CASE REPORT

OSTEOARTHRITIS OF THE HIP JOINT

Disusun Untuk Memenuhi Sebagian Tugas Kepaniteraan Klinik

Bagian Ilmu Bedah RSUD dr. H. Soewondo Kendal

Pembimbing :

dr. Wisnu Murti, Sp.OT

Disusun oleh :

Dian Rasitawati

30101306915

FAKULTAS KEDOKTERAN

UNIVERSITAS ISLAM SULTAN AGUNG

SEMARANG

2018
 HALAMAN PENGESAHAN

Nama : Dian Rasitawati

NIM : 30101306915
Fakultas : Kedokteran
Universitas : Universitas Islam Sultan Agung ( UNISSULA )
Tingkat : Program Pendidikan Profesi Dokter
Bagian : Ilmu Bedah
Judul : OSTEOARTHRITIS OF THE HIP JOINT

Semarang, Januari 2018

Mengetahui dan Menyetujui
Pembimbing Kepaniteraan Klinik
Bagian Ilmu Bedah RSUD dr. H. Soewondo Kendal

Pembimbing,

dr. Wisnu Murti, Sp.OT

 CHAPTER I

INTRODUCTION

Osteoarthritis refers to a clinical syndrome of joint pain accompanied by varying

degrees of functional limitation and reduced quality of life. It is the most common form of
arthritis, and one of the leading causes of pain and disability worldwide. The most commonly
affected peripheral joints are the knees, hips and small hand joints. Pain, reduced function
and effects on a person’s ability to carry out their day-to-day activities can be important
consequences of osteoarthritis.

Hip joint pain is one of the most common musculoskeletal complaint that brings
people to their doctor. With today's increasingly active society, the number of knee problems
is increasing. Hip joint pain has a wide variety of causes and treatments. Hip joint pain has a
wide variety of causes and treatments. cause of hip joint pain include injury, degeneration,
arthritis, and infection.

Osteoarthritis of the hip joint is a common degenerative joint condition which tends to
be progressive, debilitating and often recalcitrant to treatment. Given the rise in the incidence
of hip joint osteoarthritis in an increasingly younger patient population, along with a more
active lifestyle into later years, more effective conservative treatment options are indicated.

Osteoarthritis (OA) of the hip joint, one of the most common causes of disability,
continues to increase in prevalence as the older adult and obese populations grow. Many
other treatments are available for hip joint OA, including education, behavioural change,
physical interventions and drugs. Several management guidelines have been published over
the last few years, most of which recommend a sequential approach, using simple measure
first, such as education and advice about exercise, footwear, and weight reduction, followed
by the use of anagesics and physical therapy, reserving non-steroidal anti-inflammatory
drugs, intra-articulr interventions and surgery for the more severe cases. Often, the general
practitioner is the first to evaluate a patient with a painful hip joint that has arthritis.
Evidence-based evaluation and treatment guidelines recommend to use surgical treatment
such as Total Hip Athroplasty (THA) are considered.
 CHAPTER II

CONTENTS REVIEW

2.1 ANATOMY

The meaning of the joints is all the bone connections, both of which allow the bones
to move against each other, or can not move with each other. Anatomically, the joint is
divided by 3, there are sinartrosis, diartrosis, and amfiartrosis.

Figure 2.1 Knee Parasagital Section - Lateral to Midline

Diarthrosis is a connection between two or more bones that allows the bones to move
against each other. Among the bones jointed there is a cavity called the articulating cavity.
Diarthrosis is also called synovial joint. The joint is composed of joints (articular capsules),
joint bursa, and joints (ligament).

