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1. OSTEOARTHROSIS
PRESENTER: DR.S.H.
RANNA
PGT,ORTHOPAEDICS
MODERATOR : DR. P.S.
CHAKRABORTY
Associate prof,
orthopaedics
18-11-2015

2. 0STEOARTH
ROSIS/OSTE
OARTHRITIS
comes from three
Greek words meaning
bone, joint, and
inflammation.
refer to a group of
non inflammatory
arthritides.
suffix,-itis
means
inflammation.
it is generally agreed
that the initial events
are mechanical, not
inflammatory.

3. Definition
OA is a chronic non
inflammatory,
degenerative condition
of joints characterized
by
progressive
softening and
disintegration of
articular cartilage.
new growth of cartilage and bone at the
joint margins (osteophytes) and subchondral
sclerosis, capsular fibrosis and subchondral
cyst formations.

4. ACR definition
heterogeneous
group of condition
leads to joint
signs and
symptoms’
which are associated with
defective integrity of articular
cartilage, in addition to related
changes in the underline bone at
the joint margins.

6. EPIDEMIOLOGY
Most common
arthritis &
joint disease
¼OPD
JAPANESE,
10 million
AMERICAN
OA KNEE
BEFORE 45 YRS
: M>F
AFTER 45 YRS :
F>M
INCREASES WITH AGE

7. AETIO
LOGY
AGE GENETIC
INHERIT
ANCE
CONGENITAL
DEFECT OF
JTS
TRAUMA,INFLAM
MATION, OVERUSE
SPORTS/ LABOUR
OBESITY
MECHANICAL
STRESS
DM

8. ANATOMICAL DISTRIBUTION
• Commonly affected joints:

9. LESS COMMONLY AFFECTED JOINTS:

10. CLASSIFICATION
OA
PRIMARY OR
IDIOPATHIC
OA
GENERALISED
OA
LOCALISED
SECONDARY
OA
KNOWN
CAUSE

11. PRIMARY GENERALISED OA
INVOLVES 3 OR
MORE JOINTS.
USUALLY MIDDLE
AGED WOMAN.
PRESENTS WITH
PAIN,SWEELING,STIFF
NESS OF FINGER JTS,
1st CMC,BIG TOE MTP
JTS,THEN KNEE,HIP
FACET JTS.

12. PRIMARY LOCALISED OA
HEBERDENS NODE :
DIP JTS.
BOUCHARDS NODE
: PIP JTS without
involvement of other
jts.
GENETIC FACTORS
IMPORTANT.
FEMALE 10 Times
more than MALE.

13. SECONDARY OA

14. PATHOPHYSIOLOGY OF OSTEOARTHROSIS
Intact cartilage morphology
Increase hydration
Failure of internal collagen
that restrains the matrix gel.
Breakdown of collagenous
network
Further hydration
matrix
Cartilage
swelling occurs
Repairmechanism
EARLY
STAGE

15. Mechanical
overload persist
Repair mech.
overwhelmed
Overall pgs
degradation
Further breakdown
of collagen
Chondrocytes starts
secreting lysosomal
enzymes
Dissolves the matrix
protein
LATE
CHANGES

16. RELEASE OF
DEGRADATION
PRODUCTS INTO JTS.
SYNO
VITIS
LOSS OF SHOCK
ABSORPTION PROPERTY
Structural change in
cartilage, BLISTERING
FIBRILLATION,FISSURING
LOSS OF INTEGRITY OF
CARTILAGE

17. Mechanical forces increasingly concentrated in
subchondral bone
Increased
vascularity in
subchondral
area
Reactive
sclerosis
Focal
trabecullar
degeneration
and
subchondral
cyst
formation
What
cartilage
remains still
capable of
regeneration,
repair,
remodeling

18. Cartilage at the ends undergo
ENCHONDRAL OSSIFICATION
Spur like bony outgrowth
covered by hyaline cartilage
develops at margins of joints
OSTEOP
HYTES
Small bites of cartilage may
actually break off into joints,
leading to locking joints
JOINT
MICE

19. PATHOLOGY OF OSTEOARTHROSIS
The cardinal pathological feature of
osteoarthrosis are :
Progressive cartilage destruction.
Subarticular cyst formation.
Sclerosis of surrounding bone.
Osteophytes formation.
Capsular fibrosis.

20. Eburnation:
With progressive
disintegration of
cartilage the
underlying bone
becomes exposed
and some areas may
be polished or
burnished to ivory-
like smoothness
called eburnation.

21. OSTEOPHYTES AND JOINT MICE
Spur like bony
outgrowths covered by
hyaline cartilage, may
develop at margins of joint
& progressively enlarge
Small bits of cartilage-
covered bone, known as
joint mice, may actually
break off into the joint

22. SUBCHONDRAL CYST
CYST MAY ARISE FROM INCREASE IN
INTRASYNOVIAL PRESSURE.

23. SYNOVIAL MEMBRANE & CAPSULE
Synovial
membrane undergo
hypertrophy and
become edematous.
CAPSULES
undergoes fibrous
degeneration and
there are low-grade
chronic
inflammatory
changes.

24. Histopathology of OA
EARLY CHANGES
Increased cellularity.
Small
irregularities/splits in
the surface.
Clusters of
chondrocytes.
Metachromasia due
to depletion of PGS.
LATE CHANGES
Splits become more
extentensive.
Subchondral bone
shows osteoblastic
activity
Increased
vascularity.
Cyst formation.

