This document provides an overview of osteoarthritis. It begins by defining osteoarthritis as a type of arthritis caused by the breakdown of cartilage between bones in a joint. It then discusses the common joints affected, occurrences based on age and population, and primary versus secondary causes related to aging, injury, genetics, and other conditions. The document outlines symptoms, the etiopathogenesis of cartilage breakdown, diagnosis methods, and treatment options including non-pharmacological therapies, topical analgesics, oral medications, injections, and surgery.

1. OSTEOARTHRITIS
Presenter:
Robin Gulati

2. CONTENTS
About Osteoarthritis
Occurrences
Causes
Symptoms
Etiopathogenesis
Diagnosis
Treatment & Management

3. What is Osteoarthritis?
 Type of arthritis
 Caused by the breakdown and
eventual loss of
the cartilage of one or more
joints.
 Cartilage is a protein
substance that serves as a
"cushion" between the bones
of the joints.
 Also known as degenerative
arthritis.

4.  Osteoarthritis
commonly affects:-
Hands
Feet
Spine
Large weight-
bearing joints,
such as the hips
and knees.

5.  As defined by the American College of
Rheumatology (ACR), OA is a
heterogeneous group of condition that
leads to joint signs and symptoms which
are associated with defective integrity of
articular cartilage, in addition to related
changes in the underlying bone at the
joint margins.

6. OCCURENCES
 Before the of age 45, osteoarthritis occurs
more frequently in males.
 After 55 years of age, it occurs more
frequently in females.
 Higher incidence in the Japanese
population
 South-African blacks, East Indians, and
Southern Chinese have lower rates.

8. Primary osteoarthritis:
Have no known cause.
Secondary osteoarthritis:
When the cause of the
osteoarthritis is known.

9. CAUSES: PRIMARY OA
Aging
Water content of the cartilage increases
Protein makeup of cartilage
degenerates.
Cartilage begins to degenerate by
flaking or forming tiny crevasses.

10.  Advanced cases: Total loss of cartilage
cushion between the bones of the joints.
 Repetitive use of the worn joints over the
years can irritate and inflame the
cartilage, causing joint pain and swelling.
 Loss of the cartilage cushion causes
friction between the bones, leading to pain
and limitation of joint mobility.

11.  Inflammation of the cartilage can also
stimulate new bone outgrowths
(spurs, also referred to as osteophytes) to
form around the joints.
 Can develop in multiple members of the
same family, implying a hereditary
(genetic) basis for this condition.

13. SECONDARY OA
Caused by another disease or
condition.
Conditions that can lead to secondary
OA include:
• Obesity
• Repeated trauma or surgery to the joint
structures,
• Abnormal joints at birth (congenital
abnormalities),
• Gout
• Diabetes
• Hormone disorders

14. Obesity: Increases the mechanical stress
on the cartilage.
The most powerful risk factor, next to
aging, for osteoarthritis of the knees.
Crystal deposits in the cartilage can cause
cartilage degeneration and OA.
Uric acid crystals cause arthritis in gout,
while calcium pyrophosphate crystals cause
arthritis in pseudogout.

15. Congenital abnormalities: Vulnerable to
mechanical wear, causing early
degeneration and loss of joint cartilage.
Structural abnormalities (Hips): Present
since birth.
Hormone disturbances: Such as diabetes
and growth hormone disorders, are also
associated with early cartilage wear and
secondary osteoarthritis.

17. SYMPTOMS
1. Pain in the affected
joint(s) after repetitive
use.
2. Swelling, warmth, and
creaking of the
affected joints.
3. Pain and stiffness of
the joints after long
periods of inactivity.

18. 4. In severe OA, complete loss of the
cartilage cushion causes friction
between bones, causing pain at rest
or pain with limited motion.
5. Progressive cartilage degeneration
of the knee joints can lead to
deformity and outward curvature of
the knees, which is referred to as
being "bowlegged."
6. People with OA of the weight-
bearing joints (like the knees) can
develop a limp. The limping can
worsen as more cartilage
degenerates.

