Knee Osteoarthritis

PMR PG Teaching

1. OSTEOARTHRITIS OF THE KNEE

2. OA = JOINT FAILURE
The pathologic sine qua non -hyaline articular cartilage loss, present in a focal and, initially,
non-uniform manner.
Accompanied by increasing thickness and sclerosis of the subchondralbony plate, by
outgrowth of osteophytes at the joint margin, by stretching of the articular capsule, by mild
synovitisin many affected joints, and by weakness of muscles bridging the joint.

3. JOINT PROTECTIVE MECHANISMS AND THEIR FAILURE
Synovial fluid
Joint capsule and ligaments
Muscles and tendons
Sensory afferents
Cartilage
By providing a limit to excursion, thereby fixing the ROM
Reduces friction between articular surfaces
The ligaments, overlying skin and tendons have mechanoreceptor sensory
afferent nerves which fire at different frequencies throughout a joint's ROM,
providing feedback by way of the spinal cord to muscles and tendonsto
anticipate joint loading
Focal stress across the joint is minimized by muscle contraction that decelerates
the joint before impact and assures that when joint impact arrives, it is distributed
broadly across the joint surface.

4. CARTILAGE AND ITS ROLE IN JOINT FAILURE
Two major macromolecules in cartilage
Type 2 collagen (tensile strength)
Aggrecan(proteoglycan macromolecule
linked with hyaluronic acid, which consists
of highly negatively charged
glycosaminoglycans)

5. CARTILAGE AND ITS ROLE IN JOINT FAILURE
Mechanical and osmotic stress on
chondrocytes induces these cells to alter
gene expression and increase production of
inflammatory cytokines and matrix-
degrading enzymes
Type 2 cartilage is degraded primarily by
MMP-13 (collagenase 3)
Aggrecandegradation is by two
aggrecanases(ADAMTS-4 and ADAMTS-
5) and perhaps of MMPs

6. CARTILAGE AND ITS ROLE IN JOINT FAILURE
Both collagenase and aggrecanasesact
primarily in the territorial matrix
surrounding chondrocytesnormally
However, as the osteoarthritic process
develops, their activities and effects
spread throughout the matrix, especially
in the superficial layers of cartilage

7. CARTILAGE AND ITS ROLE IN JOINT FAILURE
The synoviumand chondrocytes synthesize
numerous growth factors and cytokines
Chief among them is interleukin (IL) 1
Transcriptional effects on chondrocytes
Stimulates proteinases
Suppresses cartilage matrix synthesis
Tumornecrosis factor (TNF) may play a
similar role

8. CARTILAGE AND ITS ROLE IN JOINT FAILURE
These cytokines also induce chondrocytes to
synthesize -
Prostaglandin E2
Nitric oxide (inhibits aggrecansynthesis
and enhances proteinase activity)
Bone morphogenicprotein 2 (BMP-2)-
stimulates anabolic activity

9. Healthy cartilage is metabolically sluggish,
with slow matrix turnover and synthesis and
degradation in balance, cartilage in early OA
or after an injury is highly metabolically
active.
It is characterized by gradual depletion of
aggrecan, an unfurling of the tightly woven
collagen matrix, and loss of type 2 collagen.
Loses its compressive stiffness
Increasing vulnerability of cartilage

10. DERANGED BIOCHEMICAL PROCESSES AND STRUCTURE
MODIFYING TREATMENTS

11. RISK FACTORS
Most potent risk factor for OA
Aged cartilage is less responsive to dynamic loading (i.e.
less matrix synthesized)
Joint protectors fail more with age
Muscles that bridge become weaker
Sensory nerve input slows with age, retarding the
feedback loop of mechanoreceptors
Ligaments stretch with age
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

12. RISK FACTORS
Hormone loss with menopause may contribute to this risk,
there is little understanding to this.
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