26. RADIOGRAPHIC GRADING OF OA
STAGE -1 NILL OR MINIMAL CHANGES/
BONY SPUR ONLY
STAGE -2 NARROWING OF JT. SPACE <
⅟2 OF NORMAL JT. SPACE
STAGE -3 NARROWING OF JT. SPACE >
⅟2 OF NORMAL JT. SPACE
STAGE -4 OBLITERATION OF JOINT
SPACE
STAGE -5 DERFORMITY OF JOINTS

28. PATHOLOGICAL GRADING OF
OSTEOARTHROSIS
GRADE-1 SOFTENING OR BLISTERING OF
JOINT CARTILAGE
GRADE -2 FRAGMENTATION OR FIBRILLATION
AN AREA < 1cm.
GRADE -3 FRAGMENTATION OR
FISSURING AN AREA >1cm.
GRADE -4 CARTILAGE FISSURING DOWN
TO THE SUBCHONDRAL
BONE.

29. SIGN AND SYMPTOMS OF
OSTEOARTHROSIS
1. PAIN: Starts insidiously and
increase slowly over months
or years.
 It is aggravated by exertion
and relieved by rest,
although with time relief on
rest is less.
In late stage pain in the bed
at night time may occur.

30. 2. STIFFNESS: Characteristically it
occurs after periods of
inactivity.
With time it becomes
constant and
progressive.
3. SWELLING: May be intermittent
suggesting of effusion.
May be continuous
suggesting capsular
thickening or large
osteophytes.

31. CREPITUS: Crunching sound or
feelings during
movements of joins.
LOSS OF FUNCTION: May be most distressing
symptoms.
Locking joints due to joint mice.
Difficulty in climbing stairs,
restriction of walking distance or
progressive inability to perform
everyday tasks.
6. DEFORMITY: It results from capsular
contracture or joint instability
but be aware that the
deformity may actually have
preceded and contributed to
the onset of osteoarthrosis.

32. INVESTIGATIONS OF OSTEOARTHROSIS
BLOOD
TEST
THERE IS NO DIAGNOSTIC LAB.
TEST FOR OA.
Osteoarthrosis is not a
systemic disease, therefore
ESR, TC, DLC are within
normal limit.
Blood tests are done for
differential diagnosis.
SYNOVIAL
FLUID

33. X-RAYS
The cardinal x-ray
features
Narrowing of joint
space.
Sclerosis subchondral
bone.
Marginal osteophytes.
Subchondral cyst.

34. MANAGEMENT OF
OSTEOARTHROSIS
CONSERVATIVE ARTHROSCOPIC
SURGICAL

35. CONSERVATIVE
1.PATIENT EDUCATION
Patient education
about the non systemic
nature of disease.
Patient should
understand the
condition and know
what they themselves
can do help.
2. LIFE STYLE
MODIFICATION
Avoid sitting on ground
with cross leg position and
sits up.
Avoid squatting.
Frequent shoe
modification due to lateral
wedging of shoe sole.
Avoid use of high heel
and up stairs.
Walking instead of
running on soft earth.
Walking within the limit
of pain.

36. 3. REDUCTION OF OVERLOADING OF
JOINTS
Slow down the rate of cartilage
loss.
Weight reduction for obese
patient.
Wearing of shock absorbing
shoes.
Using walking stick.

37. PHYSIOTHERAPY
Physiotherapy should be directed to
maintaining joint mobility and
improving muscle strength.
Range of motion /flexibility
exercises.
Zero gravity/ swimming is a good
exercise
Static muscle exercises

38. PAIN MANAGEMENT THERAPY
Hot and
cold therapy
USG
therapy
IFT, SWD
therapy etc.
 aerobic
exercise but
care should be
taken to avoid
activities which
increases
impact loading.

39. Analgesic medication:
Patient with symptomatic OA can
receive analgesic for short period of
time unless there are contraindications
ton this treatment.
Paracetamole as analgesic doses.
Other NSAIDS for acute pain for short
periods.
Oral corticosteroids usually have no
role.

40. NUTRICEUTICALS
GLUCOSEAMINE & CHONDROITIN
SULPHATE
longer period 3- 6 months.
Stimulate proteoglycan synthesis by
chondrocytes.
increases the rate of formation of new
cartilage
mild anti-inflammatory properties.

41. DIACEREIN
It is an IL-1 blocker.
Diacerein actively inhibited
the production of proteases .
Stimulate the anabolic
process of cartilage.
Administered orally 50 mg
12 hrly for 3-6 months.

42. Intra-articular injections
Hyal
uron
ic
acid
Stimulation of de novo synthesis of HA.
Inhibition of arachidonic acid release and
inhibition of IL-1 beta induced PGE2
synthesis by synoviocytes.
It influences leucocytes adherence,
proliferation, migration and phagocytosis.
It protects cellular damage caused by
reactive oxygen species.
STE
ROI
D

43. ARTHROSCOPIC TREATMENT
1. JOINT
DEBRIDGMENT &
LAVAGE
2. REMOVAL OF
LOOSE BODIES.
3. ARTHROSCOPIC
CHONDROPLASTY
.

44. AUTOGENOUS CHONDROCYTES
TRANSPLANTATION.

45. Transplantation of multiple
osteocartilagenous plugs or pegs.
Auto grafts of upto 10 mm of
diameter can be transferred into
prepared DEFECTS IN THE
FEMORAL CONDYLES.
Reported clinical results with this
technique are limited.
MOSAICPLASTY

46. MOS
AICPL
ASTY

47. CORRECTIVE OSTEOTOMY
High Tibial
Osteotomy
Realignment
osteotomy is an
option in active
patients with
symptomatic
unicompartmental
OA of the knee with
mal-alignment.

49. REPLACEMENT SURGERY
UNICONDYLAR
REPLACEMENT
TOTAL JOINT REPLACEMENT

50. THANK YOU ALL
Journey
continue..