1

CHAPTER I

INTRODUCTION

Osteoarthritis is the most common disease of the joints, and one of the most

widespread of all chronic diseases. Its prevalence increases steadily with age and by

retirement age the associated radiological changes can be observed in over half the

population. Symptoms can vary from minimal to severe pain and stiffness, but overall

the disease is responsible for considerable morbidity and is a common reason for GP

consultation. Unfortunately, it is also difficult to treat and inevitably a wide range of

potential therapies have been advocated, both by conventional and complementary

practitioners, and not necessarily with strong supporting evidence.

The high prevalence of osteoarthritis, the numerous forms of potential treatment

and the uncertainty around these all make the disorder an excellent topic for a clinical

guideline. The lack of evidence in some areas is a less favorable feature, and although

this has presented something of a challenge, the GDG has risen to this admirably. As

with all NICE guidelines, an exhaustive literature search has been performed and the

papers identified in this process have been rigorously assessed. Where it is possible to

make recommendations based on good evidence, the GDG have done so, where

evidence is not available or is weak, they have either made recommendations on the

basis of strong clinical consensus, or have advocated appropriate research.

The guideline contains a number of recommendations which are not currently

routine practice for many clinicians. While the place of paracetamol in early pain

management is confirmed, the guideline also suggests early consideration of topical

non-steroidal anti inflammatory drugs (NSAIDs) for knee and hand arthritis, and

suggests that wherever systemic NSAIDs or cyclooxygenase-2 (COX-2) inhibitors are

used, they should be coprescribed with cover from a proton pump inhibitor (PPI). This

latter recommendation will surprise many, but with PPIs now coming off patent, it is

clearly backed up by our health economic analysis. The positive role of exercise is

emphasised in contrast to the natural inclination some might have to rest when a joint is

affected by osteoarthritis. The GDG has also not shied away from negative

recommendations. They suggest that arthroscopic lavage and debridement is not

suitable therapy for

2

osteoarthritis except in clear instances where this is associated with mechanical locking

and they do not recommend the use of intra-articular hyaluronans. Elsewhere, there is

only restricted support for the use of acupuncture.

The process of producing a guideline is rarely straightforward and there have

been occasional difficulties along the way. The GDG have navigated all these with good

humour and a consistent desire to evaluate all evidence as thoroughly as they possibly

could in order to improve the management of this difficult condition. We at the NCC-

CC are grateful to them for all of their work. The guideline is a tribute to their efforts

and we hope and expect that it can be used both to practical benefit and to raise the

profile of this sometimes neglected condition.1

3

CHAPTER II

LITERATURE REVIEW

II.1.Definition

Osteoarthritis is noninflammatory degenerative joint disease marked by

degeneration of the articular cartilage, hypertrophy of bone at the margins, and changes

in the synovial membrane, accompanied by pain and stiffness. 2

II.2.Epidemiology

Osteoarthritis (OA) is the most common form of progressive joint disease

worldwide, affecting 16 million (6%) American adults. Racial differences exist for both

the prevalence and the pattern of joint involvement. Compared with whites, South

African blacks and persons of Chinese, East Indian, or Native American descent have a

lower prevalence of hip OA. Females have a higher prevalence of OA of the knees and

hands, whereas males have a higher prevalence of OA of the hips. For knee OA, the

female-to-male incidence ratio is 1.7:1.

Age is the strongest determinant of OA; the prevalence of OA at all joint sites

progressively increases with age. Estimates of the true prevalence of OA are imprecise

because of the difficulties associated with the diagnosis. Estimates based on the

radiographic evidence of knee OA are as follows: OA affects 25-30% of persons aged

45-64 years, 60% of persons older than 65 years, and more than 80% of persons older

than 75 years. 3

II.3.Etiology

The daily stresses applied to the joints, especially the weight-bearing joints (eg,

ankle, knee, hip), play an important role in causing osteoarthritis (OA). The hereditary

component has long been recognized, particularly with generalized OA; a gene for OA

has been identified and plays an important role. Potential risk factors include age,

obesity, trauma, genetics, sex hormones, muscle weakness, and environment. 3

4

Old joints and osteoarthritic joints differ. With advancing age, cartilage volume,

proteoglycan content, cartilage vascularization, and cartilage perfusion are reduced and

may result in certain characteristic radiologic features that include joint-space narrowing

and marginal osteophytes. However, biochemical and pathophysiologic findings support

the notion that age alone is an insufficient cause of OA.

Obesity increases the mechanical stress in a weight-bearing joint. It has been

strongly linked to OA of the knees and, to a lesser extent, of the hips.

Traumatic insults to the articular cartilage, ligaments, or menisci lead to abnormal

biomechanics in the joints and enhance their premature degeneration.

Menopause often increases the progression of OA; however, estrogen replacement

therapy lowers the expected rate of radiographic and clinical findings in the knees and

hips.

Muscle dysfunction compromises the body's neuromuscular protective mechanisms,

leading to increased joint motion, resulting in OA. This effect underscores the need for

continued muscle toning exercises in all individuals to prevent muscle dysfunction.

