CASE REPORT

OSTEOARTRITIS

DISUSUN OLEH

Heru Dimas Prakoso

NIM 03013092

PEMBIMBING
dr. T. Nurrobi, Sp.OT(K)Hand

KEPANITERAAN KLINIK ILMU BEDAH

FAKULTAS KEDOKTERAN UNIVERSITAS TRISAKTI
RUMAH SAKIT TNI AL Dr. MINTOHARDJO
PERIODE 08 MEI 2017 10 JULI 2017
 LEMBAR PENGESAHAN

LAPORAN KASUS
OSTEOARTRITIS

Diajukan untuk memenuhi syarat kepaniteraan klinik Ilmu bedah

Periode 08 Mei 2017 10 Juli 2017
Di Rumah Sakit Angkatan Laut dr. Mintohardjo

Disusun oleh :
Heru Dimas Prakoso
03013092

Telah diterima dan disetujui oleh dr. T. Nurrobi, Sp.OT(K)Hand, selaku dokter
pembimbing
Departemen Ilmu Bedah RS AL dr. Mintohardjo

Jakarta, Mei 2017

...................................
dr. T. Nurrobi, Sp.OT(K)Hand

2
 CONTENTS

Page
Lembar Pengesahan ..................................................................................................2
Contents ....................................................................................................................3
Chapter I Introduction ..............................................................................................4
Chapter II Case Report ..............................................................................................6
2.1 Patient's Id .............................................................................................6
2.2 History...................................................................................................6
2.3 Physical Exam .......................................................................................7
2.4 Laboratory ............................................................................................10
2.5 Resume .................................................................................................11
2.6 Working diagnosis ...............................................................................12
2.7 Differential Diagnosis ..........................................................................12
2.8 Treatment .............................................................................................12
2.9 Prognosis ..............................................................................................13
2.10 Follow Up ..........................................................................................13
Chapter III Literature Review ..................................................................................15
3.1 Anatomy...............................................................................................15
3.2 Definition .............................................................................................17
3.3 Epidemiology .......................................................................................18
3.4 Etiology and Risk Factors ....................................................................18
3.5 Pathophysiology...................................................................................21
3.6 Diagnosis..............................................................................................23
3.7 Treatment .............................................................................................24
3.8 Complication ........................................................................................26
3.9 Prognosis ..............................................................................................26
3.10 Prevention ..........................................................................................27
Chapter IV Conclusion .............................................................................................29
References ................................................................................................................30

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4
 CHAPTER I
INTRODUCTION

Osteoarthritis (OA) is an illness (the ill health identified by the person

themselves, often based on self-reported measures or physical symptoms) and a

disease (a condition that is diagnosed by a clinician). Osteoarthritis is a chronic

disease and the etiology is still unknown.(1)

Osteoarthritis is a major cause of disability in elderly populations around

the globe, especially in developed countries. The prevalence of OA is increasing

and will continue to do so as the population increases, ages, and is subject to risk

factors such as the obesity epidemic. As OA causes pain and impairs functionality

of the patient, it places a major burden on individuals, communities, health

systems, and social care systems.(2)

Osteoarthritis commonly affects middle age to elderly population. It is the

most common disease of arthritis and can occur together with other types of

arthritis. It is a disease of the entire joint, involving not only the joint lining but

also cartilage, ligaments, and bone. It is characterized by breakdown of the

cartilage, bony changes of the joints, deterioration of tendons and ligaments, and

various degrees of inflammation of the synovial.(3)

According to the World Health Organization (WHO) in 2004, it is known

that osteoarthritis affects 151 million people worldwide and reaches 24 million

people in Southeast Asia. Osteoarthritis is a chronic disease that is not known for

certain causes, but is characterized by the loss of joint cartilage in stature. This

5
disease causes pain and disability in the patient so that interfere with daily

activities.(3)

