Primary osteoarthritis is a progressive degenerative disease affecting synovial joints. It is the most common form of arthritis, usually emerging in people over age 40 and prevalence rises with age. Risk factors include age, gender, genetics, obesity, injury or repetitive joint stress. The diagnosis is based on symptoms of joint pain and stiffness, physical exam findings of crepitus and limited range of motion, and characteristic features on x-ray of joint space narrowing and bone spurs. There is currently no cure for osteoarthritis and treatment aims to reduce pain and improve joint function.

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OSTEOARTHRITIS
in Elderly
Dr Doha Rasheedy ALI
Assistant Professor of Geriatrics & Gerontology
Ain Shams University
9/24/2018

2. Definition

3. A progressive degenerative disease of synovial joints that
represents failed repair of joint damage resulting from stresses
that may be initiated by an abnormality in ANY of the joint
tissues (articular cartilage, subchondral bone, ligments,
menisci, periarticular muscles, peripheral nerves, synovium) →
breakdown of cartilage and bone.
(2009 OARSI Task Force on Defining OA: FDA OA Trial Guidance
Document 2009)

4. Epidemiology

5. 1. It is the most common condition to affect joints.
2. Osteoarthritis (OA) is one of the most prevalent condition resulting in
disability particularly in elderly population. OA is second to
cardiovascular disease as a cause of disability.
3. Usually emerge in people aged over 40, and prevalence rises with
increasing age. Until middle age, OA occurs with the same frequency
in men and women, but after age 50, symptomatic OA is more
common in women, and this difference in prevalence widens with
increasing age
4. The Framingham study found that 27% of those aged 63–70 years
had radiographic evidence of knee OA; this increased to 44% in those
over 80 years old.

6. 1. Among adults over 60, approximately 80% have radiographic
evidence of hand OA while 37% have evidence of knee OA.
2. Symptomatic OA is less prevalent, with 7% of all adults having
symptomatic hand OA and 12% of those aged 60 years or more
with symptomatic knee OA.
3. Among adults aged 45 years or more, 27% have radiographic
and 9% have symptomatic hip OA.

7. Race and ethnicity
• OA of the knee is more common in African-Americans than in non-
Hispanic whites or Mexican-Americans.
• OA of the hip is more common in people of European descent
compared to those of Asian or African descent.
• Compared to older whites in the United States, older Chinese
subjects have higher prevalence of knee OA but lower prevalence
of hip and hand OA.

8. Age-Related Changes Related
to Osteoarthritis
Age is the strongest risk factor for developing OA

9. • Although OA is common in older people, it is not universal or inevitable.
• The changes in cartilage proteoglycans are:
1. Progressive decrease in the average length of the core protein of the aggrecan molecule
2. Decreased hydrodynamic size of the aggrecan molecule via decreased length of
chondroitin sulfate chains and increase in number of keratin sulfate chains
3. Decreased proportion of aggrecans able to form aggregates with hyaluronic acid
4. Decreased size of aggregates from reduction of length of the hyaluronic acid molecule
and smaller size of the aggrecan molecules
• Decreased proprioception
• There are also age-related periarticular changes such as sarcopenia,
causing decreased ability of the bridging muscles to act as internal
shock absorbers to absorb the forces transmitted to the subchondral
bone and cartilage

10. • The commonly held notion that OA is an inevitable consequence of
aging because of the normal “wear and tear” of the joint is much
too simplistic.
• Cartilage does not simply wear out like the soles of one’s shoes.
Rather, the changes seen in OA involve the complex interaction of
genetic susceptibility, joint mechanics and injury, chondrocytes
that live a robust metabolic existence, biochemical alterations, and
the complex interplay of mediators, as well as structures that
surround the joint.

11. Risk factors

12. • OA is a complex disorder with multiple risk factors that range from
genetic (collagen gene mutations), demographic (occupation, body
weight, recreational activities), metabolic (inherited and acquired
errors of metabolism) , and biomechanical(trauma, muscle weakness,
alterations in proprioception, denervation of joints), factors to
congenital or developmental deformities of the joint.
• After age, obesity is the strongest risk factor for knee OA, particularly in
women.
• Potentially modifiable risk factors include obesity and biomechanical
factors such as repetitive or isolated traumatic injury, malalignment
(varus or valgus deformity), overload, joint instability caused by muscle
weakness, and ligamentous laxity. These risk factors are particularly
important in weight-bearing joints and may influence incidence more
than radiographic progression.

13. Genetics
• The associations between 12 chromosomes (1, 2, 4, 6, 7, 9, 11–13, 16, 19,
and X) and OA have been detected.
• Genes that code for structural proteins of the extracellular matrix of the
cartilage seem to have a significant role, especially those that code for
collagen type II (COL2A1).
• Genes that code for different interleukins (eg, IL-1A, IL-1B, IL-1RN, IL-
4R, IL-17A, IL-17F, and IL-6) may also affect genetic susceptibility to
OA.
• Other genes that have also been implicated in the development of OA
include the estrogen receptor α gene, vitamin D receptor gene, frizzled
related protein gene, asporin, and others that code for structural
proteins and proteins related to cartilage loss.

14. Occupation
• various occupations such as coal miners, pneumatic drillers, cotton
operatives, iron-workers, and elite athletes.
• Working as a farmer or as a construction worker/laborer increases
the risk of developing knee and hip OA, especially among those
who are overweight.
• Specific occupational activities such as more than 30 minutes of
squatting, more than 30 minutes of kneeling, and climbing more
than 10 flights of stairs per day increase the risk of developing
radiographic knee OA.

15. Recreational activities
• Among older adults, recreational walking, jogging, and other
recreational activities do not seem to increase the risk of
developing knee OA.
• However, certain sports are associated with increased risk of OA in
certain specific joints: American football (knees, feet, ankles);
baseball (shoulders, elbows); soccer (knees, hips, ankles); ice
hockey (knee); and boxing (carpometacarpal), for instance.
• This often accounts for the development of OA at joints not usually
affected by OA.

