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OSTEOARTHRITIS
DR MANOJ K SINGH
PGT MD PMR
PMCH PATNA
Osteoarthritis
• Osteoarthritis is a non-inflammatory,
degenerative condition of joints Characterized
by degeneration of articular cartilage and
formation of new bone i.e. osteophytes.
• Common in weight-bearing joints such as hip
and knee.
• Also seen in spine and hands.
• Both male and females are affected.
• But more common in older women i.e. above
50 yrs,particularly in 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
Ageing process in joint cartilage
Defective lubricating mechanism
Incompletely treated congenital
dislocation of hip
Classification of OA
OA
Primary OA Secondary OA
Primary OA
• More common than secondary OA
• Cause –Unknown
• Common-in elders where there is no previous
pathology.
• Its mainly due to wear and tear changes
occuring in old ages mainly in weight bearing
joints.
Secondary OA
• Due to a predisposing cause such as:
1.Injury to the joint
2.Previous infection
3.RA
4.CDH
5.Deformity
6.Obesity
7.hyperthyriodism
Types of OA
• Nodal Generalised OA
• • Crystal Associated OA
• • OA 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
Pathology
• OA is a degenerative condition primarily
affecting the articular cartilage.
1.articular cartilage
2.Bone
3.Synovial membrane
4.capsule
5.Ligament
6.muscle
Articular Cartilage
• Cartilage is the 1st structure to be affected.
• Erosion occurs,often central & frequently in wt.
bearing areas.
• Fibrillation,which causes softening,splitting and
fragmentation of the cartilage,occur in both wt.
bearing & non-wt. bearing areas.
• Collagen fibres split and there is disorganisation of
the proteoglycon collagen relationship such as H2O is
attracted into cartilage, which causes futher
softening and flaking.these flakes of cartilage break
off and may be impacted b/w the jt.surfaces causing
locking and inflammation.
Bone(Eburnation)
• Bone surface become hard & polished as
there is loss of protection from the cartilage.
• Cystic cavities form in the subchondral bone
because eburnated bone is brittle and
microfractures occur.
• Venous congestion in the subchondral bone.
• Osteophytes form at the margin of the
articular surface,which may get projected into
the jt. Or into capsule & ligament,bone of the
wt.-bearing jt.
• There is alteration in the shape of the femoral
head which becomes flat and mushroom
shaped.
• Tibial condyles become flatened.
Synovial Membrane
• Synovial membrane undergo hypertrophy and
become oedematous (which can lead to ‘cold’
effusions).
• Reduction of synovial fluid secretion results in loss of
nutrition and lubricating action of articular cartilage.
Capsule
It undergoes fibrous degeneration and there are low-
grade chronic inflammatory changes
Ligament
• Undergoes fibrous degernation
• There is low grade chronic inflammatory
changes and acc.to the aspect joint become
contracted or elongated.
Muscles
Undergoes atrophy,as pt. is not able to use the
jt. Because of pain which further limits movts.
and function.
Clinical features of OA
• Pain
• Stiffness
• Muscle spasm
• Restricted movement
• Deformity
• Muscle weakness or wasting
• Joint enlargement and instability
• Crepitus
• Joint Effusion
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.
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.
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
Special Investigations
• Blood tests: Normal
• Radiological features:
– Cartilage loss
– Subchondral sclerosis
– Cysts
– Osteophytes
Treatment Principles
• Education
• Physiotherapy
– Exercise program
– Pain relief modalities
• Aids and appliances
• Medical Treatment
• Surgical Treatment
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.
Medical Treatment
• Simple analgesics: paracetamol, low dose
ibuprofen
• NSAID’s/Coxibs PRN regular
• Intra-articular corticosteroids
• Topical treatment eg NSAID creams, capsaicin
• ‘Chondroprotective agents’
Manage and Treat Osteoarthritis Naturally
Manage and Treat Osteoarthritis Naturally
Manage and Treat Osteoarthritis Naturally

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Manage and Treat Osteoarthritis Naturally

  • 1. OSTEOARTHRITIS DR MANOJ K SINGH PGT MD PMR PMCH PATNA
  • 2. Osteoarthritis • Osteoarthritis is a non-inflammatory, degenerative condition of joints Characterized by degeneration of articular cartilage and formation of new bone i.e. osteophytes.
  • 3. • Common in weight-bearing joints such as hip and knee. • Also seen in spine and hands. • Both male and females are affected. • But more common in older women i.e. above 50 yrs,particularly in postmenopausal age.
