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BAB 1

1. Introduction
Osteoarthritis is a syndrome that has many clinical manifestation,

that differ from a patient to another patient. European Society for Clinical

and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) and

European Union Geriatric Medicine Society (EUGMS) are joined to

explore and identify different patient profiles in osteoarthritis. 1


Osteoarthritis is a disease that affects joints, therefore its surfaces

become damaged so the joint doesn’t move as smoothly as it should. The

condition is sometimes called arthrosis, osteoarthrosis, degenerative joint

disease or wear and tear.2

BAB II

1. Definition
Osteoarthritis is chronic

progressive disease that potentially affecting every articular tissue, and

may potentially lead to joint failure. Osteoarthritis is also a form of

arthritis that features the breakdown and eventual loss of the cartilage of

one or more joints. This disease may present differently in men and

women, in patients with or without trauma, in athletes, or in obese

patients. Typical clinical symptoms are pain, particularly after prolonged


activity and weight bearing, whereas stiffness is experienced after

inactivity. It is probably not a single disease but represents the final end

result of various disorders as joint failure. It is also known as degenerative

arthritis, which commonly affects the hands, feet, spine, and large weight-

bearing joints, such as the hips and knees. 1,2

2. Epidemiology
Osteoarthritis (OA) is one of the most common joint disease in

population. Osteoarthritis (OA) is the second most common

rheumatological problem and is most frequent joint disease with

prevalence of 22% to 39% in India OA of the knee joint is found in 70% of

the population over 60 years of age. Radiological evidence of OA can be


found in over 90 % of the population. Osteoarthritis of the large joints was

comparatively uncommon, with osteoarthritis of the hip found in 1.1% of

men and 2.9% of women and osteoarthritis of the knee in 0.8% of men and

5.2% of women. Bilateral knee osteoarthritis was much more common in

women than in men. The highest prevalence for osteoarthritis is seen in the

cervical spine, the lumbar spine and the distal interphalangeal joints (DIP).

Severe radiological osteoarthritis is uncommon under age 45 years, and

the prevalence does not exceed 20% in the elderly aside from in the

cervical and lumbar spine and DIP and, in women, the joints of the hands

and the knees. The incidence of osteoarthritis increases with age, and

women have higher incidences than men, especially after age 50. 2,3

3. Pathogenesis

Osteoarthritis is now conceived as the endpoint of a complex series

of events rooted in factors that have been recognized as associated with

osteoarthritis risk, in some cases, for many years. The new framework for

osteoarthritis etiology permits us to classify these factors either as drivers

of abnormal stresses on articular cartilage, including obesity, anatomic

abnormalities, or trauma; or as drivers of aberrant cartilage physiology,

including aging, genetic and metabolic factors, and inflammation (Figure

1). These sets of disease drivers induce biophysical and biochemical

changes that culminate in cartilage breakdown.3


In this review, we first briefly describe cartilage structure and the

pathophysiological mechanisms responsible for cartilage destruction,

introducing the major structural, enzymatic, and inflammatory “players” in

osteoarthritis. These mechanisms, which are well understood, have

provided the first set of targets for therapeutic approaches that extend

beyond pain relief and surgical repair to true modification of the disease

process. We then consider osteoarthritis etiology: how disease drivers

interact in the development of chondropenia, a first step on the

osteoarthritis continuum, and how they influence the balance between

cartilage synthesis and degradation. We also address events at the cellular

and molecular level, including the possible role of gap junctions in

facilitating signal transduction that promotes disease progression.3

4. Etiology
Osteoarthritis is divided into primary OA and secondary OA.

Etiology of primary OA is still unknown, while the etiology of secondary

OA is well known. Primary OA known as natural aging proccess of the

joint. By the increasing of age, the water content of cartilage will be

increased, and soon the protein of cartilage will degenerate. Here some

predicted causes of primary OA, 2,4


 Female
 Caucasian
 Obesity
 Genetics
Secondary OA is a form of osteoarthritis that is caused by another

disease or condition that affect joints. Some causes that proved to be main

cause of OA are, 2,4


 Mechanical forces: scoliosis, congenital deformity
 Metabolic and other endocrine disorders
 Prior trauma
 Prior RA and JIA or other inflammatory processes

5. Structure of Joint Cartilage

There are fve basic types of structures in the knee: 2

a. ligaments, which are passive elastic structures that can be loaded in

tension only;

b. musculotendinous units, which are active elastic structures that act

only under tension;

c. cartilage and subchondral bone, which accommodate the compressive

loads of the joint; Joint cartilage is composed by collagen (type 2),

proteoglycan (hyaluronic acid and glucoseaminoglycan, water, and

chondrocyte).