One should not confuse environmental factors as causes of OA, because these factors actually cause traumatic arthritis on a macrotraumatic or microtraumatic basis. This is especially true of individuals whose lifestyles require squatting, climbing stairs, or excessive kneeling. 3

II.4.Risk Factor

Osteoarthritis is defined not as a disease or a single condition but as a common

complex disorder

with multiple risk factors. These risk factors are broadly divisible into:

genetic factors (heritability estimates for hand, knee and hip osteoarthritis are

high at 40–60%, though the responsible genes are largely unknown)

constitutional factors (for example, aging, female sex, obesity, high bone

density)

more local, largely biomechanical risk factors (for example, joint injury,

occupational/ recreational usage, reduced muscle strength, joint laxity, joint

malalignment).

5

Importantly, many environmental/lifestyle risk factors are reversible (for

example, obesity, muscle weakness) or avoidable (for example, occupational or

recreational joint trauma) which has important implications for secondary and primary

prevention. However, the importance of individual risk factors varies, and even differs,

between joint sites. Also, risk factors for developing osteoarthritis may differ from risk

factors for progression and poor clinical outcome (eg high bone density is a risk factor

for development, but low bone density is a risk factor for progression of knee and hip

osteoarthritis). This means that knowledge, including treatments, for osteoarthritis at

one joint site cannot necessarily be extrapolated to all joint sites. 4

II.5. Pathogenesis and Pathophysiology

Pathogenesis

The main load on articular cartilage -- the major target tissue in OA -- is

produced by contraction of the muscles that stabilize or move the joint. Although

cartilage is an excellent shock absorber in terms of its bulk properties, at most sites it is

only 1 to 2 mm thick -- too thin to serve as the sole shock-absorbing structure in the

joint. Additional protective mechanisms are provided by subchondral bone and

periarticular muscles. 5

Articular cartilage serves two essential functions within the joint, both of which

are mechanical. First, it provides a remarkably smooth bearing surface, so that, with

joint movement, the bones glide effortlessly over each other. With synovial fluid as

lubricant, the coefficient of friction for cartilage rubbed against cartilage, even under

physiologic loading, is 15 times lower than that of two ice cubes passed across each

other! Second, articular cartilage prevents the concentration of stresses, so the bones do

not shatter when the joint is loaded. 5

OA develops in either of two settings: (1) the biomaterial properties of the articular

cartilage and subchondral bone are normal, but excessive loading of the joint causes the

tissues to fail, or (2) the applied load is reasonable, but the material properties of the

cartilage or bone are inferior. 5

6

Pathophysiology

The pathophysiology of OA is not completely understood, but progress is being

made. Under normal conditions, the components of the cartilage matrix are gradually

replaced. Chondrocytes are the cells responsible for this metabolism, in which synthesis

(anabolism) and destruction (catabolism) are balanced in a coordinated way. When this

process is altered, a series of changes occurs in the morphological and biomechanical

characteristics of cartilage that make it fail to perform its function. Protease inhibitors

and anti-inflammatory cytokines participate in the anabolic process, where the final

aims are the formation of the extracellular matrix and cell proliferation. Pro-

inflammatory cytokines and proteases participate in the catabolic process, which

results in the destruction of the cartilage matrix and a reduction of cell proliferation. 5

1. Proteolytic enzymes

The enzymes that play a key role in the degradation of the cartilage matrix are the

proteases, with the most common ones being the metalloproteinases, although the

serine proteases and thiol proteases also play their part. Among the metalloproteinases

involved in the degradation of the extracellular matrix, collagenase and stromelysin play

a decisive role. The collagenases are responsible for breaking down collagen’s triple

helix. Three kinds of collagenase have been identified:

1. Collagenase-1 or tissue collagenase (MMP-1): related to the inflammatory

processes of osteoarthritis.

2. Collagenase-2 (MMP-8).

3. Collagenase-3 (MMP-13): related to processes of tissue repair.

Collagenase-1 and collagenase-2 are frequently found in the surface and

intermediate layers of articular cartilage. Collagenase-3 is usually found in the deepest

layers.

The activity of the metalloproteinases is regulated by the enzymes’ physiological

inhibitors and activators. The inhibitors of the metalloproteinases are the TIMPs (tissue

inhibitors of metalloproteinase) and some of them are secreted by the chondrocytes. In

normal cartilage the metalloproteinases and their inhibitors are balanced.

7

Included among the serine proteases is the tissue plasminogen activator

(plasmin), which activates collagenase in the presence of stromelysin. There is an

inhibitor of this activity, but its levels are diminished in osteoarthritic cartilage.

Among the thiol proteases, the most important component is cathepsin B, a

lysosomal enzyme (intracellular) capable of activating the metalloproteinases. It also

has a physiological inhibitor: the inhibiting protein of the cysteine proteases. As in the

other cases, there is a lack of this inhibitor in osteoarthritic cartilage. 5

2. Cytokines, growth factors and nitric oxide

The cytokines are soluble proteins secreted by different cells in response to

specific signals. Cytokines act unlike other enzymes by regulating the activity of other

cells. They have a short half life and therefore tend to act on cells in the area adjacent to

where they are produced.

IL-1 (interleukin-1), TNF-α (tumor necrosis factor alpha) and IL-17 (interleukin-

17) participate in the catabolic program of the chondrocytes. TGF-β (transforming

growth factor beta) and IGF (insulin-like growth factor) participate in their anabolic

program. IL-6 and IL-8 (interleukin 6 and 8) are modulators of anabolic and catabolic

activity.

