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Dr. H.

Rawan Broto, SpPD (KR)


Anggauta IRA Cabang Yogyakarta
1985 Dokter Umum FK UGM
1999 Internist FK UGM
2002 Konsultan Rheumatologist FK UI
2002 Ka Subbag Reumatologi Bag PD FK UGM
2002 Sekretaris Bagian PD FK UGM
2004 Ketua SP3T Provinsi DIY
2005 Manager Operasional RS Happyland Yogya
2008 Ketua Komite Medis RS Happyland
2009 Dosen honorer FK-UMY
2012 Direktur RS Holistika Medika Yogyakarta

Penatalaksanaan
Osteoarthritis
Rawan Broto
Bagian Ilmu Penyakit
Dalam
FK UMY Jogjakarta

Arthritis affects many


older adults
Women

Men

53%

37%

Myths & Truths about OA


Myth:

Once you get arthritis,


you just have to live with it

Truth:

you can manage your


arthritis In many ways & live
comfortably

Myths & Truths about OA


Myth: No cure is available for
most forms of arthritis
Truth: However, early diagnosis &
management can help reduce
impact of arthritis

Batasan
OA adalah penyakit sendi yang ditandai
dengan berbagai sindroma, karakteristik
dengan menipisnya rawan sendi secara
progresif, disertai respon pembentukan
tulang baru/osteofit pada trabekula
subkhondral atau tepi sendi

Osteoartritis

Merupakan penyakit degeneratif ?

Konsep Wear and tear ?

Analogi dengan No acid no ulcer ?

Epidemiology
Population

Age (yrs) Female (%)

Male (%)

English

>35

70

69

US Caucasians

>40

44

43

Alaskan Eskimos

>40

24

22

Jamaican (rural)

35-64

62

54

Pima Indians

>30

74

56

Blackfoot
Indians

>30

74

61

South African
Black

>35

53

60

Epidemiologi
Indonesia:

Penelitian berbasis masyarakat


Kota

Desa

Malang*
Bandungan**

13.5%
5.4%

10.0 %

* Kalim H, cs 1994, ** Darmawan, 1992

Penelitian berbasis rumah sakit


RSCM (1991-1994) 43.8% (total pasien reumatik)
RSS (1995-2000)
54.6% (total pasien reumatik)

The prevalence is higher in women


Women are more likely to have
inflammation of the proximal
(Bouchards nodes) & distal
interphalangeal joints of the hands
(Heberdens nodes)
OA of the hip occurs more frequently
in men
African Americans experience more
severe & disabling disease than
Caucasians
Chinese have;
knee OA > hand OA > hip OA (rarely)

OSTEOARTRITIS NODULAR

Prevalensi Gambaran Radiologik OA


Dalam Populasi
70

Prevalensi (%)

60
50
40
30
20
Lutut, Laki-laki

10
0

DIP, laki-laki
Lutut, perempuan

30

40

50

Usia (tahun)

60

70

DIP, perempuan

Hal-hal Menarik dari Osteoartritis

Penyakit yang telah dikenal lama.


(lihat Jurassic Park, The lost world, mummi di Museum
Cairo)

Diagnosis relatif mudah.

Penyakit tampaknya sederhana, ternyata


kompleks.

Faktor Risiko OA

Faktor predisposisi umum:


umur, jenis kelamin, kegemukan,
hereditas, hipermobilitas, merokok,
densitas masa tulang, hormonal, penyakit
reumatik kronik

Faktor mekanik:
trauma, bentuk sendi, penggunaan sendi,
kurang gerak

Risk factors for primary OA


Old age
Obesity

Occupation

Gender

OA

Family history
Genetics

Bone injury

Joint injury
Trauma

Joint
dysplasia
Solomon L. 1997

Risk factors you cannot


change
Family

history
of disease

Risk factors you cannot


change
Family

history of
disease

Increasing

age

Risk factors you cannot


change
Family

history of
disease

Increasing
Being

age

female

Risk factors you can


change

Overuse

joint

of the

Risk factors you can


change

Overuse

of the

joint
Major

injury

Risk factors you can


change

Overuse

of the

joint
Major

injury

Overweight

Risk factors you can


change

Overuse

of the

joint
Major

injury

Overweight
Muscle

weakness

Pandangan Terbaru
Patogenesis OA

Anatomy of a normal
synovial joint
Muscle

Bone

Capsule
Ligaments hold the
bones together
Synovium
Secretes the
synovial fluid

Cartilage
Protects the
end of the bone
Synovial fluid
Lubricates the
joint capsule