Hip joint is a joint whose direction of movement is very broad or commonly called
the Ball and Socked joint. Hip joint is also the most important part in forming a person's
posture and plays an important role in every activity especially in walking. Hip joint is
formed over several bones, ligaments, and muscles in which all are interconnected and
mutually reinforcing.
Some bone forming hip joint:

1. Acetabulum
Acetabulum is a meeting between os ilium, os ischium, and os pubis which
served as a bowl joint. Coated hyalin cartilage and covered again labrium
acetabulum which is a fibro cartilage, both thickly edged and thin in the center
2. Os Femur
In the Femur Os section there are two highly related parts in the movement of
the Hip Joint joint, that part is :
A. Caput Femur
The femur cap is a half-shaped bone coated with hyalin cartilage, the fist
as a collum femoris (often fracture), the presence of trochanter major and
minor, later as the shank of the femur.
B. Collum Femur
The femur collum is a pyramidal bone processus that connects the corpus
with the femur cap and forms an angle to the medial part. The largest angle
occurs during infancy and will decrease with growth, so that at puberty
will form a curve on the corpus axis of the curve. At adulthood, the
femoral collum forms an angle of 1250 and varies depending on the
development of larger female pelvis.
 The femur collum is a pyramidal bone processus that connects the corpus with the
femur cap and forms an angle to the medial part. The largest angle occurs during infancy and
will decrease with growth, so that at puberty will form a curve on the corpus axis of the
curve. At adulthood, the femoral collum forms an angle of 1250 and varies depending on the
development of larger female pelvis.
 2.1.1 Ligaments

Ligaments are fibrous bands or connective tissue sheets that connect two or more
bones, cartilage, or structures together. One or more ligaments provide stability to the joint
during rest and movement. Excessive movements such as hyper-extension or hyper-flexion
may be limited by ligaments. Furthermore, some ligaments prevent movement in certain
directions.

There are several ligaments forming the hip joint, where these ligaments are very
strong as a link between the acetabulum and the femoral cap. There are five strongest
ligaments on the hip joint, among others:

1. Ligamentum Capitis Femoris

This ligament is enclosed by a synovial membrane extending from the
acetabuli fossa where there is a fat cushion to the femoral head, besides this
ligament contains arteria leading to the femoral head coming from r.acetabuli
abteratoria arteria. The femoral cap is supplied by A medial aurflexa and A
lateral circumphlexa.
 2. Ligamentum Pubofemoral
Derived from crista obturatoria and adjacent obturator membranes. This
ligament memamcar into the capsula articularis orbicularis zone in particular
through the road to the femoris.
3. Tranverse Acetabulum Ligament
This ligament serves to bridge the incisura acerabuli and the entire surface of
the femoral head.
4. Iliofemoral Ligament
Derived from the inferior anterior spinal iliaca and acetabulum fringe and
extending into the intertrochanterica linea. This ligament has a power of 350
kg.
5. Ischiofemoral Ligament
Derived from the ischium below and walking almost horizontally past the
femoral collum leading to the lateral pars ligament bending of the iliofemoral.
This ligamnet prevents the medial rotation of the thighs.

2.1.2 Osteokinematic Hip Joint

Hip is a joint of Ball and Socked joint so that the joint movement is very wide in all
directions, while the motion that occurs in the hip joint is:

1. Fleksi

The main driving muscles are :

a. Iliacus :

Origo : Superior 2/3 from fossa iliaca crest, anterior crest, anterior sacroiliaca,

dan iliolumbal ligament, ala of sacrum.

Insersio : tendon of psoas major, and body of femur

b. Psoas mayor :

Origo : sides of vertebral bodies and conesponding intervertebralis disc of

T12-L5 and procesus transversus of L1-L5.

