OSTEOARTHRITIS

Ika Norcahyanti
Bagian Farmasi Klinik & Komunitas
Fakultas Farmasi UNEJ
 Definisi
 kerusakan tulang rawan
(kartilago) hyalin sendi
 meningkatnya
Osteoarthritis mrp penyakit ketebalan serta sklerosis
sendi degeneratif dari lempeng tulang
 pertumbuhan osteofit
keseluruhan struktur sendi pada tepian sendi
mengalami perubahan  meregangnya kapsula
patologis sendi
 timbulnya peradangan
 melemahnya otot–otot
yang menghubungkan
sendi
Fungsi Kartilago
 memungkinkan sendi
bergerak dlm rentang
gerakan yg dibutuhkan
 mendistribusikan beban ke
semua jaringan sendi shg
mampu mencegah
kerusakan sendi
 menstabilkan sendi slm
digunakan
Komponen kartilago artikular
 air (75-80%)
 ECM (Extracelluler Complex Matrix) yg tddr kondrosit 5%
sisanya (15-20%) terbagi mjd :
 kolagen
 proteoglikan (glikosaminoglikan, kondroitin sulfat,
keratan sulfat, asam hialuronat)
 protein non kolagen
 Kondrosit
 kondrosit memiliki peranan dlm remodelling kartilago
artikular
 kondrosit distimulasi dan mensekresi sejumlah enzim yg
berperan dlm menjaga keseimbangan antara sintesis dan
degradasi dr kartilago artikular
 pd org dws kartilago artikular bersifat avaskular shg
kondrosit memerlukan nutrisi dr cairan sinovial
 Kolagen & proteoglikan
 ada 5 tipe kolagen yg terdpt pd kartilago  tipe
II,VI,IX,X,XI
 fungsi kolagen adlh utk mempertahankan kekakuan
serta menjaga volume dan bentuk dr kartilago
 proteoglikan (PG) berkombinasi dg hialuronat
berfungsi utk menjaga kandungan air pd kartilago
 Klasifikasi
osteoarthritis

primary (idiopathic) OA
the most common type, has no known cause
secondary OA
is associated with a known cause, such as trauma, metabolic
or endocrine disorders, and congenital factors
Lokasi
 Faktor Resiko
increasing age

obesity

joint trauma
genetic
predisposition
repetitive use
through work or
leisure activities
 Patofisologi
OA usually begins with damage to articular cartilage through
injury, excessive joint loading from obesity or other reasons,
or joint instability or injury

damage to cartilage increases activity of chondrocytes in

attempt to repair damage, leading to increased synthesis of
matrix constituents with cartilage swelling

normal balance between cartilage breakdown and resynthesis

is lost, with increasing destruction and cartilage loss
 Patofisologi
subchondral bone adjacent to articular cartilage undergoes
pathologic changes and releases vasoactive peptides and
matrixmetalloproteinases(MMPs)

neovascularization and increased permeability of adjacent cartilage

occur, which contribute to cartilage
loss and chondrocyte apoptosis

cartilage loss causes joint space narrowing and painful,

deformed joints
 Patofisologi
new bone formations (osteophytes) at joint margins distant from
cartilage destruction are thought to help stabilize affected joints

inflammatory changes can occur in the joint capsule and synovium

interleukin-1, prostaglandin E2, tumor necrosis factor-α (TNF-α),

and nitric oxide in synovial fluid may
also play a role

inflammatory changes result in synovial effusions and thickening

pain may result from distention of the synovial capsule by increased
joint fluid; microfracture; periosteal irritation; or damage to
ligaments, synovium, or the meniscus
 Gambaran Klinis
patients with lower
limitation of motion,
extremity involvement
stiffness, crepitus, and
may report weakness or
deformities may occur
instability
upon a rising, joint
presence of warm, red,
stiffness typically lastsless
and tender joints suggests
than 30 minutes and
inflammatory synovitis
resolves with motion

heberden and bouchard

nodes are bony
enlargements
(osteophytes) of the dip
and pip joints, respectively
 Penegakan diagnosa
For hip OA
patient
must have
hip pain
radiographic
joint space
narrowing
ESR less than
20 mm/h
radiographic
femoral or
acetabular
osteophytes
 For knee OA
age more
patient must radiographic
than 50
have knee pain osteophytes
years

morning stiffness crepitus on bony

lasting 30 motion enlargement
minutes or less

palpable
bony
joint
tenderness
warmth
 Penegakan diagnosa
ESR may be slightly elevated if inflammation is
present
Rheumatoid factor is negative
Analysis of synovial fluid reveals high viscosity
and mild leukocytosis (<2000 white blood
cells/mm3 [<2 × 109/L]) with predominantly
mononuclear cells
 Tujuan Terapi
goal of treatment

