Osteoarthritis a disease in bone .pptx

Osteoarthritis

1. Osteoarthritis

2. Osteoarthritis

Osteoarthritis is a chronic disease and the most
common of all rheumatological disorders.

It particularly affects individuals over the age of
65 years and is the major cause of hip and knee
replacements in developed countries.

Osteoarthritis (OA) is a degenerative disease of
diarthrodial (synovial) joints, characterized by

Breakdown of articular cartilage
Proliferative changes of surrounding bones

3. Osteoarthritis

* It is occurred due to the result of a complex interplay
of multiple factors including

joint integrity,

genetic predisposition,

local inflammation,

mechanical forces

cellular and biochemical processes.

4. Epidemiology
The prevalence of osteoarthritis increases with age.
Generally, osteoarthritis is uncommon under the age of 35 years
with 0.1% of people affected between the ages of 25-34 years.

80% of people affected above the age of 55 years.

Obesity is the strongest modifiable risk factor and
particularly affect the knees.
Trauma or injury due to diseases, such as rheumatoid arthritis, will
predispose a joint to developing osteoarthritis.
A strong genetic component is thought to be present, particularly
in women.
An inherited defect in type 11 collagen genes is linked to the
development of early onset poly-articular osteoarthritis.

Radiological evidence of OA can be found in over 90 % of the
nonulation.

5. Symptoms and Signs

Heberden’s

Square thumb
© Healthwise, Incorporated

Souro
NA

6. Characteristics of Osteoarthritis

@ OA is a chronic disease of the
musculoskeletal system, without systemic
involvement

e OA is mainly a non-inflammatory disease
of synovial joints

@ No joint ankylosis is observed in the
course of the disease

Souro

7. Etiology
« Osteoarthritis is a complex disease involving bone, cartilage and
the synovium.

* It is generally believed to be an imbalance in erosive and
reparative processes. ù

* There are a wide variety of factors predisposing an individual to
this condition including the following

* Increasing age and obesity

+ Gender

* Genetic predisposition

* Congenital abnormality such as Perthes disease of the hip
* Previous injury either due to sport or occupation

* Previous disease such as rheumatoid arthritis or gout

* Systemic disorders such as acromegaly

* Neuropathic joint disease such as a Charcot joint

8. Risk Factors for Primary OA

O Age

O Sex

@ Obesity

O Genetics

e Trauma (daily)

Souro
NA

9. Secondary Osteoarthritis

® Trauma

® Previous joint disorders;

e Congenital hip dislocation

e Infection: Septic arthritis, Brucella, Tb
e Inflammatory: RA

® Metabolic: Gout

® Hematologic: Hemophilia

e Endocrine: DM

Souro

10. Osteoarthritis

Normal

Souro
NA

11. Patnogenesis
* The pathogenesis of osteoarthritis has been classified into
four stages:
1. Initial repair
2. Early-stage osteoarthritis
3. Intermediate-stage osteoarthritis
4, Late-stage osteoarthritis

・ Initial repair is characterised by proliferation of chondrocytes
synthesising the extracellular matrix of bone.

・ Early stage osteoarthritis results in degradation of the extracellular
matrix as protease enzyme activity exceeds chondrocyte activity.
There is net degradation and loss of articular cartilage.

12. Pathogenesis
ㆍ Intermediate osteoarthritis is associated with a failure of

Extracellular matrix synthesis
Increased protease activity,
further increasing cartilage loss. à

* Finally, late-stage osteoarthritis may result in

Complete loss of cartilage with joint space narrowing in the
most severe of cases.

Bone outgrowths (osteophytes) appear at the joint margins, and

There is sclerosis of the adjacent bone.

Deformity is common at this stage.

13. Pathogenesis of OA

e Cytokines IL-1, IL-6, TNF-a
!
‘ e IL-1 and
e Cell destruction metalloproteases play
! an important role in

e Membrane phospholipids Cartilage destruction.

!
e Arachidonic acid e Local growth factors,
especially transforming

! growth factor (TGF) are
e Cox-1, Cox-2 involved in the formation
of osteophytes

14. Radiologic findings of OA

® Narrowing of joint space
(due to loss of cartilage)

e Osteophytes
e Subchondral (para-articular) sclerosis

e Bone cysts

15. Diagnosis of Osteoarthritis
Clinical Findings
Joint pain

mp

de
Radiologic Findings
Osteophytes
presence of joint space narrowing,
bone sclerosis,
cysts and deformity
* On arthroscopy normal cartilage is smooth, white and

glistening, while osteoarthritic cartilage is yellowed,
irregular and ulcerated.