IL-1 is the prototype of the molecule that induces a catabolic response. It

stimulates metalloproteinase expression, inhibits the proliferation of chondrocytes

induced by serum or TGF-β, and also inhibits the synthesis of collagen II and

proteoglycans. It has been observed that osteoarthritic chondrocytes can have twice as

many surface receptors of IL-1 than normal chondrocytes. 5

3. Subchondral bone in osteoarthritis

In patients with osteoarthritis, the bone mineral density of subchondral bone is

higher, there are more trabeculae and less separation between trabeculae. The

mechanical loading absorbed and transmitted by this bone appear to be converted into

biochemical signals that participate in the anabolic and catabolic programs regulating

cartilage homeostasis. 5

8

4. Synovial fluid in osteoarthritis

In patients with osteoarthritis, the synovial fluid goes through a major

inflammatory process. Large amounts of the pro-inflammatory mediators IL-1 and

TNF-α are synthesized. Collagenase, stromelysin and IL-6 have also been found in

synovial tissue. These mediators are released into the synovial fluid and finally

stimulate certain receptors on the surface of the chondrocytes, ultimately resulting in

the release more inflammatory cytokines and proteases. Both IL-1 β and TNF-α need a

mechanism of secondary messengers to perform their functions. IL-1 β stimulates both

the nitric-oxide pathway and the cyclooxygenase 2 pathway, which causes an increase

in prostaglandin E2 levels. Both pathways result in the direct or indirect destruction of

the cartilage. 5

II.6. Clinical presentations

- Joint pain : This is the main complaint that bring patients to doctor. Joint pain got worse when moving and relieved by resting.

- Barriers of joint movement : This disorders get worse with increasing pain.

- Morning stiffness : Painful or stiffness can arise after immobilization, such as sitting in a chair or a car in a long time or even after waking.

- Crepitus : This is a sense of rattling (and sometimes can be heard) on joint pain. These symptoms may arise because both the surface friction joints when the joint is moved or manipulated passively.

Joint swelling : This disorders are often seen in the knee and hand. Swelling of joints in osteoarthritis may arise because of effusion in the joints that is usually not much (<100 cc). Another reason is because of the osteofit which can alter the joint surface.

- Changes in gait : This condition is almost always associated with pain due to become the foundation of weight. mainly found in osteoarthritis of the knee, thigh joints, and osteoarthritis of the spine with spinal stenosis. in other joints, such as hand, shoulder, and wrist, osteoarthritis also cause dysfunction. This caused difficulties for elderly patients with osteoarthritis who are difficult to self-reliance.

- Signs of inflammation : Signs of inflammation in the joints may be found in osteoarthritis because of sinovitis. These signs usually occur later, often found in the knees, ankles, and small joints of the hands and feet. 6

9

Osteoarthritis of the trapeziometacarpal joints (rhizoarthritis or

osteoarthritis of the thumb)

Osteoarthritis of the trapeziometacarpal joints is a very frequent form of

osteoarthritis of the hand. It sometimes appears by itself, but is usually

associated with the presence of Heberden nodes. It is found more frequently in

women. Clinical manifestations include deformity and local joint pain that varies

in intensity; with asymptomatic forms and others involving joint effusion

accompanied by pain and marked functional impairment. This is the form of

osteoarthritis that most restricts the movements of the hand. 7

Osteoarthritis of the hip (coxarthrosis)

This is one of the most frequent and incapacitating forms of osteoarthritis. It

appears in men and women alike and is frequently the only part of the body

suffering from osteoarthritis. The main symptom is mechanical pain, located in

the groin and irradiating to surrounding areas. Pain may become intense and

cause significant function impairment, with progressive limping and marked

function limitations. Stiffness is usually experienced after resting. Mobility is

reduced. 7

Osteoarthritis of the elbow

Osteoarthritis of the elbow is not frequent and is usually secondary to trauma or

a previous joint disease. The symptoms are pain and moderate limitation of

mobility. 7

Osteoarthritis of the shoulder (omarthritis)

Osteoarthritis of the shoulder is not frequent, but is still the second cause of

shoulder pain. It is usually also associated with trauma or a previous joint

disease. The symptoms are pain which, when intense, is accompanied by

stiffness and limited mobility. 7

Osteoarthritis of the ankle

10

Osteoarthritis of the ankle is not frequent, despite being a weight-bearing joint.

The primary form is rare (some experts even hold that it does not exist). When

the secondary form appears, it is usually associated with fractures, trauma and

inflammatory diseases. The clinical symptoms are mechanical pain, stiffness

after resting and loss of function, which may sometimes be severe and require

surgery. 7

The symptoms and severity of OA vary from person to person. Severe OA can

make it difficult to perform the activities needed for daily living, leading to

fatigue, anxiety and depression. 7

II.7. Diagnosis of osteoarthritis

The symptoms of osteoarthritis depend on the joints affected, but have some characteristics in common.

