DAFTAR RIWAYAT HIDUP

Nama
: dr Zusron Fuadi, SpOT
T/TL
: Ponorogo, 26 Juni 1977
Alamat
: Perum Bumi Mas Blok GG-12 Madiun Jawa Timur
Agama
: Islam
Status Perkawinan
: Menikah
Pendidikan : Program Pendidikan Dokter Spesialis Orthopaedi dan
Traumatologi FK UNS Surakarta
Riwayat Pendidkan:
SDN Maron II Kauman Ponorogo, 1983-1989
SMPN 1 Ponorogo, 1989-1992
SMAN 1 Ponorogo, 1992-1995
FK Universitas Airlangga Surabaya, 1995-2001
PPDS 1 Orthopaedi dan Traumatologi FK UNS Surakarta, 2007-2012
Riwayat Pekerjaan:
Klinik 24 jam Platuk Indah Surabaya, 2002-2003
Klinik 24 jam Sidomulyo Surabaya, 2002-2003
Klinik JW Marriot Hotel Surabaya, 2002-2003
BKU Muhammadiyah Siti Khodijah Gurah Kediri, 2002-2003
RS Soedono Madiun, 2003-2006
RSUD Kota Madiun, 2013-sekarang
RS Griya Husada, 2013-sekarang
RSUD Sayidiman Magetan, 2013-sekarang
RS At-Tin Husada Ngawi, 2014-sekarang

OSTEOARTHRITIS
dr ZUSRON FUADI SpOT

OSTEOARTHRITIS
= OSTEOARTHROSIS
= DEGENERATIVE JOINT DISEASE

DEFINITION
Osteoarthritis (OA) is a degenerative
disease of diarthrodial (synovial)
joints, characterized by
Breakdown of articular cartilage
and proliferative changes of
surrounding bones

EPIDEMIOLOGY
Osteoarthritis(OA) is the most
common joint disease
OA of the knee joint is found in 70% of
the population over 60 years of age
Radiological evidence of OA can be
found in over 90 % of the population

Nearly 27 million Americans older than

25 years of age have OA.
By 2030, nearly 20% of Americans
(approximately 72 million people) will
surpass 65 years of age and be at high
risk for OA.
Indonesia: 15,5% (male), 12,7%
(female)

Under the age of 45, male OA patients

out number females. After that age, it is
more common in women.
It is also more likely to develop in
overweight people and people with jobs
that stress certain joints.

ANATOMI

CHARACTERISTICS OF OA
OA is a chronic disease of the
musculoskeletal system, without
systemic involvement
OA is mainly a noninflammatory
disease of synovial joints

CLASSIFICATION OF OA
Primary OA

Etiology is unknown

Secondary OA

Etiology is known

RISK FACTORS FOR PRIMARY

OA
Age
Sex
Obesity
Genetics

SECONDARY OSTOARTHRITIS
Trauma
Previous joint disorders;
Congenital hip dislocation
Infection: Septic arthritis, TB
Inflammatory: RA, AS
Metabolic: Gout
Hematologic: Hemophilia
Endocrine: DM

ETIOLOGY OF OA
Cartilage properties
Biomechanical problem

Morphology of Primary OA

STRUCTURE OF JOINT
CARTILAGE
Collagen (Type 2)
Proteoglycan
- Hyaluronic acid
- Glycoseaminoglycan

Water
Condrocyte
Regeneration and Degeneration

ETIOPATHOGENESIS OF OA
Age,gender
Local
Genetic
biochemical
Other factors

OA
effects

ETIOPATHOGENESIS OF OA
Dysfunction of joint cartilage
Condrocyte function: 1- Degredative enzymes
(metalloproteases)
2- Inhibitors
Degeneration and regeneration functions are
balanced
IL-1 , degredative enzymes + synovial
inflammation results: Breakdown of cartilage

PATHOGENESIS OF OA
Cytokines

IL-1, IL-6, TNF-

Cell destruction
Membrane phospholipids
Arachidonic acid
Cox-1, Cox-2

IL-1 and metalloproteases have been

found to play an important role in
cartilage destruction.
Local growth factors, especially
transforming growth factor (TGF) are
involved in the formation of
osteophytes

PATHOLOGY OF OA
Fibrillation
Eburnation
Osteophytes
Subcondral cysts

Peripheral Joints
Hands
Feet

LABORATORY FINDINGS OF
OA
There are no pathognomonic laboratory
findings for OA
Laboratory analysis is performed for
differential diagnosis

RADIOLOGIC FINDINGS OF OA
Narrowing of joint space
(due to loss of cartilage)
Osteophytes
Subchondral (paraarticular) sclerosis
Bone cysts

RADIOLOGIC FINDINGS?
GRADE 1 - 4?

DIAGNOSIS OF OA
CLINICAL FINDINGS
Joint pain
+
RADIOLOGIC FINDINGS
Osteophytes

X-RAY OF HIP OA

MATUR SUWUN