Insersio : Leser trochanter of femur

 While other muscles associated with the motion of flexion :

Sartorius :

Origo : anterior superior iliac spine, upper aspec of iliac notch

Insersio : Proksimal aspec of medial surface tibia

2. Ekstensi

a. Gluteus Maksimus

Origo : Posterior gluteal line of ilium, iliac crest, dorsum of sacrum and cocyx,

saerotuberous ligament

Insersio : iliotibial tract, gluteal tuberositas femur

 Semitendinosus :

Origo : ishial tuberositas

Insersio : Proksimal aspect of medial surface tibia

 Semimembrannosus

Origo : ischial tuberositas

Insersio : Medial condilus tibia

b. Biceps Femoris :

Origo : Ischial tuberositas, lateral tip of linea aspec femur and lateral

intermuscular septum

Insersio : Lateral aspect of head fibula

3. Abduksi

a. Gluteus medius

Origo : outer surface ilium antara and posterior and anterior gluteal lines

Insersio : Greater trohanter femur

b. Gluteal Minimus :
 Origo : outer surface ilium between anterior and posterior gluteal lines

Insersio : greater trohanter femur

While other muscles associated with this movement are :

Tensor Facia Latae

Origo : anterior superior iliac spine, anterior aspect of auterlip ofiliac crest

Insertio: illiotibial tractus aproximately 1/3 down the tight

4. Adduksi

a. Adductor Magnus

Origo  : inferior rami of pubis dan ischium ischial tuberosity

Insertio : a line fro great trochanter  to linea aspera femur, linea aspera, adductor

tubercole, medial supracondilare line of femur

b. Adductor longus

Origo : Anterior aspec of pubis

Insersio : Linea aspera along middle 1/3 femur

c. Adductor brevis

Origo : Inferior ramus of pubis

Insersio : line lesser trohanter to linea aspera, upper portion of linea aspera

d. Pectineus

Origo : pectineal line of pubis

Insersio : Line from lesser trohanter to linea aspera

e. Gracilis

Origo : Body and ramus of pubis

Insersio : proksimal aspecct of medial surface tibia

5. Medial rotasi

a. Tensor facia latae

 b. Gluteaus minimus

c. Gluteus medius

6. Lateral rotasi

a. Piriformis

Origo : anterior suface sacrum, sacrotuberous ligament

Insersio : Freater trohanter femur

b. Gemellus superior

Origo : iscial tuberositas

Insersio : Greater trohanter femur

c. Obturator internus :

Origo : Obturatory membran and forament, inner surface of pelvis, inferior rami

of pubis and ischium

Insersio : greater trohanter femur

d. Obturator Eksternus :