Tendon
Dieppe P. 1998

Normal Articular cartilage


components and structure
Collagen and proteoglycan
aggregates provide tensile
strength, elasticity and
recoil
Chondrocytes regulate the
synthesis and degradation of
cartilage by secreting
enzymes
Tide mark separates articular
cartilage from calcified
cartilage

Bone Area of detail

Articular cartilage in action


No load

Light load

Unaffected
cartilage

Light
contact

Heavy load Rebounding

Cartilage

Cartilage
distortion

Cartilage
and bone
rebound when
weight is
removed

Characteristics of OA
Normal joint

OA joint

Thickening
of capsule

Modest, patchy
chronic synovitis

Cartilage:
Pitted and frayed surface
Loss of elasticity
Cartilage may wear away
completely

Bone ends thicken


Bony outgrowths
(osteophytes) form
Bone fragments may
float in the joint space
Fluid filled cysts may
form in the bone
Dieppe P. 1998

Articular cartilage in OA
Erosion

Collagen fibre structure is altered and the


number and quality of proteoglycan
aggregates decreases
More chondrocytes are produced resulting in
an imbalance in the synthesis and degradation
of cartilage components

Cartilage surface cracks and erodes.


Small fragments break off into synovial
fluid
Eventually the bone becomes exposed

Bone Area of detail

Softening Stage

Fibrillation Stage

Fragmentation Stage

Joint =

Bone + Cartilage +
Synovial Fluid

Perubahan pada tulang

Perubahan pada cartilago

Perubahan pada cartilago

Joint tissues involved in OA

PATOGENESIS OA
Bukan sekedar Wear and Tear :

Ada perbedaan dengan perubahan rawan


sendi akibat proses penuaan (aging process)
Dapat terjadi pada hewan muda yang
dirangsang dengan zat kimia / trauma
Perubahan-perubahan patologi berkaitan
dengan perubahan kimiawi matriks

Obesity,
Developmental
and anatomic
abnormalities
Bony remodeling
and micro
fracture

Aging

Stresses
Abnormal

Cartilage
abnormal

Inflammation
Administration of
toxins

Normal
cartilage

Loss of joint
stability

Genetic and
metabolic
disease

Immune
response

Trauma

Theory A Biomaterial
failure
collagen network
fracture
Proteoglycan
unravelling

Theory B
Cell injury
Increase of degradative responses
Inhibitors reduced
Proteolytic enzymes increased
Destruction of prteoglycans collagen
and other proteins

Cartilage breakdown

RAWAN SENDI NORMAL

KOMPONEN MATRIKS EKSTRASELULER TERUS


MENERUS TURN-OVER

PROTEOGLIKAN LEBIH CEPAT DEGRADASI DARI


KOLAGEN

DILEPASKAN FRAGMEN PROTEOGLIKAN

BAGIAN YANG CLEAVAGE : INTI PROTEIN DEKAT G1


DAN G2

IKATAN HA-GLIKOSAMINOGLIKAN TERLEPAS

RAWAN SENDI OA

Terdapat gangguan keseimbangan degradasi


dan sintesis (anabolik dengan katabolik)
Walaupun ada sintesis (growth hormon) tetapi
kualitas rawan sendi terbentuk buruk
Stadium akhir: sintesis proteoglikan
merosot, fungsi khondrosit
sangat menurun.
Peranan IL-1 sangat besar yaitu merangsang
sekresi enzym katabolik stromelysin,
kolagenase, gelatinase & tissue plasminogen
inhibitor

Remodelling in OA

Hyaluronic acid
acid
Hyaluronic
Bone

Cartilage
HA

Capsule

Chondrocytes
HA

Synovial
lining

Osteoblast

Osteoclast

Bone
Synthesis: Synoviocyte, chondrocyte

Hyaluronan in OA Synovial fluid

Hialuronan membentuk selubung yang berfungsi


sebagai perisai viskoelastik guna melindungi
kartilago tulang rawan dan sinovium dari stress
mekanik, radikal bebas dan proses inflamasi.
Hialuronan
membentuk
kerangka
agregat
proteoglican
yang
sangat
penting
untuk
integritas struktur dan fungsi dari tulang rawan
sendi.

