Osteoarthritis lecture

Prof G.S PATNAIK
MS(ortho), FAOI(USA),FACS
Consultant Orthopedic Surgeon
11/17/2020www.drgspatnaik.com 1

Epidemology
 Most common form of arthritis worldwide
 Occurs most in women and in adults over
age 45
 Occurs in 80% of people over 55 years of
age
 Affects >40 million people in US (1 in 6)
 23% experience limitation of activities
 Cost in medical care and lost wages ~$95
billion
(Elders, 2000; Loeser et al, 2001; Merskey et al, 1994)

• “Osteoarthritis (OA) is a degenerative joint
disease, occurring primarily in older
persons, characterized by erosion of the
articular cartilage, hypertrophy of bone at
the margins (i.e., osteophytes),
subchondral sclerosis, and a range of
biochemical and morphologic alterations of
the synovial membrane and joint capsule.
• Pathologic changes in the late stages of OA
include softening, ulceration, and focal
disintegration of the articular cartilage;
synovial inflammation also can occur.”

Harris: Kelley's Textbook of Rheumatology, 7th ed.
“Despite its prevalence, the precise
etiology, pathogenesis, and progression of
OA remain beyond our understanding…”

 Progressive loss of articular cartilage
 Chondrocytes produce metalloproteinases
that degrade cartilage and cause fissuring,
pitting, erosion, and denuded areas
 Subchondral bone thickens and
osteophytes, or bone spurs, form
 Synovium thickened (contains moderate
amount of lymphocytes, plasma cells)
 Joint capsule and ligaments hypertrophied
(Loesser et al, 2001; Wall et al, 1994)

 Deep aching pain, poorly localized
 May occur in one or two joints or be generalized
 Pain occurs in involved joint and is relieved by rest
 Joint stiffness in morning and after periods of inactivity
 Aching “night pain” is common
 If pain is severe on activity and asymptomatic at rest,
evaluate for neurogenic claudication
(Loesser et al, 2001)

Cartilage is aneural, so the joint pain
must arise from other structures:
 Subchondral bone: microfractures,
meduallary hypertension with bone angina
 Osteophytes: stretching of nerve endings
in the periosteum
 Ligaments: stretch
 Joint capsule: inflammation, distention
 Synovium: inflammation
 Periarticular muscle: spasm
 Neuronal plasticity( central sensitization)

 Biomechanical
Forces?
◦ OA is mechanically driven
 Biochemical Forces?
◦ Chemically mediated
◦ Cytokine activation

 Risk Factors and Possible
Causes:
◦ Age
◦ Female versus Male sex
◦ Obesity
◦ Lack of Osteoporosis
◦ Occupation
◦ Sports Activities
◦ Prior injury
◦ Muscle weakness
◦ Propioceptive deficits
◦ Acromegaly
◦ Calcium crystal deposition disease

• History: age, functionality, degree of
pain, stiffness, time of occurrence (e.g.,
morning, at rest, during activity)
• Physical examination: range of motion,
tenderness, bony enlargement of joint
• Laboratory findings: radiograph, CBC,
synovial fluid analysis
(Loesser et al, 2001; Manek et al, 2000)

 Radiographic Criteria:
◦ Loss of joint space
◦ Subchondral sclerosis or
cyst formation
◦ Presence of new bone
formation or osteophytes
 Bone demineralization,
osteopenia, extra-
articular changes would
suggest other
diagnoses.

Mild-to-moderate pain Paracetamol/ NSAIDs
Moderate-to-severe pain Tramadol and Paracetamol
combination
Severe arthritis pain: COX-2
drugs and non-specific
NSAIDs do not provide
substantial relief
Strong Opioids
Drug therapy ineffective and
function severely impaired
Surgical Treatment
11/17/2020www.drgspatnaik.com
12
First, perform a comprehensive assessment of pain and function
(ACR, 2000; APS, 2002; Manek et al, 2000)

 Is Paracetamol
effective for
Osteoarthritis?
 Is Paracetamol the
drug of choice?
 Is it safe?

Acetaminophen has clearly been demonstrated to be
effective in the treatment of the pain of OA when c/w
placebo, with a NNT of 3.6 for 50% pain reduction
when using 1000mg.
Acetaminophen is the drug of choice in both the
ACR and EULAR guidelines.
Acetaminophen has been demonstrated to be
safe in doses up to 4gm/day.

Cochrane Review 1997: no evidence to assess clinical
differences among the various NSAIDs. Decisions should be
made upon safety, acceptability and cost.
No…as OA is principally non-inflammatory NSAIDs should
clearly be titrated for clinical effect.
Consensus expert opinion and clinical data appear to state that in the
treatment of mild to moderate osteoarthritis acetaminophen and NSAIDs
have comparable efficacy.
There is no reliable evidence in human models by clinical
trials that NSAIDs are either chondroprotective or
chondrodestructive.

• What are those COX enzymes
again?
– COX breaks down
arachadonic acid into
prostaglandins.
– COX1: responsible for normal
physiologic processes like GI
protection and platelet
aggregation.
– COX2: involved in the inflammatory
response.
– These new drugs are either
called COX2 inhibitors or COX1
sparing.
– COX3 and so on are coming!

