bilateral osteoarthritis

8/10/2019 Bilateral Osteoarthritis

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BILATERAL

OSTEOARTHRITISCASE REPORT

Presented by:

Myra Leslie S. Viloria SPTGenrev Navales SPT


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Osteoarthritis is the most common type of j

affecting more than 20 million individuals in

States alone (see Epidemiology).

It represents a heterogeneous group of condit

in common histopathologic and radiologic ch

be thought of as a degenerative disorder

biochemical breakdown of articular (hyaline) ca

synovial joints.However, the current view holds that osteoarth

not only the articular cartilage but also the

organ, including the subchondral bone and syno


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Osteoarthritis predominantly involves the

bearing joints, including the knees, hips, ce

distal interphalangeal (DIPand lumbosacral s

feet. Other commonly affected joints inproximal interphalangeal (PIP), and carpom

(CMC) joints

Although osteoarthritis was previously thoug

caused largely by excessive wear and tear, ievidence points to the contributions of

mechanics and inflammation.

Therefore, the term degenerative joint dise

longer appropriate in referring to osteoarthrit


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Historically, osteoarthritis has been divided into

secondary forms, though this division is somewh

Secondary osteoarthritis is conceptually easier t

understand: It refers to disease of the synovial joresults from some predisposing condition that h

altered the joint tissues (eg, trauma to articular

subchondral bone). Secondary osteoarthritis can

relatively young individuals (see Etiology)


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uyjThe definition of primary osteoarthritis is more

Although this form of osteoarthritis is related to

process and typically occurs in older individuals

the broadest sense of the term, an idiopathicphenomenon, occurring in previously intact join

having no apparent initiating factor


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uyj Some clinicians limit the term primary osteoarthe joints of the hands (specifically, the DIP an

joints and the joints at the base of the thumb)

include the knees, hips, and spine (apophyseal

articulations) as well.


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uyjAs underlying causes of osteoarthritis are disco

the term primary, or idiopathic, osteoarthritis

become obsolete. For instance, many investiga

believe that most cases of primary osteoarthrihip may, in fact, be due to subtle or even

unrecognizable congenital or developmental d

No specific laboratory abnormalities are assoc

osteoarthritis. Rather, it is typically diagnosed

basis of clinical findings, with or without radio

studies


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uyjAnatomy

Joints can be classified in either functional or

structural terms. A functional classification, ba

movement, would categorize joints as follows:

Synarthroses (immovable)Amphiarthroses (slightly moveable)

Diarthroses (freely moveable)


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uyj A structural classification would categorize joinas follows:

Synovial

Fibrous

Cartilaginous


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uyjNormal synovial joints allow a significant am

motion along their extremely smooth

surface. These joints are composed of the fo

Articular cartilage

Subchondral bone

Synovial membrane

Synovial fluidJoint capsule


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uyj The normal articular surface of synovial jointsof articular cartilage (composed of chond

surrounded by an extracellular matrix that

various macromolecules, most imp

proteoglycans and collagen. The cartilage f

joint function and protects the underlying sub

bone by distributing large loads, maintain

contact stresses, and reducing friction at the jo


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uyj Synovial fluid is formed through a ultrafiltration process by cells that form the sy

membrane (synoviocytes). Synovial cells

manufacture hyaluronic acid (HA, also know

hyaluronate), a glycosaminoglycan that is the

noncellular component of synovial fluid. Sy

fluid supplies nutrients to the avascular art

cartilage; it also provides the viscosity needabsorb shock from slow movements, as well a

elasticity required to absorb shock from

movements.


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uyjPathophysiology

Primary and secondary osteoarthritis are not

separable on a pathologic basis, though bilat

symmetry is often seen in cases of primary

osteoarthritis, particularly when the hands a

affected.[2, 21] Traditionally, osteoarthritis w

thought to affect primarily the articular cartilsynovial joints; however, pathophysiologic ch

are also known to occur in the synovial fluid,

as in the underlying (subchondral) bone, the

overlying joint capsule, and other joint tissue


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uyjAlthough osteoarthritis has been classified as

noninflammatory arthritis, increasing evidenc

has shown that inflammation occurs as

cytokines and metalloproteinases are releasedinto the joint. These agents are involved in the

excessive matrix degradation that characterize

cartilage degeneration in osteoarthritis.[26]

Therefore, it is no longer appropriate to use th

term degenerative joint disease when referrinto osteoarthritis


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uyj In early osteoarthritis, swelling of the cusually occurs, because of the increased synt

proteoglycans; this reflects an effort

chondrocytes to repair cartilage damage. Th

may last for years or decades and is characte

hypertrophic repair of the articular cartilage.