INFLAMASI PADA
OSTEOARTRITIS

USAHA PEMBERSIHAN DEBRIS

KERADANGAN DEBRIS : KONDROITIN SULFAT


DAPAT MENGAKTIFKAN FAKTOR HAGEMAN
------ JALUR KININ

KERADANGAN KARENA ARTRITIS LAIN :


CONTOH : MILWAUKEE SHOULDER SYNDROM

PERAN IL-1 DAN TNF ALFA

Inflamasi pada Osteoarthritis

Reduction of synovial membrane inflammation

Before treatment
After treatment

Kerusakan pada Osteoartritis


Metabolisme

khondrosit
Kerusakan jaringan kolagen
Peningkatan kadar air
Penurunan proteoglikan
Penurunan kualitas kolagen,
proteoglikan

Classification of OA
Primary

OA

Most common form


Is rare before age 40 years, prevalence increases
with age
Knee joint most often affected
Genetic predisposition, particularly for hand arthritis

Secondary

OA

Preceded by a predisposing disorder such as joint


trauma
Occurs in any joint

Solomon L. 1997

primary OA (idiopathic)

secondary OA

Predominant form & occurs in


absence of precipitating event
& assumes a certain pattern;
Localized (involving one or
two sites)
Generalized (involving three
or more sites)
Erosive

occurs when the disease is caused by


congenital, developmental disorders,
inflammatory, metabolic, or
endocrine diseases, e.g.:
Mechanical injury of joint
(Congenital or posttraumatic)
Prior inflammatory disease (RA,
chronic gouty arthritis, etc )
Metabolic disorder (Pagets disease)
Endocrinopathies (DM, obesity, sex
hormone abnormalities)
Neuropathic disorders
Intraarticular corticosteroid overuse
others

Localized OA is distinguished from


generalized disease by the number
of sites involved
Erosive disease is characterized by
an erosive pattern of bone destruction
and marked proliferation of
interphalangeal joints of the hands.

Signs and symptoms of OA


Signs

Symptoms

Loss of joint space

Use-related joint pain

Joint grinding/grating

Joint stiffness after periods


of inactivity

Bony outgrowths
(osteophytes)
Joint deformities e.g.
Heberdens nodes

Loss of joint movement/difficulty


performing certain tasks
Joint locking/giving way
Feeling of instability
Restricted/painful movements

Oxford Handbook of Clinical Medicine. 1998

Gambaran Klinis
Nyeri sendi: jalan, naik tangga, waktu
malam, gerak lutut, kadang waktu diam
(seperti sakit gigi di lutut).
Hambatan gerak
Pembesaran sendi
Tanda keradangan minimal
Krepitus
Sendi yang sering terkena: lutut, koksa,
DIP, pergelangan kaki, tulang belakang.

Finger deformities in OA
Deformities

occur at:
The base of the thumb
(Bouchards nodes)
The middle joint of a finger
(Bouchards nodes)
The finger tip
(Heberdens nodules)

Heberdens nodules
in a patient with OA
Sciencephoto.com

OA Primer

OA Sekunder

Laboratory Tests
No specific laboratory test or value is
diagnostic for OA.
The erythrocyte sedimentation rate (ESR)
and hematologic & chemistry panels are
usually unremarkable.
Aspirated synovial fluid (if obtained) often
displays leukocytosis & high viscosity.
Other Diagnostic Tests
Radiologic evidence may be misleading
because structural evidence of OA
correlates poorly with symptoms.
Radiographic changes are often absent in
early OA.
As the disease progresses, joint-space
narrowing, subchondral bone sclerosis,
& osteophytes may be detected.
In late OA, there is gross deformity and
possibly effusions.

Gambaran klinis (lanjutan)


Secara klinis:
Berat ringan gejala tidak
berkorelasi dengan
gambaran radiologik
gambaran artroskopi

Gambaran radiologik OA
Indeks Kellgren dan Lawrence (KL)

KL-0
KL-1 (penyempitan celah sendi)
KL-2 (osteofit)
KL-3 (pembesaran tulang)
KL-4 (deformitas)

Osteofit

Celah sendi
menyempit

Celah sendi

Nyeri sendi degeneratif:

Peningkatan tekanan interoseus akibat degenerasi rawan sendi akan


menekan reseptor nociceptif

Mekanisme lain melalui reaksi nyeri inflamatif yang sama misal


khondroitin sulfat merangsang XII mencetuskan jalur kinin

Infiltrasi sel MN dan hiperplasia vaskuler.