  • 4. 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
  • 5. Ageing process in joint cartilage Defective lubricating mechanism Incompletely treated congenital dislocation of hip
  • 6.
  • 7.
  • 9. Primary OA • More common than secondary OA • Cause –Unknown • Common-in elders where there is no previous pathology. • Its mainly due to wear and tear changes occuring in old ages mainly in weight bearing joints.
  • 10. Secondary OA • Due to a predisposing cause such as: 1.Injury to the joint 2.Previous infection 3.RA 4.CDH 5.Deformity 6.Obesity 7.hyperthyriodism
  • 11. Types of OA • Nodal Generalised OA • • Crystal Associated OA • • OA of Premature Onset
  • 12. Nodal Generalised OA • • Heberden’s nodes • • Bouchard’s nodes • • CMC of thumb • • Hallux • valgus/rigidus • • Knees & hips • • Apophyseal joints
  • 13. Crystal Associated OA • Calcium pyrophosphate • dihydrate occurs • mainly in elderly • women, and principally • affects the knee
  • 14. Pathology • OA is a degenerative condition primarily affecting the articular cartilage. 1.articular cartilage 2.Bone 3.Synovial membrane 4.capsule 5.Ligament 6.muscle
  • 15. Articular Cartilage • Cartilage is the 1st structure to be affected. • Erosion occurs,often central & frequently in wt. bearing areas. • Fibrillation,which causes softening,splitting and fragmentation of the cartilage,occur in both wt. bearing & non-wt. bearing areas. • Collagen fibres split and there is disorganisation of the proteoglycon collagen relationship such as H2O is attracted into cartilage, which causes futher softening and flaking.these flakes of cartilage break off and may be impacted b/w the jt.surfaces causing locking and inflammation.
  • 16. Bone(Eburnation) • Bone surface become hard & polished as there is loss of protection from the cartilage. • Cystic cavities form in the subchondral bone because eburnated bone is brittle and microfractures occur. • Venous congestion in the subchondral bone.
  • 17. • Osteophytes form at the margin of the articular surface,which may get projected into the jt. Or into capsule & ligament,bone of the wt.-bearing jt. • There is alteration in the shape of the femoral head which becomes flat and mushroom shaped. • Tibial condyles become flatened.
  • 18. Synovial Membrane • Synovial membrane undergo hypertrophy and become oedematous (which can lead to ‘cold’ effusions). • Reduction of synovial fluid secretion results in loss of nutrition and lubricating action of articular cartilage. Capsule It undergoes fibrous degeneration and there are low- grade chronic inflammatory changes
  • 19. Ligament • Undergoes fibrous degernation • There is low grade chronic inflammatory changes and acc.to the aspect joint become contracted or elongated. Muscles Undergoes atrophy,as pt. is not able to use the jt. Because of pain which further limits movts. and function.
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  • 22. Clinical features of OA • Pain • Stiffness • Muscle spasm • Restricted movement • Deformity • Muscle weakness or wasting • Joint enlargement and instability • Crepitus • Joint Effusion
  • 23.
  • 24. Clinical features 3 • Deformities – Soft tissue swelling: • mild synovitis • small effusions – Osteophytes – Joint laxity – Asymmetrical joint destruction leading to angulation
  • 25. 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.
  • 26. 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.
  • 27. 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
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  • 30. Special Investigations • Blood tests: Normal • Radiological features: – Cartilage loss – Subchondral sclerosis – Cysts – Osteophytes
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  • 33. Treatment Principles • Education • Physiotherapy – Exercise program – Pain relief modalities • Aids and appliances • Medical Treatment • Surgical Treatment
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  • 35. Exercise • Encourage full range low impact movements eg swimming, cycling • Avoid – Prolonged loading – Activities that cause pain – Contact sports – High impact sports eg running
  • 36. 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.
  • 37. 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.
  • 38. Aids and appliances • Braces / splints • Special shoes/insoles • Mobility aids • Aids: dressing, reaching, tap openers, kitchen aids • Taping of patella in patello femoral OA
  • 39. 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.
  • 40. 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.
  • 41. Medical Treatment • Simple analgesics: paracetamol, low dose ibuprofen • NSAID’s/Coxibs PRN regular • Intra-articular corticosteroids • Topical treatment eg NSAID creams, capsaicin • ‘Chondroprotective agents’