Table 2.3 ACR classification of OA of the knee*7

Clinical

1. Knee pain for most days of prior monty

2. Crepitus on active joint motion

3. Morning stiffness <30 min in duration

4. Age>38 years

5. Bony enlargement of the knee on examination

OA present if items 1, 2, 3, 4, or 1, 2, 5 or 1, 4, 5 are present

Clinical and radiological

1. Knee pain for most days of prior month

2. Osteophytes at joint margins (X-ray)

3. Synovial fluid typical of osteoarthritis (laboratory)

4. Age > 40 years

11

5. Morning stiffness <30 min

6. Crepitus on active joint motion

OA present if items 1, 2 or 1, 3, 5, 6 or 1, 4, 5, 6 are present

*Modified from Altman (1986) (1), Altman (1991)

ACR classification of OA of the hip7

Clinical and radiological

1. Hip pain for most days of the prior month

2. Erythrocyte sedimentation rate # 20 mm/h (laboratory)

3. Radiographic fermoral and/or acetabular osteophytes

4. Radiographic hip joint space narrowing

OA present if items 1, 2, 3, or 1, 2, 4 or 1, 3, 4 are present

ACR classification of OA of the hand7

1. Heberden nodes (enlarged lymph of distal interphalangs joints)

2. Bauchard nodes (enlarged lymph of proximal interphalangs joints)

ACR classification of OA of the spine7

In addition to the typical symptoms of the disease, osteoarthritis of the spine

involves neurological symptoms caused by compression of spinal nerve

roots.

Diagnostic imaging

There is no laboratory test that is specific for osteoarthritis. Treatment is usually based on the results of diagnostic imaging. In patients with OA, x rays may indicate narrowed joint spaces, abnormal density of the bone, and the presence of subchondral cysts or bone spurs. The patient's symptoms, however, do not always correlate with x ray findings. Magnetic resonance imaging (MRI) and computed tomography scans (CT scans) can be used to determine more precisely the location and extent of cartilage damage. 8

12

II.8. Radiography Findings

One important characteristic of primary osteoarthritis is that different abnormalities are found in the pressure (ie, contact) and nonpressure areas of the affected joint. In the highly stressed (ie, pressure) areas of the joint, radiographs can depict joint space loss, as well as subchondral bony sclerosis and cyst formation. In the areas without high contact pressures, osteophytes can be detected. Bilateral symmetry is often seen in cases of primary osteoarthritis, particularly when the hands are affected. 9

Figure 1 is an X-ray of a normal knee with normal space between the bones of the upper and lower leg. Figure 2 shows bone spurs and a narrowed joint space caused by osteoarthritis.

The most widely using classification schemes for OA are based on the radiological appearance of the joint. The radiological hallmarks of OA are osteophyte formation, joint space narrowing, sclerosis and cyst formation. Severity may be graded based on the 0-4 scale developed by Kellgren and Lawrence. The scoring system is based on comparing films with those in a standard atlas of radiographs. Tables 1 and 2 below describe the categories for osteoarthritis of the knee and hip. Based solely on radiographic findings, osteoarthritis can be classified as: 0-absent 1-doubtful, 2- minimal, 3-moderate, and 4-severe. Studies commonly use either grades 2-4 or grades 3-4 for establishing OA, resulting in greatly differing prevalence estimates. Including grade 2 results in estimates 4-17 times higher for OA of the knee and 2-8 times higher for the hip. 7

13

Table 2.1 Radiographic grades of severity for osteoarthritis of the knee (atlas of standard radiographs, 1963) 7

Grade Verbal description

Grade 1 Doubtful narrowing of joint space and possible osteophytic lipping.

Grade 2 Definite osteophytes and possible narrowing of joint space.

Grade 3 Moderate multiple osteophytes, definit narrowing of joint space, and some sclerosis and possible deformity of bone ends.

Grade 4 Large osteophytes, marked narrowing of joint space, severe sclerosis, and definite deformity of bone ends.

14

Table 2.2 Radiographic grades of severity for osteoarthritis of the hip (atlas of standard radiographs, 1963) 7

Grade Verbal description

Grade 1 Doubtful narrowing of joint space medially and possible osteophytes around femoral head.

Grade 2 Definite narrowing of joint space inferiorly, definite osteophyes, and slight sclerosis.

Grade 3 Marked narrowing of joint pace, slight osteophytes, some sclerosis and cyst formation, and deformity of femoral head and acetabulum.

Grade 4 Gross loss of joint space with sclerosis and cysts, marked deformity of femoral head and acetabulum, and large osteophytes.

With the onset of osteoarthritis, articular cartilage loses its smooth texture and becomes coarsened. This change leads to a sharp increase in frictional forces. Subsequently, cracks and tears, which lead to cartilage softening and flaking, are noted histologically. The net loss of articular cartilage appears as a reduction of the joint space on radiographs.

In major weight-bearing joints, a greater loss of joint space occurs at those areas subjected to the greatest pressures; this effect is in contrast to that of inflammatory arthritides, in which uniform joint-space narrowing is the rule. In the osteoarthritic knee, for example, one commonly observes the greatest loss of joint space in the medial femorotibial compartment (see Image 1), although the lateral femorotibial compartment and patellofemoral compartment may also be affected. Collapse of the medial or lateral compartments may result in varus or valgus deformities, respectively. Hence, weight-bearing radiographs are preferred for evaluation of the osteoarthritic knee to depict such deformities, as well as to provide an accurate assessment of joint-space narrowing. 9

15

Image 1: Standing anteroposterior (AP) radiograph of the knees reveals bilateral medial femorotibial compartment narrowing and sharpening of the tibial spines; this finding is typical of osteoarthritis.