19. 5. Osteoarthritis of the
cervical spine or lumbar
spine causes pain in the
neck or low back.
Bony spurs, called
osteophytes, that
form along the
arthritic spine can
irritate spinal
nerves, causing
severe
pain, numbness, and
tingling of the
affected parts of the
body.

20. 6. Formation of hard, bony
enlargements of the small
joints of the fingers.
 The bony deformity is a
result of the bone
spurs from the
osteoarthritis in that
joint.
7. Appearance of finger nodes
 Classic bony enlargement
of the small joint at the
end of the fingers is
called a Heberden's node
 Common bony knob
(node) occurs at the
middle joint of the fingers
in many patients with
osteoarthritis and is
called a Bouchard's node.

21. ETIOPATHOGENESIS
 Cartilage matrix: made up of:-
a. Proteoglycans (chondrotin sulfate)
b. Glycosaminoglycans (carbohydrates
that contain amino sugars found in
proteoglycans)
c. Chondrocytes
d. Collagen

22. 1. Proteoglycans
 Huge molecules made up of protein and
sugars that are woven around and
through collagen fibres forming a dense
netting inside the cartilage.
 These molecules make cartilage so
resilient that it can stretch and then
bounce back when moved. They also trap
water molecules much like a sponge.

23. 2. Chondrocytes
 Special cells sprinkled throughout the
matrix.
 They are the only cells found within the
matrix and are continually producing new
collagen and proteoglycan molecules.
 Also responsible for releasing enzymes
that dispose off ageing collagen and
proteoglycan molecules that have
surpassed their usefulness.

24. 3. Collagen
 Provides elasticity and the ability to
absorb shock at the joints.
 Creates a framework to hold the
proteoglycans in place and can be referred
to as the "glue" that holds the cartilage
matrix together.

25. Abnormal integrin expression
Modified chondrocyte synthesis
Imbalance of destructive cytokines over regulatory
factors
Degradation of cartilage matrix due to activity of
cytokines by increased production of MMP
No adequate synthesis of inhibitors
Metalloproteinases activated
Loss of articular cartilage

26.  A key role is played by cell/extra-cellular
matrix (ECM) interactions, which are
mediated by cell surface integrins.
 Integrins modulate cell/ECM
signalling, essential for regulating growth
and differentiation and maintaining
cartilage homeostasis.
 During OA, abnormal integrin expression
alters cell/ECM signalling and modifies
chondrocyte synthesis, with the following
imbalance of destructive cytokines over
regulatory factors.

27.  IL-1, TNF-alpha and other pro-catabolic
cytokines activate the enzymatic
degradation of cartilage matrix and are
not counterbalanced by adequate
synthesis of inhibitors.
 Enzymes involved in ECM breakdown:
Metalloproteinases (MMPs), activated by
an amplifying cascade.
 MMP activity is partially inhibited by the
tissue inhibitors of MMPs (TIMPs), whose
synthesis is low compared with MMP
production in OA cartilage.

28.  Intriguing is the role of growth factors
such as TGF-beta and others, which do
not simply repair the tissue damage
induced by catabolic factors, but play an
important role in OA pathogenesis

31. DIAGNOSIS
 No blood test for the diagnosis of
osteoarthritis
 Blood tests are performed to exclude
diseases that can cause secondary
osteoarthritis.
 X-rays: Loss of joint cartilage, narrowing
of the joint space between adjacent
bones, and bone spur formation.

33.  Arthrocentesis
(Joint aspiration):
Sterile needle is
used to remove
joint fluid for
analysis.
Joint fluid analysis
is useful in
excluding
gout, infection, an
d other causes of
arthritis.

34.  Arthroscopy: A
surgical technique
whereby a doctor
inserts a viewing
tube into the joint
space to detect the
abnormalities of
and damage to the
cartilage and
ligaments.