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As osteoarthritis progresses, however, theproteoglycans eventually drops very low, cacartilage to soften and lose elasticity and ther

compromising joint surface integrity. Microscopicand fibrillations (vertical clefts) develop along thsmooth articular cartilage on the surface of an osjoint. Over time, the loss of cartilage results in lspace.


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uyjIn major weight-bearing joints of perso

osteoarthritis, a greater loss of joint space

those areas experiencing the highest loads. T

contrasts with that of inflammatory arthritidesuniform joint-space narrowing is the rule.

In the osteoarthritic knee, for example, the gre

of joint space is commonly seen in th

femorotibial compartment, though the

femorotibial compartment and pate

compartment may also be affected. Collaps

medial or lateral compartments may result in

valgus deformities, respectively.


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uyjErosion of the damaged cartilage in an oste

joint progresses until the underlying bone is

Bone denuded of its protective cartilage con

articulate with the opposing surface. Eventuincreasing stresses exceed the biomechani

strength of the bone. The subchondral bone

with vascular invasion and increased c

becoming thickened and dense (a process k

eburnation) at areas of pressure.[27


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uyj The traumatized subchondral bone mayundergo cystic degeneration, which is attrib

either to osseous necrosis secondary to c

impaction or to the intrusion of synovial

Osteoarthritic cysts are also referred

subchondral cysts, pseudocysts, or geode

preferred European term) and may range fro

20 mm in diameter. Osteoarthritic cysts acetabulum (see the image below) are termed

cyst


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uyj

This radiograph demonstrates osteoarthritis of t

hip, including the finding of sclerosis at the supeof the acetabulum. Frequently, osteoarthritis at

bilateral finding, but it may occur unilaterally in

individual who has a previous history of hip trau

was confined to that one side.


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uyj At areas along the articular margin, vascularizof subchondral marrow, osseous metaplasia o

synovial connective tissue, and ossifying

cartilaginous protrusions lead to irregular

outgrowth of new bone (osteophytes).

Fragmentation of these osteophytes or of the

articular cartilage itself results in the presence

intra-articular loose bodies (joint mice).


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uyjAlong with joint damage, osteoarthritis may als

lead to pathophysiologic changes in associated

ligaments and the neuromuscular apparatus. Fo

example, lateral collateral ligament complexabnormalities are common in knee osteoarthri


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uyjPain mechanisms in osteoarthritis

Pain, the main presenting symptom of osteoarthritis, is presumed to

combination of mechanisms, including the following:

Osteophytic periosteal elevation

Vascular congestion of subchondral bone, leading to increased intraosseo

Synovitis with activation of synovial membrane nociceptors

Fatigue in muscles that cross the joint

Overall joint contracture

Joint effusion and stretching of the joint capsule

Torn menisciInflammation of periarticular bursae

Periarticular muscle spasm

Psychological factors

Crepitus (a rough or crunchy sensation)

Central pain sensitization


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uyjWhen the spine is involved in osteoarthritis

especially the lumbar spine, the associated

changes are very commonly seen from L3

through L5. Symptoms include pain, stiffnessand occasional radicular pain from spina

stenosis. Foraminal narrowing is caused by

facet arthritic changes that result in

compression of the nerve roots. Acquiredspondylolisthesis is a common complication o

arthritis of the lumbar spine


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uyjThe daily stresses applied to the joints, esp

weight-bearing joints (eg, ankle, knee, and hiimportant role in the development of ost

Most investigators believe that degenerative

in osteoarthritis primarily begin in the articula

as a result of either excessive loading of a he

or relatively normal loading of a previously

joint. External forces accelerate the catabolic

the chondrocytes and further disrupt the ca

matrix

Etiology

Ri k f t f t th iti i l d th f ll


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Risk factors for osteoarthritis include the follo

33, 34, 35] :

Age

Obesity[36, 37, 38]

Trauma

Genetics (significant family history)

Reduced levels of sex hormones

Muscle weakness[39]Repetitive use (ie, jobs requiring heavy labor a

bending)[40]

Infection

Crystal deposition

AcromegalyP i i fl t th iti ( b t t


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g yPrevious inflammatory arthritis (eg, burnt-out r

arthritis)Heritable metabolic causes (eg, alkhemochromatosis, and Wilson

Hemoglobinopathies (eg, sickle cell disethalassemia)Neuropathic disorders leading to a Charcotsyringomyelia, tabes dorsalis, and Underlying morphologic risk factors (eg, condislocation and slipped femoral capital Disorders of bone (eg, Paget disease and

necrosis)Previous surgical procedures (eg, meniscectom

Advancing age


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g g

With advancing age come reductions in cavolume, proteoglycan content, cartilagevascularization, and cartilage perfusion. Thchanges may result in certain characteristicradiologic features, including a narrowed jospace and marginal osteophytes. Howeverbiochemical and pathophysiologic findings

support the notion that age alone is aninsufficient cause of osteoarthritis.


