
• Paracetamol + NSAID 27.4%
• Paracetamol + other analgesic 4.2%
• NSAID + other analgesic 1.4%
• Paracet.+NSAID+other analg. 3.5%

Denoeud et al. Fisrt line treatment of knee OA in out patients in France: adherence to the EULAR 2000 recommendations and factors
influencing adherence.bmjjournals.com.9Febr.2006.
 Summary
• Inflammation is represent a complex interaction of phatogenic
agents, parenchymal cell ang tissue components, the vasculature,
and both plasma and cellular component of blood.
• Inflammation is the central point of the pathogenesis of rheumatic ds
• OA is a condition that represents a complex of interactive
degradative and reparative processes in cartilage and bone with
secondary inflammatory changes in synovium
• The pathologic changes of OA are an abnormalities of cartilago,
subchondral bone, chronis synovitis and surrounding tissue.
• It needs comprehensive management
• Eleminate the etiological factors
• Education is important (Self management programe)
• Drug : only for symptomatic therapy, simple analgetic, NSAID
• DMOAD?
Thank You
 OSTEOARTHRITIS (OA) :

a condition that represents a complex of

interactive
degradative and reparative processes
in cartilage and bone
with secondary inflammatory changes.

Poole AR and Howell DS, Etiopathogenesis of OA. Osteoarthritis. 3d Edt. Diagnosis and Medical/Surgical Management.
WB Saunder Comp.2005
 Principal in Making Clinical Diagnosis

• Clinicall data :
Joint (arthritis) or outside the joint
Monoarticular, oligoarticular, or poliarticular
With ekstraarticular symptoms
Acute or chronic condition
Age, sex, hereditary, occupation
• Supporting data
Selective, depends on working diagnosis
Radiology : joint predilection
Laboratory : non specific or spesific
 Clinical Diagnosis

• History taking :
Chief complain : pain on knee joint
Basic seven
Foundamental four
Making diagnosis and DD
• Physical examination
Inspection : swelling
Palpation : joint pain
efussion (Bulging sign or ballotement
test)
Movement : disturbance of movement, ankylose
Auscultation : crepitation
• Supporting diagnosis
Rontgen : osteophyte
Nonpharmacologic management
of patients with osteoarthritis of the knee*
*) Hochberg MC et al, Guidline for the medical management of OA. Arthritis & Rheumatism. 38(11):1541-1546.1995.

_ Patient education
Self management programme (e.g. Arthritis Self-Help Course)
Health professional social support via telepone contact
Weight loss of overweight
Physical therapy
Range of motion exercises
Quadriceps strengthning exercises
Assistive devices for ambulation
Occupational thrapy
Joint protection and energy conservation
Assistive devices for ADLs and JADLs
Aerobic exercise programs
Astroscophic examination of knee joint
Plain Photo of OA on the Knee

Cartilago :
Narrowing joint space
Chondrocalsinosis
Focal articular contour irregularity
Bone
Osteophyte
Subchondral sclerosis
loose bodies, etc
Surrounding Tissue
Swelling
Atrophy os fibrous tissue
Myocytic ossification
Ectopic calsification
 DMOADs
(Diseases Modifying OA Drugs)

• Expected to have role in pathogenesis

• There people claimed that DMOAD could
reduced destruction or could increase cartilago
formation
• Glucosamine ?
• To date, no medicine proven as a DMOADS yet
• In future : Biologic agents (Il-1-Ra)

Brandt.Non-surgical treatment of OA, a half century of 'advances, ard.bmjjournals.com,1 Febr.2006

ACRFP
 NORMAL vs. OA JOINT
Normal knee Osteoarthritic knee

thickened capsule
capsule
cyst formation
cartilage sclerosis in
subchondral bone
synovium
fibrillated cartilage

bone synovial hypertrophy

osteophyte formation

ACRFP
Terapi alternatif ? • Accupunture
• TENS
• Pulse electromagnetic
field
• Refleksi
• dan lain-lain
Principal management of Rheumatic disease