Origo : rami of pubis and ischium, outer surface of obturatory membran

Insersio : Greater trohanter femur

e. Quadrratus femoris

Origo : ischial tubrosity

Insersio : quadrate tuberosity femur

2.2 OSTEOARTRITIS HIP JOINT

2.2.1 Definition
Osteoarthritis is a degenerative noninflammantory joint disease common in
elderly people. While other definitions say that osteoarthritis is a chronic
degenerative joint disease with joint cartilage damage in the form of
disintegration and progressive use, followed by an increase in the edge of
bone and joint cartilage called osteophytes, followed by fibrosis in the
joint capsule.
2.2.2 Epidemiology
Incidence of osteoarthritis increases with the aging process and is
especially found in the age above 50 years. In Indonesia, the prevalence of
OA in 2007 reached 36.5 million. It is estimated that 40% of the
population aged over 70 years suffer from OA and 80% of OA patients
have limited mobility in varying degrees of mild to severe which result in
reduced quality of life due to high prevalence. It is estimated that 1-2
million elderly people in Indonesia suffer from disability due to OA. The
radiologically visible appearance of knee OA reaches 15.5% in men and
12.7% in women aged 40-60 years.
2.2.3 Risk Factor
Risk factors for osteoarthritis are influenced by:
 Age
Generally found in elderly (above 50 years), because in the elderly
formation of chondroitin sulphate which is the basic substance of
cartilage is reduced and cartrosis fibrosis can occur.
 Weight
The higher a person's weight, the more likely a person is to have
osteoarthritis. This is because along with the increase in body weight,
the burden to be received joints on the body the greater. The load
received by the joint will put pressure on the affected part of the joint,
for example on the pelvis and knees.
 Gender
This disorder can be found in both men and women where primary
osteoarthritis is more common in postmenopausal women whereas
secondary osteoarthritis is more common in men.
 Genetics
Genetic factors also play a role in the occurrence of hip OA. It is
associated with abnormalities of the genetic code for inherited
collagen synthesis, such as the presence of mutations in the
procollagen II gene or other structural genes for joint cartilage
structures such as collagen type IX and XII, binding proteins, or
 proteoglycans. Bone inherited disorders affect the shape and stability
of the joints that can cause osteoarthritis.
 Trauma and occupational factors
Trauma to joints or overuse of joints, especially intra-articular
fractures or joint dislocations. Athletes and people with jobs that
require repetitive motion have a higher risk of osteoarthritis due to
injury and increased pressure on certain joints. In addition, it occurs
also in the joints where the bone has been cracked and has been
performed surgery.
 Metabolic or endocrine factors
Patients with hypertension, hyperuricemia and diabetes are more
susceptible to osteoarthritis.
 Muscle weakness
Weakness in the muscles surrounding the joints can lead to
osteoarthritis. Muscle weakness can be reduced due to age,
inactivation due to pain or due to inflammation of the joints.
 Weather or climate
Symptoms more often occur after contact with cold or humid weather.
 Race is more common in Asians especially China, Europe and
America than blacks.
 Nutrition
Normal metabolism of bone depends on the presence of vitamin D.
Low levels of vitamin D in the tissues can impair the ability of the
bone to respond optimally to the process of osteoarthritis and will
affect its development. The likelihood of vitamin D has a direct effect
on the chondrocytes in cartilage that have osteoarthritis, proved to
reshape vitamin D receptors.
 Diet
One type of OA that is common in Siberia is called Kashin-Beck
disease that may be caused by ingestion of a toxin called fusarin.
2.2.4 Classification

Osteoarthritis can be divided into two types, namely:

1. Primary osteoarthritis
 Primary osteoarthritis is not known clearly the cause, it can affect one or
several joints. This type of osteoarthritis is predominantly found in white,
middle-aged and generally poly-articular women with acute pain
accompanied by a burning sensation in the distal interfalangeal part that
subsequently occurs in bone swelling called the Hebreden node.
2. Secondary osteoarthritis
Secondary osteoarthritis can be caused by a disease that causes damage to
the synovial resulting in secondary osteoarthritis. Some of the conditions
that can lead to secondary osteoarthritis are:
 Trauma / instability
Secondary osteoarthritis occurs due to fracture in the joint area
after menisectomy, lower legs are not equal in length, the presence
of hypermobility and joint instability, misalignment and
incompatibility of joint surfaces.
 Genetic / developmental factors
The presence of genetic abnormalities and developmental
abnormalities such as epiphyseal dysplasia, acetabular dysplasia,
Legg-Calve-Perthes disease, congenital hip joint dislocation and
slipped epiphysis.
 Metabolic / endocrine diseases
Secondary osteoarthritis may also be caused by metabolic /
endocrine diseases such as okronosis, acromegaly,
mucopolysaccharidosis, crystal deposition or after an inflammation
of the joint, eg rheumatoid arthritis or inflammation by
inflammation.
 Osteonecrosis
Osteoarthritis can develop due to femoral head osteonecrosis by
various causes, such as Caisson disease, sickle cell disease.
A. Classification of OA based on Etiology
Based on etiology, OA can occur in primary (idiopathic) and secondary. The
classification of OA based on etiology can be seen in the table below :
B. Classification of osteoarthritis based on the location of affected joints