Radiographs of the entire lower extremity (ie, load-line views) are also useful for demonstrating varus or valgus malalignment. Axial projections are best for evaluating the patellofemoral joint. When the patellofemoral compartment is involved, the lateral facet of the patella is more frequently affected than the medial facet, and lateral patellar subluxation may be noted. Osteoarthritic changes of the patellofemoral articulation may be seen on lateral projections. 9

16

Right knee x-ray which showed signs of osteoarthritis - reduction in knee joint space, sclerosis of articular margin and osteophyte formation. Left knee x-ray that showed similar signs but to a lesser degree. 9

This 52 year old gentleman complaint of chronic bilateral knee pain worst on the right compared to the left.

In the osteoarthritic hip, the superior aspect of the joint is typically the most narrowed (see Image 2); axial and medial migration of the femoral head is less commonly seen. In the small joints of the hand, radiographs often show narrowing of the entire joint (see Image 3). In some cases, the interphalangeal joint may be asymmetrically affected, and radial or ulnar deviation at the joint may be appreciated; volar subluxation, as seen with rheumatoid arthritis, seldom occurs. Valgus deformity often accompanies osteoarthritis of the first metatarsophalangeal joint (see Image 4). 9

17

Image 2: Anteroposterior (AP) radiograph of the hip reveals severe superior migration of the femoral head (which reflects loss of articular cartilage), subchondral sclerosis, prominent osteophytes, and a large Egger cyst in the superior acetabulum. Mild flattening of the superior aspect of the femoral head is present.

Image 3: Posteroanterior (PA) radiograph of the hand reveals narrowing, osteophytes, and subchondral cysts affecting the distal interphalangeal joints; this finding is typical of osteoarthritis.

18

Image 4: Radiograph of the foot reveals narrowing, subchondral sclerosis, and osteophyte formation affecting the first metatarsophalangeal joint. A mild valgus deformity is present as well.

As the cartilage is worn away, friction causes the exposed subchondral bone to become smooth and polished, giving it a shiny surface (eburnation). The bone also becomes rebuttressed and sclerotic, a finding that is seen radiographically, generally after visible joint space narrowing occurs. As degeneration progresses, sclerosis becomes more marked, infiltrating deeper into the bone. Sclerosis is often the most prominent radiographic finding when osteoarthritis affects the facet joints of the spine (see Image 5).

19

Image 5: Oblique projection demonstrates gradual narrowing and sclerosis of the facet joints as one progresses down the lumbar spine.

Cyst formation is a fundamental radiographic finding in patients with osteoarthritis. Osteoarthritic cysts are also referred to as subchondral cysts, pseudocysts, or geodes, the preferred European term. These lesions are generally 2-20 mm in diameter. On radiographic examination, communication with the articular space may or may not be seen. Osteoarthritic pseudocysts in the acetabulum are termed Egger cysts (see Image 2).

Later in the disease, the subchondral bone weakens and compresses; bony collapse may be seen radiographically. This finding is commonly seen in advanced cases of osteoarthritis of the hip, in which flattening of the superior aspect of the femoral head typically occurs (see Image 2).

The fundamental radiographic finding in the less-stressed areas of the osteoarthritic joint is osteophytosis. Osteophytes are mushroom-shaped bony outgrowths that are generally seen at the margins of the joint. These outgrowths are capped by cartilage that gradually ossifies. The osteophytes vary in size and may be smooth or jagged. In the knee, sharpening of the tibial spines and the more typical marginal osteophytes may be present (see Image 6). 9

Image 6: Standing radiograph of the knee reveals narrowing of the medial and lateral femorotibial compartments with marginal osteophytes.

A bony prominence, known as the Parson bump, may develop just anterior to the tibial spines (see Image 7). Growth of osteophytes is one of the best indicators of disease progression. Fractured osteophytes result in intra-articular loose bodies. Flexed views

20

(ie, tunnel views, skier views) of the knees often demonstrate these loose bodies particularly well. 9

Image 7: Lateral radiograph of the knee reveals patellofemoral compartment narrowing and osteophytosis. A prominent Parson bump is also seen. Large ossified intra-articular bodies are evident.

As stated previously, primary osteoarthritis is most commonly seen in the hands. Bilateral symmetry is generally observed, with multiple fingers on each hand affected. Heberden nodes refer to bony prominences at the distal interphalangeal joints, whereas similar bony outgrowths at the proximal interphalangeal joints are called Bouchard nodes. Although they are generally present simultaneously, Heberden nodes are more common. On frontal radiographs, medial or lateral subluxation may accompany the wavy joint surface. In most patients with osteoarthritis of the interphalangeal joints, the first carpometacarpal joint is also affected (see Image 8), often with some degree of radial subluxation of the metacarpal. The scaphotrapezium and scaphotrapezoid joints may also be affected (see Image 9). 9

21

Image 8: Radiograph demonstrates narrowing and osteophytosis affecting the first carpometacarpal joint.

Image 9: Close-up radiograph of the wrist shows osteoarthritic changes at the first carpometacarpal joint, with severe narrowing and sclerosis of the trapezium-scaphoid and trapezoid-scaphoid (triscaphe) articulations.

22

Computed Tomography

CT is rarely used for the diagnosis of primary osteoarthritis, although it may be used for the diagnosis of malalignment of the patellofemoral joint or the foot and ankle joints. It may also be useful in evaluating the osseous detail of the vertebral column, particularly the facet joints (see Image 10).9

Image 10: Transverse CT scan image obtained through the lower lumbar spine shows sclerosis of the facet joints.