The total prevalence of OA in the United States 1 of 7 adults has the sign

of OA. In Europe about 1.3 - 1.8 million people have the sign of OA. Totally,

about 10% to 15% people above 60 years old suffering OA.(3) Based on data from

the World Health Organization (WHO), people with osteoarthritis in Indonesia

recorded 8.1% of the total population.(3) As many as 29% of them go to doctor for

check, and the rest or 71% take pain relief medication. In Central Java, the

incidence of osteoarthritis is 5.1% of all citizen.(11)

It is estimated that 40% of the population aged over 70 years suffer from

osteoarthritis, and 80% of osteoarthritis patients have limited movement in

varying degrees from mild to severe which results in reduced quality of life due to

high prevalence. Because of its chronic-progressive nature, osteoarthritis has a

large socio-economic impact, both in developed and developing countries. An

estimated 1 to 2 million elderly people in Indonesia suffer from disability due to

osteoarthritis.(11)

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 CHAPTER II
CASE REPORT

2.1 Patient's Id
Name : Mrs. A
Date of Birth/Age:18-8-1965/ 57
Gender : Female
Address : Central Jakarta
Job : Housewife
Religion : Islam
Marital Status : Married
Education : Primary School
Insurance : BPJS
Date of Entry : 22 May 2017

2.2 History
1. Chief Complain
Pain in the left knee joint since 2 years ago.

2. Other Complain
-
3. Recent Health History
Patient complained of pain in the knee joint since 2 years ago. The pain
perceived lost arising and moved from front side to back side. Pain felt by the
patient was pulsed and impaled needle. Patient also has morning stiffness and
soon after wake up she felt difficult to move the left knee. When she tried to move
the left knee, she felt hard to bent. The pain gets heavier when the patient folds
her knee and moves her leg but slightly decreases with rest. Initially, the patient
admitted of getting pain and difficult to walk when the she wants to move from
her bed to another room. She also stated that when the left knee is moved, there
was a crackling sound. Patients still often do house work such as sweeping and

7
cooking, but since the knee was painful patient can only walk casually around the
house.

4. Past Health History

Hypertension (+), DM (-), Asthma (-), Allergy (-), Uric Acid (-)
5. Family Health History
OA in right knee 5 years ago, surgery
Hypertension (+)
DM (-)
6. Habit
House cleaning
7. Medication History
Acetaminophen 3 x 500 mg

2.3 Physical examination

General condition : Fair
Conscious stage : Compos mentis
Nutritional status : Good, BMI= 26.7 (overweight)
(BW/BH= 60kg/150 cm)
Vital sign : Blood tension : 150/90mmHg
Pulse rate : 82x/ min
Respiration rate : 20x/min
Temperature : 36.7C

General Status
1. Skin
Colour : yellowish, not pale, cyanosis (-), Icteric (-), rash (-)
Lesion : no lession such as macule, papule, pustule or other secondary
lession like keloid and scar on other parts of the body
Turgor : good
Temperature : warm

8
2. Eye
Shape : normal, symethrical, exopthalmos (-), enopthalmos (-)
Palpebrae : normal, ptosis (-), lagofthalmos (-), oedema (-), bleeding (-),
blepharitis (-), xanthelasma (-)
Movement : good, strabismus (-), nistagmus (-)
Sclera : icteric (-)
Pupil : round, isokhor, diameter 3mm, direct light reflex (+) ODS,
indirect light reflex (+) ODS

3. Ear
Shape : normotia
Ear canal : good
Cerument : not found in ADS

4. Nose
Shape : normal, no deformity
Septum : in medial, symetrical
Nasal Mucose : hyperemia (-), nasal concha eutrophy
Nasal cavity : bleeding (-)

5. Mouth and throat

Lips : normal, pale (-), cyanosis (-)
Teeth : average hygiene
Buccal mucose: hyperemia (-)
Tongue : normoglosia, typhoid tounge (-)
Tonsils : T1/T1, hyperemia (-)
Pharynx : hyperemia (-), symetrical pharynx arch, uvule in the middle

6. Cervical
Venous congestive : (-), JVP 5+2cm H2O

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Thyroid gland : no enlargement, symetrical
Trachea : medial

