osteoarhritis knee is very common in old age even and even in middle age. i

1. Presenter –Dr Sourabh Kumar

2. Definition
• Osteoarthritis is a non-inflammatory, degenerative
condition of joints Characterized by degeneration of
articular cartilage and formation of new bone i.e.
osteophytes.
• It is one of the main joint of the lower limb, and for
the routine daily activities of the person it is a very
important joint.

3. Classification of
OA
OA
Primary OA Secondary OA

4. Primary OA
• More common than secondary OA
• Cause –Unknown
• Common-in elders where there is no previous pathology.
• Its mainly due to wear and tear changes occuring in old ages
mainly in weight bearing joints.
Secondary OA
Due to a predisposing cause such as:
1.Injury to the joint
2.Previous infection
3.RA
4.CDH
5.Deformity
6.Obesity
7.hyperthyriodism

5. Epidemiolog
y
• Knee OAmost common cause of disability in adults
• Decreased work productivity, frequent sick days
• Highest medical expenses of all arthritis conditions
• Due to habit of sitting cross-legged and squatting OAis more prevalent in
India.
• Symptomatic Knee OA
– More than 11% of persons > 64yr

6. The knee joint is formed by femur, tibia and patella.
Anatomy

8. Normal Knee
Physiology
• Cartilage- Sponge like action (deformation and reformation)
Beneficial for the joint function
Facilitates blood supply of the joint
• Synovial Fluid- Lubrication of the joint and the articular cartilage
(secreted by the synovial membrane around the joint)
Smoothens the articular surface
• Healthy cartilage and good lubrication is necessary for smooth functioning
and pain free movement of the joint
• Good mechanical axis is also necessary for smooth knee function

9. • Protein Diet
• Multi-vitamins and multi- minerals
• Green vegetables
• Antioxidants, are necessary for repair of day to day wear and tear of the
cartilage and maintainance of healthy cartilage

10. Pathology
OAis a degenerative condition primarily affecting the articular
cartilage.
1. Articular cartilage
2. Bone
3. Synovial membrane
4. Capsule
5. Ligament
6. Muscle

11. Articular Cartilage-
• The lower end of the femur ( condyle of the femur) is covered by thick
articular cartilage about 0.5-1 cm in thickness. Similarly, upper end of the tibia
(condyle of the tibia) is also covered by 0.5-1 cm thick articular cartilage.
• Articular cartilage is a smooth, shiny and elastic structure and it serves the
function of a shock absorber.
• Cartilage is the 1st structure to be affected.
• Erosion occurs,often central & frequently in wt. bearing areas.
Right: Early OAwith area of cartilage loss in
the center.
Left: More advanced changes with extensive
cartilage loss and exposed underlying bone

12. Changes in
Bone
• Bone surface become hard & polished as there is loss of protection from
the cartilage.
• Cystic cavities form in the subchondral bone because eburnated bone is
brittle and microfractures occur.
• Venous congestion in the subchondral bone.
• Osteophytes form at the margin of the articular surface,which may get
projected into the jt. Or into capsule & ligament,bone of the wt.-bearing jt.
• Tibial condyles become flatened, medial tibial condyle is more affected and
depressed as the weight bearing line passes medially. Thus, giving rise to
varus deformity.

13. A patient with typical OA of the
knees. In the normal standing
posture there is a mild varus
angulation of the knee joints due to
symmetrical OA of the medial
tibiofemoral compartments
Knee joint Effusion

14. Synovial
Membrane-
• Synovial membrane undergo hypertrophy and become oedematous (which can
lead to ‘cold’effusions).
• Reduction of synovial fluid secretion results in loss of nutrition and lubricating
action of articular cartilage.
Capsule
• It undergoes fibrous degeneration and there are low-grade chronic
inflammatory changes.

15. Ligaments
-
• Undergoes fibrous degernation
• There is low grade chronic inflammatory changes and acc.to the aspect joint
become contracted or elongated.
Muscles
Undergoes atrophy,as pt. is not able to use the jt. Because of pain which further
limits movts. and function.

