DEGENERATIF_BEDAH_DASAR osteoarthritis .PPT

therieffendi 8 views 79 slides Oct 21, 2025
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About This Presentation

degenrative


Slide Content

PRABEDAH / RIO / 2006 1
Degenerative
Disorder of
Bone and Joints
Department of Orthopaedic and Traumatology
Medical Faculty Airlangga University /
Dr.Soetomo General Hospital
Surabaya.

PRABEDAH / RIO / 2006 2

PRABEDAH / RIO / 2006 3
What is degenerative disorder ?
a : progressive deterioration of
physical characters from a level
representing the norm of earlier
generations or forms
b : deterioration of a tissue or an organ
in which its function is diminished
or its structure is impaired
Merriam Webster dictionary

PRABEDAH / RIO / 2006 4
Painful Knees
Osteoarthritis
Rheumatoid
Trauma
Others

PRABEDAH / RIO / 2006 5
OA referred to
•Degenerative arthritis
•Osteoarthrosis
•Degenerative joint disease
•Hypertrophic arthritis

PRABEDAH / RIO / 2006 6
Background
•Osteoarthritis (OA) is a chronic,
degenerative disorder of multifactorial
aetiology, characterised by loss of articular
cartilage and periarticular bone remodelling.
•OA is the most common form of progressive
joint disease

PRABEDAH / RIO / 2006 7
Background…
•Age is the strongest determinant of OA.
–OA affects 25-30% of persons aged 45-64
years,
–60% of persons older than 65 years, and
–affects more than 80% of persons older than 75
years.

PRABEDAH / RIO / 2006 8
Pattern of joint
involvement in
osteoarthritis.

PRABEDAH / RIO / 2006 9
Causes
•Primary OA is idiopathic
•Secondary OA:
–Previous trauma (ie, posttraumatic OA)
–Infection
–Crystal deposition
–Previous rheumatoid arthritis (ie, burnt-out
rheumatoid arthritis)

PRABEDAH / RIO / 2006 10
The viscious cycle of degenerative arthritis
MECHANICAL
OR
CHEMICAL INJURY
PROTEOGLYCAN
DEPLETION
LOSS OF
ELASTICITY
MECHANICAL
STRESS
FIBRILLATION
ENZYME
RELEASE
ENZYME
RELEASE
SYNOVITIS
CELL DEATH &
PROTEOGLYCAN
DEBRISE

PRABEDAH / RIO / 2006 11
Cytokines – joint inflammation
IL-1
(from synoviocytes, chondrocytes,
neutrophils, monocytes, etc)
CHONDROCYTES
Stromelysin (L)
Collagenase (L)
Stromelysin (A)
Collagenase (A)
Plasmin (A)
Plasminogen
(from serum &
synovial fluid)
Proteoglycan
Matrix
Protein
Collagen
MATRIX
Inhibitor Activator (L) Latent Enzyme (A) Active Enzyme Activation Inhibition Proteolytic Action
TIMP
PAI-1
TPA

PRABEDAH / RIO / 2006 12
PATHOGENESIS
Changed chondrocyte
function/release of
destructive enzyme
Mechahnical
stress
Alteration of
proteoglycan
matrix
Alteration of
collagen matrix
Symptomatic OA
Cartilage
destruction
Mineralization
Cartilage changes
Synovial
Inflammation
Genetic
Predisposition
Multiple
aetiological factors

PRABEDAH / RIO / 2006 13
Diagnosing OA
 History
 Signs & Symptoms
 Radiology
 Laboratory findings

PRABEDAH / RIO / 2006 14
Symptoms characteristic of
osteoarthritis
Pain
Deep, aching, poorly localized
Early, pain with use; later, pain at rest
Stiffness
Localized to involved joints
Rarely exceeds 15 to 30 minutes’ duration
Related to weather change
Crepitus, crackling
Limitation of joint motion
Giving way of weight-bearing joints

PRABEDAH / RIO / 2006 15
Signs of osteoarthritis
Tenderness on palpation
May involve widely separated areas of the joint
Pain on passive motion
Crepitus, crunching on joint motion
Joint enlargement---due to
Cartliage and bone proliferative spur formation, or
Synovitis with acute flares or after prolonged disease
Limitation of motion--due to
Joint surface incongruity
Muscle spasm and contracture
Mechanical block (osteophytes, loose bodies)
Deformity, subluxation (seen late)--due to
Cartilage loss
Subchondral bone collapse
Bone cysts
Bony overgrowth
Muscle artophy
Rarely, ankylosis

PRABEDAH / RIO / 2006 16
Anatomy of Normal Knee

PRABEDAH / RIO / 2006 17
Tibia Femoral
Angle
Genu Varum
and
Flexion Contracture

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Radiology (Twersky)
1. Narrowing joint space + subchondral bone sclerosis
2. Altered shape of bone ends
3. Cystic formation
4. Osteophyte
5. Periarticular calcification
6. Mal alignment
Mild OA : any 2 of these findings
Moderate OA : any 3 of these findings
Severe OA : any 4 of these findings

PRABEDAH / RIO / 2006 19
Radiographic changes on OA

PRABEDAH / RIO / 2006 20
Relationship between radiologic evidence of osteoarthritis
of the knee and clinical manifestations by age group
(Modified from Lawrence et al, 1966)