16. Primary RF:
• Age
• Gender
• Genetic
• Obesity
• High bone mass
• Mechanical : repetitive bone use
squatting
Secondary RF:
• Injury to joint: traumatic or
inflammatory.
RH A, Ankylosing spondylitis, septic A, Gout,
Psoariatic A, Avascular necrosis
• Heamoartharosis
• Congenital/developmental
• Neuropahic joint
DM, tabes dorsalis
• Metabolic
(wilson heamochromatosis, amyloidosis, cushing,
acromegaly, hypothyroidism )
Calcium pyrophosphate disease (CPPD) should be suspected when OA is seen in atypical joints such as the
metacarpophalangeal (MCP) joints, wrists, elbows, and shoulders

17. Pathogenesis

18. • OA can be best defined as failed repair of joint damage that has
been caused by abnormal intra- and extraarticular processes
involving a combination of biomechanical, biochemical, and
genetic factors mediated by a variety of pathways, rather than a
degenerative process.
• A single or a variety of insults to the joints, including
biomechanical trauma, chronic inflammation, and genetic and
metabolic factors, can trigger or contribute to the cascade of events
that lead to OA

19. In the earliest stage of OA, fibrillation of the superficial layer of the articular
cartilage may be observed. Eventually, the fibrillation extends to the subchondral
bone, the cartilage fragments into the joint, the matrix degrades, and the
cartilage is completely lost, leaving a denuded bone
1. Chondrocytes and synovial cells release matrix metalloproteinase (MMP) enzymes, such as
collagenases, stromelysins and gelatinases, which are responsible for cartilage
degradation.
2. these MMPs may be susceptible to MMP inhibitors, synthesis of MMPs is enhanced and the
inhibitors are overwhelmed in OA.
3. Cytokines have been implicated in the regulation of this process. Interleukin-1 (IL-1), a
catabolic cytokine, is known to suppress type 2 cartilage synthesis and to induce proteases.
IL-1 level and cell sensitivity are increased in OA.
4. Anabolic cytokines, such as insulin-like growth factor-1 and transforming growth factor β, on
the other hand, are found in decreased levels in the serum and synovial fluid of OA patients.
5. The complement system may also stimulate inflammatory mediators and enzymes that can
contribute to the pathogenesis of inflammatory OA.
6. Nitric oxide, known to activate MMPs in articular cartilage, may also mediate the
osteoarthritic development process.
7. Supported by epidemiologic studies, sex-related hormones have also been considered to
play a role in the development of OA, especially in women.

20. • Several other factors have also been implicated in the
development of OA. Crystals, including calcium pyrophosphate
dihydrate and basic calcium phosphate crystals, have been
identified in the synovial fluid of OA joints. Besides their ability to
induce inflammation, their role in the pathogenesis of OA remains
unclear

21. • OA is now viewed as a dynamic process with episodic progress.
• Chondrocyte dysfunction leads to metalloproteinase enzyme release causing collagen and
proteoglycan degradation.
• Synovial inflammation is present, with production of cytokines such as IL-1 and TNF- A that
also induce metalloproteinase production.
• Chondrocyte activation with the release of the pro-inflammatory cytokines IL-1β, tumour
necrosis factor alpha (TNFa) and the matrix metalloproteinase stromelysin (MMP-3) can
follow mechanical stimulation of cartilage and there is evidence for elevation of
collagenase-1 (MMP-1), collagenase-2 (MMP-8) and collagenase-3 (MMP13) in
osteoarthritic human cartilage.
• Local growth factors, especially transforming growth factor (TGF) are involved in the
formation of osteophytes
• It affects all joint structures:
The disease processes affect articular cartilage, subchondral bone, synovium, capsule and ligaments.
Ultimately, cartilage degenerates with fibrillation, fissures, ulceration and full thickness loss of joint
surface

23. MACROSTRUCTURAL CHAGNES
• Loss of articular cartilage
• Subchondral cyst
• Osteophytes
• Sclerosis
• Muscle wasting
Pathological change
• Cartilage fibrillation, erosion
• Subchondral new bone
• Myxoid degeneration
• Trabecular compression

24. MACROSTRUCTURAL CHAGNES
• The osteoarthritic joint is characterized by degradation and loss of
the articular cartilage, thickening of the subchondral bone
accompanied by formation of bone marrow lesions and cysts,
osteophytes at the joint margins, variable degrees of synovitis with
synovial hypertrophy, meniscal degeneration (knee), and
thickening of the joint capsule.

25. TYPES

26. TYPES
• PRIMARY (Idiopathic) OA:
• Affect DIP, PIP, 1st carpometacarpal, knee, hip , spine.
• Localized OA or Generalized OA (affect 3 or more joints)
• SECONDARY OA:
• Affect less common joints as wrist, metacarpophalangeal, shoulder.
• EROSIVE OA:
• Hand episodic flare, female

27. SECONDARY CAUSES OF OSTEOARTHRITIS
• Anatomical abnormalities: Bone dysplasia, congenital hip
dislocation
• Metabolic/endocrine: Diabetes mellitus, hemochromatosis,
acromegaly, hyperparathyroidism, ochronosis
• Crystal deposition disease: Gout, pseudogout
• Inflammatory arthritis: Rheumatoid arthritis, systemic lupus
erythematosus, seronegative spondyloarthropathy, juvenile
idiopathic arthritis
• Trauma: Fracture, surgery, infection
• Others: Avascular necrosis, neuropathic charcot joints

28. Diagnosis

29. • The diagnosis is based on history (ie, symptoms of joint pain, often
with transient morning stiffness), physical examination (ie, crepitus,
bony tenderness and bony enlargement) and characteristic
radiographic features (ie, joint space narrowing with osteophytes).
• OA usually has an insidious onset and chronic course. OA is a
progressive disorder that takes many years to cause significant
disability. Unfortunately, there is no cure
• It affects the distal interphalangeal (DIP) joints, causing
characteristic Heberden’s nodes, and the proximal interphalangeal
(PIP) joints, causing Bouchard’s nodes.