16. Clinical manifestations
Osteoarthritis is traditionally classified by etiology into
1. Idiopathic form (depending on the number of joints involved)
i. localized osteoarthritis
ii. Generalised osteoarthritis
2.Secondary forms.

i. Localised osteoarthritis
a. Most commonly affects the hands, feet, hip, knees and spine,
b. less commonly affects the shoulder temporo-mandibular
sacroiliac and wrist joints.

* Pain is increased by movement and loading on the joint, and may
radiate beyond the joint itself, as in leg pain associated with
spinal disease, and knee pain radiating from the hip.

17. Clinical manifestations

・ Stiffness in the early morning lasts for less than 30 min, after
periods of rest and throughout the day.

* Inthe hands, the most commonly affected joints are the distal
interphalangeal joints or Heberden's nodes, the proximal
interphalangeal joints (Bouchard's nodes) and the base of the
thumb, the first carpometacarpal joint.

* Hip pain is particularly felt in the groin.

18. OA of Knee Joint (Gonarthrosis)

e More common in obese females

® over 50 years of age

e Joint stiffness (<30 minutes)

® Mechanical pain

e Physical examination findings: Crepitus
e Pain on pressure

e Painful ROM and functional limitation

e Limitation of ROM in later stages of OA (first
extension)

e Laboratory analysis within normal limits

Souro
NA

19. OA of Hip Joint

e More common in males over 40 years of age
e Joint stiffness

e Pain of hip, gluteal and groin areas radiating
to the knee.

e Mechanical pain
® Limited walking function

Souro
NA

20. Treatment of OA

e Symptomatic treatment
e Structure modifying treatment

e Surgical treatment

Souro
NA

21. Symptomatic treatment

à

e Decrease of joint loading
- Weight loss if over weight or obese
- Splinting
- Walking sticks

e Exercises- Strengthening exercises to improve muscle
strength and aerobic fitness training

- Swimming
- Walking
- Strengthening

e Patient education, advice and access to information
Souro

NA

22. Structure modifying treatment
e Hyaluronic acid injection (HA) °
Hyaluronan is an endogenous molecule found in the

synovial fluid. Its key functions are to increase viscosity of
synovial fluid and lubrication within the joint.

Synthetic intra-articular injections of hyaluronan are thought
to provide pain relief and improve joint function.

e Glycose amino glycans (GAG) and chondroitin

e Paracetamol (first line drug for relief of pain)

@ Topical NSAIDs, capsaicin and rubefacients are widely
used for local relief of pain and Inflammation.

23. Non-Pharmacologic Treatment of OA

® Patient education

e Weight loss (if overweight)
e Aerobic exercise programs
e Physical therapy

e Range-of-motion exercises
Muscle-strengthening exercises

® Assistive devices for ambulation
Patellar taping
Appropriate footwear

e Occupational therapy
e Joint protection and energy conservation

Souro
NA

24. Indications of surgical intervention
e Severe joint pain,

resistant to conservative treatment
methods

e Limitation of daily living activities

e Deformity, angular deviations, instability

Souro
NA

25. RA vs. OA

Rheumatoid Arthritis Osteoarthritis

Age of onset
2
Speed of onset
Distribution
Joints affected

Duration of morning
stiffness

Systemic symptoms

Can happen at any age

Rapid- weeks to months
Symmetrical polyarthritis
Small joints of hands and
feet

Stiffness worse in the
morning >1hour

Fatigue, fever, night
sweats

Usually later in life
Slow- over years
Initially asymmetrical

monoarthritis >polyarthritis

Weight bearing joints- knees,
hips

Stiffness <1hour and worse
at the end of the day (after
activity)

Souro
NA

26. Management

Oral NSAIDs
including COX-2
inhibitors

Opioids

Intra-articular
corticosteroid
injections

Education, advice,
information access

Strengthening exercise,
aerobic fitness training

Weight loss if
overweight/obese

Manual therapy
(manipulation
and stretching)