2.2.5 Pathogenesis
Joints consist of joint, joint and synovial joints (joint membranes). Joints
are composed of extracellular matrix of collagen tissue (types I, II, III, V
and XI), proteoglycans and water and cellular components, especially
collagen chondrocytes arranged as elongated and elastic longitudinal
bonds so as to maintain joint function in restraining body load pressure.
Proteoglycan in prone joints is a sugar protein (glycoprotein) consisting of
linked N bonds and O linked oligosaccharides. The addition of sulfate
groups causes various kinds of proteoglycans. Proteoglycans consist of
90% agregan, in which the agregan consists of 2 components of
 glycosaminoglycans ie chondroitin sulfate and sulfate-solvent which are
bound by hyaluronan acid.
At a young age the formation of chondroitin sulfate is more than keratin
sulphate. The combination of collagen, agregan (kondoritin sulphate) and
hyaluronan acid will cause the joint to become elastic and resistant to
withstand the pressure of the body load. Besides prone to joints, there are
also fluids (lubricants) and bursa and ligaments that can strengthen joint
structure.
With age (> 38 years) the production of chondroitin sulphate will decrease,
otherwise keratin sulfate increases. As a result, the joint is less susceptible
or elastic in the face of various mechanical pressures. When precipitated
with micro trauma to the joint (working with load, trauma, up and down
stairs), the elastic and strong joint structure is altered. Happen micro injury
is prone to joints which is the beginning of inflammation joints. If the
trauma continues, an inflammatory mediator, prostaglandin, cytokine (IL-
1beta) free radical nitrite oxide (NO) and proteolytic enzymes, all of which
cause damage to joint-prone structures. NO and IL-1beta will inhibit the
formation of collagen and proteoglycans. Other negative effects, NO and
IL-1beta can activate proteolytic enzymes (matrix metallo proteinase)
resulting in gradation of joint-prone tissue especially collagen and cause
chondrocytes death. Thus in osteoarthritis local inflammation occurs with
joint-prone degradation with collagen damage and degradation of
proteoglycan structure. The result of degradation of the joints into the
lymph system and blood into the liver and then excreted through the urine.
Instead repair joints can be done by the growth hormone insulin like
growth factor and transforming growth factor produced by chondrocytes.
In osteoarthritis, degradation is greater than formation. Finally arise pain,
swelling and joint dysfunction. Advanced phase will occur compensated
with bone growth under joint-prone due to growth hormone stimulation.
The bone under the joint prone to hypertrophy and hard (osteofit), this
hard bone will actually cause the elasticity of the joints more reduced
again so that will increase damage to joints.
2.2.6 Clinical Manifestations
 Symptoms
 a. Pain is a common symptom. Often widespread or possibly
reffered to distant locations, examples of knee pain in hip OA.
Pain appears suddenly and increases slowly over a month or
year. Pain increases with activity and improves with rest. At an
advanced stage, the patient feels pain during sleep at night.
There are several possible causes of pain: synovial
inflammation, painful capsule fibrosis, stretched tissue
stretching, muscle fatigue and bone suppression due to blood
vessel congestion and intraosseous hypertension.
b. Stiffness, often occurs, characteristic occurs after the period of
inactivity but over time becomes constant and progressive.
c. Loss of function, difficulty up the stairs, limitations of running
distance, progressive incapacity to perform daily tasks
 Signs
a. Swelling, can occur due to effusion in the joints, usually not
much (<100 cc). Another reason is osteophytes, which can alter
the surface of the joint.
b. Deformity, may arise due to prolonged joint contractures,
altered joint surfaces.
c. Movements are limited, often existing even in early
(radiologically) OA. It usually gets worse with the severity of
the disease until the joints can only be shaken and become
contractures. Motion obstacles can be concentric (all direction
of movement) or eccentric (one direction of movement only).
Movement disorders in the joints are mainly due to fibrosis of
the capsule, osteophytes or joint surface irregularity.
d. Crepitus, initially just a feeling of something broken or broken
by the patient. With the severity of the disease, crepitations can
be heard for a certain distance. These symptoms may arise
because of the friction of both surfaces of the bones at the time
the joint is moved or passively manipulated.
2.2.7 Diagnosis
 The American College of Rheumatology sets the criteria for the diagnosis
of idiopathic pelvic OA based on clinical and radiological examinations as
follows:

Table 2.2.1 Diagnosis Criteria of Pelvic OA

2.2.8 Clinical feature

The diagnosis of OA apart from clinical features can also be established by
radiological features, narrowing the gap between the joints, the formation
of osteophytes, the formation of cysts, and subchondral sclerosis.
Figure 2.2.2 X-ray radiological imaging of pelvic osteoarthritis.
Information:
a. Up arrow (right): anteroposterior view indicates narrowing of joint
crack
b. Right arrow: lateral view shows sclerosis marked by osteophyte
formation
c. Left Arrow: found subchondral cyst

Based on these radiographic images, Kellgren and Lawrence divide OA

into four degrees :

a. Grade 0: normal
b. Grade 1: normal joint, there is little osteofit
c. Grade 2: osteophytes in two sites with subcondral sclerosis, normal
joint cleft, there are subcondral cysts
d. Grade 3: moderate osteophytes, there is a deformity in the bone line,
there is narrowing of the joint crevice
e. Grade 4: there are many osteophytes, no joint cleft, there are
subcondral cysts and sclerosis
 Table 2.2.3 Grading according to Kellgren-Lawrence criteria
2.2.9 Management
The goal of treating patients with osteoarthritis is 5:
1. Relieves pain
2. Optimize joint function
3. Reduce dependence on others and improve quality of life
4. Inhibits disease progression
5. Prevent the occurrence of complications
 Conservative (nonpoperative) / EARLY TREATMENT
A. Nonpharmacological
a. Education, telling the patient about his illness and to keep his illness
from getting worse.
b. Modification of lifestyle, such as losing weight.
c. Activity modification
d. Medical rehabilitation / physiotherapy
Medical rehabilitation programs that are often performed on OA can be:
- Hot therapy
Deep heat therapy, ie heat can penetrate to the deeper tissues that reach
the muscles, bones, and joints. In the case of OA used SWD (short
wave diathermi) and USD (ultra sound diathermi). Therapeutic heat in
vasodilating effects that can reduce or eliminate pain.
 - Electrical therapy
What is used is TENS (Transcutaneous Electrical Nerve Stimulation).
TENS is a modality used to reduce or eliminate pain through increased
threshold of excitatory pain.
- Muscle strengthening exercises
Exercise is known to improve and maintain joint motion, strengthen
muscles, improve static and dynamic resistance and improve overall
function. Exercises consist of passive exercises, active, endurance,
stretching and recreation.
- Orthotic Prosthetic
Used to restore function, prevent and correct defects, support weight
and support sick limbs. In patients with OA is usually done plan the
use of knee brace or knee support.
B. Pharmacological
1. Analgesic, acetaminophen is the drug of choice for mild to moderate
arthritis.
2. Non-steroids anti-inflammatory drugs (NSAIDs). NSAIDs are powerful
prostaglandin inhibitors that reduce vascular congestion in subchondral
bone. The disadvantage, can cause gastrointestinal irritation and in some
patients leads to ulcers and bleeding.
3. Topical, NSAIDs and capsaicin.
4. Intraarticular injection
Intra articular or periarticular injection is not the primary choice in the
treatment of osteoarthritis. Care is required and selectivity in the use of
this therapy modality, given the detrimental effects of both local and
systemic. There are basically 2 indications of intra articular injection ie
symptomatic treatment with steroids and viscosupplementation with
hyaluronan for modification of the course of the disease.
- Local injections of intra-articular corticosteroids may also be given to
OA patients who are unlikely to be given NSAIDs (renal failure,
gastrointestinal bleeding) or may be administered with NSAIDs in
order to reduce the amount of NSAIDs administered. Intraarticular
local injection is not recommended in cases with a strongest prediction
of infective arthritis (pussy, clouding or leukocytes> 30,000 / mm3).
 The frequency of intraarticular steroid injections is recommended not
too often ie maximal given 2 or 3 times a year. This restriction is due
to the administration of steroid injections that are too frequent to
potentially increase joint damage or cause arthritis pseudo
Charcotarthropathy.
- Hyaluronic acid is also called viscosupplement because one of the
benefits of this drug is to improve the viscosity of synovial fluid.
Hyaluronic acid is important in the formation of cartilage matrix
through aggregation with proteoglycans.
 Operative
1. INTERMEDIATE
If symptoms increase despite conservative therapy then some operative
treatment is necessary. This is a procedure performed primarily in young
patients who are not ready for joint replacement therapy. For knee OA, joint
debridement (removing osteophytes, cartilage) can be performed
arthroscopically.
2. LATE
Progressive joint destruction with increased pain, instability and deformity
(one of the heavy support joints), usually requires a reconstruction
operation.
Arthroplasty (Joint replacement) Joint replacement surgery or arthroplasty is
an orthopedic surgical procedure in which arthritis or surface joint
dysfunction is replaced by orthopedic prosthesis.
 Figure 2.2.1 Total Hip Joint Replacement