Image 11: Transverse CT scan image obtained through the superior aspect of the hip reveals joint narrowing, osteophyte formation, and subchondral cysts typical of osteoarthritis.

23

Magnetic Resonance Imaging

MRI can depict many of the same findings of osteoarthritis as those depicted on radiographs, including joint narrowing, subchondral osseous changes, and osteophytes (see Image 12). However, radiographs remain the imaging method of choice in the diagnosis of osteoarthritis, because they are more cost-effective than other methods and because they can be obtained more readily and quickly. Unlike radiography, MRI can depict articular cartilage directly; this feature of MRI has been the subject of multiple research studies over the past several years, particularly focusing on the cartilage of the knee. A variety of pulse sequences have been described, but the most commonly used include spoiled gradient-recalled echo (SPGR) and fast spin-echo imaging. 9

Image 12: T1-weighted coronal MRI of the knee shows typical findings of osteoarthritis, including narrowing and subchondral changes at the medial femorotibial compartment and osteophyte formation.

24

Image 13: Sagittal 3-dimensional gradient-echo fat-saturated MRI of the knee reveals full-thickness thinning of the articular cartilage of the lateral femoral condyle posteriorly with underlying degenerative subchondral marrow changes.

Joint-fluid aspiration: The synovial fluid can be analyzed when viscosity is high and cellularity is low. This analysis is particularly useful for ruling out the existence of other inflammatory or microcrystalline processes.10,11

Blood analysis: Blood disorders are not common in osteoarthritic patients, unless there is an associated disease. The sedimentation rate is usually normal except in cases of primary osteoarthritis, when it is moderately high. The results of systematic analysis (hemogram, urine, biochemistry parameters, etc.) are normal.10,11

II.9. Differential Diagnosis

1. BursitisDifferentiating signs/symptoms :

Greater trochanteric bursitis in the hip and pes anserine bursitis in the knee present with pain over the lateral aspect of the hip and over the medial aspect of the knee, respectively. There is also local tenderness in these areas that is usually absent in simple OA.

Differentiating test :Local anaesthetic and corticosteroid injection might be therapeutic and diagnostic if it relieves symptoms to a significant degree.

2. GoutDifferentiating signs/symptoms : The onset of arthritis in gout is usually more acute and over a period of a few hours,

but could mimic an exacerbation of acute OA. Gout or pseudogout often co-exists in the same joint. In acute attacks of crystal

arthritis, the affected joint is usually red, hot, and acutely tender.

25

Gout commonly involves the foot, especially the first metatarsophalangeal (MTP) joint, although it may affect almost any joint.

Differentiating test :Arthrocentesis and joint fluid analysis, which shows leukocytes >2000 cells/mm^3, and

the presence of sodium monourate crystals.

Foot OA

3. PseudogoutDifferentiating signs/symptoms :

26

The onset of arthritis in gout is usually more acute and over a period of a few hours, but could mimic an exacerbation of acute OA.

Gout or pseudogout often co-exists in the same joint. In acute attacks of crystal arthritis, the affected joint is usually red, hot, and acutely tender.

Gout commonly involves the foot, especially the first metatarsophalangeal (MTP) joint, although it may affect almost any joint.

Differentiating test :Arthrocentesis and joint fluid analysis, which shows leukocytes >2000 cells/mm^3, and the presence of pyrophosphate crystals.

Pseudogout Knee OA

4. Rheumatoid Arthritis (RA)Differentiating signs/symptoms : It is usually straightforward to differentiate RA from OA based on the number and

distribution of the involved joints. RA usually causes a symmetrical small joint polyarthritis in the hands, particularly

affecting the MCP joints and sparing the DIP joints. Patients with acute RA may also feel generally unwell, with fatigue and low mood.

Differentiating test :In RA, ESR and CRP are abnormal and rheumatoid factor and anti-cyclic citrullinated antibodies are positive. Typical RA erosive changes are seen on x-ray, MRI, or ultrasound.

5. Psoriatic Arthritis

27

Differentiating signs/symptoms : Psoriatic arthritis can occur in the absence of skin psoriasis and often affects the DIP

joints. In psoriatic arthritis, the joint involvement is usually asymmetrical, but inflammatory

OA can be difficult to distinguish from some cases of psoriatic arthritis with only DIP involvement.

Differentiating test :In psoriatic arthritis, x-ray shows typical erosive changes.

Magnetic resonance image of index finger: psoriatic arthritis (mutilans form). Shown is a T2 weighted fat suppressed sagittal image of the index finger in a patient with PsA (mutilans form). Focal increased signal (probable erosion) is seen at the base of the middle phalanx (long thin arrow). There is synovitis at the proximal interphalangeal joint (long thick arrow) plus increased signal in the overlying soft tissues indicating oedema (short thick arrow). There is also diffuse bone oedema (short thin arrows) involving the head of the proximal phalanx and extending distally down the shaft.

6. Avascular Necrosis (AVN)Differentiating signs/symptoms :

This is common in the hip and knee joints. The onset is subacute and there is usually a risk factor such as corticosteroid use. Early on, the joint examination is unremarkable, except for possible localised bony tenderness in the knee.

