OSTEOARTHRITIS

 Osteoarthritis is the result of mechanical and

biological events that destabilise the normal
process of degradation and synthesis of
articular cartilage chondrocytes, extracellular
matrix and subchondral bone.

These changes lead to deterioration of

articular cartilage.
Definition
 Osteoarthritis is a chronic disorder of synovial
joints in which there is progressive softening &
disintegration of articular cartilage & bone at the
joint margins(osteophytes),cyst formation &
sclerosis in the subchondral bone, mild synovitis &
capsular fibrosis.
 The most common sites are hip, knee ,&hand
 Defined as
Degenerative, non inflammatory joint disease
characterised by destruction of articular cartilage
and formation of new bone at the joint surface and
bone margins.

O- Old age
A- Arthritis

Women >Men

Weightbearing joints: knee, hip, ankle and spine.

Finger jonts may also be affectected (1st MCP and
DIP).
 Types
The two types of OA are:
 Primary OA : it occurs in old age, mainly (in hip
&knee).in a generlised variety trapezio-metacrpel
joint of the thumb & the distal interphlangeal joints
of the fingers are also affected. Primary OA is more
common than secondary OA.

 Secondary OA : in this there is an underlying

primary disease of the joint which leads to
degeneration of the joint, often many years later.
Types
 Primary: age
joints:
occupation
prolonged standing
sports
genetics and heredity factors

 Secondary: underlying primary disease

age: adolesents
joint
predisposing factors
congenital maldevelopment
previous trauma
obesity
internal derangemnts:loose bodies
Risk factors
 Joint dysplasia
 Trauma
 Occupation
 Bone density
 Obesity
 Family history
 Pathology
 The first osteoarthritic change in articular cartilage, which
has been confirmed in humans, is an increase in water
content,.

 The proteoglycans has been allowed to swell with water

far beyond normal. in addition, there are changes in the
newly synthesized proteoglycan.

 In later stages of disease progression, proteoglycans are

lost, which diminishes the water content of cartilage. As
proteoglycans are lost, articular cartilage loses its
compressive stiffness & elasticity, which in turn, results in
transmission of compressive forces to underlying bone.
 Cont……
 Changes in cartilage proteoglycan will also –vely affect the
ability of cartilage to form a squeeze film over its surface
during joint loading.

 Collagen synthesis is increased initially, although there is a

shift from type 2 to type 1 ,found in skin & fibrous tissue.

 As the cartilage is destroyed, joint space narrows.

 The 1st noticable change in the cartilage is the mild fraying

or “flaking” of superficial collagen fibers. Deeper fraying or
“fibrillation”, of the upper 3rd of cartilage follows in areas
of greater weight bearing.
 Cont…
 The cartilage may degenerate to the point that
subchondral bone is exposed. Sub chondral bone can thus
become sclerotic & stiffer than normal bone.

 These changes in the cartilage and bone result in

increased friction, decreased shock absorption & greater
impact loading of the joint .

 The traditional view of OA is that the disease process

starts with an unrepaired injury to the ac; however, there
is also evidence that reduced compliance in bone &
periarticular structures may initiate the degenerative
process.
Pathology
Articular cartilage is affected

increase in water content and depletion of proteoglycans from cartilage matrix

WT bearing

loss of water & fibrillation of cartilage

exposing the underlying bone

further rubbing

Eburnation: subchondral bone becomes

hard and glossy

Formation of cysts and scerosis due to

micro fractures

Margins hypertrophy: Osteophyte formation

Clinical features

 Pain
 Swelling
 Restricted ROM and stiffness
 Severe cases would be disabling to do daily
activities
 Painful ROM
 Deformity
 Coarse crepitus
 Loose bodies: locking & giving way
 Loss of terminal flexion of knee
Radiological findings