13. RISK FACTORS
Highly heritable disease, but varies by joint.
50% percent of the hand and hip OA is attributable to
inheritance
However, this is 30% in knee OA
Emerging evidence has identified high risk genetic mutations
e.g. polymorphism within Growth Differentiation Factor 5
geneDecreases GDF5 (normally has anabolic effects on the
synthesis of cartilage matrix)
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

14. RISK FACTORS
Fracture through the joint surface
Avascular necrosis
Tears of ligamentous and fibrocartilaginousstructures,
such as the ACL and meniscus (knee) and labrum(hip)
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

15. RISK FACTORS
Weakness in the quadriceps muscles bridging the knee
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle weak
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

16. RISK FACTORS
The role of bone in serving as a shock absorber for impact
load is not well understood, but persons with increased bone
density are at high risk of OA
Suggests that resistance of bone to impact during joint use
may play a role in disease development
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increased bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

17. RISK FACTORS
Malalignmentincreases stress on a focal area of cartilage,
which then breaks down
Varusknees -exceedingly high risk of cartilage loss in the
medial or inner compartment
Valgus malalignmentpredisposes to rapid cartilage loss in the
lateral compartment.
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

18. RISK FACTORS
Patients have impaired proprioception across their knees, and
this may predispose them to further disease progression
Several studies have shown that proprioceptive acuity in OA
knee may be improved with interventions as simple as an
elastic bandage, neoprene sleeve, bracing, or exercise
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive deficit
Loading
factors
•Obesity
•Injurious physical
activities

19. RISK FACTORS
It is a stronger risk factor for disease in women than in men,
Not only is obesity a risk factor for OA in weight-bearing
joints, but obese persons have more severe symptoms from
the disease
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious physical
activities

20. RISK FACTORS
Workers performing repetitive tasks as part of their
occupations for many years are at high risk of OA in those
joints
One reason why workers may get disease is that during
long days at work, their muscles may gradually become
exhausted, no longer serving as effective joint protectors
In a study, compared to non runners, professional runners
in Olympics had high risks of both knee and hip OA
Systemic
factors
•Increased age
•Female
•Genetics
Local
factors
•Previous damage
•Bridging muscle
weakness
•Increasing bone density
•Mal-alignment
•Proprioceptive
deficiencies
Loading
factors
•Obesity
•Injurious phys. activity

21. SOURCES OF PAIN
Cartilage is aneural. Its loss in a joint is not accompanied by pain.
Thus, pain in OA likely arises from innervated structures in the joint
Synovium,
Ligaments
Joint capsule
Muscles
Subchondralbone.
Most of these are not visualized by the x-ray, and the severity of x-ray changes in OA correlates poorly
with pain severity.

22. SOURCES OF PAIN
Based on MRI studies in OA knees comparing those with and without pain
likely sources of pain include
Synovial inflammation
Joint effusions -Capsular stretching from fluid in the joint stimulates
nociceptive fibres
Bone marrow edema–it signals the presence of microcracksand scar,
which are the consequences of trauma. May stimulate bone nociceptive
fibers
Osteophytes -When they grow, neurovascular innervation penetrates
through the base of the bone and into the developing osteophyte
Outside the joint also, including bursae-Common sources of pain near
the knee are anserine bursitis and iliotibialband syndrome.

23. CLINICAL FEATURES
Joint pain -activity-related.
Pain comes on either during or just after joint use and then gradually resolves. Examples include knee or
hip pain with going up or down stairs, pain in weight-bearing joints when walking, and, for hand OA,
pain when cooking.
Early in disease, pain is episodic, triggered often by a day or two of overactive use of a diseased joint
As disease progresses, the pain becomes continuous and even begins to be bothersome at night.
Stiffness of the affected joint may be prominent, but morning stiffness is usually brief (<30 min).
In knees, buckling may occur, in part, due to weakness of Quads

24. CLINICAL FEATURES
No blood tests are routinely indicated for workup of patients with OA unless symptoms and signs
suggest inflammatory arthritis.
Examination of the synovial fluid is often more helpful diagnostically than an x-ray. If the synovial fluid
white count is >1000 per L, inflammatory arthritis or gout or pseudogoutare likely, the latter two being
also identified by the presence of crystals.