PRABEDAH / RIO / 2006 21
Laboratory
Primary OA
No specific findings
ESR ?
C-reactive protein ?
Secondary OA
Specific lab.studies
Synovial fluid

PRABEDAH / RIO / 2006 22
Main factors in pathogenesis according to osteoarthritis location
Intrinsic factors extrinsic factors
Age SexHeredity Obesity mation trauma DisturbancesAngulation
Inflam- MechanicalDysplasia or
Fingers : Distal + ++ ++
Interphalangeal joints
and nodal generalized
OA
Finger : Proximal + + ++
interphalangeal joints
and non-nodal
generalized OA
First carpometacarpal joint + + +
First metatarsophalangeal (+)
joint
Hip (+) ++
Knee (+) + + + ++
Shoulder (+) + +
Ankle +
Wrist +
From Peyron JG : Semin Arthritis Rheum 8 : 288-306, 1979

PRABEDAH / RIO / 2006 23
Management of Arthritis
Surgical option usually considered after
failure of conservative management
or
As a primary option in selected patients
Patient’s & Surgeon’s expectation has changed

PRABEDAH / RIO / 2006 24
Surgical Treatment-The
Options!
Normal cartilage Osteoarthritic cartilage

PRABEDAH / RIO / 2006 25
•Synovectomy
•Debridement
•Osteotomy
•Total joint replacement
Surgical Management

PRABEDAH / RIO / 2006 26
Non arthroplasty- Osteotomy
Pre - Op Post - Op

PRABEDAH / RIO / 2006 27
In normal knee :
mechanical ~ anatomical axis
WB point : medial plateau+2 cm
WB distribution :
70% medial plateau
30% lateral plateau

PRABEDAH / RIO / 2006 28

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PRABEDAH / RIO / 2006 30

Correction osteotomy
To correct :
–Mal alignment
–Mal biomechanic
–Mal distribution of load
–Mal stress on cartilage

Realignment by osteotomy

PRABEDAH / RIO / 2006 31
Pre – Op X-Ray Both Knee
Up Right Weight Bearing Position

PRABEDAH / RIO / 2006 32
Bilateral Varus Knee ( AP view)

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Bilateral Varus Knee ( Lateral view )

PRABEDAH / RIO / 2006 35
Post Operative HTO in
Bilateral Knee

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Valgus Knee
Mal Alignment

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Total Knee Replacement

PRABEDAH / RIO / 2006 44
Intra Operative

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PRE-OP
POST-OP

PRABEDAH / RIO / 2006 46
Evaluation – 7 years POD
PRE-OP
POST-OP

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18 y.o 65 y.o

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PRABEDAH / RIO / 2006 55
Spondylolisthesis
Spondylos = spina, Olisthenein = to slip
Forward slip of the spine
Mostly occur between L4-L5 or L5-S1

PRABEDAH / RIO / 2006 56
Degenerative spondylolisthesis
Incidence
- male: female = 1:5
- after age 40
Etiology
disc and facets degeneration
Pain
- local
- claudicatio
- sciatica

PRABEDAH / RIO / 2006 57
Clinical picture
Symptoms
Pain :
- LBP
- sciatica
Physical exam.
degree of slip and L-S kyphosis
--> physical manifest

PRABEDAH / RIO / 2006 58
Local palpation
Leg raising -- m.paraspinal spasm
forward flexion – m.hamstring spasm
slip > 50% :
- L-S kyphosis
- trunk shortening
- hyperlordosis Th-L
- body’s center of gravity
To stand erect :
- trunk
- hip & knee

PRABEDAH / RIO / 2006 59
62 yrs. Man. L4 spondylolisthesis / radiculopathy, LBP
L3/4
L4/5
3
5
3
4
4

PRABEDAH / RIO / 2006 60
OSTEOARTHRITIS

PRABEDAH / RIO / 2006 61
Degenerative lumbar
diseases are quite
common pathology in
orthopedic field.

PRABEDAH / RIO / 2006 62
L5/S1 Hernia at shoulder

PRABEDAH / RIO / 2006 63
52 yrs. Man. L5 spondylolysis / rt-radiculopathy, LBP
5
4
L5/S
L4/5

PRABEDAH / RIO / 2006 64
Facet osteoarthritis
•3 times more common in women
•Each degree of increased extension leads to
4% increase in peak pressure
•X-ray changes of OA not easily seen
•Facet joints small unlike the knee

PRABEDAH / RIO / 2006 65

PRABEDAH / RIO / 2006 66
Spinal stenosis
•Narrowing of the spinal canal causing
mechanical compression of spinal cord or
nerve roots.
•Congenital or degenerative stenosis
•Central or root canal stenosis
•Thickened ligamentum flavum, osteophyte
•Critical spinal canal size

PRABEDAH / RIO / 2006 67

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Causes
•Unknown

PRABEDAH / RIO / 2006 70
Pathology
Phase
ROM
Pain

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Civilization….. Brought to you by the human thumb
• The thumb has become the power digit
“The thumb presents the last and best proof that the principles of adaptation which
evinces design in creation”
- Sir Charles Bell

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Clinical Features
•1/3 woman over 40 will have x-
ray changes
•Pain , CMC joint stiffness
•Tenderness over CMC joint
•‘ Grind ‘ test positive
•Localized or systemic ( RA ,
gout )

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