CASE REPORT

OSTEOARTHRITIS

Pembimbing:

dr. Tjahja Nurrobi, Sp.OT (K) Hand, M.Kes

Disusun oleh:

Ainus Saadi Rizal

030.13.009

KEPANITERAAN ILMU KLINIK BEDAH

FAKULTAS KEDOKTERAN UNIVERSITAS TRISAKTI

RSAL DR. MINTOHARDJO

PERIODE 23 JULI – 29 SEPTEMBER 2018

JAKARTA
 LEMBAR PENGESAHAN

LAPORAN KASUS
OSTEOARTRITIS

Diajukan untuk memenuhi syarat kepaniteraan klinik Ilmu bedah

Periode 23 Juli – 29 September 2018
Di Rumah Sakit Angkatan Laut dr. Mintohardjo

Disusun oleh :
Ainus Saadi Rizal
030.13.009

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

Jakarta, 13 September 2018

dr. Tjahja Nurrobi, Sp.OT (K) Hand, M.Kes

i
 KATA PENGANTAR

Puji syukur kehadirat Tuhan Yang Maha Esa karena atas berkat dan

rahmat-Nya, penulis dapat menyelesaikan laporan kasus yang berjudul

“Osteoarthritis”. Penulisan laporan kasus ini dilaksanakan dalam rangka

memenuhi sebagian persyaratan salah satu tugas kepaniteraan ilmu klinik Bedah

di Rumah Sakit Angkatan Laut Dr. Mintohardjo periode 23 Juli – 29 September

2018. Penulisan laporan kasus ini tidak akan selesai tanpa dukungan dan

bimbingan berbagai pihak. Oleh karena itu, penulis mengucapkan terima kasih

kepada dr. Tjahja Nurrobi, Sp.OT (K) Hand, M.Kes selaku dokter pembimbing

yang telah menyediakan waktu, tenaga, dan ilmunya untuk mengarahkan penulis

dalam penyusunan referat ini.

Penulis menyadari bahwa penulisan laporan kasus ini masih jauh dari

sempurna. Oleh karena itu, kritik dan saran sangat penulis perlukan demi

melengkapi laporan kasus ini. Akhir kata, semoga Tuhan membalas kebaikan

semua pihak dan laporan kasus ini hendaknya membawa manfaat bagi

pengembangan ilmu pengetahuan, profesi, dan masyarakat luas.

ii
 CONTENTS

HALAMAN JUDUL
LEMBAR PENGESAHAN ...................................................................i
KATA PENGANTAR ......................................................................... ii
CONTENTS ........................................................................................ iii
LIST OF IMAGES ...............................................................................iv
CHAPTER I CASE REPORT............................................................... 1
1.1 Identity ............................................................................................ 1
1.2 Anamnesis ....................................................................................... 1
1.3 Physical Examination ...................................................................... 1
1.4 Laboratory ....................................................................................... 3
1.5 Resume ............................................................................................ 5
1.6 Working diagnosis .......................................................................... 5
1.7 Differential diagnosis ...................................................................... 5
1.8 Treatment ........................................................................................ 5
1.9 Prognosis ......................................................................................... 5
1.10 Follow Up Post Operation............................................................. 6
CHAPTER II LITERATURE REVIEW ............................................... 7
2.1 Anatomy .......................................................................................... 7
2.2 Definition ........................................................................................ 9
2.3 Epidemiology .................................................................................. 9
2.4 Risk Factor .................................................................................... 10
2.5 Aetiology ....................................................................................... 10
2.6 Patophysiology .............................................................................. 11
2.7 Symptoms ...................................................................................... 13
2.8 Diagnosis and Investigations ........................................................ 14
2.9 Treatment ...................................................................................... 14
2.10 Prevention ................................................................................... 15
CHAPTER III CONCLUSION ........................................................... 17
REFERENCES.................................................................................... 18

iii
 LIST OF IMAGES

Image I. Anatomy of Knee ........................................................................ 7

