bilateral osteoarthritis
TRANSCRIPT
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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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