Differentiating test :MRI is the most sensitive test in AVN. In the early stages, localised subchondral oedema is characteristic. In 50% of all cases, accompanying joint effusion may be found. Due to necrosis of the cells of bone marrow and bone fibrovascular tissue, reactions with hyperaemia can be delineated. 12

28

II.10. Treatment

Treatment for OA of the knee aims to alleviate pain and improve function in order to mitigate reduction in activity (American College of Rheumatology, 2000; Felson, 2006). However, most treatments do not modify the natural history or progression of OA, and thus are not considered curative. Nonsurgical modalities include education, exercise, weight loss, and various supportive devices; acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen; nutritional supplements (glucosamine and chondroitin); and, intra-articular viscosupplements. 13,14,15,16

Guidelines for the medical management of osteoarthritis emphasize the role of both nonpharmacologic and pharmacologic therapies (American College of Rheumatology, 2000; Jordan, Arden, Doherty, et al., 2003). Initial management involves nonpharmacologic therapies, including education, exercise, various appliances and braces, and weight reduction. 13,14,15,16

Acetaminophen is recommended as first-line pharmacologic therapy. If pain relief is inadequate with acetaminophen, analgesic-dose NSAIDs may be used (e.g., ibuprofen, naproxen). If symptom response to a lower NSAID dosage is inadequate, higher, anti-inflammatory, doses may be used. Intra-articular corticosteroid injection may be considered when relief from NSAIDs is insufficient or the patient is at risk from gastrointestinal adverse effects. Injection of corticosteroids is frequently limited to three to four times per year per joint because of concern about the possibility of progressive cartilage damage through repeated injection in the weightbearing joints (Neustadt, 1992). 13,14,15,16

If symptom relief is inadequate with conservative measures, invasive treatments may be considered. Operative treatments for symptomatic OA of the knee include arthroscopic lavage and cartilage debridement, osteotomy, and, ultimately, total joint arthroplasty (Day, 2005). 13,14,15,16

Surgical procedures intended to repair or restore articular cartilage in the knee, including abrasion arthroplasty, microfracture techniques, autologous chondrocyte implantation, and others, are appropriate only for younger patients with focal cartilage defects secondary to injury (Clarke and Scott, 2003). 13,14,15,16

29

NON-pharmalogical THERAPIES

Non- pharmalogical are a very important part of the treatment of osteoarthritis.

Exercise. When done properly, exercise can help to decrease OA symptoms and make you feel better overall. If done improperly, exercise can “flare” your arthritis. Therefore, an exercise program should be done under the guidance of a trained physiotherapist. 14

Heat and Cold

Heat is one of the oldest treatments to provide relief from muscle and joint pain. When heat therapy is used it can reduce joint pain, stiffness and muscle spasm. Heat promotes blood circulation, which nourishes and detoxifies muscle fibers. You can purchase “hot packs” made of silicate gel, beans, or corn (i.e. magic bags) or use a hot water bottle. Place a damp towel on the skin to improve heat conduction and apply the “hot pack” for 10-15 minutes. Heat should be comfortably warm. The heat should not feel like it is burning your skin. If heat is too hot, add one or two towels between the heat source and body part, or remove heat. Continuously inspect the area that is being heated. The area will appear red and possibly sweaty. If, however, the heat has caused pain in the area, it should be removed and discontinued until you consult with your physiotherapist. Heat can be re-applied after leaving it off for the same period of time for which it was applied. All redness should be gone before re-applying. In order to avoid making symptoms worse, heat should not be applied to an already inflamed joint. 14

Cold applied to inflamed joints reduces pain and swelling by constricting blood flow. Gel packs, a bag of frozen vegetables, or crushed ice in a bag are good “cold packs”. Place a moist towel between the pack and the skin to improve conduction of cold and apply the cold pack for 10-15 minutes. The skin underlying the cold pack will redden; check the skin frequently for signs of overcooling (blanched, white skin). Leave at least two hours between cold applications. You should not use ice if you have circulatory problems such as Raynaud’s disease. 15

Protecting your Joints. You should always use your joints in ways that avoid excess stress. This allows you to experience less pain, perform tasks more easily, and protect your joints from damage. 14

Relaxation & Coping Skills. Developing good relaxation and coping skills can help you maintain balance in your life giving you a greater feeling of control over your arthritis and a more positive outlook. Relaxing the muscles around a sore joint reduces pain. There are many ways to relax. Try deep breathing exercises. Listen to music or relaxation tapes. Meditate or pray. Another way to relax is to imagine, or visualize, a pleasant activity such as lying on the beach, or sitting in front of a

30

fireplace. For more information on these skills, you can participate in the Arthritis Self-Management Program or see a psychologist, social worker or arthritis therapist.