It is one form of procedure that has recently been selected for OA in patients with
intolerable symptoms, signs of loss of function, and severe restriction of daily activity. For
hip and knee OA in middle age and older patients, total joint replacement with modern
techniques is promising for 15 years or more. Joint replacement depends on engineering
skills, implant design, appropriate tools and postoperative care.

Artificial joints can help:

 Reduce joint pain.

 Restore or maintain joint motion.
 Improve the look and alignment of the joints.
 Enhance overall.

Total Hip Replacement

a. Cemented Total Hip Replacement

 In this method of fixation, bone cement is used to attach the artificial hip joint to the
femur bone. Bone cement does not function like a glue, but as a filler material. Up to
now, the most widely used bone-cement material is polymethylmethacrylate
(PMMA), which was introduced by Sir John Chanrley in the early 1960s.

b. Cementless Total Hip Replacement

Cementless THR, also called uncemented THR was introduced in early 1980. THR
method is developed because the cemented THR has a deficiency. First, filling cement
bone into the femur during operation can cause disturbance to the circulation and may
block blood flow. Secondly, bone cement takes an average of 10 minutes to gouge. In
this time, there is the possibility of artificial hip joint changing position. Third, bone
cement may crack and cause a shift from the implant. For cementless artificial hip
joints, the surface of the artificial hip joint system is crude. This is to produce good
friction between artificial hp joint and cortical so that it can be mounted more stable.
In this method there are also shortcomings. First, when the artificial hip joint is
attached to the bone, the substance of the bone gets pushed into the blood circulation
system and blocks the blood circulation. Femur can be broken during operation due to
large loads.
c. Hybrid Total Hip Replacement
In this method, combining between cementeless and cemented THR methods. This
combination produces cementless acetabular cup with femoral stem fitted with
cement. Methods can reduce stem damage or failure from 30-40% to 3-4%