educate patient, family members, and caregivers

relieve pain and stiffness
maintain or improve joint mobility
limit functional impairment
maintain or improve quality of life
Tata Laksana Terapi
(Knee & Hip OA)
Tata Laksana
Terapi
(Hand OA)
 Tata Laksana Terapi
(Knee & Hip OA)
 Acetaminophen is a preferred first-line treatment
 it may be less effective than oral nonsteroidal anti-
inflammatory drugs (NSAIDs) but has less risk of serious
gastrointestinal (GI) and cardiovascular events
 If a patient fails acetaminophen, nonselective NSAIDs or
cyclooxygenase-2 (COX-2) selective inhibitors (eg,
celecoxib) are recommended
 COX-2 inhibitors pose less risk for adverse GI events than
nonselective NSAIDs, but this advantage may not be
sustained beyond 6 months and is substantially reduced
for patients taking aspirin
 PPIs and misoprostol reduce adverse GI events in patients
taking NSAIDs
 Tata Laksana Terapi
(Knee & Hip OA)
 For knee OA, topical NSAIDs are recommended if
acetaminophen fails and are preferred over oral NSAIDs
in patients older than 75 years
 Topical NSAIDs provide similar pain relief with fewer
adverse GI events than oral NSAIDs but may be
associated with adverse events at the application site
 Intra-articular (IA) corticosteroid injections are
recommended for both hip and knee OA when analgesia
with acetaminophen or NSAIDs is suboptimal
 Injections can be given with concomitant oral analgesics
for additional pain control
 Do not administer injections more frequently than once
every 3 months to minimize systemic adverse effects
 Tata Laksana Terapi
(Knee & Hip OA)
 Tramadol is recommended for hip and knee OA in
patients who have failed scheduled full-dose
acetaminophen and topical NSAIDs, who are not
appropriate candidates for oral NSAIDs, and who are not
able to receive IA corticosteroids.
 Tramadol can be added to partially effective
acetaminophen or oral NSAID therapy
 Opioids should be considered in patients not responding
adequately to nonpharmacologic and first-line
pharmacologic therapies
 Patients who are at high surgical risk
and cannot undergo joint arthroplasty are also candidates
for opioid therapy
 Tata Laksana Terapi
(Knee & Hip OA)
 Duloxetine can be used as adjunctive treatment in patients
with partial response to first-line analgesics (acetaminophen,
oral NSAIDs)
 It may be a preferred second-line medication in patients with
both neuropathic and musculoskeletal OA pain
 IA hyaluronic acid is not routinely recommended for knee OA
pain
 Injections do not provide clinically meaningful improvement
and may be associated with serious adverse events (eg,
increased pain, joint swelling, and stiffness)
 Glucosamine and/or chondroitin and topical rubefacients (eg,
methyl salicylate, trolamine salicylate) lack uniform efficacy for
hip and knee pain and are not preferred treatment options
 Tata Laksana Terapi
(Hand OA)
Topical NSAIDs are a first-line option for hand OA
Diclofenac has efficacy similar to oral ibuprofen and oral
diclofenac with fewer adverse GI events
Oral NSAIDs are an alternative first-line treatment for
patients who cannot tolerate the local skin reactions or
who received inadequate relief from topical NSAIDs
Capsaicin cream is an alternative first-line treatment and
demonstrates modest improvement in pain scores
It is a reasonable option for patients unable to take oral
NSAIDs
 Tata Laksana Terapi
(Hand OA)
Adverse effects are primarily skin irritation and burning
Tramadol is an alternative first-line treatment and is a
reasonable choice for patients who do not respond to
topical therapy and are not candidates for oral NSAIDs
because of high GI, cardiovascular, or renal risks
Tramadol may also be used in combination with partially
effective acetaminophen, topical therapy, or oral NSAIDs
 Oral &
topical
analgesics
 IA
corticosteroids
& NSAID
NSAID
 Evaluasi Terapi
 To monitor efficacy, assess baseline pain with a visual
analog scale, and assess range of motion for affected
joints with flexion, extension, abduction, or adduction

 Depending on the joint(s) affected, measurement of grip

strength and 50-ft walking time can help assess hand and
hip/knee OA, respectively

 Baseline radiographs can document extent of joint

involvement and follow disease progression with therapy
 Evaluasi Terapi
 Ask patients about adverse effects from medications.
Monitor for signs of drugrelated effects, such as skin rash,
headaches, drowsiness, weight gain, or hypertension
from NSAIDs

 Obtain baseline serum creatinine, hematology profile,

and serum transaminases with repeat levels at 6- to 12-
month intervals to identify specific toxicities to the
kidney, liver, GI tract, or bone marrow
☺Terima Kasih☺