Diet. There are many claims about diets which help or “cure” arthritis. Most of the information is confusing and claims made are usually not supported by scientific evidence. Simply put, there is no diet that has been proven to significantly improve osteoarthritis. Until there is more conclusive evidence, use a common sense approach by eating a well-balanced diet aimed at maintaining a healthy weight. 14

Massage. Massage is widely used for pain relief, but its results are open to question. At best, massage may relieve muscle ache or tension by increasing blood flow, but that benefit is relatively short-lived. Massage should be avoided when joints are especially tender or inflamed, since it can actually worsen your condition at such times. If you’re having a massage done by a professional, make sure he or she understands that, because of your arthritis, you want only the gentlest procedure. 14

II.11. Complication

The general complication of OA include loss of range of motion, extremity deformity due to asimmetric loss of joint space, subluxation, ankylosis or complete bony fusion of a joint, and intrarticular loose bodies related to subchondral fracture.17

II.12. Prognosis

The prognosis of osteoarthritis depends on joint envolved and severity. No proven disease/ structure-modifying drugs for osteoarthritis currently exist; thus, the medication-based regimen is directed at symptom relief. 17

31

CHAPTER III

SUMMARY

Osteoarthritis is a noninflammatory degenerative joint disease marked by

degeneration of the articular cartilage, hypertrophy of bone at the margins, and

changes in the synovial membrane, accompanied by pain and stiffness.

Osteoarthritis affects 25-30% of persons aged 45-64 years, 60% of persons older

than 65 years, and more than 80% of persons older than 75 years. Females have a

higher prevalence of OA of the knees and hands, whereas males have a higher

prevalence of OA of the hips. For knee OA, the female-to-male incidence ratio is

1.7:1.

The symptoms may vary from joint pain, limited joint movement, morning

stiffness, crepitus, joint swelling to signs of inflammation. Severe OA can make it

difficult to perform the activities needed for daily living, leading to fatigue, anxiety

and depression.

There is no laboratory test that is specific for osteoarthritis. Treatment is usually

based on the results of diagnostic imaging. In patients with OA, x rays may indicate

narrowed joint spaces, abnormal density of the bone, and the presence of

subchondral cysts or bone spurs. The patient's symptoms, however, do not always

correlate with x ray findings. Magnetic resonance imaging (MRI) and computed

tomography scans (CT scans) can be used to determine more precisely the location

and extent of cartilage damage.

The general complication of OA include loss of range of motion, extremity

deformity due to asimmetric loss of joint space, subluxation, ankylosis or complete

bony fusion of a joint, and intrarticular loose bodies related to subchondral fracture.

The prognosis of osteoarthritis depends on joint envolved and severity. No proven disease/ structure-modifying drugs for osteoarthritis currently exist; thus, the medication-based regimen is directed at symptom relief.

32

REFERENCES

1. Stacy, G.S., and Basu, P.A., 2009. Osteoarthritis, Primary. Available from:

http://emedicine.medscape.com/article/392096-overview [Accessed on 19

March 2011]

2. Lozada, C.J., and Steigelfest, Eli., 2010. Osteoarthritis. Available from:

http://emedicine.medscape.com/article/330487-overview [Accessed on 19

March 2011]

3. Siddiqui , F.H., and Laborde, J.M., 2011. Osteoarthritis. Available from:

http://emedicine.medscape.com/article/1270114-overview [Accessed on 19

March 2011]

4. Higgins, Bernard., 2008. Osteoarthritis National clinical guideline for care and

management in adults. Sudbury, Suffolk: The Lavenham Press Ltd, 1-4

5. Brandt, KD. Osteoarthritis . In : Kasper DL, Braunwald E, Fauci AS, Hauser SL

(eds) Harrison’s Principles of Internal Medicine. 16th ed. Mc Graw-Hill. New

York 2005

6. Soeroso, J., Isbagio, H., Kalim, H., Broto, R., dan Pramudiyo, R., 2006,

Osteoartritis, Dalam: Sudoyo, W., Setiohadi, B., Alwi, I., Simadibrata, M.,

Setiati, S.,, ed. Ilmu Penyakit Dalam. Jakarta: Pusat Penerbitan Ilmu Penyakit

Dalam FKUI, 1195-1201.

7. Symmons, D., Mathers, and C., Pfleger, B., 2000, Global burden of

osteoarthritis in the year 2000. Available from:

www.who.int/healthinfo/statistics/bod_rheumatoidarthritis.pdf [Accessed on 13

March 2011]

8. http://health.stateuniversity.com/pages/1102/Osteoarthritis.html

9. Stacy, G.S. and Basu, P.A., 2009.

http://emedicine.medscape.com/article/392096-imaging

10. http://www.csbioactive.com/doc_p.php?op=p_ostheo3&id=7

11. Osteoarthritis Differential Diagnosis, Available from:

http://bestpractice.bmj.com/best-practice/monograph/192/diagnosis/differential.html

33

[ accessed on 18 March 2011]

12. Samson, D.J., Grant, M.D., Ratko, T.A., Bonnell, C.J., Ziegler, K.M., 2007.

Treatment of Primary and Secondary Osteoarthritis of the Knee. AHRQ

Publication,7 (12) 11

13. The Arthritis Society, 2007. Osteoarthritis. Available at http:// www.arthritis.ca

14. Hinton, R..L., Davis, A.W., Thomas, S.F., 2002. Osteoarthritis: Diagnosis and

Therapeutic Consideration. American Family Physician, 65; (5), 844-846

15. Zhang, W., et al., 2008. OARSI recommendations for the management of hip

and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines.

Osteoarthritis and Cartilage, 16, 137-162

16. http://www.levelofhealth.com/osteoarthritis/osteoarthritis-understanding-the-

pathophysiology-genetics-and-treatments-complications.html

17. Lozada, J.C., and Steigelfest, E, 2010. Osteoarthrtitis. Available at

http://emedicine.medscape.com/article/330487-followup