35.  Careful analysis of the
location, duration, and character of the
joint symptoms and the appearance of the
joints.
 Bony enlargement of the joints from spur
formations: Presence of Heberden's
nodes, Bouchard's nodes

36. TREATMENT & MANAGEMENT
Non-Pharmacological
Pharmacological

37. NON-PHARMACOLOGICAL
 Diet control with weight reduction.
 Avoiding activities that exert excessive
stress on the joint cartilage
 Rest, exercise, physical and occupational
therapy, and mechanical support devices.

38.  Exercise:
Strengthens the muscular
support around the joints.
Prevents the joints from
"freezing up" and
improves and maintains
joint mobility.
Helps with weight
reduction and promotes
endurance.

39. PHARMACLOGICAL
Topical analgesics
NSAIDS
Opioid analgesics
Intra-articular injection
Surgical Treatment

40. TOPICAL ANALGESICS:
Capsiacin
For patients who cannot tolerate
systemic therapy.
Pain relief
Recommended 4 times daily
Long term adherence: twice daily

41. NSAIDS
1. Paracetamol:
First choice
Divided doses, at regular intervals, with
the total daily dose not exceeding 4 g.
Should be used with caution in patients
who have liver disease and those with a
history of excessive alcohol
consumption.

42. 2.Cyclo-oxygenase-2-specific inhibitors
Aspirin, Acetaminophen, Coxibs, Oxicams
Choice between NSAIDs and COX-
2 inhibitors should be made after carefully
assessing the risk of serious upper-GI
complications and discussing with patients
the risk of serious thrombotic
cardiovascular events.

43.  For patients with impaired renal
function, NSAIDs and COX-2 inhibitors
should only be prescribed after very
careful consideration.
 Plasma sodium, potassium and creatinine
levels, blood pressure and the presence of
oedema should be checked at baseline
and regular intervals.

44. OPIOID ANALGESICS
 Combination of codeine and paracetamol
provides better analgesia than paracetamol
alone.
 Nausea, vomiting, dizziness and
constipation lead to discontinuation of this
combination in up to a third of patients.

45.  Tramadol (centrally acting synthetic
opioid) inhibits the reuptake of serotonin
and noradrenaline.
 Generally well tolerated, but is
contraindicated in seizure disorders, as it
lowers the seizure threshold, and in
combination with selective serotonin
reuptake inhibitors because of the risk of
serotoninergic syndrome.

46. Glucosamine and chondroitin:
 Glucosamine sulfate (GS) and chondroitin
sulfate (CS) are derivatives of
glycosaminoglycans found in articular
cartilage.
 Oral GS confirm a 20%–25% reduction in
pain in patients with mild to moderate
primary knee OA but not so effective in
severe cases.
 GS is contraindicated in seafood allergy.
 Topical application of GS and CS may be
effective in reducing pain from knee OA

47. INTRA-ARTICULAR INJECTION
1. Viscosupplementation (Hyaluronate
Injections):
Hyaluronic acid helps in reconstitution
of synovial fluid temporarily improving
its elasticity and viscosity and
enhancing joint function
Given as a weekly intra-articular
injection for 3 weeks

48. 2.Glucocorticoids:
A modest and short-lived reduction in
pain.
Some patients have a dramatic and
sustained response.
Iatrogenic infection is rare if aseptic
technique is used.
Common side effects include flushing
(40%), worsening hyperglycaemia and
post-injection flare (thought to be
inflammation in response to
glucocorticoid crystals).
Single joint not be injected more than
three times a year.

49. SURGICAL TREATMENT
 Patients must be medically fit and able to
participate in a rehabilitation program
postoperatively.
 Total joint arthroplasty relieves pain and
improves function over at least 10 years.
 Total joint arthroplasties do deteriorate
over time, and may require revision.
 Revision arthroplasty is a more
complicated procedure, so arthroplasty
may be best postponed in younger
patients with OA.

51. HAPPY JOINTS
HAPPY HEALTH