Image II. Epidemiology of Years Lived with Disability......................... 10
Image III. Comparasion of a Healthy and Generate OA Joint ................ 12
Image IV. Practical Guideline approaching toward the diagnosis of
knee OA .................................................................................................. 14

iv
 CHAPTER I
CASE REPORT

1.1 Identity
Name : Tn. D S
Gender : Laki-laki
Age : 52 years old
Date of birth : 11th January 1965
Address : Komp TNI AL, Block C15 No.I, Sukamanah,
Jonggol. Bogor
Religion : Muslim
Work : TNI AL
Education : High school
Marital status : Married
Date of hospital admission : 20th August 2018
Medical record number : 170468

1.2 Anamnesis
Autoanamnesis
Main complaint Crooked shape of right knee
Additional Difficult to walk for a long time
complaint
History of the Patient come to the hospital with suggest to be operated for
disease repair the shape of right knee. Patient have been fracture
for right knee 17th december 2017 and has been surgery
28th december 2017. After operated patient still using cane
for walking for 4 months, after that time patient not use the
cane for walk but still difficult to walk. Everytime he feel
pain on right knee when he walking. 20 august 2018 the
patient come to Mintohardjo Navy Hospital for operation
right knee. For a long time patient feel uncomfortable to
walk because pain and limitation of motion.
History of the Heart disease (+), hypertension (-), diabetes mellitus (-)
past disease
History of the None
family disease
Medical history The heart disease have been healed
Socioeconomy Patient get treatment with BPJS
history

1.3 Physical Examination

General condition : Fair
Conscious stage : Compos mentis
Nutritional status : Good, BMI= 30.86 (overweight)
(BW/BH= 82kg/163 cm)
Vital sign : Blood tension : 150/80mmHg

1
 Pulse rate : 107x/ min
Respiration rate : 20x/min
Temperature : 37,1°C

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

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

3. Ear
Shape : normotia
Ear canal : good
Cerument : 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
Thyroid gland : no enlargement, symetrical
Trachea : medial

2
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 : symetrical, no widening vein
Palpation : tenderness (-)
Percussion : tympanic in 4 quadrants
Auscultation : bowel sound: (+), bruit (-)

Extremities
Upper : No deformity, warm akral +/+ , oedema -/-, CRT < 2", clubbing
finger (-)
Lower : For right knee: Elastic bandage + drain, warm akral +/+, oedema
-/-, tenderness +/-, pain +/-

Localize status:
Genu dextra
Look : Elatic bandage + drain
Feel : Tenderness (+), skin temp: warm
Move : Pain on RoM, Limitation on RoM

1.4 Laboratory
Laboratory findings (20th august 2018)
Lab Checking Result Unit Normal Value
Leukocyte 8400 /μL 5.000 - 10.000
Eritrocyte 4.92 million/ μL 4,2 - 5,4
Haemoglobin 15.4 g/dL 12 - 14

3
Haematokrit 44 % 37 - 42
Trombocyte 299.000 thousand/ μL 150.000 - 450.000
ESR 8 Mm/hour <10
Diferential count
Basophil 0 % 0-1
Eosinophil 4 % 1-3
Rod neutrophil 0 % 2-6
Segment 56 % 50-70
neutrophil
Lymphocyte 33 % 20-40
Monocyte 7 % 2-8
Bleeding Time 2'30 minute 1' - 3'
Clotting time 11'30 minute 5' - 15'
Blood glucose at a 173 mg/dL < 200
time

Laboratory findings (21th august 2018)

Blood glucose at a 184 mg/dL <200
time

Radiology
Genu dextra AP/Lateral

4
 1.5 Resume

Everytime he feel pain on right knee when he walking. 20 august 2018 the patient
come to Mintohardjo Navy Hospital for operation right knee. For a long time
patient feel uncomfortable to walk because pain and limitation of motion. From
physical diagnosis found genu dextra look: elastic bandage + drain, feel:
tenderness (+), oedem (-), eritema (-), skin temp: warm, move: pain on range of
motion, limitation on range of motion.