30. Symptoms
• Patients with OA most commonly present with pain in the joint. Pain tends to worsen
with increased activity or weight-bearing and to improve with rest. “mechanical”
pain
• The onset of the symptoms of OA is usually insidious, beginning in only 1 or a few
joints.
• Early in the disease, patients may complain of pain that is sharp, intermittent, and
unpredictable.
• As the disease progress, the pain becomes more constant and aching in nature.
• The pain is typically related to activity, but late in the disease, pain may be noted
with progressively less activity, possibly occurring even at rest and at night
• Rest pain is present in approximately 50% and night pain in about 30%.
• Nociceptor pain can become persistent, and persistent pain is often associated with
central neurogenic sensitization, thereby establishing a peripherally stimulated, but
centrally mediated, chronic pain syndrome.

31. • There are several potential mechanisms for pain; none are completely
understood.
• Pain may arise from:
1. inflammatory mediators or
2. intraarticular hypertension
3. stimulating capsular, periosteal, and synovial nerve fibers.
4. Pain may also arise from enthesopathy or bursitis that can
accompany structural alteration, muscle weakness, and altered joint
use.

32. • Stiffness:
1. Difficulty initiating movement in a joint or decreased or painful movement
in a joint.
2. Morning stiffness, commonly seen in the more inflammatory types of
arthritis like rheumatoid arthritis, may be present but is usually of shorter
duration (less than 30 minutes) and limited to fewer joints.
3. Joint stiffness may recur following periods of inactivity, a phenomenon
termed gelling. This is usually quite short-lived, lasting minutes, and
improves after the joint is “worked out.”
• Patients may also report joint locking or joint instability.
• In addition to chronic pain and disability, sleep disturbance, fatigue
and depression are also prominent features of OA in the older
population.

33. • Knee OA patients may complain of localized or diffuse knee pain. They may
have difficulty climbing the stairs or walking for even short periods of time.
• Hip OA patients may complain of pain in the anterior hip or inguinal area.
Less commonly, their pain may also be felt laterally (ie, in the trochanter) or
referred to the knee. They may have difficulty crossing their legs or putting on
a pair of shoes.
• Hand OA patients may report of pain involving the DIP, PIP and first CMC
joints. Gripping, pinching, holding, or lifting objects may be particularly
challenging in patients with symptomatic hand OA.
• OA of the cervical spine can cause neck pain, upper extremity radicular pain
and occipital headaches.
• OA of the lumbar spine can cause lower back pain that may radiate into the
posterior thigh and worsen with bending ipsilateral to the involved joint.

34. Signs
• OA patients may have a completely normal physical examination
• Or
1. joint-line tenderness, crepitus or grating sensation, and osteophytes
,particularly in the hands at the distal interphalangeal (DIP) joints and the
proximal interphalangeal (PIP) joints.
2. A varying amount of joint effusion and/or soft-tissue swelling can be present,
but tends to be intermittent without warmth.
3. As OA progresses, range of joint motion becomes diminished, and joint
deformity and/or joint laxity may develop.
4. Knee OA: The joint fluid may migrate into the semimembranosus bursa
posteriorly, causing swelling along the posterior knee known as the popliteal or
“Baker’s” cyst. Knee varus (“bow-legged”) or valgus (“knock-kneed”) deformities
may be observed later in the disease.
5. Hip OA patients may also develop an antalgic gait in which the stance phase of
the gait is abnormally shortened on the affected hip joint

35. Clinical picture
1. Mechanical pain: on activity relieved by rest
2. Stiffness: less than 30 minutes.
3. Gel effect: reemergence of stiffness after rest
4. Bony swelling, Deformity (late)
5. Crepitus
6. Tenderness
7. Limitation of ROM (late)
8. Locked joint
9. Buckling
Osteoarthritis is often asymmetric. A patient may have severe, debilitating osteoarthritis
of one knee with almost normal function of the opposite leg.

36. Nodal generalized OA
This common condition is characterized by ( 3 or more joints) :
1. polyarticular finger involvement
2. Heberden’s nodes (distal interphalangeal joint)
3. Bouchard’s nodes (proximal interphalangeal joint)
predisposition to OA of knee, hip, and spine
good functional outcome in the hands
female preponderance
peak onset around the menopause
strong family history.
There is a tendency to greater distal joint disease. The first carpometacarpal (CMC),
metacarpophalangeal (MCP), and interphalangeal (IP) joints of the thumb are also
often involved, as are the index and middle MCP. The more proximal joints of the
hand and wrist are otherwise relatively spared.

44. Erosive OA
1. hand interphalangeal involvement
2. tendency to joint ankylosis
3. florid inflammation (episodic)
4. radiographic subchondral erosive change.
• IP joint instability is common. Given the additional risk of ankylosis,
• functional impairment is more likely than nodal OA.
• The principal hallmark of the condition is subchondral erosive change that
can lead to remodeling.

48. • The Gull-wing appearance (also known as seagull erosions) is seen in
erosive osteoarthritis, typically on posteroanterior (PA) radiographs.
• The combination of cartilage space loss, central subchondral
erosions, and marginal osteophyte proliferation results in a gull-wing
appearance.