7. Lymphatic vessels
Cervical : no enlargement
Axilla : no enlargement
Inguinal : no enlargement

8. Thorax
Lungs
Inspection : symetrical movement, no retraction, thoracoabdominal type,
Palpation : symetrical movement, vocal fremitus balance in hemithorax
Percussion : sonor in both hemithorax, lung liver border ICS VI linea
midclavicularis dextra,
lung stomach border in ICS VIII linea axillaris anterior
Auscultation : SNV +/+, Rhonki (-), Wheezing (-)

Heart
Inspection : no thrill, no ictus cordis
Palpation : ictus cordis on ICS V, linea midclavicularis sinistra
Percussion : right heart: ICS III-V linea sternalis dextra,
left heart: ICS V, 1 cm lateral linea midclavicularis sinistra,
upper heart: ICS II linea sternalis sinistra
Auscultation : HS I,II regular, murmur (-), gallop (-)

Abdomen
Inspection : symetricall, no widening vein
Palpation : tenderness (-)
Percussion : tympanic in 4 quadrants
Auscultation : bowel sound: (+), bruit (-)

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Extremities
Upper : No deformity, warm akral +/+ , oedema -/-, CRT < 2", clubbing finger (-)
Lower : No deformity, warm akral +/+, oedema -/-

Localize status:
Genu sinistra
Look : Edema (+)
Feel : Crepitaion (+), tenderness (+), ballotement (+), skin temp: warm
Move : Pain on RoM, Limitation on RoM

2.4 Laboratory
Laboratory findings
Lab Checking Result Unit Normal Value
Leukocyte 7400 /L 5.000 - 10.000
Eritrocyte 4.70 million/ L 4,2 - 5,4
Haemoglobin 13.3 g/dL 12 - 14
Haematokrit 41 % 37 - 42
Trombocyte 338.000 thousand/ L 150.000 - 450.000
Bleeding Time 2'30 minute 1' - 3'
Clotting time 11'30 minute 5' - 15'
Blood glucose at a 165 mg/dL < 200
time

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Radiology
Genu sinistra AP/Lateral

Joint intact
Enclosing joint gap in medial part
Sclerotic joint surface with spur formation

2.5 Resume
Patient complained of pain in the knee joint since 2 years ago. The pain
perceived lost arising and moved from front side to back side. Pain felt by the
patient was pulsed and impaled needle. Patient also has morning stiffness and
soon after wake up she felt difficult to move the left knee. From physical
diagnosis found high blood pressure, Edema (+) on the left knee, crepitus on the

12
left knee, ternderness (+), ballotement (+), skin temp: warm, pain on RoM, and
limitation on RoM. Joint intac, enclosing joint gap in medial part, sclerotic joint
surface with spur formation

2.6 Working diagnosis

Osteoarthritis

2.7 Differential diagnosis

Gout arthritis, rheumatoid artritis

2.8 Treatment
1. Artrhoscopy
Preparing for Surgery:
Preoperative tests may include blood tests or an electrocardiogram (EKG).
Spinal anesthesia.
Aseptic and antiseptic in knee area
Cover the leg with surgical draping that exposes the prepared incision site
Positioning device is sometimes placed on the leg to help stabilize the
knee while the arthroscopic procedure takes place.
Procedure:
Made a few small incisions, called "portals,"
A sterile solution will be used to fill the knee joint and rinse away any
cloudy fluid
This helps to see the structures inside the knee clearly and in great detail
The surgeon's first task is to properly diagnose the problem
Insert the arthroscope and use the image projected on the screen to guide it
If surgical treatment is needed, your surgeon will insert tiny instruments
through other small incisions.
Specialized instruments are used for tasks like shaving, cutting, grasping,
and meniscal repair
Closure :
The length of the surgery will depend upon the findings and the treatment
necessary
The surgeon may close each incision with a stitch or steri-strips (small
bandaids)
Then cover the knee with a soft bandage.
2. Post artrhoscopy

