OsteoarthritisOsteoarthritis
Osteoarthritis is a non-inflammatory, Osteoarthritis is a non-inflammatory,
degenerative condition of joints degenerative condition of joints
Characterized by degeneration of articular Characterized by degeneration of articular
cartilage and formation of new bone i.e. cartilage and formation of new bone i.e.
osteophytes.osteophytes.
Common in weight-bearing joints such as Common in weight-bearing joints such as
hip and knee.hip and knee.
Also seen in spine and hands.Also seen in spine and hands.
Both male and females are affected.Both male and females are affected.
But more common in older women i.e. But more common in older women i.e.
above 50 yrs,particularly in above 50 yrs,particularly in
postmenopausal age.postmenopausal age.
Risk factors
Obesity esp OA knee
Abnormal mechanical loading
eg.meniscectomy, instability
Inherited type II collagen defects in
premature polyarticular OA
Inheritance in nodal OA
Occupation eg farmers
Infection:Non-gonococcal septic arthritis
Hereditary
Poor posture
Injured joints
Ageing process in joint cartilage
Defective lubricating mechanism
Incompletely treated congenital
dislocation of hip
Classification of OAClassification of OA
OA
Primary OA Secondary OA
Primary OAPrimary OA
More common than secondary OAMore common than secondary OA
Cause –UnknownCause –Unknown
Common-in elders where there is no Common-in elders where there is no
previous pathology.previous pathology.
Its mainly due to wear and tear changes Its mainly due to wear and tear changes
occuring in old ages mainly in weight occuring in old ages mainly in weight
bearing joints.bearing joints.
Secondary OASecondary OA
Due to a predisposing cause such as:Due to a predisposing cause such as:
1.Injury to the joint1.Injury to the joint
2.Previous infection2.Previous infection
3.RA3.RA
4.CDH4.CDH
5.Deformity5.Deformity
6.Obesity6.Obesity
7.hyperthyriodism7.hyperthyriodism
Types of OATypes of OA
Nodal Generalised OANodal Generalised OA
• • Crystal Associated OACrystal Associated OA
• • OA of Premature OnsetOA of Premature Onset
Nodal Generalised OA
•• Heberden’s nodes
•• Bouchard’s nodes
•• CMC of thumb
•• Hallux
•valgus/rigidus
•• Knees & hips
•• Apophyseal joints
Crystal Associated OA
•Calcium pyrophosphate
•dihydrate occurs
•mainly in elderly
•women, and principally
•affects the knee
OA of Premature Onset
•• Previous meniscectomy
•• Haemochromatosis
PathologyPathology
OA is a degenerative condition primarily OA is a degenerative condition primarily
affecting the articular cartilage. affecting the articular cartilage.
1.articular cartilage1.articular cartilage
2.Bone2.Bone
3.Synovial membrane3.Synovial membrane
4.capsule4.capsule
5.Ligament5.Ligament
6.muscle6.muscle
Articular CartilageArticular Cartilage
Cartilage is the 1Cartilage is the 1
stst
structure to be affected. structure to be affected.
ErosionErosion occurs,often central & frequently in wt. occurs,often central & frequently in wt.
bearing areas.bearing areas.
FibrillationFibrillation,which causes softening,splitting and ,which causes softening,splitting and
fragmentation of the cartilage,occur in both wt. fragmentation of the cartilage,occur in both wt.
bearing & non-wt. bearing areas.bearing & non-wt. bearing areas.
Collagen fibresCollagen fibres split and there is disorganisation split and there is disorganisation
of the proteoglycon collagen relationship such of the proteoglycon collagen relationship such
as H2O is attracted into cartilage, which causes as H2O is attracted into cartilage, which causes
futher softening and flaking.these flakes of futher softening and flaking.these flakes of
cartilage break off and may be impacted b/w the cartilage break off and may be impacted b/w the
jt.surfaces causing locking and inflammation.jt.surfaces causing locking and inflammation.
Right: Early OA with
area of cartilage loss in
the center.
Left: More advanced
changes with extensive
cartilage loss and
exposed underlying
bone
Arthroscopic appearances
in OA of the knee joint:
fibrillated surface of the
cartilage on the medial
femoral condyle
Bone(Eburnation)Bone(Eburnation)
Bone surface become hard & polished as Bone surface become hard & polished as
there is loss of protection from the there is loss of protection from the
cartilage.cartilage.
Cystic cavities form in the subchondral Cystic cavities form in the subchondral
bone because eburnated bone is brittle bone because eburnated bone is brittle
and microfractures occur.and microfractures occur.
Venous congestion in the subchondral Venous congestion in the subchondral
bone.bone.
Gross superior view of a
femoral head from a
patient with radiographic
stage I OA. This shows an
area of complete cartilage
loss, with polishing or
eburnation of the
underlying bone.
Osteophytes form at the margin of the Osteophytes form at the margin of the
articular surface,which may get projected articular surface,which may get projected
into the jt. Or into capsule & ligament,bone into the jt. Or into capsule & ligament,bone
of the wt.-bearing jt.of the wt.-bearing jt.
There is alteration in the shape of the There is alteration in the shape of the
femoral head which becomes flat and femoral head which becomes flat and
mushroom shaped.mushroom shaped.
Tibial condyles become flatened.Tibial condyles become flatened.