 April 6, 2005
◦ The three COX2 agents are associated with an
increased risk of serious adverse CV events
c/w placebo.
◦ Data from large clinical trials do not
demonstrate a significant increased CV risk of
the COX2 agents over the non-selective
NSAIDs.
◦ The COX2 agents reduce the incidence of GI
ulcers visualized at endoscopy.
◦ Box warning label for all prescription NSAIDs
including increased risk of CV events.

 High risk identification:
◦ Age >65 years
◦ Anti-coagulant use
◦ Prior GI bleeding
◦ Use of oral steroids
 H. Pylori
◦ If history of GI bleed, test and
treat
◦ If asymptomatic, consider “test
and treat”
 Treatment options:
◦ NSAID and PPI
◦ If no inflammation
,Tramadol/paracetamol
combination

• Is there a role for opioid
analgesia in
osteoarhtritis?
• Is there a role for chronic
therapy with opioid
analgesics?

Yes…all the guidelines and UpToDate recommend
considering narcotic analgesia for acute exacerbations
unresponsive to conventional therapy. Tramadol is
specifically identified by the ACR as well as UpToDate
as the initial agent of choice.
Yes…some patients may require chronic therapy with
Tramadol. ACR guidelines support Tramadol
therapy when other treatments have failed or are not
appropriate. American Pain Society guidelines for
nonmalignant pain should be followed.

Elliott M. Antman, MD; Joel S. Bennett, MD;
Alan Daugherty, et al: Circulation.
2007;115:1634-1642.

• Glucosamine sulfate and chondroitin sulfate
are particularly popular treatments for
osteoarthritis.
• Several early studies demonstrated that
glucosamine was superior to placebo and
comparable to NSAIDs for knee OA.
(manufacturer supported)
• Other studies measuring changes in joint
space narrowing suggested a
“chondroprotective” effect against articular11/17/2020www.drgspatnaik.com 25

• How does it work?
– Thought to stimulate
chondrocytes to make
proteoglycans.
– Thought to possibly inhibit
cartilage catabolic enzymatic
activity.
– Some hypothesize the sulfate
may be key to the effect.
– Real mechanism of action is
largely unknown.

• Cochrane Review 2005: WOMAC outcomes of
pain, stiffness and function did not show a
superiority of glucosamine over placebo for both
Rotta and non-Rotta preparations of
glucosamine. Glucosamine was as safe as placebo
• NIH multi-centered trial:
– Glucosamine and chondroitin alone or in
combination did not reduce pain effectively in the
overall group of patients
– Exploratory analyses suggest that the combination
of glucosamine and chondroitin may be effective
in the subgroup of patients with moderate-to-
severe knee pain
– European trials that showed a benefit with glucosamine
used as glucosamine sulfate; most of the American
trials—including GAIT—used glucosamine hydrochloride
Clegg DO et al. (2006), N Engl J Med 354(8):795-808

 Using Glucosamine:
◦ Safe, however, questions exist as
to adverse effects, purity and
efficacy..
◦ Trial of 1500 mg/d for 6 to 8
weeks is not unreasonable in an
informed patient.

 Synovial fluid is an ultrafiltrate
of plasma modified by the
addition of hyaluronic acid (HA),
which is produced by the
synovium.
 In osteoarthritis, the HA is
decreased and compromised.
 Exogenous supplementation of
intraarticular HA is thought to
support changes in the
character of synovial fluid.

• What’s the Evidence?
– Cochrane Review 2005
• Viscosupplementation is an effective
treatment for OA of the knee with
beneficial effects: on pain, function
and patient global assessment; and at
different post injection periods but
especially at the 5 to 13 week post
injection period.
– Questions?
• Is HA superior to corticosteroid
injections or saline injections?
• Do HA injections result in lower
utilization of NSAIDs?

 Using Hyalgan:
◦ Indications: indicated for the treatment
of osteoarthritis not responsive to non-
pharmacologic measures and to simple
analgesics.
◦ Requires sterile technique, remove joint
effusion if present prior to injection.
◦ Three to five weekly injections
recommended.
 Is it safe?
◦ No concern of inhibition of
prostaglandins.
◦ Post-injection synovitis is described, and
can last up to three weeks.

 Severe symptomatic OA that
has failed to respond to non-
surgical management.
 Evidence on clinical assessment
of either:
◦ Loose bodies
◦ Mechanical symptoms: locking,
giving way, or catching.

Indications for osteotomy
– Age less than 60 years
– Unicompartmental arthritis
– 10 to 15 degrees of varus
deformity on weight bearing
radiographs
– Preoperative motion arc of
at least 90 degrees
– Flexion contracture less
than 15 degrees
– Ability and motivation to
effectively and safely
perform rehabilitation

 The main indication for total
knee arthroplasty is for
relief of pain associated
with arthritis of the knee in
patients who have failed
non-operative treatments.
- American Academy of
Orthopedics

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