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uyjObesity

Obesity increases the mechanical stress in a weight-bearing jo

has been strongly linked to osteoarthritis of the knees and,

lesser extent, of the hips. A study that evaluated the associa

between body mass index (BMI) over 14 years and knee pa

year 15 in 594 women found that a higher BMI at year 1 a

significant increase in BMI over 15 years were predicto

bilateral knee pain at year 15.[38] The association between

increase and knee pain was independent of radiographic chang

In addition to its mechanical effects, obesity may be an

inflammatory risk factor for osteoarthritis. Obesity is associate

with increased levels (both systemic and intra-articular) of

adipokines (cytokines derived from adipose tissue), which may

promote chronic, low-grade inflammation in joints.[41]


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uyj Muscle dysfunction compromises thneuromuscular protective mechanisms, l

increased joint motion and ultimately re

osteoarthritis. This effect underscores thecontinued muscle toning exercises as a

preventing muscle dysfunction.

Valgus malalignment at the knee has been

increase the incidence and risk of ra

progression of knee osteoarthritis involving

compartment.[43]


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uyj GeneticsA hereditary component, particularly

osteoarthritis presentations involving mu

joints, has long been recognized.[44, 45, Several genes have been directly associated

osteoarthritis,[47] and many more have

determined to be associated with contrib

factors, such as excessive inflammation obesity.


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uyjEpidemiology

United States and international statistics

Osteoarthritis affects more than 20

individuals in the United States, though stfigures are influenced by how the cond

definedthat is, by self-report, by radiogra

symptomatic criteria, or by a combinat

these.[53] On the basis of the radiographic

for osteoarthritis, more 50% of adults older t

years are affected by the disease


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uyjAge-related demographics

Primary osteoarthritis is a common disorder of the

and patients are often asymptomatic. Approximat

90% of individuals older than 65 years have evide

radiographic primary osteoarthritis.[54]

Symptoms typically do not become noticeable until a

the age of 50 years. The prevalence of the disease inc

dramatically among persons older than 50 years, like

because of age-related alterations in collagen and

proteoglycans that decrease the tensile strength of th

cartilage and because of a diminished nutrient supply

cartilage.[5

S l t d d hi


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uyjSex-related demographics

In individuals older than 55 years, the preva

osteoarthritis is higher among women than

men.[54]

Women are especially susceptible to osteoar

the DIP joints of the fingers. Women a

osteoarthritis of the knee joints more freque

men do, with a female-to-male incidence ratioWomen are also more prone to erosive osteo

with a female-to-male ratio of about 12:1.


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uyj Race-related demographics

Interethnic differences in the prevalence of ost

have been noted.[55] The disorder is more pNative Americans than in the general populatio

of the hip is seen less frequently in Chinese pat

Hong Kong than in age-matched white po

Symptomatic knee osteoarthritis is extremely c

China.[


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uyj

Prognosis


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uyj The prognosis in patients with osteoarthritis dependjoints involved and on the severity of the condit

proven disease- or structure-modifying dru

osteoarthritis are currently known; consepharmacologic treatment is directed at symptom reli

A systematic review found the following clinical featu

be associated with more rapid progression of knee

osteoarthritis[58] :

Older age

Higher BMI

Varus deformity

Multiple involved joints

Patient Education


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uyjPatient Education

Educate patients on the natural history of

management options for osteoarthritis, emphasizin

benefits of exercise and weight loss. Explaindifferences between osteoarthritis and more ra

progressive arthritides, such as rheumatoid arthritis

Several Arthritis Foundation studies have demonst

that education in osteoarthritis benefits the paThrough education, patients can learn and imple

strategies for reducing pain and improving joint fun

Emphasize the need for physician follow-up visits.

History


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uyjHistory

The progression of osteoarthritis is characterist

slow, occurring over several years or decades. O

period, the patient can become less and less ac

thus more susceptible to morbidities related to

decreasing physical activity (including potentia

gain).

Early in the disease process, the joints may app

normal. However, the patients gait may be ant

weight-bearing joints are involved.