Penebalan kapsul sendi menimbulkan rasa nyeri dan spasme otot

Serpihan rawan juga bersifat antigenik.

Inilah proses kronisitas inflamasi pada OA

Kajian Pasien dengan OA


Sumber Nyeri:

mekanik - berkaitan dengan penggunaan sendi

Inflamasi - kekakuan, nyeri diperberat dengan


istirahat

Nyeri malam hari - Hipertensi intraoseus

Nyeri memburuk dengan cepat - Pikirkan sepsis,

avascular necrosis, fraktur, atau sinovitis kristal.

Kajian Pasien dengan OA


Pemeriksaan Klinis:

Sumber nyeri dari persendian atau sekitar


sendi?

Nyeri menyeluruh? pertimbangkan fibromyalgia

Adakah deformitas?

Adakah kelemahan otot?

Tanda Inflamasi atau efusi lokal?

OA generalisata atau lokal?

Pencegahan

Identifikasi faktor risiko untuk


terjadinya OA.

Modifikasi faktor risiko seperti


berat badan (obesitas) dan trauma
minor berulang.

Perubahan Gaya Hidup


Umum
Pertahankan berat badan optimal / ideal.
Pertahankan aktifitas dan olah raga teratur.
Pertahankan pendekatan positif.
Khusus
Penguatan otot.
Berikan perhatian terhadap disabilitas
spesifik (belanja, pekerjaan di rumah dan
pekerjaan).

Balanced Diet

Helps manage weight

Extra pressure on some joints may aggravate


your arthritis

Stay

healthy

Exercise is important
Strengthening
Aerobic
Stretching

Aerobic Exercises
Walking, Biking

Improve cardiovascular fitness


Helps control weight
May help reduce inflammation
in joints
For those worried about
advancement of arthritis, a
Swedish study showed no
progression of arthritis with
moderate exercise.

Walking Aides

Cane

Walker

Helps keep you balanced so you dont hurt other joints.

Exercices
Suppress the signal
transduction
pathways of
proinflammatory/cata
bolic mediators

Treatment is individualized (medical history,


physical examination, radiographic findings,
distribution & severity of joint involvement &
response to previous treatment

Goals

of therapy include

(1) educating the patient and caregivers


(2) relieving pain
(3) maintaining or restoring mobility
(4) minimizing functional impairment
(5) Preserving joint integrity
(6) improving quality of life.

OA Medications !
NSAIDs
Nutritional Therapies
Non Traditional therapy
Future Therapies

Patient Perspectives !!!

Doctor
Perspectives !!!

Medications
Analgesics,

pain relievers,
may provide
temporary relief
of arthritis pain.
Must know what
the side effect

Farmakoterapi
OAINS : hanya menekan nyeri dan inflamasi, tidak
dapat menghentikan perjalanan penyakit
Kortikosteroid oral: tidak lazim diberikan pada OA
Steroid injeksi IA diberikan dengan temporary
Hyaluronan diberikan dengan pertimbangan tertentu
DMARD (Disease Modified Anti-Rheumatic Drugs
atau DC-ART (Disease Controlled Anti-Rheumatic
Therapy) : dapat mengontrol dan menghentikan
perjalanan penyakit

ACR 2000 GuidlinesDrug Therapy Options in Osteoarthritis


Baseline program
(Weight loss/exercise)
Mild/moderate
Pain

Moderate/severe
pain/inflammation

Acetaminophen

Steroids IA

COX-2 specific
Inhibitors

OTC NSAIDs
Tramadol
Propoxyphene
Opioids

Hyaluronans
(Hyalgan)

Traditional NSAIDs
(plus gastrorptection)

Surgery

PENGOBATAN SIMPTOMATIK
Jangka Pendek

Obat anti inflamasi non steroid (NSAIDs)


Analgetikum (Opioid, non-opioid)
Muscle relaxan (eperison,dll)

Terapi medikamentosa penyakit


reumatik :

Penting pemilihan NSAIDs secara rasional

Perlu pemahaman mekanisme kerja NSAIDs

Perlu pemberian NSAIDs ?

Pemilihan NSAIDs : perlu pertimbangan-pertimbangan


tertentu

Tujuan : pengobatan yang efektif, aman / bebas dari efek


samping yang merugikan

NSAIDs mana ?
Sulit dijawab dengan singkat

Perhatikan perbedaan :
- Efektifitas pada berbagai individu Individual
- Efektifitas dan dosis optimal pada penyakit yang berbeda
- Farmakokinetik
- Efek samping
- Kepatuhan penderita
- Harga obat
- Lain-lain : faktor yang mempengaruhi perjalanan suatu obat
sebelum mencapai target organ, misalnya interaksi
dengan makanan, interaksi dengan obat lain,
bioavailibilitas dsb.

