1. OSTEOARTHRITIS
And Crystal Induced
Arthropathies
Dr Humaira Achakzai

2. DEFINITION
Osteoarthritis OA is a degenerative
disease of (synovial) joints,
characterized by
Breakdown of articular cartilage
Proliferative changes of surrounding
bones

3. EPIDEMIOLOGY
Osteoarthritis(OA) is the most
common joint disease
OA of the knee joint is found in 70% of
the population over 60 years of age
Radiological evidence of OA can be
found in over 90 % of the population

4. LIMITED FUNCTION
OA may cause functional loss (Activites
of daily living)
Most important cause of disability in
old age
Major indication for joint replacement
surgery

5. CHARACTERISTICS OF OA
OA is a chronic disease of the
musculoskeletal system, without
systemic involvement
OA is mainly a noninflammatory
disease of synovial joints
No joint ankylosis is observed in the
course of the disease

6. CLASSIFICATION OF OA
Primary OA Secondary OA
Etiology is unknown Etiology is known

7. RISK FACTORS FOR PRIMARY
OA
Age
Sex
Obesity
Genetics
Trauma (daily)

8. SECONDARY OSTOARTHRITIS
☛Results from problems that can cause cartilage
damage
1.Physical trauma (external, internal, biomechanical
derangements,
2.Inflammatory disorders
a. inflammatory arthritis (e.g. rheumatoid arthritis)
b. joint infection
c. gout, pseudogout
3. Metabolic disorders
a. hemochromatosis (excess iron)
b. Wilson’s Disease (excess copper)
4. Endocrine disorders
a.Diabetes
b.acromegaly

9. Pathophysiology
☛The earliest and most characteristic feature of OA is Cartilage Damage
1-Cartilage
 a. Covers the ends of articulated bones,
 b. Provides a low-friction interface greatly capable of absorbing shock,
 c. Physical characteristics result from collagen
fibers (50% of the dry weight of cartilage) intermingled with proteoglycans
2-. Collagen
 Hyaline (joint) cartilage -Type II collagen.
Gives cartilage tensile strength and allows it to resist shear forces during motion under load
Altered cartilage in OA contains increased amounts of Type collagen (normally found in
skin, bones, tendons)
Constrains the negatively charged, highly hydrated proteoglycans. This produces a large
swelling pressure and gives cartilage its elasticity and resistance to compression. Under
high-load conditions, proteoglycans release water and lubricate the cartilage surface
(hydrostatic lubrication)
3-Proteoglycans
a. Complex macromolecules than bind a large number of water molecules in cartilage
b. Markedly diminished in osteoarthritic cartilage
c. Enzymatic damage by matrix metalloproteases is an important cause of osteoarthritis
and early damage significantly impacts proteoglycans
d. Immobilization causes decreased proteoglycan synthesis and aggregation, further
diminishing normal cartilage function

10. Pathophysiology….Contd
4-BONE
a. Bony degeneration is also a universal
b. Includes localized increases in bone density (scelorisis) and
new bone formation osteophytes
Unknown whether cartilage abnormalities cause bone
degeneration

11. Morphology of Primary OA

12. Primary Generalized OA

14. LABORATORY FINDINGS OF
OA
There are no pathognomonic laboratory
findings for OA
Laboratory analysis is performed for
differential diagnosis

15. RADIOLOGIC FINDINGS OF
OA
Narrowing of joint space
(due to loss of cartilage)
Osteophytes
Subchondral (paraarticular) sclerosis
Bone cysts

17. RADIOLOGIC GRADE OF OA
G1 Normal
G2 Mild
G3 Moderate
G4 Severe
Kellgren Lawrence Classification

18. DIAGNOSIS OF OA
CLINICAL FINDINGS
Joint pain
+
RADIOLOGIC FINDINGS
Osteophytes

19. SIGNS AND SYMPTOMS
Joint pain - degenerative
Stiffness following inactivity – 30 min
Limitation of ROM – later stages
Deformity – restricition of ADL

20. OA OF KNEE JOINT (GONARTHROSIS)
More common in obese females
over 50 years of age
Joint stiffness (<30 minutes)
Mechanical pain
Physical examination findings: Crepitus
Pain on pressure
Painful ROM and functional limitation
Limitation of ROM in later stages of OA (first
extension)
Laboratory analysis within normal limits

21. GENU VALGUM - ORTHOSIS

24. OA OF HIP JOINT
More common in males over 40 years
of age
Joint stiffness
Pain of hip, gluteal and groin areas
radiating to the knee (N obturatorius)
Mechanical pain
Limited walking function

25. X-RAY OF HIP OA

26. Peripheral Joints
Hands
Feet

27. Treatment Concepts
1. Patient education
2. Reinforce importance of exercise to maintain strength and ROM
Exercises
- Swimming
- Walking
- Strengthening
3. Physical modalities:
a. Decrease of joint loading
- Weight control
- Splinting
- Walking sticks
b. muscle strengthening
4.Analgesics
a. acetaminophen
b. non-steroidal anti-inflammatory drugs
5.Corticosteroid injections
6. Joint replacement surgery for end stage disease
7. On the horizon:
a. autologous cartilage grafts
b. stem cells to grow new cartilage