Osteophyte at margin of articular
surface
Synovial MembraneSynovial Membrane
Synovial membrane undergo hypertrophy and Synovial membrane undergo hypertrophy and
become oedematous (become oedematous (which can lead to ‘cold’ which can lead to ‘cold’
effusions)effusions)..
Reduction of synovial fluid secretion results in Reduction of synovial fluid secretion results in
loss of nutrition and lubricating action of articular loss of nutrition and lubricating action of articular
cartilage.cartilage.
CapsuleCapsule
It undergoes fibrous degeneration and there are It undergoes fibrous degeneration and there are
low-grade chronic inflammatory changeslow-grade chronic inflammatory changes
LigamentLigament
Undergoes fibrous degernationUndergoes fibrous degernation
There is low grade chronic inflammatory There is low grade chronic inflammatory
changes and acc.to the aspect joint changes and acc.to the aspect joint
become contracted or elongated.become contracted or elongated.
MusclesMuscles
Undergoes atrophy,as pt. is not able to use Undergoes atrophy,as pt. is not able to use
the jt. Because of pain which further limits the jt. Because of pain which further limits
movts. and function. movts. and function.
Clinical features of OAClinical features of OA
PainPain
StiffnessStiffness
Muscle spasmMuscle spasm
Restricted movementRestricted movement
DeformityDeformity
Muscle weakness or wastingMuscle weakness or wasting
Joint enlargement and instabilityJoint enlargement and instability
CrepitusCrepitus
• • Joint Joint EffusionEffusion
Clinical features 1
•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
Clinical features
•Pain and tenderness (cont)
–Types of pain
•Mechanical: increases with use of the joint
•Inflammatory phases
•Rest pain later on in 50%
•Night pain in 30% later on
Clinical features 2
•Movement abnormalities
–‘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.
Clinical features 3
•Deformities
–Soft tissue swelling:
•mild synovitis
•small effusions
–Osteophytes
–Joint laxity
–Asymmetrical joint destruction leading to
angulation
Osteoarthritis of the DIP
joints. This patient has
the typical clinical
findings of advanced
OA of the DIP joints,
including large firm
swellings (Heberden’s
nodes), some of which
are tender and red due
to associated
inflammation of the
periarticular tissues as
well as the joint.
Knee joint effusion
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.
Pseudolaxity due to
cartilage loss. The
joint is not loaded in
the first photograph
Unstable distal
interphalangeal
joints in OA. The
examiner is able to
push the joint from
side to side due to
gross instability, a
common finding in
late interphalangeal
joint OA.
Radiographic Classification
Stage 1 Bony spur only
Stage 2 Narrowing of jt.
Space,less than half of
the normal jt. space
Stage 3 Narrowing of jt.
Space,more than half
of the normal jt. space
Stage 4 Obliteration of jt. space
Stage 5 Subluxation or
sec.lateral arthrosis
Distribution of OA of the
hip joint. OA can
maximally affect the
superior pole, inferior
pole, posterior part or
other segments of the
hip joint. Superior pole
involvement, with a
tendency for the head
of the femur to sublux
superolaterally, is the
commonest pattern.
Involvement of the
whole joint (concentric
OA) is relatively
uncommon.
Special Investigations
•Blood tests: Normal
•Radiological features:
–Cartilage loss
–Subchondral sclerosis
–Cysts
–Osteophytes
Management
Treatment Principles
•Education
•Physiotherapy
–Exercise program
–Pain relief modalities
•Aids and appliances
•Medical Treatment
•Surgical Treatment
Education
•Nonsystemic nature of disease
•Prevent overloading of joint. Obesity!!
•Appropriate use of treatment modalities
–Importance of exercise program
–Aids, apliances, braces
–Medial treatments
–Surgical treatments
Exercise
•Will not ‘wear the joint out’
•Important for cartilage nutrition
•Some evidence that lack of exercise leads
to progression of OA
Exercise
•Encourage full range low impact
movements eg swimming, cycling
•Avoid
–Prolonged loading
–Activities that cause pain
–Contact sports
–High impact sports eg running
Quadriceps exercises
for knee OA.
Quadriceps exercises
are of proven value for
pain relief and
improving function, and
everyone with knee OA
should be taught the
correct techniques and
encouraged to make
these exercises a
lifetime habit. There is a
weight on the ankle.
Use of transcutaneous
nerve stimulation
(TENS) as an adjunct to
other therapy for pain
relief at the knee joint.
The use of
acupuncture, TENS and
other local techniques
to aid pain relief in
difficult cases of OA is
often worthwhile.
Aids and appliances
•Braces / splints
•Special shoes/insoles
•Mobility aids
•Aids: dressing, reaching, tap openers,
kitchen aids
•Taping of patella in patello femoral OA
Use of a cane, stick or other walking aid. This patient,
who has hip OA, has found that she can reduce the
pain in her damaged left hip by leaning on the stick in
the right hand as she walks. The reduction in loading
can be huge, and the effect on symptoms and
confidence with walking very beneficial.
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.
A patient with OA of the
carpometacarpal joint of
the left thumb
undergoing
arthrocentesis for
injection of a depot
corticosteroid
preparation. The
operator is distracting
the patient’s thumb to
open up the joint space.
Joint replacement surgery
•Indications: pain affecting work, sleep,
walking and leisure activities
•Complications
–sepsis
–loosening
–lifespan of materials (mechanical failure)