49. Knee OA
• Classic clinical criteria —
• The classic criteria method for OA of the knee is based upon the presence
of knee pain plus at least three of the following six clinical characteristics
1. Greater than 50 years of age
2. Morning stiffness for less than 30 minutes
3. Crepitus on active motion of the knee
4. Bony tenderness
5. Bony enlargement
6. No palpable warmth

50. OSTEOARTHRITIS OF THE HAND
• The diagnosis of OA of the hand
• including hand aching or stiffness plus at least three of the following
four features:
1. Hard tissue enlargement of 2 or more of 10 selected joints. The 10
selected joints are the second and third distal interphalangeal (DIP)
joints, the second and third proximal interphalangeal (PIP) joints, and
the first carpometacarpal (CMC) of both hands
2. Hard enlargement of two or more DIP joints
3. Fewer than three swollen metacarpophalangeal (MCP) joints
4. Deformity of at least 1 of the 10 selected joints

51. OSTEOARTHRITIS OF THE HIP
• the presence of hip pain plus at least two of the following three features:
1. ESR of less than 20 mm/h
2. Radiographic osteophytes (femoral or acetabular)
3. Joint space narrowing on radiography (superior, axial or medial)

52. Spine
• Spinal involvement in OA is most common at spinal levels C5, T8, and L3, which
represent the areas of greatest spinal flexibility.
• Two syndromes of clinical importance are due to OA of the lumbar apophyseal joints:
1. cervical spine, osteophytes arising from the margins of the vertebral body (cervical
spondylosis) may compromise the spinal canal. When sufficiently advanced, cervical
spinal cord compression may result.
2. Lumbar apophyseal osteophytes (lumbar spondylosis) can cause spinal stenosis if
they encroach into the intervertebral foramina and/or the spinal canal. The
resultant symptoms of low back pain with lower extremity radiation worsen with
exertion, thereby mimicking vascular claudication, but may more rapidly resolve
with rest
• Spondylolisthesis, a slipping of one vertebral body on another, typically affecting the
apophyseal joints at L4 to L5, may occur with severe OA.

53. Natural history of OA
• Progression in the knee may take many years. Cohort studies have found
that radiographic deterioration occurs in one-third.
• Progression of hip disease is variable. A Danish study found that 66% of
hips worsened radiologically over 10 years, although symptomatic
improvement was common.
• Hand disease is relapsing and remitting with episodic inflammatory phases
associated with redness and swelling. Flares then reduce in frequency, and
pain also improves.

55. Radiologic findings

56. X-rays
• Osteoarthritis can be clinically diagnosed primarily based on history
and physical examination. Conventional radiography may be used to
confirm the diagnosis, but it is often not necessary
• Radiologic findings frequently do not correlate with clinical
symptomatology; thus, decisions regarding surgical intervention rely
more upon functional limitations, especially in the elderly, than on
radiographic findings.
• Radiographic features of OA include joint space narrowing,
osteophytes, subchondral sclerosis, subchondral cysts, and altered bone
contours.
• Joint space loss is typically nonuniform and asymmetric.
• Scoring systems, such as the Kellgren-Lawrence grading system, have
been developed to assess OA disease severity using joint radiographs.

58. Scoring systems
In 1957, Kellgren and Lawrence developed a classification system that sets out a
series of radiological features that are considered evidence of osteoarthritis,
and divides the disease into five grades:
0 – None
1 – Doubtful
2 – Minimal
3 – Moderate
4 – Severe

59. Radiographic classification of osteoarthritis:
Grade 1: doubtful joint space narrowing (JSN) and possible osteophytic
lipping.
B, Grade 2: definite osteophytes and possible JSN.
C, Grade 3: moderate multiple osteophytes, definite JSN, some sclerosis,
possible bone end deformity.
D, Grade 4: large osteophytes, marked JSN, severe sclerosis definite
deformity of bone ends.

64. Erosive OA

71. Severe spine OA
spondylolisthesis

75. MRI
• allowed the detection of preradiographic OA. It has demonstrated
that bone marrow lesions, meniscal damage and synovitis are
important features of OA.
• allows visualization of bone and soft tissue structures. MRI allows
visualization of subchondral cyst-like lesions, subchondral bone attrition,
joint effusion, synovitis (with or without contrast enhancement), and
meniscal damage. Integrity of ligaments, periarticular cysts and bursae, and
osteophytes may also be assessed through MRI.
• MRI is not necessary to diagnose OA. However, it should be considered to
evaluate mechanical symptoms of locking or sudden weakness in the
knees, instability of the hip and impingement symptoms of the shoulder.

76. Laboratory Studies

77. Laboratory testing
• Usually is not required to make the diagnosis.
• Markers of inflammation, such as erythrocyte sedimentation rate and C-
reactive protein level, are typically normal.
• Immunologic tests, such as antinuclear antibodies and rheumatoid factor,
should not be ordered unless there is evidence of joint inflammation or
synovitis, which makes autoimmune arthritis a more likely diagnosis.
• A uric acid level is recommended only if gout is suspected. Because false-
positive results are possible.
• When a patient presents with acute joint pain with synovial effusion, joint
aspiration and synovial fluidfanalysis should be performed to rule out
infectious etiology or crystalline disease. Synovial fluid findings in OA usually
suggest a minimally inflammatory (white blood cell count <2000/mm3) or
noninflammatory process.

78. New markers
• There are potential markers of tissue destruction and inflammation
that may be of use clinically in the future.
• A number of biochemical markers are under investigation to help with
diagnosis and to determine risk of progression or response to
therapy.
1. cartilage oligomeric matrix protein (COMP)
2. pyridinoline and bone sialoprotein
3. metalloproteinases
4. hylauronan.

79. Differential Diagnosis

80. Differential Diagnosis
• Before making a clinical diagnosis of OA, other diseases should
be excluded. At the very least, OA should be distinguished from
referred pain, inflammatory arthritis conditions (eg, rheumatoid
arthritis, gout, pseudogout), and periarticular bursitis (eg,
trochanteric bursitis of the hip, pes anserine bursitis of the
knee).

81. MANAGEMENT

83. The goals of therapy for OA
1. to reduce pain
2. to slow progression
3. improve function and quality of life
• OA management should be tailored to the individual patient, and
optimal management likely includes a combination of the different
treatment modalities.

84. lifestyle modifications
• Like many other chronic diseases, lifestyle modifications play an
important part of the therapeutic approach of OA.
• Non-pharmacologic approaches are by far the most important
therapies for OA.
• The patient education, exercise programs, weight reduction, and
wedge insoles all offer additional benefit in combination with an
analgesic or nonsteroidal anti-inflammatory drug (NSAID).