13
 bedrest
monitoring vital sign
intravenous fluid
analgesic
control to polyclinic
3. Medication
Na diclofenac: 3 x 1
Ceftriaxone

2.9 Prognosis
Ad vitam: bonam
Ad Sanationam: dubia ad bonam
Ad Funcionam: dubia ad bonam

2.10 Follow up post operation

Date Subjective and Objective Treatment

22/May/2017 S: pain in the left leg almost 2 years (+), IVFD RL 20 dpm
GC / Consciousness : Fair / composmentis
VS : BP : 150/90 mmHg
RR : 20 x/ min
Pulse : 82 x/ min
T : 36.70C
VAS : 5
Oedema (+), eritema (-), limitation ROM

22/May/2017 S: pain in the left leg(+),Anxious for IVFD RL 20 dpm

tomorrow surgery Sodium Diclofenac 3x1
GC / Consciousness : Fair / composmentis Ceftriaxone 2gr
VS : BP : 150/90 mmHg
RR : 20 x/ min
Pulse : 86 x/ min
T : 36.90C
VAS : 5
Oedema (+), eritema (-), limitation ROM

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23/May/2017 S: Pain (+) IVFD RL 20 dpm
GC / Consciousness : Fair / composmentis Sodium Diclofenac 3x1
VS : BP : 150/90 mmHg Ceftriaxone
RR : 20 x/ min Control next week
Pulse : 85 x/ min
T : 36.80C
VAS : 5
Oedema (+), eritema (-), limitation ROM

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 CHAPTER III
LITERATUR REVIEW

3.1 Anatomy
The knee joint is a complex hinge joint formerly described as ginglymus
(meaning hinge). The joint is inherently unstable because of its articular
morphology but stability is provided static and dynamic stabilizers. The static
stabilizers formed by numbers of ligaments that hold the joint. The dynamic
stabilizers formed by muscles acting across the joint.(4)
Joint protectors include: joint capsule and ligaments, muscle, sensory
afferents, and underlying bone. Joint capsule and ligaments serve as joint
protectors by providing a limit to excursion, thereby fixing the range of joint
motion.(4)
The medial and lateral menisci are fibrocartilagenous structures that help
in deepening the joint surface and also act as shock absorption. The medial and
the lateral collateral ligaments prevent translation in the mediolateral plane. The
medial collateral ligament is a broad, flat, membranous band located near the
posterior aspect, which is attached to the medial condyle of the femur superiorly
and to the medial condyle and the medial surface of the tibia inferiorly.(5) The
ligament is composed of a superficial and a deep layer, the deep layer being
intimately adherent to the medial meniscus. The lateral collateral ligament, on the
other hand, is a rounded, fibrous, cord-like structure, which is attached to the
lateral femoral condyle superiorly and to the head of the fibula inferiorly.(6)
The cruciate ligaments are located in the center of the joint, closer to the
posterior than the anterior surface. The anterior cruciate ligament is attached to
the tibial spine and passes upwards, backwards and laterally to attach to the
medial and posterior aspect of the lateral femoral condyle. Its primary function is
to prevent anterior translation of the tibia on the femur.(5) The posterior cruciate
ligament arises from the posterior aspect of the tibia and passes upward, forward
and medially to insert on the anterior aspect of the medial femoral condyle. Its
main function is to prevent posterior translation of the femur on the tibia.(5)

16
 Image 1. Knee Anatomy(7)

Image 2. Knee Anatomy(7)

The joint is covered by a synovial membrane throughout and has a number
of bursae surrounding it. Synovial fluid reduces friction between articulating
cartilage surfaces, thereby serving as a major protector against friction-induced
cartilage tear.(6) This lubrication function depends on the molecule lubricin, a
mucinous glycoprotein secreted by synovial fibroblasts whose concentration
diminishes after joint injury and in the face of synovial inflammation. Synovial
fluid supplies nutrients to the avascular articular cartilage, it also provides the