1.6 Working diagnosis

Osteoarthritis genu dextra

1.7 Differential diagnosis

Rheumatoid arthritis
Gout arthritis

1.8 Treatment
Medication:
Ketorolac 3 x 30 mg iv
Tramadol 2 x 100 mg iv
Ondancentron 3 x 4 iv

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

1.10 Follow up post operation

Date Subjective and Objective Treatment

22 august 2018 S: pain in the right knee IVFD RL 20 dpm

GC / Consciousness : Fair / composmentis Attached drain

VS : BP : 140/90 mmHg
RR : 20 x/ min
Pulse : 92 x/ min
T : 37,0 0C
VAS : 4
Oedema (-), eritema (-), limitation ROM

5
 CHAPTER II
LITERATUR REVIEW

2.1 Anatomy
The knee joint is the largest and most complex joint in the body. Despite
its single joint cavity, the knee consists of three joints in one: an intermediate one
between the patella and the lower end of the femur (the femoropatellar joint), and
lateral and medial joints (collectively known as the tibiofemoral joint) between
the femoral condyles above and the C-shaped menisci, or semilunar cartilages, of
the tibia below.1

Image I. Anatomy of Knee1

Besides deepening the shallow tibial articular surfaces, the menisci help
prevent side-to-side rocking of the femur on the tibia and absorb shock

6
transmitted to the knee joint. However, the menisci are attached only at their outer
margins and are frequently torn free.1
The tibiofemoral joint acts primarily as a hinge, permitting flexion and
extension. However, structurally it is a bicondylar joint. Some rotation is possible
when the knee is partly flexed, and when the knee is extending. But, when the
knee is fully extended, side-to-side movements and rotation are strongly resisted
by ligaments and the menisci. The femoropatellar joint is a plane joint, and the
patella glides across the distal end of the femur during knee flexion.1
The knee joint is unique in that its joint cavity is only partially enclosed by
a capsule. The relatively thin articular capsule is present only on the sides and
posterior aspects of the knee, where it covers the bulk of the femoral and tibial
condyles. Anteriorly, where the capsule is absent, three broad ligaments run from
the patella to the tibia below. These are the patellar ligament flanked by the
medial and lateral patellar retinacula (ret˘-nak ı u-lah; “retainers”), which merge
imperceptibly into the articular capsule on each side. The patellar ligament and
retinacula are actually continuations of the tendon of the bulky quadriceps muscle
of the anterior thigh. Physicians tap the patellar ligament to test the knee-jerk
reflex.1
The synovial cavity of the knee joint has a complicated shape, with several
extensions that lead into “blind alleys.” At least a dozen bursae are associated
with this joint. For example, notice the subcutaneous prepatellar bursa, which is
often injured when the knee is bumped anteriorly.1
All three types of joint ligaments stabilize and strengthen the capsule of
the knee joint. The ligaments of two of the types, capsular and extracapsular, all
act to prevent hyperextension of the knee and are stretched taut when the knee is
extended. These include the following:
1. The extracapsular fibular and tibial collateral ligaments are also critical
in preventing lateral or medial rotation when the knee is extended. The
broad, flat tibial collateral ligament runs from the medial epicondyle of the
femur to the medial condyle of the tibial shaft below and is fused to the
medial meniscus
2. The oblique popliteal ligament (poplı˘-teal) is actually part of the tendon
of the semimembranosus muscle that fuses with the joint capsule and helps
stabilize the posterior aspect of the knee joint
3. The arcuate popliteal ligament arcs superiorly from the head of the
fibula over the popliteus muscle and reinforces the joint capsule
posteriorly
The knee’s intracapsular ligaments are called cruciate ligaments
(kroosheat) because they cross each other, forming an X (cruci = cross) in the
notch between the femoral condyles. They act as restraining straps to help prevent
anteriorposterior displacement of the articular surfaces and to secure the
articulating bones when we stand. Although these ligaments are in the joint
capsule, they are outside the synovial cavity, and synovial membrane nearly
covers their surfaces. Note that the two cruciate ligaments both run superiorly to
the femur and are named for their tibial attachment site.1