85. Patient Education
• it is important to establish and communicate realistic objectives for
each patient.
• An important goal of therapy is to reduce stress on joints by weight
reduction if indicated, strengthening of the muscles around involved joints,
improving flexibility and proprioception, joint protection strategies,
including improving joint mechanics, and the use of assistive devices and
orthotics.
• It is critical to focus the patient’s attention on enhancement and
preservation of functional ability, such as walking, dressing, and
living independently.
• the emphasis should be on maintaining adherence to
nonpharmacologic and pharmacologic therapies.

86. Weight loss
• Weight loss in overweight and obese individuals with OA of the lower limb
is recommended by all existing guidelines for knee and hip OA
management.
• A realistic goal is weight loss of more than 5% to be achieved within a 20-
week period
• Weight reduction has been shown to improve knee OA-related pain,
stiffness, and disability. Studies also suggest similar benefits in patients
with hip OA, but the evidence is not as strong as for knee OA.
• The combination of diet and modest exercise in older adults with knee OA
has been known to be most effective in weight control. However, weight
loss in the overweight, inactive older patient is a particular problem as
weight loss without exercise can cause inadvertent decrease in muscle
mass (sarcopenia).

87. Exercise
• Rehabilitation that increases muscle strength has been shown to be associated with
decreased joint pain and disability without exacerbation of knee OA pain. Stretching
and flexibility exercises are also key elements in exercise programs for people with
OA
• Exercise is an important intervention, to build muscle strength, encourage weight loss,
improve endurance and joint proprioception.
• A Cochrane review of exercise for osteoarthritis of the knee concluded that land-based
exercise can result in short-term reduction of pain and improvement in physical function. A
similar Cochrane review of water-based exercise for knee and hip osteoarthritis showed
improvement, but the results were not as robust
• Swimming is an especially good exercise that provides conditioning and strengthening
without weight bearing that may exacerbate an already painful joint.
• For patients with advanced OA, range of motion and isometric strengthening exercise can
initially be prescribed, and an exercise regimen may progress sequentially through isotonic
strengthening, aerobic exercises, and, ultimately, to recreational exercise. Extra attention is
needed for the older patient to enhance both safety and compliance with an exercise program

88. Other nonpharmacologic modalities
• Biomechanical Approaches:
• directed toward reducing the load in affected joints include the use of
walking aids, wedged insoles that change the angle of the legs, shock
absorbing footwear that reduce impact, and a heel lift if one leg is shorter
than the other.
1. medial wedge insoles for valgus knee OA, subtalar strapped lateral
insoles for varus knee OA, medially directed patellar taping,
2. Knee bracing was recommended by EULAR, but ACR has no
recommendation because of conflicting data on efficacy.
3. Patients may benefit from using a cane in one hand for OA of the
contralateral hip or knee, but it needs to be properly fitted (ie, when
standing, the elbow should be bent to approximately 20 degrees).

89. Varus (bowlegged) vs Valgus (knock-kneed)
G2 Unloader Brace

90. • bracing and splinting to help support painful or unstable joints.
• Knee orthoses have been shown to improve knee proprioception.
Use of an elastic knee bandage improves proprioception, probably
because the bandage stimulates superficial skin receptors, free
nerve endings, and hair end organs that would react strongly to
bandage movement on skin.
• Knee cages around the knee may provide some stability when ligamentous
laxity is pronounced
• Pillows should never be placed under the knees at night because of the risk
of developing flexion contracture
• a brace and a neoprene sleeve have additional beneficial effect for knee OA
compared with medical treatment alone. A brace tends to be more
effective than a neoprene sleeve,

91. • Laterally wedged insoles can provide symptomatic benefit and
decrease lateral thrust in the knee of patients with medial
compartment OA. They can also potentially reduce NSAID usage. In
parallel, medially wedged insoles can be beneficial for patients with
lateral compartment knee OA. Comfort, fit, and adherence are all
reasons that the use and benefit from orthotics have been limited.

92. HAND OA - RESTING SPLINT

93. Physical therapy modalities
• Therapeutic ultrasound (significant reduction of pain)
• Transcutaneous electrical nerve stimulation (no significant reduction
of pain) Dose-dependent inhibition of nociceptive nerve transmission
• manual therapy
• application of heat and/or cold modalities temporary benefits
• stretching/traction

94. HEAT AND COLD
• Heat and cold modalities have been used for many years in the
treatment of OA despite the paucity of adequate controlled,
randomized clinical studies. Moist superficial heat can raise the
threshold for pain, produce analgesia by acting on free nerve
endings and decrease muscle spasm

95. Acupuncture
• A meta-analysis on the effectiveness of acupuncture for osteoarthritis
of the knee found only short-term benefit which the authors
described as clinically irrelevant.

96. COMPLEMENTARY AND
ALTERNATIVE MEDICINE

97. Nutraceuticals: Glucosamine/ Chondroitin
• The combination of glucosamine and chondroitin, appeared to be
effective for moderate to severe osteoarthritis of the knee.
Chondroitin alone did not show benefit for osteoarthritis of the knee
or hip in a meta-analysis.
• The amounts generally administered are glucosamine 1500
mg/day and chondroitin sulfate 1200 mg/day

98. Other alternative therapy
• Other nutraceuticals that have been tried in the management of OA
include flavocoxid, S-adenosylmethionine (SAM-e), Boswellia,
collagen hydrolysate, Avocado-soybean, curcuma (tumeric), ginger,
and evening primrose oil, but each of these have very limited
evidence of efficacy
• There is some evidence that avocado/ soybean unsaponifiable (ASU)
supplementation, evening primrose oil, and omega-3 fish oils
improve pain.
• the supplement S-adenosylmethionine (SAM-e) to reduce functional
limitation. The effectiveness of SAM-e is comparable to that of
NSAIDs in some studies but with fewer adverse effects.