 Loss of joint space

 Sclerosis (in in cellularity and bone
deposition)
 Subchondral cysts (synovial fluid into the
bone)
 Ostoephytes
 Bone collapse
 Loose bodies
 Deformities and malalignment
Examination
 Tenderness on the joint line
 Crepitus on moving the joint
 Irregular or enlarged looking joints due to
formation of peripheral osteophytes.
 Deformity-varus of the knee,flexion-abduction-
external rotation of the hip.
 Effusion-rare & transient
 Terminal limitation of joint movement.
 Subluxation detected on ligament testing.
 Wasting of quadriceps femoris muscle.
 Complications
 Capsular herniation : OA of knee is sometimes
associated with marked effusion & herniation of
posterior capsule(baker’s cyst)
 Loose bodies : cartilage & bone fragments may give
rise to loose bodies, resulting in episodes of locking.
 Rotator cuff dysfunction : OA of AC joint may cause
cuff impingement, tendinitis or cuff tears.
 Spinal stenosis
 spondylolisthesis
 Management
 Drug therapy in OA has no effect on disease
progression
The goals of drug therapy in patients with OA are to
 Relieve pain & Decrease inflammation
 Oral analgesics, NSAIDS & coricosteroid injections are
the primary medications used in OA management.
Knee
 Conservative:physical
therapy,analgaesics,chondroitin,glucosamine
 HTO
 Unicompartmental osteoarthritis
 Total knee arthroplasty
 Arthrodeses
 Arthroscopic debridement.
Hip
 Osteotomies
 THR
 Arthrodeses
 Physiotherapy management
General principles of treatment are:
 Prevention
 To control pain
 To prevent further damage
 To improve ROM
 To improve strength ,endurance & muscle function
 To improve the functional status of the involved joint
& the whole body-with correct ergonomic control
The method of management vary with each joint, its
function & degree of its involvement.
 Common sites of OA & their
management
 OA of hip: common cause of disability due to stiffness
& pain
 The objective of physiotherapy is to provide painless &
functionally active hip joint.
 Control of pain: In acute phase muscle spasm causes
pain, this can be relieved by ice massage, ice packs, or
hydrocollator packs.
gentle intermittent traction
deep heating modalities like US,PSWD,TENS etc
 Joint mobilization: initially relaxed PROM exercises are
ideal.
 progress to small range assisted free active movts using
stationary bicycle or roller skates in restricted range.
 Maitland techniques of low grade mobilization.
 Hydrotherapy
 Pnf techniques,provided they are not painfull.
 Muscle strengthening:improving strength &
endurance,which offer stability to the body in weight
bearing & transfers,like gluteal muscles shoild be
initiated.
 Gait reeducation
 OA of knee
 The major problems are: pain, instability, deformity, &
functional inadequacy.
 Management:
 Self care & self help methods
 During acute phase of exacerbations pain control can
be managed effectively by cryotherapy,
hydropacks,TENS,US,PSWD,
 chronic pain can be adequately relieved by deep
thermotherapy.
 Exercise programme:
-iisometrics
-Quantitative progressive excs
-free relaxed movts
-isokinetic excs
-SLR
-hamstring stretching
-posture ,gait & assistive devices
-wedge insole
The proper control of excs ,rest & self care are the most
important measures to limit imbalances b/w
mechanical stresses & improvement in the ability of
tissues to adequately withstand such stresses.
 OA of the hand
During acute phase of exacerbations:
 Rest in splint with elevation
 Relaxed PROM excs once in a day to Maintain ROM
 Small range active movts with max relaxation without
exerting any stress on the involved joint are imp.
 Cryotherapy,TENS,US,etc for pain relief.
 Mobilization :when acute symptos subside,vigorous
mobilization to improve ROM.,strength & endurance
of hand function is initiated.use of corrective splint ,till
adequate control of hand function is returned.
Bibliography
 Apley’s system of orthopaedics and fractures
 Physical rehabilitation-susan b o’sullivan
 Essential orthopaedics –maheshwari
 Essentials of orthopaedics & applied
physiotherapy-jayant joshi
 Thank you