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.