99. Balneotherapy
• spa therapy or mineral baths.
• mineral baths were of some benefit to patients with osteoarthritis,
but the authors addressed methodologic flaws in the studies and
urged caution in interpreting the findings.

100. Pharmacologic Management

101. Topical
• Topical NSAIDs:
• Topical 1% diclofenac gel (2–4 g every 6 hours). They have a high margin of
safety and are not associated with acute renal failure or gastrointestinal (GI)
adverse events. Thus, they may be particularly useful in patients with
cardiac, renal or GI comorbidities. However, they may also be less
efficacious than oral NSAIDs.
• Capsaicin and rubefacients:
• Topical capsaicin (0.025% or 0.075% every 6–8 hours) may also provide significant
pain relief. activates and sensitizes peripheral c-nociceptors.
• Rubefacients containing salicylates (eg, trolamine salicylate, hydroxyethyl salicylate,
diethylamine salicylate) may also be used as adjunctive agents, despite scant
supportive data. Skin burning, stinging, and erythema are potential side effects.
may be useful for treatment of symptomatic osteoarthritis in the hands
and knees.

102. Acetaminophen
• acetaminophen is better than placebo for treating mild osteoarthritis, but
less than nonsteroidal anti-inflammatory drugs (NSAIDs), but with fewer
gastrointestinal adverse effects.
• Dose: 650 to 1,000 mg up to four times per day.
• Although most patients have tried acetaminophen prior to visiting the
physician, they rarely have tried the maximum recommended dose (4
g/day). It is important to note that the Food and Drug Administration has
reduced the maximum daily dose of acetaminophen to 3 g/day.
• Hepatotoxicity is a potential side effect, but this is primarily seen only
in patients with concurrent alcohol abuse or when used with other
hepatotoxic drugs.
• When acetaminophen fails to control symptoms, the use of NSAIDs or
intraarticular corticosteroid injections is recommended

103. Nonsteroidal Antiinflammatory Drug and
Cyclooxygenase-2 Inhibitors
• When acetaminophen fails to control symptoms, or if symptoms are
moderate to severe, NSAID therapy is recommended.
• NSAIDs as a class are superior to acetaminophen for treating osteoarthritis.
• NSAIDs inhibit the activity of cyclooxygenase (COX) -1 and -2 enzymes,
providing analgesic and antiinflammatory effects. They can be very helpful for
OA patients who minimally respond to acetaminophen alone and with
moderate-to-severe levels of pain
• adverse effects include gastrointestinal bleeding, renal dysfunction, and
blood pressure elevation.
• Cyclooxygenase-2 inhibitors, such as celecoxib (Celebrex), have an improved
safety profile for gastrointestinal adverse effects but are costly and confer an
increased cardiovascular risk.

104. Traditional NSAIDs
1. Omit alcohol.
2. Take with food and water.
3. Watch for over-the-counter (OTC) NSAIDs adding to prescribed amount consumed.
4. Keep the dose low. Consider using OTC NSAID, in which the dose is lower than by
prescription.
5. Consider stopping the medication if the patient is dehydrated.
6. Older patients should be monitored for gastrointestinal side effects, and serum creatinine
should be checked periodically.
7. Consider combining NSAIDs with H2-blockers, PPIs, or misoprostol (at least 800 micrograms
units).
8. Salicylate levels should be measured in serum when more than 3600 mg per day are
consumed.
9. Nonacetylated salicylates lack cardiovascular protective effect, but have less risk for peptic
ulcers.
10. Combination of angiotensin-converting enzyme (ACE) inhibitors and NSAIDs may be
nephrotoxic.

105. • Short-acting NSAIDs, such as ibuprofen (400 mg every 4–6 hours) are widely available, but
patients may find greater levels of relief with longer acting NSAIDs, such as diclofenac (50 mg
every 8 hours), naproxen (500 mg every 12 hours), or nabumetone (500–750 mg every 8–12
hours); these may be of particular use for short periods during disease flares. Patients may be
started on a low-cost NSAID with a short half-life, such as ibuprofen or naproxen. If they have
minimal response after a few weeks, then the medication dosage may be maximized. Switching
to a different NSAID is another OA treatment management option
• Long-term use of NSAIDs may be problematic, particularly among the elderly. The selective
COX-2 inhibitors are as efficacious as standard NSAIDs, but there remains concern over
cardiovascular safety; they should be used with caution and avoided in patients with
cardiovascular risk factors.
• Patients with chronic kidney disease (CKD) stage IV or V (estimated glomerular filtration rate
less than 30 cc/min) should avoid NSAIDs. Nonacetylated salicylates, sulindac and nabumetone
appear to be less nephrotoxic than other NSAIDs
• Patients with cardiovascular disease are also at increased risk for cardiovascular adverse events
(eg, myocardial infarct or stroke) associated with NSAIDs. Patients should be made aware of
such risks. Finally, concomitant use of low-dose aspirin and short-acting NSAIDs (eg, ibuprofen)
may also render aspirin less effective when used for cardioprotection and stroke prevention.
Other types of NSAIDs should be considered in OA patients taking low-dose aspirin.

106. COX-2 Inhibitors
• A COX-2 inhibitor (ie, celecoxib) or a COX-2 selective NSAID (eg, meloxicam) can be a better
treatment option for a subset of OA patients.
• COX-2 inhibitors are no better at relieving pain than traditional NSAIDs.
• Older patients are at risk of cardiovascular events (MI, Stroke) with NSAIDs (traditional
and COX-2 inhibitors).
• COX-2 may increase blood pressure and edema, and cause more renal failure than
traditional NSAIDs.
• COX-2 has fewer gastrointestinal complications than traditional NSAIDs.
• COX-2 can be combined with aspirin, but the risks of gastrointestinal problems increase.
• Monitoring of COX-2 is more important in the elderly population, and side effects and
recommendations are similar to that of traditional NSAIDs.