7
 The anterior cruciate ligament attaches to the anterior intercondylar area of
the tibia. From there it passes posteriorly, laterally, and upward to attach to the
femur on the medial side of its lateral condyle. This ligament prevents forward
sliding of the tibia on the femur and checks hyperextension of the knee. It is
somewhat lax when the knee is flexed, and taut when the knee is extended.1
The stronger posterior cruciate ligament is attached to the posterior
intercondylar area of the tibia and passes anteriorly, medially, and superiorly to
attach to the femur on the lateral side of the medial condyle. This ligament
prevents backward displacement of the tibia or forward sliding of the femur.1
The knee capsule is heavily reinforced by muscle tendons. Most important
are the strong tendons of the quadriceps muscles of the anterior thigh and the
tendon of the semimembranosus muscle posteriorly. The greater the strength and
tone of these muscles, the less the chance of knee injury.1
The knees have a built-in locking device that provides steady support for
the body in the standing position. As we begin to stand up, the wheel-shaped
femoral condyles roll like ball bearings across the tibial condyles and the flexed
leg begins to extend at the knee. Because the lateral femoral condyle stops rolling
before the medial condyle stops, the femur spins (rotates) medially on the tibia,
until the cruciate and collateral ligaments of the knee are twisted and taut and the
menisci are compressed. The tension in the ligaments effectively locks the joint
into a rigid structure that cannot be flexed again until it is unlocked. This
unlocking is accomplished by the popliteus muscle. It rotates the femur laterally
on the tibia, causing the ligaments to become untwisted and slack.1

2.2 Definition
Osteoarthritis is characterized by the breakdown of cartilage in joints. As
cartilage deteriorates, the bones of the joint begin to run against one another,
causing stiffness and pain, which often impairs movement. Osteoarthritis also can
damage ligaments, menisci, and muscles. Bone or cartilage fragments may float in
the joint space, causing irritation and pain. Bone spurs, or osteophytes, may also
develop, causing additional pain and potentially damaging surrounding tissues.2
Osteoarthritis is a non-inflammatory condition that is characterised by
progressive damage and loss of the articular cartilage. The progressive nature of
the disease process is the result of the body’s innate inability to regenerate hyaline
articular cartilage. Osteoarthritis is termed as primary or secondary depending
upon whether a predisposing cause can be identified for its development.3

2.3 Epidemiology
Around the world, an estimated 10%-15% of adults over 60 have some
degree of osteoarthritis. It most commonly affects the joints in the knee, hands,
feet, and spine, and is also relatively common in other joints such as the shoulder
and hip joints.1
Osteoarthritis is the single most common cause of disability in older
adults. It ranks as the fifth highest cause of years lost to disability in the whole
population in high-income countries, and the ninth highest cause in low- and
middle-income countries. It accounts for 50% of the entire musculoskeletal

8
disease burden, and thus is considered the highest-burden condition within the
musculoskeletal group of diseases, which also includes rheumatoid arthritis and
osteoporosis. Radiographic evidence of knee osteoarthritis is present in
approximately 30% of men and women over the age of 65. Worldwide estimates
are that 9.6% of men and 18.0% of women over the age of 60 years have
symptomatic osteoarthritis. Approximately 80% of those with OA will have
limitations in movement, and 25% cannot perform their major activities of daily
life.1

Image II. Epidemiology of Years Lived with Disability1

2.4 Risk Factor

A multitude of factors including genetic, biochemical and mechanical
influences have been implicated in the development of primary osteoarthritis.
Despite these theories the exact mechanism for the development of primary
osteoarthritis remains unknown and it is thereby termed idiopathic.3

2.5 Aetiology
Aetiology of osteoarthritis:
Primary:
 Cause unknown, termed idiopathic
 Femoroacetabular impingement implicated as a possible cause
Secondary:
 Trauma
 AVN
 Perthes’ disease
 Developmental dysplasia of the hip
 Slipped capital femoral epiphysis
 Septic arthritis
There are two types of osteoarthritis: primary and secondary. Primary

9
 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.3 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 aetiology is different than that of primary OA, the resulting
symptoms and pathology are the same.3