17
viscosity needed to absorb shock from slow movements, as well as the elasticity
required to absorb shock from rapid movements.(6)
The dynamic stabilisers of the knee joint consist of the quadriceps femoris
crossing it anteriorly, the biceps femoris and popliteus laterally, the sartorius,
gracilis, semitendinosus and semimembranosus medially, and the popliteus
posteriorly.(5,6)

Image 3. Knee Anatomy(7)

3.2 Definition
Osteoarthritis (OA) is a common degenerative disorder of the articular
cartilage associated with hypertrophic changes in the bone. Indonesian
Rheumatology Association said osteoarthritis is a degenerative joint disease
resulting from chronic inflammation process in the joint and the bone around it.(8)

18
There are two types of osteoarthritis:
Primary osteoarthritis is a chronic degenerative disease that is related to,
but not caused by, aging. As a person ages, the water content of their cartilage
decreases, thus weakening it and making it less resilient and more susceptible to
degradation. There are strong indications that genetic inheritance is a factor, as up
to 60% of all OA cases are thought to result from genetic factors.(9)
Secondary arthritis tends to show up earlier in life, often due to a specific
cause such as an injury, a job that requires kneeling or squatting for extended
amounts of time, diabetes, or obesity. But though the etiology is different than
that of primary OA, the resulting symptoms and pathology are the same.(9)

3.3 Epidemiology
Osteoarthritis (OA) is the most common joint disorder in the United
States. Symptomatic knee OA occurs in 10% men and 13% in women aged 60
years or older. The number of people affected with symptomatic OA is likely to
increase due to the aging of the population and the obesity epidemic.(10)
In Asia, China and India have the highest number of OA patient according
to data and mostly occur in the knee.(10) In Indonesia, based on RISKESDAS 2013
East Nusa Tenggara has the highest prevalence of joint disorder compare to other
province in Indonesia.(11) About 33% of elderly had complains about degenerative
disorder, like gout arthritis, osteoarthritis, hypertension, diabetes mellitus.(12)

3.4 Etiology and Risk Factors

The daily stresses applied to the knee joints, also act as the weight-bearing
joints, play an important role in the development of osteoarthritis. Most
researchers believe that degenerative alterations in osteoarthritis primarily begin
in the articular cartilage, as a result of either excessive loading of a healthy joint
or relatively normal loading of a previously disturbed joint. External forces
accelerate the catabolic effects of the chondrocytes and further disrupt the
cartilaginous matrix.(13)

19
 There are several risk factors that affect osteoarthritis, for simple it can be
divided into two factor those are predisposing factors and biomechanical
factors:(14)
A. Predisposing Factors
1. Demographic Factors
i. Age(8)
From all of risk factors for the onset of osteoarthritis, the aging factor is
the strongest. The aging process is considered a cause of increased weakness
around the joints, decreased joint flexibility, cartilage calcification and lowered
chondrocyte function, all of which support the occurrence of OA. Study have
showed that 27% of people aged 63-70 years had radiographic evidence suffered
from knee OA, which increased by 40% at age 80 or older.

ii. Gender(8)
The prevalence of OA in men before age 50 is higher than for women, but
after age more than 50 years the prevalence of women is higher in OA than in
men. This is associated with a significant reduction in the hormone estrogen in
women.

iii. Ethnicity(12)
The prevalence of knee OA in patients in European and American
countries was no different, whereas one study proved that African-American race
had a 2-fold greater risk of knee OA than Caucasians. Asian populations also have
a higher risk of knee OA than Caucasians. Another study concluded that colored
populations were more prone to OA than were white.

2. Genetic Factors(12)
Hereditary factors also play a role in the onset of osteoarthritis. The
presence of mutations in the pro-collagen gene or other structural genes for
elements of joint cartilage such as collagen, proteoglycans play a role in the
emergence of familial tendencies in osteoarthritis.