108. NSAIDs Side Effects
• Patients should be well informed of adverse effects, including peptic ulcer, gastrointestinal bleeding, renal
dysfunction, edema, abnormal liver function tests, elevated blood pressure, and the potential
cardiovascular risk when the therapy is initiated.
• Presence of multiple comorbidities and the risk of NSAID-associated gastrointestinal (GI) side effects
limit their use in older patients, those on aspirin or anticoagulants, and those on concomitant use of
glucocorticoids. The risk of GI side effects is greatest in the first month of use.
• Central nervous system dysfunction in older adults can occur even with the standard dosages,
particularly with indomethacin.
• Nephrotoxicity is more likely to occur in patients with preexisting diabetes mellitus, congestive heart
failure, liver cirrhosis, diuretic therapy, or chronic kidney disease while using an NSAID. The
nonacetylated salicylates, sulindac, and nabumetone appear to be less toxic to the kidney.
• Short-acting NSAIDs, such as ibuprofen, interfere with the desirable antiplatelet effects of low-dose
aspirin and should not be administered within 3 hours of aspirin.
• The risk of GI bleeding can be lessened by use of a cyclooxygenase-2 selective inhibitors (eg, celecoxib
or meloxicam) or concomitant use of a proton pump inhibitor or misoprostol. However, gastroprotective
agents are not protective below the ligament of Treitz and lower GI bleeding risk, which is common with
NSAID use in older adults, remains high even with use of these agents. The potential reduction in GI
risks cannot justify the use of cyclooxygenase inhibitors as an initial agent, given concerns about the
increased risk of cardiovascular events and their cost. Furthermore, in the presence of low-dose aspirin,
reduction of GI adverse effects may not be maintained.

109. Opioids
• Opioids should be prescribed first at low dosages and carefully monitored to
evaluate for potential dependence. Opioids also may cause chronic
constipation and can place older patients at risk of falls.
• Tramadol is a weak μ-opioid receptor inhibitor and inhibits the reuptake of
serotonin and norepinephrine. It can significantly relieve pain in patients with
hand, knee or hip OA. Patients may be started on 25 mg daily, and the dosage
may be increased, thereafter. Just like other narcotic agents, it can also cause
nausea, dizziness, somnolence, and vomiting. Long-term use may also lead to
physical dependence. However, respiratory depression and constipation are
considered less of a problem with tramadol.
• Stronger opioid: such as oxycodone, hydrocodone, or morphine sulfate,
Because of the potential for abuse, opioids should be an option only if the
patient has not responded to acetaminophen or NSAID with severe pain and
contraindication to surgery.

110. serotonin and norepinephrine reuptake
inhibitor
• duloxetine may also be useful for control of the pain associated with
osteoarthritis.

111. Disease-modifying osteoarthritis drugs
• At present, there are no DMOAD therapies available in the market.
• Many studies have focused primarily on preventing hyaline cartilage loss.
Because the pathogenesis of OA involves multiple tissues, more recent studies
are also targeting other tissues including the subchondral bone.
• DMOADs that are under investigation have an anticatabolic effect on cartilage
and may also structurally modify subchondral bone. These include calcitonin,
bisphosphonates, inducible nitric oxide synthase inhibitors, interleukin-1β
antagonists, matrix metalloproteinase inhibitors, aggrecanase inhibitors, and
doxycycline.
• Others, such as strontium ranelate, BMP-7 and FGF-18, have an anabolic effect
on cartilage.
• Most of these experimental therapies are given systemically, but some are
administered intra-articularly

112. Diacerein
• Diacerein Is Being Studied as Disease-Modifier for Osteoarthritis.
• Diacerein has been studied to treat osteoarthritis of the knees and hips.
Diacerein is an anti-inflammatory medication that works differently from the
typical NSAIDS. Diacerein blocks interleukin-1, as opposed to inhibiting the
cyclooxygenase (COX) pathway as NSAIDs do.
• dose of 50 mg twice a day.
• The most common side effect associated with diacerein was diarrhea.

113. Intra-articular injections of corticosteroids or
hyaluronic acid
• Intra-articular injections of corticosteroids are very useful in treating inflammatory disease flares, and
may result in sustained symptom improvement, although response duration is variable. (short-term
relief lasting four to eight weeks )
• Many practitioners also add local anesthetic, although there is no clear evidence that this improves
the efficacy of the treatment. Most data are available for knee OA. Infection is rare ( < 1 in 10,000
incidence), but care should be taken to clean overlying skin, and injection through infected/psoriatic
skin should be avoided. Other side effects to warn patients about are skin depigmentation and fat
atrophy. It is advised that patients receive no more than 2 or 3 injections per year.
• The efficacy of intra-articular injection of hyaluronic acid derivatives a large molecular weight
glycosaminoglycan which is a constituent of synovial fluid (visco-supplementation) is controversial,
although it may provide prolonged relief in some cases.(The treatment effect often lasted for up to
four months )
• Viscosupplementation can lead to significant reduction in pain, improvement in physical function, and
reduction in stiffness, needs to be administered at weekly intervals for 3 to 5 weeks. There is a small
risk of postinjection reactive inflammatory synovitis and a slight risk of joint infection
• corticosteroids had a better short-term response rate and were equal to hyaluronic acid in the
intermediate four- to eight-week range, but were inferior to hyaluronic acid after eight weeks from
the time of injection

114. Growth factor injections and/or platelet rich
plasma
• The clinical use of platelet-rich plasma has been proposed as a
therapeutic alternative in patients with osteoarthrosis,
administering it by means of intra-articular injections directly in
the knees of the affected patients. Most of the studies
performed so far show promising results, with pain reduction
and an improvement in joint function. A couple of years ago,
studies on controlled randomised trials began to be published.
These provided improved clinical evidence about the first non-
controlled trials or the ones in which series of cases were
analysed.