2.6 Pathophysiology
Macroscopically, normal hyaline articular cartilage is a rather unruffled
white to yellowish overlay coating the articulating joint surface. The synovial
fluid makes it to appear slippery and provides its gliding properties.
Microscopically, hyaline cartilage consists of evenly stained (“hyaline”) collagen-
and proteoglycan-rich extracellular matrix with sparsely distributed cartilage cells
(“chondrocytes”). The cells represent less than 5% of the total volume of articular
cartilage but are of obvious importance for the maintenance of the tissue.
Chondrocytes are surrounded in most parts by a specialized pericellular matrix
forming a biomechanical and biochemical interface between the rigid
interterritorial matrix and the cells. The mechanical properties ofarticular cartilage
largely depend on the biochemical composition of the extensive interterritorial
(extracellular) cartilage matrix.4
Macroscopically, OA cartilage is often yellowish or brownish, is typically
soft, and is often swollen. The surface shows roughening in the early stages and
overt fibrillation and matrix loss in the later stages until the eburnated subchondral
bone plate is visible. These changes can be seen and graded radiographically and
can be visualized in more detail on the histologic level. Thus, microscopically, the
surface shows undulations (roughening) in the early and overt fissures and splits
as well as matrix loss in the later disease stages until the subchondral bone plate
becomes visible. Besides the total destruction of matrix areas, also the degradation
of matrix molecules plays an important role preceding and driving the final loss of
the respective matrix areas: loss of toluidine blue staining reflecting the loss of
proteoglycans in damaged cartilage areas). Apart from the degradation of
molecular components, destabilization of supramolecular structures also takes
place. For example, destabilization of the collagen network results in
microscopically and, finally, macroscopically visible matrix destruction. Both
mechanical wear and enzymatic degradation appear to play a pivotal role during
the disease process. Together, these cause the destruction of the cartilage matrix
on the molecular (e.g., proteoglycan depletion) and the macromolecular (e.g.,
network loosening), explaining the changes observed on the microscopic (e.g.,
fissures) and the macroscopic level (e.g., cartilage tear).4

10
 Image III. Comparasion of a Healthy and Generate OA Joint4

At the margins of joints frequently (osteo)cartilaginous outgrowths appear

(chondro-osteophytes). They are best considered as a process of secondary
chondroneogenesis in the adult. Osteophytes derive from mesenchymal precursor
cells within periosteal or synovial tissue and often merge with or overgrow the
original articular cartilage. Thus, in this process, mesenchymal precursor cells
differentiate into chondrocytes. A similar, but less structured process is observed
in the areas of the eburnated bone, in which the articular cartilage is completely
torn off. Here, mesenchymal multipotential stem cells of the bone marrow
undergo also chondrogenic differentiation: metaplastic cartilage in forms of
nodules or “tufts” is found either within the bone marrow or at the naked bone
surface.4
Osteophytes could be considered as endogenous repair attempts in
degenerating joints and might be a physiologic response to mechanical
overloading by increasing the articulating joint surface, thus having a supportive
function. However, they are mainly found in non–weightbearing areas and their
mechanical stability and biologic benefit are questionable. To date, the molecular
mechanisms in the development of osteophytes are largely unknown. Mechanical
or biochemical stimuli could play a central role. However, most osteophytes do
not take part in the articulating process and are subsequently not exposed to major
mechanical load. Thus, it is more likely that growth factors play a dominant role
in the induction and promotion of osteophyte formation. For example, the
exogenous application of transforming growth factor-β (TGF-β) and bone

11
morphogenetic protein-2 (BMP-2) into knee joints of adult mice leads to
significant osteophyte formation.4

2.7 Symptomps
The main symptoms are pain, loss of ability, and “joint stiffness after
exercise or use.” These symptoms are often aggravated by activity or rigorous
exercise and relieved during rest, though the disease may eventually progress to
the point where the patient even feels pain when resting, and some people report
pain so intense that it wakes them up when they are sleeping.2
The most consistent symptom is pain in the groin followed by limitation of
movement. Groin pain occurs secondary to irritation of the obturator nerve, which
crosses the hip joint. The pain may also radiate down to the knee joint and in
some cases the only presenting feature may be a painful knee. In the early stages
of the disease, pain is activity related but as the disease progresses the patient also
complains of pain at rest.3
The patient frequently complains of night pain and may also find it
difficult to get into a comfortable position while sleeping. Functionally, most have
difficulty in putting on their shoes/socks and getting into and out ofa bath or a car.
As the pain increases the joint gradually loses its movement because of muscle
spasm, reluctance to move the joint and fibrosis of the capsule. Clinical
examination may reveal gluteal muscle wasting and an effusion with crepitus
anteriorly.3
There may also be a limp with a positive Trendelenburg’s sign. Shortening
is a consistent feature and by the time that most patients present to the surgeon
they are using a walking stick in the opposite hand for support. There is limitation
of movement, particularly rotation in the earlier stages of the disease process; in
the later stages of the disease the limb is in a position of fixed external rotation,
adduction and flexion.3
Pain. Stiffness. Deformity. Pain increases in severity as the disease
progresses. Sleep is often disturbed. Synovial thickening and bony enlargement of
joint because of osteophytes. Effusions. Tenderness. Loss of movement. Crepitus.
Fixed deformities. Disturbances of gait.5