25. ACR RADIOLOGIC AND CLINICAL CRITERIA FOR OA

26. THE WOMAC (WESTERN ONTARIO AND MCMASTER UNIVERSITIES) INDEX
TO MONITOR THE COURSE OF THE DISEASE OR EFFECTIVENESS OF
MEDICATIONS
Pain:
(1) walking
(2) stair climbing
(3) nocturnal
(4) rest
(5) weight bearing
(7) getting in or out of car
(8) going shopping
(9) putting on socks
(10) rising from bed
(11) taking off socks
(12) lying in bed
(13) Getting in and out of bath
(14) sitting
(15) getting on or off toilet
(16) heavy domestic duties
(17) light domestic duties
Stiffness:
(1) morning stiffness
(2) stiffness occurring later in the day
Physical function:
(1) descending stairs
(2) ascending stairs
(3) rising from sitting
(4) standing
(5) bending to floor
(6) walking on flat surface

27. Interpretation:
• minimum total score: 0
• maximum total score: 96
• minimum pain subscore: 0
• maximum pain subscore: 20
• minimum stiffness subscore: 0
• maximum stiffness subscore: 8
• minimum physical function subscore: 0
• maximum physical function subscore: 68
Scoring and Interpretation -Response Points
none 0
slight 1
moderate 2
severe 3
extreme 4
THE WOMAC (WESTERN ONTARIO AND MCMASTER UNIVERSITIES) INDEX
TO MONITOR THE COURSE OF THE DISEASE OR EFFECTIVENESS OF
MEDICATIONS

28. RADIOGRAPHS AND OTHER MODALITIES
Knee joint using the extended-knee radiograph, which
is a bilateral AP image acquired while the patient is
weight-bearing
Kellgren-Lawrence Grading Scale
Grade 1: doubtful narrowing of joint space and
possible osteophyticlipping
Grade 2: definite osteophytes, definite narrowing of
joint space
Grade 3: moderate multiple osteophytes, definite
narrowing of joints space, some sclerosis and possible
deformity of bone contour
Grade 4: large osteophytes, marked narrowing of joint
space, severe sclerosis and definite deformity of bone
contour
OTHERS
MRI useful to exclude AVN, stress fractures, occult
fractures, inflammatory arthropathy
Ultrasound is gaining popularity and is finding
increasing role in detecting small effusions, earl
cartilage changes. It also is an adjunct for accurate
aspiration and intraarticularinjections

29. MANAGEMENT

31. NON-PHARMACOLOGIC RECOMMENDATIONS FOR THE
MANAGEMENT OF KNEE OA -ACR
Strongly recommended-
Participate in cardiovascular (aerobic) and/or resistance land-based exercise
Participate in aquatic exercise
Lose weight (for persons who are overweight)

32. NON-PHARMACOLOGIC RECOMMENDATIONS FOR THE
MANAGEMENT OF KNEE OA -ACR
Conditionally recommended -
Receive physical therapy with supervised exercise
Psychosocial interventions
Use medially directed patellar taping
Wear medially wedged insoles if they have lateral compartment OA
Wear laterally wedged insoles if they have medial compartment OA
Use of thermal agents
Walking aids
Be treated with traditional Chinese acupuncture*
Be instructed in the use of transcutaneous electrical stimulation*

33. NON-PHARMACOLOGIC RECOMMENDATIONS FOR THE
MANAGEMENT OF KNEE OA
No recommendations regarding:
Participation in balance exercises, either alone or in combination with strengthening exercises
Wearing knee braces
Using laterally directed patellar taping