116. TANEZUMAB
• the inhibition of nerve growth factor in patients with OA can reduce pain, but is
associated with adverse effects that limit its clinical use.
• The administration of a range of doses of tanezumab, a monoclonal antibody
that inhibits nerve growth factor, significantly reduced knee pain while walking,
compared with placebo, in a randomized trial involving 450 patients with OA of
the knee (45 to 62 versus 22 percent)
• Reversible abnormalities in sensation occurred in some of the treated patients.
• Trials of tanezumab were halted, however, by the US Food and Drug
Administration (FDA) on June 22, 2010 because of the development of
progressively worsening OA associated with bone necrosis in at least 16 patients
from one of the trials for OA of the hip and knee. All of these patients required
total joint arthroplasty of the affected joints. The joint failure in these patients is
presumed to be related to injury from excessive use allowed by the absence of
joint pain.
• Further study would be required to determine if this or similar agents have a role
in the treatment of OA or other painful conditions.

117. Other agents
• Colchicine has been tried in patients who have inflammatory OA that is
refractory to NSAIDs and/or intraarticular glucocorticoids and who
have evidence of CPPD crystals. Hydroxychloroquine has also been
tried anecdotally in patients with inflammatory or erosive OA that has
been unresponsive to NSAIDs.
• Hydroxychloroquine has been used infrequently in patients with
inflammatory or erosive OA.
• One report retrospectively reviewed charts of patients with erosive OA
who were treated with hydroxychloroquine because of symptoms that
were unresponsive to NSAIDs.
• hydroxychloroquine was felt to be effective in six of eight patients.
• Prospective, randomized, double-blind studies of large numbers of
patients are needed in order to confirm these initial observations.

118. SURGICAL INTERVENTION

119. • Surgery should be reserved for patients whose symptoms have not
responded to other treatments.
• The well-accepted indication for surgery is continued pain and
disability despite optimal conservative treatment.
• The most effective surgical intervention is total joint replacement,
with excellent patient outcomes following total joint replacement of
the hip, knee, and shoulder.
• Arthroscopy and osteotomy may be helpful in some cases.

120. Arthroplasty
• consists of the surgical removal of joint surface and the insertion of
a metal and plastic prosthesis .
• unicompartmental and total knee replacement surgery
• The prosthesis is held in place by cement or by bone ingrowth into a
porous coating on the prosthesis.
• The use of cement results in faster pain relief, but bone ingrowth may
provide a more durable bond; accordingly, prostheses with a porous
coating are used in younger patients.

121. • Unicompartmental knee arthroplasty involves replacement of a part
or section of the knee that is arthritic.
• It may be considered in patients with discrete knee pain and disease
that is localized to the medial compartment. Compared to total knee
arthroplasty, it may also improve knee pain and function but requires
a smaller surgical incision. Consequently, there is less postoperative
pain, and hospital stay is shorter. The rehabilitation process also
tends to be more rapid. Postsurgical complications, such as deep
vein thrombosis and infection, are also fewer with unicompartmental
than with total knee replacement surgery.
• The concern about unicompartmental knee arthroplasty, though, is
that it may make subsequent total knee replacement surgery more
complex.

122. • Total joint replacement surgery is an irreversible procedure used in those
with severe OA who have failed conservative treatment modalities. It is
usually selected for those with OA of the hip, knee or shoulder. Patients
who undergo surgery often attain substantial improvements in pain and
physical functioning.
• Maximal improvements are usually observed in the first 3 to 6 months with
long-term benefit plateauing after 9 to 12 months. Quality of life indicators
following joint replacement also improve approximately a year after
surgery.
• With current advances, the implant typically lasts 15 years or more.
• Arthroplasty revision may be required due to aseptic loosening or infection.
Risk of revision is also higher in patients with OA younger than 65 years
than in those aged 65 years or older

124. Arthroscopic debridement and joint
lavage
• Arthroscopic debridement is the removal of loose bodies, debris,
mobile fragments of articular cartilage, unstable torn menisci, and
impinging osteophytes. The procedure variably includes joint lavage.
While it is a relatively common procedure, its practice is highly
controversial. While a few uncontrolled studies have demonstrated
short-term efficacy, most studies have shown that it is no better than
placebo in providing symptomatic benefit for knee OA. These
procedures are not recommended as treatment options in the AAOS
and OARSI OA management guidelines.

125. Osteotomy
• High tibial osteotomy is a potential surgical treatment for knee OA. It is
appropriate for unilateral knee OA with varus malalignment. Realignment of
the varus deformity would reduce stress on the medial compartment of the
knee by redistributing the weight of the body from the arthritic medial
compartment to the healthier lateral compartment.
• The procedure can reduce pain, improve function, and delay the need for
joint replacement. Overall failure rate at 10 years is approximately 25%.
• Intertrochanteric varus or valgus osteotomy has been used for hip OA
treatment for nearly a century. Pelvic or femoral osteotomies have also been
used to correct the biomechanics and joint congruency in young patients
with hip dysplasias to prevent the development of hip OA. Evidence in the
efficacy of these procedures, however, is limited.

126. Joint fusion
• Joint fusion surgery, also known as arthrodesis, may be selected in
patients with severe OA of the wrist, ankle, or first MTP joint.
• It may also be used as a salvage procedure when knee joint
replacement has failed.
• During the procedure, two bones on each end of a joint are fused,
eliminating the joint itself. While a fused joint loses flexibility, it can
bear weight better and may be completely pain free.

127. PREVENTION

128. PREVENTION
• There are currently no therapies known to prevent the progression of
joint damage due to OA.
• current research efforts are trying to identify preclinical biochemical
and imaging biomarkers that will provide opportunities to diagnose
and treat OA earlier. Hence, we may eventually prevent the
development and further progression of the disease.
• There are also known potential theoretical targets for primary and
secondary prevention of OA. These include addressing weight
gain/obesity, joint injuries/trauma related to recreational and/or
occupational activities, as well as structurally abnormal joints.

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