 Arthrodesis
Arthrodesis, also known as artificial ankylosis or syndesis is an artificial
induction of joint repeatability between two bones through surgery. This is done
to relieve pain in joints that can not be managed by pain medication, splints or
usual treatments. The typical causes of the pain are fractures that disrupt joints
and arthritis. This is most often done on the joints in the spine, hands, ankles,
and legs. Historically, knee and hip arthrodesis was also performed as a pain
relief procedure, but with great success achieved in hip and knee arthroplasty,
the arthrodesis of large joints failed as a major procedure and is now only used
as the last procedure in some failed arthroplasty.
2.2.10 Prognosis
The prognosis in patients with OA depends on the joint damage involved
and the severity of the disease. Pharmacologic therapy is only intended to
relieve symptoms. Patients who have undergone joint replacement have a
good prognosis. Prosthesa joints need to be revised after 10-15 years since
 joint replacement. Younger patients and more active patients need to be
revised more frequently while the majority of elderly patients do not
require revisions.
2.2.11 Complications
This disease if not received good and proper handling, it requires a variety
of new problems that teriadi due to the disease process itself. Like the spur
(osteofit) so that the process of destruction of joint cartilage. The
subcondral bone gradually punctures the metaphysis of the tibia and femur
bones as a result of complications such as pain, varus and valgus legs,
atrophy of meniscus quadriceps femoris muscle weakness, decreased
structural resistance and complications of varus and valgus deformity.
Ternganggunya daily activities such as activities of worship, squatting,
sitting, bendiri and road.
 CHAPTER III
PATIENT’S STATUS
 CHAPTER IV
DISCUSSION

Osteoarthritis refers to a clinical syndrome of joint pain accompanied by varying

degrees of functional limitation and reduced quality of life. It is the most common form of
arthritis, and one of the leading causes of pain and disability worldwide. The most commonly
affected peripheral joints are the knees, hips and small hand joints. Pain, reduced function
and effects on a person’s ability to carry out their day-to-day activities can be important
consequences of osteoarthritis.

From the foregoing outline it should be apparent that the division of OA into
‘primary’ (when there is no obsvious antecedent factor) and ‘secondary’ (when it follows a
demonstrable abnormality) is somewhat artificial. This is borne out in clinical practice:
patient with secondary OA of the hip joint following meniscectomy have been found also to
have a higher than usual incidence of ‘primary’ OA in other joint. Perhaps primary,
generalized factors (genetic, metabolec or endocrine) alter the physical properties of cartilage
and there by determine who is likely to develop OA, while secondary factors such as
anatomical defects or trauma specify when and where it will occur. OA is, ultimately, more
process than disease, occuring in any condition which causes a disparity between the
mechanical stress to which articular cartilage is exposed and the ability of the cartilage to
with stand that stress. These patients, based on history, the patient was a woman aged 64
years working as a house-assitant since 10 years ago and she got fall down from the chair
when she cleaned home so her collum femur was fracture and then she got an orif treatment.
After 2 years she felt pain in her hip joint. In addition, of the physical examination of patients
were overweight. This conditions is a risk factor for the occurrence of secondary OA. So it
can be concluded that the cause of OA in these patients is not including the primary risk
factor of OA.
 CHAPTER V
CONCLUSSION

Osteoarthritis (OA) is a chronic joint disorder caused by an imbalance between

degradation and synthesis of joint cartilage as well as an extracellular, chondrocytes and
subcondral matrix in old age. This can be regarded as a degenerative disorder arising from the
biochemical destruction of articular (hyaline) cartilage in the synovial joint. The prevalence
of this disease increases sharply with age. OA of the hip joint is more suffered by women
than men, because of the broader female pelvic size.

Osteoarthritis is classified into two primary osteoarthritis and secondary osteoarthritis.

Primary osteoarthritis is not known clearly the cause, it can affect one or several joints.
Secondary osteoarthritis can be caused by circumstances that cause damage to the synovia
such as trauma, genetic factors, metabolic diseases and osteonecrosis.

Diagnosis of osteoarthritis can be established through anamnesis, physical

examination and investigation. For radiological examination, standard radiological evaluation
methods used are plain photographs.

Management can be done conservatively or operatively. Conservative management

can be done by treating pain such as analgesic administration, NSAID and topical
medicament with physiotherapy, lifestyle modification and activity. The goal of treatment in
OA patients is to reduce symptoms and prevent the occurrence of contractures or muscle
atrophy.

Important education is to convince the patient to be self-reliant, not necessarily

dependent on others even though OA is incurable, but the quality of life of the patient can be
improved and an understanding of therapeutic grounds is necessary to ensure the success of
osteoarthritis therapy.
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