d. meniscus, which are crescentic fbrocartilaginous pads that attach to the

intercondylar area and periphery of the tibial plateau; and

e. the bursae.
6. Diagnosis
Diagnosis of osteoarthritis is described by clinical findings and also

radiologic findings. The clinical fndings of osteoarthritis are characteristic

to each stage of the disorder. Physical examinations should include all

relevant tests, including inspection and palpation, range of movement and

special functional tests when required, such as meniscus tests, ligament

stability and gait analysis.2,3


Plain flms should be obtained in at least two planes: anteroposterior

and lateral. The main radiographic features associated with osteoarthritis

are osteophytes, narrowing of the joint space due to articular cartilage loss

and several changes in the subchondral bone, such as sclerosis, cysts,

shape changes and loss ofbone volume.2,3


7. Signs and Symptoms
The symptoms of osteoarthritis tend to develop slowly. Pain or

soreness is often noticed when the patient move certain joints repetitively

or when the patients been inactive for a prolonged period. The pain in

weight-bearing joints is usually worsened by standing and walking is and

relieved by rest. Although it is typically intermittent, pain can become

constant. The affected joints may also be stiff or creaky and occured most

often in the morning. Typically, osteoarthritis leads to morning stiffness

that resolves in 30 minutes. When osteoarthritis affects the hands, some

people develop bony enlargements in the fingers, which may or may not

cause pain. In the later stages patient will aso experience limitation of

ROM and some will have deformity that restrict daily activity. Effusion,

bony swelling or both, crepitus (defned as a sensation of crackling or

crunching), is also commonly felt on passive or active movement of an


affected joint. For long term effect, soft tissue contractures can result in

varus (inward) or valgus (outward) knee deformity and lead to joint

instability. 2,3,4

8.

Additional Examination
Laboratory Findings
There are no pathognomonic laboratory findings for OA. Laboratory

analysis is only performed for differential diagnosis 2


Radiologic Findings
 Narrowing of joint space (due to loss of cartilage)
 Osteophytes
 Subchondral (paraarticular) sclerosis
 Bone cysts
Kellgren Lawrence Classification
9. Treatment

The goal of treatment in osteoarthritis is to reduce joint pain and

inflammation while improving and maintaining joint function. There is no

treatment to stop the erosion of cartilage in the joints, but there are ways to

improve joint function. One of these is physical therapy to increase

flexibility and strengthen the muscles around the affected joints. The
therapist may also apply hot or cold therapies such as compresses to

relieve pain. To obese or overweight patients, one of the most effective

ways to relieve pain in the knee or hip joints is to shed a few pounds of

weight.1,2

Pharmacotherapy

Structure modifying: Hyaluronic Acid injection (HA), Glycose

Amino Glycans (GAG) over-the-counter pain and anti-inflammatory

medication, such as aspirin, ibuprofen, or acetaminophen, and pain-

relieving creams or sprays can also help when applied directly to the sore

area.2,3

Exercise

Exercise is essential for all people with knee osteoarthritis. Meta-

analyses have found small-to-moderate effects in pain and function with

exercise, similar to those achieved with analgesics and nonsteroidal anti-

inflammatory drugs (NSAIDs). High-intensity, home-based strength

training can produce substantial improvements in strength, pain, physical

function and quality of life in people with knee osteoarthritis. Muscle

rehabilitation plays an important role in disease management in general

and in reducing symptoms and improving function in particular. 2,3

Diet

Most of OA patients have elevated blood cholesterol, so it is better

to reduce the intake of foods high in satyrated fat. Another suggested diet
is consuming more food containing antioxidant that can be found in food

with high vitamin A, C, and E. Vitamin D is also essential for bone and

cartilage growth. It is also important have daily sun exposure (10-15

minutes) to increase vitamin D level

Surgery

If osteoarthritis interferes significantly with everyday life and the

symptoms don't improve with physical therapy or medication, joint

replacement surgery is an option. This procedure is used on those with

severe OA and need to replace a damaged joint with an artificial one. The

knee and hip are the joints that are replaced most often. 2,3
References

1. What is Osteoarthritis?. 2014. National Institute of Arthritis and

Musculoskeletal and Skin Disease. Bethesda: National Institutes of

Health
2. Arden, Nigel et al. 2018. Atlas of Osteoarthritis 2nd ed. European

Society for Clinical and Economic Aspects of Osteoporosis,

Osteoarthritis and Musculoskeletal Diseases. London: Springer Health

Care.
3. Mahajan et al. Osteoarthritis. 2005. Journal of The Association of

Physicians of India vol 53.


4. Osteoarthritis of The Knee. 2013. Arthritis Research UK.
5. British Dieteric Association. 2017. Diet and Osteoarthritis.

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