34. PHARMACOLOGIC RECOMMENDATIONS FOR KNEE OA -ACR
Conditionally recommend
Acetaminophen
Oral NSAIDs and Topical NSAIDs
Tramadol
Intraarticularcorticosteroid injections
Conditionally recommend that patients with knee OA should not use the following:
Chondroitin sulfate
Glucosamine
Topical capsaicin
No recommendations regarding the use of
Intraarticularhyaluronates, and duloxetine

35. Acetaminophen Up to 1 g qid
Oral NSAIDs and COX-2
inhibitors
a
Naproxen 375–500 mg bid
Salsalate 1500 mg bid
Ibuprofen 600–800 mg 3–4 times a day
Topical NSAIDs
DiclofenacNa 1% gel 4gm qid(for knees)
Capsaicin 0.025–0.075% cream qid
Opiates Various
Intraarticularinjections
Hyaluronans
Steroids
Varies from 3–5 weekly injections
depending on preparation

36. NEUTRACEUTICALS
Two nutritional supplements –Glucosaminesand chondroitin sulphate
Some studies have shown that they stimulate glycosaminesand proteoglycan synthesis
They might also inhibit IL-1 and TNF medicated NO production

37. PLATELETRICH PLASMA INJECTIONS
Wang-Saegusaet alinvestigated 312 patients with knee OA. The patients were given 3 injections of
plasma-rich plasma at 2-week intervals. At 6 months, the patients reported a significant improvement in
pain, stiffness, function.
Theories to explain the mechanism -
Proliferation of autologous chondrocytes and mesenchymalstem cells were demonstrated after platelet-
rich plasma exposure in an ovine model
Increased hyaluronic acid secretion has also been noted in the presence of platelet-rich rather than
platelet-poor preparation
Human osteoarthritic chondrocytes exposed to platelet-rich plasma demonstrated less interleukin-1β-
induced inhibition of collagen 2 and aggrecangene expression, and diminished nuclear factor-B
activation, which are pathways involved in osteoarthritis pathogenesis.
Thus studies suggest that platelet-rich plasma may play a role in improving clinical outcomes
in patients with early onset osteoarthritis at both 6 months and 1 year

38. SURGICAL PROCEDURES
Débridement,
Osteochondralor chondrocyte transplantation
High tibialosteotomy
Distal femoral osteotomy
Arthroplasty
Arthrodesis
Because of the progressive nature of the disease, many patients eventually require operative
treatment

39. DÉBRIDEMENT
Open Arthroscopic
Less postop pain
Shorter rehab
Symptoms recur
Painful
Often 6 months
of postop rehab
Rarely used
Osteophytes excision
Loose bodies removal
Chondroplasty
Damaged menisci removal

40. DÉBRIDEMENT
Osteophytes excision
Loose bodies removal
Chondroplasty
Damaged menisci removal
Simple smoothing chondroplasty
Abrasion chondroplasty
surgery of the articular cartilage
•Loose fragments removed
•Area and edges smoothed over using mechanized
shaver
Articular surface damaged such that underlying bone is
exposed
Superficial abrasion of the bone surface by a rotatory 4.5mm
burr. bleeding surface over the next 6 weeks forms
scar tissue substitute for the original articular cartilage
6 week period using crutches for the recovery and healing

41. DÉBRIDEMENT
Osteophytes excision
Loose bodies removal
Chondroplasty
Damaged menisci removal
The abrasion chondroplastyhas largely been
replaced by the micro-fracture technique
Pierce exposed bone with a pick 
Bleeding of the underlying bone but preserves
the structure of the bone surface
6 weeks on crutches is still necessary to allow
proper healing of the defect after surgery

42. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
Osteochondralcylinder of a non-weight-bearing part of
the femur condyle harvested transplanted in the
defective portion of a weight-bearing part
Single large bone plug or multiple small plugs
(mosaicplasty)

43. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
For larger lesions (2 to 3.5 cm)
Allografts from a fresh osteoarticularsize-matched
hemicondyle
Disadvantage -patients must be “on call” for immediate
surgery when a suitable graft becomes available

44. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
For larger lesions (2 to 3.5 cm)
Allografts from a fresh osteoarticularsize-matched
hemicondyle
Disadvantage -patients must be “on call” for immediate
surgery when a suitable graft becomes available

45. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
For larger lesions (2 to 3.5 cm)
Allografts from a fresh osteoarticularsize-matched
hemicondyle
Disadvantage -patients must be “on call” for immediate
surgery when a suitable graft becomes available

46. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
For larger lesions (2 to 3.5 cm)
Allografts from a fresh osteoarticularsize-matched
hemicondyle
Disadvantage -patients must be “on call” for immediate
surgery when a suitable graft becomes available

47. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
•Lesions up to 10 cm or for multiple lesions.
•Small amount of articular cartilage removed for growing of
the autologous chondrocytes cells cultured 3 to 6
weeks implant the cells in the chondraldefect under
periosteal graft

48. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
•Lesions up to 10 cm or for multiple lesions.
•Small amount of articular cartilage removed for growing of
the autologous chondrocytes cells cultured 3 to 6
weeks implant the cells in the chondraldefect under
periosteal graft

49. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
•Lesions up to 10 cm or for multiple lesions.
•Small amount of articular cartilage removed for growing of
the autologous chondrocytes cells cultured 3 to 6
weeks implant the cells in the chondraldefect under
periosteal graft

50. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
•Lesions up to 10 cm or for multiple lesions.
•Small amount of articular cartilage removed for growing of
the autologous chondrocytes cells cultured 3 to 6
weeks implant the cells in the chondraldefect under
periosteal graft

51. OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral
AutograftTransplant
System (OATS)
Osteochondral
allografting
Autologous
chondrocyte
implantation (ACI)
Satisfactory short-term results have been
reported
•However data are insufficient
•Indications are limited and include isolated,
full-thickness, grade IV femoral defect.
•Patients must be willing to restrict activity for
12 months to allow the new cartilage to
mature

52. PROXIMAL TIBIAL OSTEOTOMY
Well-established procedure for unicompartmentalOA knee
Varusor valgus deformities cause an abnormal distribution of the weight-bearing stresses
Most common is varusposition degenerative changes in the medial part
Biomechanical rationale in unicompartmentalOA is “unloading”

53. PROXIMAL TIBIAL OSTEOTOMY
Indications -
Pain and disability resulting from OA that significantly interfere with high-demand employment or
recreation
Evidence on weight-bearing X-ray of degenerative arthritis that is confined to onecompartment
(corresponding varusor valgus deformity)
Able to use crutches/walker and have sufficient muscle strength and motivation to carry out a rehab
program

54. PROXIMAL TIBIAL OSTEOTOMY
Contraindications -
Narrowing of lateral compartment cartilage space
Lateral tibialsubluxation of more than 1 cm
Medial compartment tibialbone loss of more than 2 or 3 mm
Flexion contracture of more than 15 degrees
Knee flexion of less than 90 degrees
More than 20 degrees of correction needed
Inflammatory arthritis
Significant peripheral vascular disease.

55. TOTAL KNEE ARTHROPLASTY AFTER PROXIMAL TIBIAL OSTEOTOMY
At 10 to 15 years after proximal tibialosteotomy, 40% of patients require conversion to total
knee arthroplasty. Most series of total knee arthroplastiesafter proximal tibialosteotomies report
slightly lower rates of good and excellent clinical results than those reported for primary total knee
arthroplasty.
DISTAL FEMORAL OSTEOTOMY
If the valgus deformity at the knee is more than 12 to 15 degrees, or the plane of the knee
joint deviates from the horizontal by more than 10 degrees,
Coventry recommended a distal femoral varusosteotomy rather than a proximal tibialvarus
osteotomy.

56. THANK YOU