20
3. Lifestyle Factors(8)
i. Smoking Habits
Smoking can damage cells and inhibit proliferation of joint cartilage cells
and also increase the oxidant stress that affects cartilage loss. Smoking can
increase the carbon monoxide content in the blood, causing tissue deficiency and
can inhibit cartilage formation.

ii. Consumption of Vitamin D

People who do not regularly consume foods containing vitamin D have a
three-times increased risk of knee OA.

4. Metabolic Factors
i. Obesity
Excessive weight turns out to increase mechanical pressure in the body's
weight-bearing joints, and more often causes osteoarthritis of the knee.

ii. Osteoporosis
The relationship between knee OA and osteoporosis supports the theory
that an abnormal bone mechanical movement will accelerate cartilage damage.

iii. Other Illnesses

OA of the knee has been shown to be associated with diabetes mellitus,
hypertension and hyperuricemia, with the non-obese patient.

B. Biomechanical Factors(8)
1. History of Knee Trauma
Acute knee injury including a tear in the krusiatum and meniscus
ligaments is a risk factor for the occurrence of knee OA. Meniscectomy

21
2. Anatomical Disorders
Risk factors for knee OA include localized abnormalities in knee joints
such as genu varus, genu valgus, Legg - Calve -Perthes disease and acetabulum
dysplasia.

3. Work
Osteoarthritis is commonly found in heavy physical workers, especially
those with multiple knee-strength powers (farmers, labor, etc.)

4. Physical Activity
Heavy physical activity such as standing longer (2 hours or more daily),
lifting heavy items (10 kg - 50 kg for 10 or more times each week), pushing heavy
objects (10 kg - 50 kg for 10 times or more each week are risk factors for knee
OA. Sports that probably have high risk for knee injury such as football may
increase the risk of OA.

3.5 Pathophysiology
Occurrence of OA cannot be separated from many joints that exist in
human body. A total of 230 joints connect 206 bones that allow for movement. To
protect bone from friction, inside the body there is cartilage. However, due to
various risk factors, there is erosion of cartilage and reduced of fluid in the joints.
Cartilage itself serves to reduce vibration between bones. Cartilage consists of
soft tissue collagen that serves to strengthen the joints, proteoglycans that make
the tissue elastic and water (70%) that bearing, lubricants and giving nutrition.(13)
Chondrocytes are cells whose job is to form proteoglycans and collagen in
the joint-cartilage. Osteoarthritis results from the failure to synthesize a qualified
matrix and maintains a balance between the degradation and synthesis of
extracellular matrices, including the excessive production of collagen type I, III,
VI and X and short proteoglycan synthesis. This results in changes in the diameter

22
and orientation of the collagen fibers that alter the biomechanics of the cartilage,
resulting in joint cartilage losing its unique compressibility properties.(13)
In addition to chondrocytes, synoviocytes also play roles in the
pathogenesis of OA, especially after synovitis, which causes pain and discomfort.
Inflammatory synoviocytes produce Matrix Metalloproteinases (MMPs) and
various cytokines to be released into the joint cavity and damage the joint-prone
matrix and activate chondrocytes. Ultimately the subcondral bone will also play a
role, where the osteoblasts will be aroused and produce proteolytic enzymes.(13)
Agrecanase is an enzyme that will break down proteoglycans in a joint-
prone matrix called an aggression. There are two types of agrekanase: agronomase
1 (ADAMTs-4) and agrecanase 2 (ADAMTs-11). MMPs are produced by
chondrocytes, then activated through a cascade involving serine proteinases
(plasminogen activator, plamsinogen, plasmin), free radicals and some membrane
type MMPs. This enzymatic cascade is controlled by various inhibitors, including
TIMPs and plasminogen activator inhibitors. Other enzymes that contribute to the
destruction of type II collagen and proteoglycans are katepsin, which acts at low
pH, including aspartate protein (katepsin D) and cysteine proteinases (katepsin B,
H, K, L and S) that are encapsulated in the lysosome of chondrocytes.
Hyaluronidase is not present in the joints, but other glycosidases play a role in
destroying proteoglycans.(13)
Various cytokines contribute to stimulate the chondrocytes in producing
destructive enzymes prone to joints. Proinflammatory cytokines will attach to
receptors on the surface of chondrocytes and synoviocytes and cause transcription
of the MMP gene so that the enzyme production increases. The most important
cytokines are IL-1, as well as regulatory cytokines (IL-6, IL-8, LIFI) and cytokine
inhibitors (IL-4, IL-10, IL-13 and IFN-). This cytokine inhibitor with IL-Ira may
inhibit the secretion of various MMPs and increase TIMPs secretion. In addition,
IL-4 and IL-13 may also counteract the metabolic effects of IL-1. IL-1 also plays
a role in reducing collagen type II and IX synthesis and improves the synthesis of
collagen types I and III, resulting in poor quality prone matrix.(14)