PERTIMBANGAN PEMBERIAN NSAIDs


Pertanyaan yang harus dijawab sebelum menuliskan resep NSAIDs :
1. Apakah penderita benar-benar memerlukan NSAIDs ?
2. Apakah keluhan penderita dapat diobati dengan analgesik saja ?
3. Adakah faktor risiko pada penderita yang perlu diperhatikan ?
4. Apakah diperlukan NSAIDs dosis tinggi ?
5. Bagaimana kombinasi NSAIDs dengan obat-obat lain seperti :
- NSAIDs lain
- analgesik
- analog prostaglandin
- antasida, antagonis H2 atau proton pump inhibitor

NSAID menekan proses inflamasi


- Tidak mempengaruhi perjalanan penyakit
- Kerusakan sendi atau organ lain akibat penyakit reumatik
berjalan terus

Mekanisme Kerja Lain NSAIDs:

Penghambatan kemotaksis terhadap sel-sel yang terlibat


dalam proses inflamasi

Daya antagonis terhadap mediator lain

Stabilisasi membran lisosom

Penghambatan biosintesis mukopolisakarida

Mempengaruhi translokasi Ca++

Penghambatan terhadap produksi kolagen

Penekanan fungsi limfosit

Disease Modifying Osteoarthritis


Drugs (DMOAD)

Tetrasiklin
Glycosaminoglycan polysulfuric acid
(GAPS)
Glycosaminoglycan peptide complexes
Pentosan polysulfate
Growth factors and sitokin (TGF-b)
Terapi genetik
Transplantasi stem cell
Osteochondral Graft
Anti TNF Alfa (Etanercept)

a. Topical NSAIDs

b. Counterirritants

VISCOSUPLEMENT
Advantages :
Safe and effective
Better than placebo
As effective as
NSAID
Improves patient
assessed pain
Low rate of
complication

Disadvantages :
Patient with more
severe radiographic
grade have responded
less
Potential adverse
event (rare): joint
effusion, joint swelling,
arthralgia, joint warm,
injection site erythema

Wang CT et al. J.Bone Joint SurbAm 2004.86A.538-545. Kemper F et al.CurrMed ResOpn2005.21.1261-1269. LussierA et al.
J Rheumatol1996.23.1579-1583. VadVB et al.Arch Phys Rehab 2003.84.634-637. PetrellaRJ et al. Arch Intern Med
2002.162.292-298

KOMPLIKASI INJEKSI INTRAARTIKULER


Infeksi

1 dari 1000-16.000 injeksi


Perdarahan
Kerusakan rawan sendi
Nekrosis aseptik
Atrofi kulit dan jaringan subkutan
Ruptur tendo atau ligamentum

New concepts in OA medicines


Bio synthesis activity of chondrosit
Inhibiting cytokin and free radical
Inhibiting enzymes that account for joint
damage
Removing lipid deposit in subchondral
vascular
Increasing sinovial hyaluronan
(Kalim, 1999)

Recent advances
Weight loss 3,9 kg improves symptom of OA
Quadriceps exercises are beneficial in
patients with OA of the knee
Cox-2 selective drugs reduce the incidence of
ulcers
The prevalence of OA necessitates a shared
care approach to management between
general practitioners and hospital specialist
Several non surgical interventions to alleviate
pain and disability : education, social support,
physiotherapy and occupational therapy

Other Interventions

Surgical : Osteotomy, Arthroplasty

Cartilage cell replacement

Stem cell transplantation

Enzym engineering

Nutritional Supplements : Glukosamin,


Chondroitin sulfate, vit D and C

Tujuannya mengoreksi deformitas


Osteotomy, arthroplasty
Sangat menolong pasien muda
(Lavorgna et al., 1999)

Replaced Hip X-ray

Total Knee
Joint
Replacement

End surface of femur


replaced with metal
End surface of tibia
replaced with metal
Plastic liner is inserted
between femur and tibia
Patella is resurfaced
with plastic
The entire knee is not
removed as myth and lore
would have it.
This is a resurfacing
procedure.

Total Knee
Replacement

Canina Raphael of Minnara Cattery Yogyakarta

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