28. STRUCTURE MODIFYING
TREATMENT
Hyaluronic acid injection (HA)
Glycose amino glycans (GAG)

29. PRIMARY PREVENTION OF
OA ??
Regular exercises
Weight control
Prevention of trauma

30. HAND OA - RESTING SPLINT

32. INDICATIONS OF SURGICAL
INTERVENTION
Severe joint pain, resistant to
conservative treatment methods
Limitation of daily living activities
Deformity, angular deviations,
instability

33. CRYSTALLINE-INDUCED
INFLAMMATORY ARTHRITIS
A. Gout (acute gouty arthropathy)
☛Gout is a disease of hyperuricemia
1. Clinical Features
 a. Generally affects men over age 30
 b. Presents as an acute attack of highly inflammatory monoarticular arthritis
c. Most commonly involved joint is the great toe
 i. 50% first attack
 ii. 90% eventually
d. Other common joints (in order of frequency): ankle, knee, wrist, finger, elbow
e. 50% recurrence within the first year (90-95% by 10 years)
f. Risk of clinical gout increases with serum urate level

34. Differential Diagnosis
 a. Infection!
 acute gout often looks like cellulitis
 b. Inflamed bunion (bursitis)
 c. Trauma
 d. Psoriatic arthritis
 e.Reactive arthritis
 f. Pseudogout

35. 3. Etiology
a. Acute inflammation is caused by monosodium urate (MSU) crystals
b. Saturation of urate at 37°C is 7.0mg/dl –close to normal serum level
c. Most patients with gout are under excretors rather than overproducers
of urate
d. Serum urate levels rise in males at puberty and in females at
menopause
e. Causes of hyperuricemia
 i. Overproduction
 - increased purine biosynthesis
 - inherited enzyme defects
 - increased nucleic acid turnover
 •myeloproliferative diseases
 •hemolytic anemias
 •psoriasis (increased skin
 turnover)
 •increased breakdown of
 adenosine triphosphate (ATP

36. Causes of hyperuricemia
i. Overproduction
 - increased purine biosynthesis
 - inherited enzyme defects
 - increased nucleic acid turnover
 myeloproliferative diseases
 •hemolytic anemias
 •psoriasis (increased skin
 turnover)
 increased breakdown of adenosine triphosphate (ATP
 severe illness
 strenuous exercise
 excessive ethanol consumption
ii. Underexcretion (decreased renal clearance)
- intrinsic renal disease (decreased filtration, decreased secretion, or both)
•renal insufficiency
•gout
•lead nephropathy
•endocrinopathy
(hypothyroidism, hyper- and
hypoparathyroidism)
- competition for excretion by organic acids
•drugs (e.g. thiazides, nicotinic acid, low-dose salicylates)
•lactic acid (e.g. lactic acidosis, heavy ethanol use)
•ketosis

37. Diagnosis
a. Aspiration of synovial fluid
b. Demonstration of needle-shaped
crystals
with negative birefringence (frequently
inside
polymorphonuclear WBCs) on polarized
microscopy

38. Treatment Concepts
a. Don’t treat asymptomatic hyperuricemia.
b. For acute attacks:
 i. Non-steroidal anti-inflammatory drugs
 (NSAIDS) or corticosteroids (systemic or intra-articular)
 ii. High-dose colchicine is an outdated treatment approach
c. For prevention of acute attacks:
 i. Urate-lowering agents are available that increase urinary excretion of uric acid or inhibit metabolic
production of uric acid
B. Pseudogout
1. Clinical

39. Pseudogout
Clinical features
a. Acute, inflammatory, gout-like attacks that occur secondary to calcium
pyrophosphate dihydrate (CPPD) crystals.
b. Patients are typically older (60’s-70’s)
c. Male/Female incidence is about 1:1
d. Knee is to pseudogout as big toe is to gout (wrist is also common)
e. Trauma (e.g. surgery) is a common trigger
Laboratory Data
 a. Serum calcium level usually normal.
 b. Inflammatory synovial fluid; usually containing rhomboid shaped crystals with positive
birefringence
 c. Radiographs typically show linear deposition of CPPD in hyaline cartilage or fibrocartilage
“chondrocalcinosis”
.Associated Conditions
 a. Hyperparathyroidism
 b. Hemochromatosis
 c. Hypothyroidism
 d. Gout
 e. Hypomagnesemia
 f. Hypophosphatasia

40. Treatment concepts
a. NSAID
b. intra-articular steroids
c. low-dose colchicine may help prevents
attacks

41. Diagnosis of Crystalline
Arthropathy
1. Birefringent Crystals
 a. Refraction (bending) of light by an optically active structure yields two perpendicular rays (one fast
and one slow) → “birefringence”
 b. The optical orientation (sign) of the fast and slow wave of a birefringent crystal isdetermined by
using a first order redretardation plate (compensator)
2. “Positive” birefrigence
 a. Crystal appears blue when its longitudinal axis is parallel to the direction of slow vibration of light in
the compensator (the direction of slow vibration is marked on the compensator)
 b. Crystal appears yellow when it is perpendicular to the compensator's slow ray
 c. Calcium pyrophosphate dihydrate has weakly positive birefringence
3. "Negative” birefrigence
 a. Crystal appears yellow when its longitudinal axis is parallel to the compensator's slow ray
 b. Crystal is blue when perpendicular to the compensator's slow ray
 c. Monosodium urate has strong negative birefringence

43. QUESTIONS?