23
3.6 Diagnosis
Diagnostic criteria / classification of knee OA using criteria from
American College of Rheumatology (15) is listed on the table:

Clinical + Laboratory Clinical & Radiographic Clinical

Knee + at least 5 of the Knee pain + at least 1 of Knee pain + at least 3 of
following: the following: the following:
- Age > 50 years old - Age > 50 years old - Age > 50 years old
- Morning stiffness < 30 - Morning stiffness < 30 - Morning stiffness < 30
Minutes Minutes Minutes
- Crepitus - Crepitus - Crepitus
- Bony Tenderness + - Bony Tenderness
- Bony enlargement Osteophytes - Bony enlargement
- No palpable warmth - No palpable warmth
- ESR < 40mm/h
- RF < 1:40
-Synovial fluid consistent
with OA
Table 1. ACR Criteria for the diagnosis of knee OA

The degree of knee osteoarthritis is assessed to be five degrees by Kellgren and

Lawrence, namely:
- Degree 0 : there is no picture of osteoarthritis.
- Degree 1 : osteoarthritis is dubious with a picture of a normal joint, but
there is minimal osteophytes.
- Degree 2 : minimal osteoarthritis with osteophytes in 2 places, no
sclerosis and subchondral cysts, as well as fine joint gap.

24
- Degree 3 : moderate osteoarthritis with moderate osteophytes, tip bone
deformities, and narrow joint gap.
- Degree 4 : severe osteoarthritis with large osteophytes, bone deformities,
joint gap disappear, as well as present of sclerosis and subchondral cysts.

3.7 Treatment
The aims of the management of patients with osteoarthritis are: (17)
1. Relieves pain
2. Optimize joint function
3. Reduce dependence on others and improve quality of life
4. Inhibits the progression of disease
5. Prevent the occurrence of complications

Pillar therapy in patients with osteoarthritis are:(17)

Nonpharmacological:
1. Lifestyle modification
2. Education
3. Regular breaks aimed at reducing the use of burden on the joints
4. Modify the activity
5. Lose weight
6. Medical rehabilitation / physiotherapy
a. Exercise static and strengthen the muscles
b. Physiotherapy, which is useful for reducing pain, strengthening
muscles, and increase the area of joint movement
7. Use of tools.

Pharmacological:(18)
1. Systemic
a. Analgesic
Non narcotics: paracetamol
Opioids (codeine, tramadol)

25
b. Non-steroidal anti-inflammatory (NSAIDs)
Oral
Injection
Suppository
c. DMOADs (disease modifying OA drugs)
Among the nutraceuticals currently available in Indonesia are Glucosamine
sulfate and Chondroitin sulfate.

2. Topical(18)
a. Cream rubefacients and capsaicin.
Several preparations have been available in Indonesia in a way that is generally
counter-irritant.
b. NSAIDs Creams
Some of which can be used are pyoxicam gel, and diclofenac sodium.
Intraarticular / intra-lesion injection
Basically there are 2 indications of intraarticular injections namely
symptomatic treatment with steroids, and viscosuplementation with hyaluronic for
modification of the course of the disease. Some intraarticular injection
preparations, including:
a. Steroids (triamcinolone hexacetonide and methyl prednisolone)
Only given if one or two joints are experiencing pain and inflammation that are
less responsive to NSAIDs, cannot tolerate NSAIDs or there are comorbidities
that are contraindicated in the administration of NSAIDs.
Dosage for large joints such as knee 40-50 mg / injection, while for small joints
usually used a dose of 10 mg.
b. Hyaluronic: high molecular weight and low molecular weight
Given 5 to 6 times at intervals of one week each 2 to 2.5 ml Hyaluronic. Stocks in
Indonesia include Hyalgan and Osflex.