12
2.8 Diagnosis and Investigations

Image IV. 2016 ACR revised Criteria for early diagnosis of knee OA6

a. In the presence of 3 points out of 10 with at least 1 point from Domain II

along with all entry criteria, the diagnosis of knee OA can be established
b. Exclusion criteria are including: 1) moderate to significant knee synovitis
2) Hot or red knee 3) history and/or physical examination findings compatible
with the internal derangement of knee
c. Knee pain that is initiated or increased with knee activity/exercise and
finished or decreased wtih knee resting
d. Clear fluid with normal viscosity accompanied by WBC count less than
2000/mm3 with less than 25% PMN
e. It must be ignored in the presence of osteophyte in knee X-Ray6

Image V. Practical Guideline approaching toward the diagnosis of knee OA6

Radiographs: narrowing of joint space, subchondral bone sclerosis, subchondral

cysts, osteophytes, evidence of other underlying pathology. Symptoms do not
necessarily correlate with the severity of radiological changes.5

2.9 Treatment
There is no specific pharmacological therapy for osteoarthritis; however,
conservative treatment with non-steroidal antiinflammatories, glucosamine
sulphate, regular exercise and physiotherapy to improve muscle strength and
range of movement, and modification of lifestyle with loss of weight does help.

13
Also, patients are encouraged to use a walking stick in the opposite hand to
offload the affected joint. The indications for surgery are relentless pain,
limitation of lifestyle and activities of daily living, and failure of conservative
treatment.3
The surgical options include an arthrodesis, an osteotomy or a joint
replacement in the form of a resurfacing arthroplasty or a total joint replacement.
The choice of a particular procedure is based upon the age of the patient, the
lifestyle and activity status and the stage of the disease. The principle behind each
of these procedures is described in Surgical procedures of the hip. The dictum that
patients should receive a joint replacement only in the end stage of osteoarthritis
when they are in severe pain and activities of daily living are markedly restricted
has certainly evolved over the last decade. More and more joint replacements are
now being performed based on limitation of lifestyle and individual needs,
thereby making it a truly life-improving operation.3
Principles of treatment involve pain relief, improvement of mobility and
correction of deformity. Management may be conservative or surgical.
Conservative. Analgesia: start with mild analgesia, e.g. paracetamol; NSAIDs are
usually required eventually.5
 Lose weight
 Walking stick or shoe raise
 Physiotherapy, i.e. heat treatment or short-wave diathermy
 Changing occupation to a lighter job.

Surgical. Disturbance of sleep, severe uncontrolled pain and gross lack of

mobility are indications for surgery.5 The following procedures may be
undertaken depending upon the level of symptoms and joint involved:
 Arthroscopy or open debridement: occasionally synovectomy and removal
of osteophytes can give temporary relief.
 Replacement arthroplasty most joints can be replaced by artificial joints,
e.g. hip and knee.
 Osteotomy: weight-bearing axis redistributes weight commonly to the
lateral side. Pain relief is often dramatic and failure of the procedure is slow.
 Excision arthroplasty: for small joints, e.g. small toes.
 Arthrodesis: surgical fusion of the joint, relieves pain, e.g. first MTP joint
in hallux rigidus.5

2.10 Prevention
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.1 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.

14
 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.

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. Tertiary prevention Tertiary prevention focuses on
minimizing the compilations of disease once it has been diagnosed.1
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 behavioural interventions, rehabilitation services, and
medical or surgical treatments.1

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 CHAPTER III
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.1
One major reason for this gap is because there is a lack of effective
biomarkers and diagnostics for OA, which makes it difficult to diagnose, track
progression of, and monitor improvements in the patient’s condition. These issues
are especially important to address because OA is a condition that requires long-
term careful management, so detailed information regarding the effectiveness of
medicines is essential. Future research should be directed at addressing this gap in
diagnostics and biomarkers which will improve disease monitoring and allow the
development of medicines that can reverse the progression of this high-burden
condition.1

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