16. Risk
Factors
• Age (>45 yrs)
• Female (more common in post-menopausal women)
• Obesity ( most important modifiable)
• Previous knee injury (specially previous trauma and sports injury)
• Lower extremity malalignment
• Habit of squatting and sitting cross-legged
• High impact activities
• Muscle weakness
• Osteoporosis

17. Diagnosis of Knee
OA
Tests
• FBC, ESR, RF
• Arthrocentesis
• X-rays (3 views)
– Weight-bearingAP
– Lateral
– Tangential Patellar (Sunrise)
• MRI

18. • Clinical symptoms
Pain
Joint Stiffness
Swelling
Crepitus
Varus Deformity
Synovial Thickening and effusion
• Synovial fluid
1. WBC<2000/mm3
2. Clear color
3. High Viscosity
• X-rays
1. Osteophytes
2. Loss of joint space
3. Subchondral sclerosis
4. Subchondral cysts

19. Pain and
Tenderness
– Usually slow onset of discomfort, with gradual and intermittent increase
– Pain is more on wt. bearing due to stress on the synovial membrane & later
on due to bone surface,which r rich in nerve endings coming in contact.
-Initially relieved by rest but later on disturb sleep.
-Diffuse/ sharp and stabbing local pain
– Types of pain
• Mechanical: increases with use of the joint
• Inflammatory phases
• Rest pain later on in 50%
• Night pain in 30% later on

20. Joint
Stiffness-
– ‘Gelling’: stiffness after periods of inactivity, passes over within minutes
(approx 15min.) of using joint again
– Coarse crepitus: palpate/hear (due to flaked cartilage & eburnated bone ends)
– Reduced ROM: capsular thickening and bony changes in joint,ms. Spasm or
soft tissue contracture.

22. Kellegren Lawrence
Grading

24. Managemen
t
• Weight loss
– Nutrition referral
• Exercise Program (improves cartilage nutrition, muscle strength and
prevents progression of OAand deformity)
– Physiotherapy
– Quadriceps strengthening
– ROM exercises
– Low impact activities e.g. swimming, biking
– Avoid high stress activities (eg- jumping, running etc)
• Ambulatory assist devices
– Cane
– Walker
• Insoles
• Unloader knee braces

25. Medical
Management
• Chondroprotective agents - Glucosamine/Chondroitin/Collagen
polypeptide/Diacerin/Rosehip Powder (help in cartilage repair)
• Acetaminophen
• NSAIDs (Diclofenac,Aceclofenac, Indomethacin, Nimesulide)
• Cox-2 inhibitors ( Celecoxib, Etoricoxib)
• Opioids(Tramadol)
• Intraarticular injections
– Glucocorticoids
– Hyaluronans
• Anti-Osteoporotic treatment( Bisphosphonates, Calcium, Vit D3)
• Anti- Oxidants ( VitA, C, E, Se, Mn, Zn)

26. Management: Algorithm
Lifestyle Modifications Acetaminophen
NSAIDs
Opioids
Celecoxib
Steroid Injections
Hyaluronan Injections
Surgical Referral

27. The use of shoes and insoles to reduce
impact loading on lower limb joints.
Modern sports shoes (‘trainers’) often
have appropriate insoles.Alternatively,
special heel or shoe insoles of sorbithane
or viscoelastic materials can be used.
They may help relieve pain as well as
reducing the peak impact load on the
joints during walking.

28. Surgical
Management
High Tibial Osteotomy
• Indication:
– Unicompartmental arthritis
– Genu varus or valgus
• Realign mechanical axis
• Age < 60yo
• < 15 degrees deformity19

29. Partial Knee
Arthroplasty
• Indication:
– Unicompartmental arthritis
• Ligaments spared
• Increased ROM
• Faster recovery
• Prosthesis 10-yr survival: 84%

30. Total Knee Arthroplasty
• Indication:
– Pain during rest is the strongest indication
– Diffuse arthritis
– Severe pain
– Functional impairment
• Pain relief > functional gain
• ACL sacrificed
• PCL also may be sacrificed
• Prosthesis 10-yr survival: 90%