1. OSTEOARTHRITIS
Dr Doha Rasheedy ALI
Lecturer of Geriatrics & Gerontology
Ain Shams University

2. Definition
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)

3. Epidemiology
• It is the most common condition to affect joints.
• Osteoarthritis (OA) is one of the most prevalent
condition resulting in disability particularly in elderly
population.
• Usually emerge in people aged over 40, and
prevalence rises with increasing age.
• In the elderly in the West, OA is second to
cardiovascular disease as a cause of disability.
• 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.

4. 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

5. PATHOGENESIS

6. Risk factors
Primary:
• Age
• Gender
• Genetic
• Obesity
• High bone mass
• Mechanical : repetitive
bone use squatting
Secondary:
• 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 )

8. • 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

9. 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

11. MACROSTRUCTURAL CHAGNES
• Loss of articular cartilage
• Subchondral cyst
• Osteophytes
• Sclerosis
• Muscle wasting

12. Pathological change
• Cartilage fibrillation, erosion
• Subchondral new bone
• Myxoid degeneration
• Trabecular compression

13. Nodal generalized OA
This common condition is characterized by ( 3 or more joints) :
polyarticular finger involvement
Heberden’s nodes (distal interphalangeal joint)
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.

20. Erosive OA
1. hand interphalangeal involvement
2. tendency to joint ankylosis
3. florid inflammation (episodic)
4. radiographic subchondral erosive change.
• Unlike nodal OA, proximal and distal IP joints are
equally involved and, less frequently, the MCPs.
• 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.

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

26. 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

27. 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

28. 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)

29. 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.

30. • 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.

31. 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.

32. • Patients with noninflammatory OA generally have pain
and disability-related complaints as their only
symptoms. Physical findings in affected joints include
tenderness, bony prominence, and crepitus.
• Patients with inflammatory OA complain of articular
swelling, morning stiffness lasting for more than 30
minutes, and night pain. Signs of inflammation include
joint effusion on examination or radiography, warmth
on palpation of the joint, and synovitis on arthroscopic
examination

34. Investigations
• OA is a clinical and radiological diagnosis. There
are no specific laboratory tests.
• Radiographs correlate poorly with symptoms and
clinical function.
• MRI may be better at identifying early loss of
articular cartilage, but this and other imaging
modalities have not been well validated for the
evaluation of osteoarthritis.
• synovial fluid analysis may be useful to exclude
other causes of joint pain, such as pseudogout.

36. Radiography
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

37. 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.

42. Erosive OA

50. Severe spine OA
spondylolisthesis

54. 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.
• ordering some of these tests may add unnecessary
confusion if the pretest probability of gout or an
autoimmune arthritis is low

55. New markers
• There are potential markers of tissue
destruction and inflammation that may be of
use clinically in the future.
1. cartilage oligomeric matrix protein (COMP)
2. pyridinoline and bone sialoprotein
3. metalloproteinases
4. hylauronan.

56. Differential Diagnosis
• Rheumatoid arthritis
• Gout
• Psuedogout
• Psoaritic arthritis

57. TREATMENT OF OA
• Symptomatic treatment or Structure
modifying treatment
• Pharmacologic, non-pharmacologic ,
and Surgical treatment

59. NON-PHARMACOLOGIC
TREATMENT

60. Exercise
• 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

61. physical therapy modalities
• Therapeutic ultrasound (significant reduction
of pain)
• Transcutaneous electrical nerve stimulation
(no significant reduction of pain)

62. Management: Lifestyle
Varus (bowlegged) vs Valgus (knock-kneed)
G2 Unloader Brace

63. HAND OA - RESTING SPLINT

64. Weight Reduction
• weight loss of 5 percent from baseline was
sufficient to reduce disability.
• Additionally, pain and disability were reduced
if patients lost more than 6 kg.
• Aerobic exercise is important for weight loss,
but can be challenging in persons with
osteoarthritis of weight-bearing joints.
Swimming, elliptical training, cycling, and
upper body exercise may help in such cases.

65. Assistive devices
• bracing and splinting to help support painful
or unstable joints.
• A cane can help reduce the weight load in
persons with hip or knee osteoarthritis, but it
needs to be properly fitted and used on the
side contralateral to the affected joint

66. PHARMACOLOGIC

67. Topical
• Topical 1% diclofenac gel (2–4 g every 6
hours).
• Topical capsaicin (0.025% or 0.075% every 6–8
hours) may also provide significant pain relief.
may be useful for treatment of symptomatic
osteoarthritis in the hands and knees.

68. Acetaminophen
• acetaminophen is better than placebo for
treating mild osteoarthritis, and equal to
nonsteroidal anti-inflammatory drugs
(NSAIDs), but with fewer gastrointestinal
adverse effects.
• Dose: 650 to 1,000 mg up to four times per
day.

69. NSAID therapy
• 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.
• 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.

70. • 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.
• 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.

72. Opioids
• Because of the potential for abuse, opioids
should be an option only if the patient has not
responded to acetaminophen or NSAID.
• 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 and duloxetine may also be useful for
control of the pain associated with osteoarthritis.

73. 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.

74. ANTIMALARIAL DRUGS
• 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.

75. 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 (visco-
supplementation) is controversial, although it may provide prolonged relief
in some cases.(The treatment effect often lasted for up to four months )
• 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

76. • Growth factor injections and/or platelet rich
plasma

77. 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.

78. COMPLEMENTARY AND
ALTERNATIVE MEDICINE

79. 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.

80. 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

81. 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.

82. Other alternative therapy
• There is some evidence that avocado/
soybean unsaponifiable (ASU)
supplementation, evening primrose oil, and
omega-3 fish oils improve pain.

83. 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.

84. (SAM-e)
• 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.

85. SURGICAL

86. • 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 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.

87. • Arthroplasty consists of the surgical removal of
joint surface and the insertion of a metal and
plastic prosthesis .
• 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.

89. QUESTIONS?