4. Surgery(18)

26
Before decided to do surgical therapy, it should first consider the risks and
benefits. Consideration of operative action when:
a. Deformity causes disruption of mobilization
b. Pain that cannot be overcome with medicine and rehabilitative

There are 2 types of surgical therapy: Realignment osteotomy and replacement

joint. Kinds of knee joint surgery for osteoarthritis:(18)
a. Partial replacement
b. High tibial osteotomy: for young people
c. Patella & condyle resurfacing
d. Minimally constrained total replacement: joint stability is performed in part by
the original ligament and partly by the artificial joint.
e. Cinstrained joint: fixed hinges: used when there is missing bone and severe
instability.
f. Total knee replacement, if acquired pain, deformity, instability resulting from
rheumatoid or osteoarthritis.

3.8 Complication
Complications can occur when osteoarthritis is not treated seriously, such
as: Chronic complications of significant bone malfunction, the worst is the
occurrence of paralysis.(19)

3.9 Prognosis
OA is the degenerative and irreversible disease. Measuring the
development of morbidity can also assess the prognosis of OA. Subject with
definite knee OA, especially if associated with complaints of knee pain, were at
significantly greater risk of developing mobility and lower extremity disability
than subjects with normal knee radiography.(20)

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3.10 Prevention(21)
Because no highly effective pharmaceutical treatments exist and surgical options
are expensive and not widely available, prevention is a major strategy in
addressing the disease burden of osteoarthritis.
A. Primary prevention
Only a limited number of primary interventions have been identified for
osteoarthritis, including:
Weight control: Obesity is considered a risk factor for OA. Thus,
maintaining or reducing weight through altered diet and increased physical
exercise can lower the risk of developing OA.
Occupational injury prevention: Avoidance of repetitive joint use and
proper management of related injuries can help prevent arthritis.
Sports injury prevention: Taking the necessary precautions to prevent
injury such as warming up and using proper equipment can help reduce
joint injuries.
Misalignment: Improper alignment of the knee or hip can contribute to
osteoarthritis and proper treatment such as orthotics or bracing can help
reduce the risk of developing the disease.

B. Secondary prevention
The aim of secondary prevention is early diagnosis which allows for
effective and appropriate interventions that will minimize the health consequences
of the disease. Recently, research into bone and cartilage degradation has
identified biochemical markers that may be used to identify OA early in the
progression of the disease.
However, not enough is known about these biochemical markers to
implement them in clinical practice. Currently, identification of arthritis is
primarily done with X-rays or other imaging methods. But access to well-
equipped health care facilities with X-ray technology is limited in many parts of
the world.

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C. Tertiary prevention
Tertiary prevention focuses on minimizing the compilations of disease
once it has been diagnosed. Such strategies for osteoarthritis are aimed at reducing
pain and disability, and improving quality of life. Tertiary prevention strategies
for OA include self-management (weight control, physical activity, and
education), home help programs, cognitive behavioral interventions, rehabilitation
services, and medical or surgical treatments.

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 CHAPTER IV
CONCLUSION

Osteoarthritis is a chronic progressive disease that is one of the leading

causes of disability among elderly populations throughout the world. It causes
pain, disability and impaired movement, which places a large burden (both in
terms of health and economics) on individuals, communities, and health systems.
While there are several therapies available for symptomatic treatment that
mitigate pain, there are no medicines that can reverse or halt the progression of
the disease. This pharmaceutical gap must be addressed in order to reduce the
burden of OA.

30
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