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uyjPain is usually the initial source of morbi

osteoarthritis, with the diseasesprimary symptom

deep, achy joint pain exacerbated by extensive us

reduced range of motion and crepitus are fre

present. Stiffness during rest (gelling) may develo

morning joint stiffness usually lasting for less t

minutes.

Initially, pain can be relieved by rest and may resp

simple analgesics. However, joints may become u

as the osteoarthritis progresses; therefore, the pa

become more prominent (even during rest) and m

respond to medications.

Physical Examination


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uyjy

Physical examination findings in patien

osteoarthritis are mostly limited to the

joints.[59, 60, 61] Reduced range of motcrepitus are frequently present.

Malalignment with a bony enlargement ma

Most cases of osteoarthritis do not involve e

or warmth over the affected joint(s); how

bland effusion may be present. Limitation

motion or muscle atrophy around a more

affected joint may occur.

O h i i f h h d f ff


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uyj Osteoarthritis of the hand most often affedistal interphalangeal (DIP) joints but also ty

involves the proximal interphalangeal (PIP) joi

the joints at the base of the thumb. Heberdenwhich represent palpable osteophytes in t

joints, are more characteristic in women than

Inflammatory changes are typically absent or

not pronounced

Progression of Osteoarthritis


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uyjProgression of Osteoarthritis

The etiopathogenesis of osteoarthritis has been divid

stages as follows:

Stage 1Proteolytic breakdown of the cartilage matr

Stage 2 Fibrillation and erosion of the cartilage

develop, with subsequent release of proteoglyc

collagen fragments into the synovial fluid

Stage 3 Breakdown products of cartilage induce ainflammatory response in the synovium, which

contributes to further cartilage breakdown

Several systems have been advocated for u


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uyjSeveral systems have been advocated for u

grading of focal cartilage change; however,

description of the extent of disease (ie, surfac

thickness, or full-thickness irregularity with o

underlying subchondral bone change) is

sufficient and prevents the confusion that may

numeric grading systems. Such systems are in

intended more for research purposes than for cl

Certain diseases are often categorized as s

primary osteoarthritis. These include primary g

osteoarthritis (PGOA), erosive osteoarthr

chondromalacia patellae

Several systems have been advocated for use i


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uyjy

grading of focal cartilage change; however, a s

description of the extent of disease (ie, surface, p

thickness, or full-thickness irregularity with or w

underlying subchondral bone change) is gensufficient and prevents the confusion that may occu

numeric grading systems. Such systems are in any

intended more for research purposes than for clinica

Certain diseases are often categorized as subseprimary osteoarthritis. These include primary gener

osteoarthritis (PGOA), erosive osteoarthritis,

chondromalacia patellae


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uyj Rheumatoid arthritis

Rheumatoid arthritis predominantly affects the w

as the metacarpophalangeal (MCP) and proximalinterphalangeal (PIP) joints. It rarely, if ever, involv

interphalangeal (DIP) joints or the lumbosacral spi


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jSystemic inflammation (elevated eryth


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uyjy ( y

sedimentation rate [ESR] or C-reactive protein

level)

Positive serologies (rheumatoid factor [RF] or

cyclic citrullinated peptide [anti-CCP] antibodies

Inflammatory joint fluid with a predominan

polymorphonuclear leukocytes (PMNs)

Elevated white blood cell (WBC) count

j


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uyj Additional arthritides

Back pain may result from spondyloarthropathy

from osteoarthritis with sacroiliac and lumbosac

spine involvement. Clinical history and character

radiographic findings can be used to differentiat

these disorders.

j Secondary osteoarthritis must be conside


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uyj Secondary osteoarthritis must be consideindividuals with any of the following:

ChondrocalcinosisHistory of joint trauma

Metabolic bone disorders

Hypermobility syndromes

Neuropathic diseases

jThe following disorders should also be consid


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uyjThe following disorders should also be consid

the differential diagnosis:

Crystalline arthropathies (ie, gout and pseudogoInflammatory arthritis (eg, rheumatoid arthritis

Seronegative spondyloarthropathies (eg, p

arthritis and reactive arthritis)

Septic arthritis or postinfectious arthropathy

Fibromyalgia

Tendonitis

jIn patients with knee pain, other disorders to conside


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uyj differential diagnosis are patellofemoral syndromprepatellar bursitis.

Differential DiagnosesAnkylosing Spondylitis

Avascular Necrosis

Fibromyalgia

Gout and Pseudogout

Imaging in Neuropathic Arthropathy (Charcot Joint)Lyme Disease

Patellofemoral Arthritis

Psoriatic Arthritis

Rheumatoid Arthritis

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bilateral osteoarthritis

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