OSTEOARTHRITIS

09/25/09
CLINICAL FEATURES

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 Consensus definition of OA
 OA disease are manifested by morphologic, biochemical,
molecular, and biomechanical changes of both cells and matrix
which lead to a softening, fibrillation and eburnation of sub-
chondral bone, osteophytes, and sub-chondral cysts.

 Clinically evident characterized by joint pain, tenderness,

limitation of movement, crepitus, occasional effusion, and
variable degrees of inflammation without systemic effect.

Kuettner KE, et al. Am Acad Orthop Surg,1999

 Joints Commonly Involved
in Osteoarthritis

· Osteoarthritis principally affects weight-

bearing joints in the knees and hips.
· Also affects the feet, ankles, distal
interphalangeal joints, proximal
interphalangeal joints, first
carpometacarpal joints, cervical spine, and
lower spine

APS. Guideline for the Management of Pain in Osteoarthritis, Rheumatoid Arthritis, and Juvenile Chronic Arthritis. 2nd ed. Glenview, Ill:
American Pain Society; 2002.
 Distribution of OA of the hands
Swanson AB, Swanson G. Clin Rheum Dis 1985
5
distribusi

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Sendi Normal dan Perubahannya Pada OA

Tulang subkhondral
Tekstur tulang menebal dan ireguler,
subkhondral normal tampak sklerostik dan
pembentukan kista

Rawan sendi Kapsul mengalami

normal, tebal dan fibrosis, distorsi dan
rata penebalan

Fibrilasi, kerusakan dan

berkurangnya volume
Ujung tulang rata
rawan sendi
Sinovium normal
dengan selapis sel Sinovitis kronik
tunggal

Pertumbuhan osteofit,
Kapsul sendi tebal dan penebalan jaringan
ikat lunak
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 Common symptoms and sign of OA

Symptoms Signs

Pain Crepitus
Stiffness Restricted movement
Alteration in shape Tenderness - joint line
Functional impairment - periarticular
+ anxiety, depression Bony swelling
Deformity
Muscle wasting / weakness
+ effusions, increased warmth
+ instability

O’Reilly S, Doherty M. in OA Oxford Press 1998 8

Osteoartritis sendi lutut

Kista subkondral

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OARSI recommendations for the management
of hip and knee
osteoarthritis, Part II: OARSI evidence-based,
expert consensus
guidelines (2008)
 OARSI recommendations
for the management of hip and knee OA
1. Optimal management of OA requires a combination of non-
pharmacological and pharmacological modalities. SOR: 96%
(95% CI 93-99)
2. Patients with hip and knee OA should be encouraged to
undertake, and continue to undertake, regular aerobic,
muscle strengthening and range of motion exercises. SOR:
96% (95% CI 93-99)
3. Patients with hip and knee OA, who are overweight, should
be encouraged to lose weight and maintain their weight at a
lower level. SOR: 96% (95% CI 92-100)
 OARSI recommendations
for the management of hip and knee OA

4. Acetaminophen can be an effective initial oral analgesic for

treatment of mild to moderate pain in patients with knee or
hip OA. In the absence of an adequate response, or in the
presence of severe pain and/or inflammation, alternative
pharmacologic therapy should be considered based on
relative efficacy and safety, as well as concomitant
medications and comorbidities. SOR: 92% (95% CI 88e99)
5. In patients with symptomatic hip or knee OA, non-steroidal
anti-inflammatory drugs (NSAIDs) should be used at the
lowest effective dose but their long-term use should be
avoided if possible. SOR: 93% (95% CI 88e99)
 OARSI recommendations
for the management of hip and knee OA

• 6. Intra-articular (IA) injections with corticosteroids can be

used in the treatment of hip or knee OA, and should be
considered particularly when patients havemoderate to
severe pain not responding satisfactorily to oral
analgesic/anti-inflammatory agents and in patients with
symptomatic knee OA with effusions or other physical signs of
local inflammation. SOR: 78% (95% CI 61e95)
• Injections of IA hyaluronate may be useful in patients with
knee or hip OA. They are characterised by delayed onset, but
prolonged duration, of symptomatic benefit when compared
to IA injections of corticosteroids. SOR: 64% (95% CI 43e85)
 RHEUMATOID ARTRITIS
• Chronic systemic autoimmune inflammatory
disease , especially affected small joint, leading
to joint destruction and disability
• Joint destruction mostly in first 2 year
• ‘‘Early aggressive treatment with DMARDs is
needed to achieve the greatest effect on long
term outcome’’
• Prevalence: - 1 % (USA)
• - 0.2 - 0.6 % (Asia)
• Female : male = 3 : 1
 RA is Characterised by Synovitis and
Joint Destruction
Inflamed
NORMAL RA synovial
Synovial
membrane membrane

Major cell types:

• T lymphocytes
• macrophages
Pannus
Cartilage Minor cell types:
• fibroblasts
• plasma cells
• endothelium
• dendritic cells

Synovial Major cell type:

Capsule fluid • neutrophils

Cartilage thinning
Adapted from Feldmann M, et al. Ann Rev Immunol. 1996;14:397-440;
Pincus T. Drugs. 1995;50(suppl 1):1-14; Tak P, Bresnihan B. Arthritis Rheum. 2000;43:2619-2633.
Rheumatoid arthritis (RA) is a chronic and progressive inflammatory disease,
characterised by synovitis and joint destruction, 1 and often results in significant
disability and premature mortality.2
The pathogenesis of this chronic autoimmune disease is mediated by an interdependent
network of cytokines, prostanoids, and proteolytic enzymes.3 Cytokines possess
proinflammatory and immunosuppressive anti-inflammatory properties that regulate
immune responses.1
An imbalance between proinflammatory and anti-inflammatory effects is thought to
contribute to the chronic nature of RA. Hence, the current pathogenetic model for RA is
one of a chronic, tissue-specific inflammatory process to which a variety of immune
responses can contribute.1
This slide depicts the unique pathophysiological elements of RA that arise from
interactions between
–the variety of leucocytes that invade the joint, and
–the native cellular components of joint tissue.
 Rheumatoid Arthritis:
Goal of Treatment

• Remission
1. Pain control
2. Maintan joint fuction for essential and daily
activity
3. Optimize QOL
4. Prevent or inhibit joint destruction
 Rheumatoid arthritis : Therapy
• Education
• Non pharmacologic : diet, exercise, rehabilitation
• Pharmacologic :
– NSAIDs
– DMARD :
• Conventional
• Biologic
– Glucocorticoid
• Surgery
• Others
 NSAIDs
• The NSAIDs are used to modify the symptoms of RA.
• The use of NSAIDs is recommended at disease onset, when a new
DMARD is introduced, and occasionally when uncontrolled
isolated symptoms persist despite good response to a DMARD.
• The need for continuous use of NSAIDs in a patient with RA
should be interpreted as inadequate control of inflammatory
activity and should, therefore, lead to reassessment of the
DMARD regimen.
 NSAIDs
• All NSAIDs should be used at the full dose for at
least 1 week before considering the treatment to
have failed. Once symptoms have been
controlled, the minimum effective dose should be
used.
• There is no evidence that some NSAIDs are better
than others, but vary in their potential
gastrointestinal, liver and cardio-renal toxicity;
therefore, when choosing the agent and dose,
healthcare professionals should take into account
individual patient risk factors