Osteoarthritis is a degenerative joint disease characterized by breakdown of cartilage. It most commonly affects weight-bearing joints like the knee, hip, and hand. Risk factors include age, obesity, previous injury, and genetics. Symptoms include pain, stiffness, swelling, and decreased range of motion. Diagnosis is based on x-rays showing joint space narrowing, osteophytes, and bone changes. Treatment focuses on reducing pain and inflammation with medications and physical therapy. For advanced disease, options include joint injections, bracing, and surgery like arthroscopy, joint replacement, or fusion.

1. Osteoarthritis
Moderator: Assoc Prof Dr Suresh Uprety
Presenter: Dr Ajay shah
MS orthopedics
1st year Resident

2. Content
• Anatomy
• Introduction
• Aetiology and risk factors
• Pathogenesis
• Pathology
• Symptoms and Signs
• Investigations
• Management

3. ANATOMY
 Usually a condition of synovial joints
 Components
 Articular cartilage
 Synovial membrane
• Synoviocytes
• Produce lubricants, hyaluronic acid,
cytokines and growth factors

4. Fibrous capsule
• Lined by synovial membrane
• Continuous with the periosteum
• Provide stability throughout the ROM of joints
Synovial Fluid
• Viscous slippery fluid rich in albumin and hyaluronic acid
Intra articular discs of fibrocartilage
• Hip joint- labrum-deepens the articulation
• Knee joint-mensci- improve congruency
• Protect from both compressive and shear forces

5. Introduction
• Osteoarthritis, non-inflammatory degenerative
joint disorder characterized by degeneration of
cartilage that results in structural and
functional failure of synovial joints.
• Most common type of joint disorder
• Intrinsic disease of cartilage in which
chondrocytes respond to biochemical and
mechanical stresses resulting in breakdown of
matrix.

6. Joints involvement
Knee joint
• MC joint to involve
• MC sites: anteromedial compartment- Tibiofemoral joint
lateral facet- Patellofemoral joint
 Hip joint
• Superolateral aspect of joint
Hand
• Distal interphalangeal joints, PIP joints
 Feet -1ST MTP
Spine
• Facet joints of cervical and lumbosacral spine

7. Prevalence
• Internationally, OA is the most common articular
disease
• On the basis of the radiographic criteria for
osteoarthritis more than 50% of adults older
than 65 years are affected by the disease
• In individual older than 55 years, the prevalence
of OA is higher among women than among men
• Leading cause of chronic disability in those older
than 70 years, costing US greater than $100
billion annually

8. Types of OA
1 Primary/Idiopathic
• When there is no obvious predisposing factors
• Common form of OA
• Its mainly due to wear and tear changes occurring in old ages mainly in weight
bearing joints
2 Secondary OA
• When degenerative joint changes occur in response to recognizable local or
systemic factors

9. Causes of secondary OA
• Developmental
Developmental dysplasia of hip
Legg-calves perthe’s disease
Epiphyseal dysplasia
• Mechanical
Hypermobility syndromes
Leg length discrepancy
Mal-alignment
• Trauma (acute or chronic)
Sports injury
Iatrogenic
Occupational
Accidental
• Metabolic
Hemochromatosis
Gout
Pseudogout
Calcium crystal deposition

10. • Endocrine
Acromegaly
Hyperparathyroidism
Hypothyroidism
• Inflammatory
Any systemic rheumatic disease
Septic arthritis
• Miscellaneous
Hemophilia
Osteonecrosis
Paget’s disease
Neuropathic arthropathy

11. OA Variants
Atrophic destructive OA including
rapidly progressive hip OA and
Milwaukee shoulder
 Rapid period with joint damage progresses
to extensive bone loss
Whole head of femur and humerus may
disappear

12. • Hypertrophic OA
Particularly common at hip and knee joints
Characterized by massive osteophyte formation
It may be associated with
 calcium pyrophosphate dehydrate crystal deposition
 diffuse idiopathic skeletal hyperstosis (DISH)

13. • Erosive inflammatory OA of
interphalangeal joints
Involves terminal interphalangeal joints of hands
Associated with signs of inflammation and
development of joint erosions.
Radiograph shows erosion of joint
( sea gull appearance)

14. • Kashin Beck disease
Rare polyarticular form of OA
Joint pain, polyarticular swelling and deformity from childhood
Adults have short stature
Radiographs reveal distorted epiphyses and tubular long bones

15. Risk factors
• Systemic predisposition
Genetics
Age
Gender
Diet and obesity
• Local biomechanical factors
Abnormal joint shape and size
Previous injury
Neuromuscular problems
Obesity
Loading/occupational factors
• Bone mineral density

16. Pathogenesis

18. Pathological Changes
• Focal areas of loss of articular cartilage
• Bone growth at the joint margins
• Sclerosis of underlying bone
• Cyst formation in underlying bone
• Loss of bone
• Varying degrees of synovial inflammation
• Fibrosis and thickening of joint capsule

19. Gross Appearance

20. Microscopic Features

21. Symptoms and signs at different joint sites
Knee Joint
• MC site medial patellofemoral joint
• Pain: globally over knee and proximal tibia
• In isolated patellofemoral OA, pain is anteriorly over knee and is often worst
during ascending and descending stairs
• Symptoms of instability
• Swelling and stiffness

22. • Antalgic gait
• Weakness/Wasting of quadriceps muscles
• Varus deformity
• Restricted extension and flexion
• Audible crepitus

23. Hip joint
• Pain usually felt in groin, radiates down anterolateral aspect of thigh
• Pain is worse on exercise and walking distance is reduced
• Morning and rest stiffness
• Antalgic gait
• Weakness of hip abductors
• Restricted internal rotation with flexion

24. Hand joint
• MC affected joints are DIPs and thumb base
( radiocarpal and radiotrapezoid joints)
• Strongly associated with knee OA and genetic
predisposition, suggesting as feature of
generalized OA
• More common in women and often start
around the time of menopause( sometimes
called as menopausal OA)

25. • Bouchard's nodes are a classic sign of OA of the
hand.
• Named after the French pathologist Charles-
Joseph Bouchard, who studied arthritis patients
in the 19th century.
• Bouchard nodes are bony enlargements of the
proximal interphalangeal (PIP) joints.
• Heberden’s nodes are similar bony swellings
that develop at the distal interphalangeal (DIP)
joint. Bouchard's nodes are less common than
Heberden's nodes.

26. FOOT
• Hallux rigidus: 1st MTP joint OA
• Pain and tenderness over
dorsum of joint
• Limited dorsiflexon secondary to
large osteophytes
• Stiffness of 1st MTP joint and
compensatory hyperextension of
IP joint
• Grind test

27. Investigations
• Plain Radiographhs
Four cardinal signs
Joint space narrowing
Osteophytes formation
Subchondral bone cysts
Sclerosis of underlying bone

28. Kellgren and lawrence

29. • Grade 0 : Normal
• Grade 1: Minimal osteophyte, doubtful significance
• Grade 2: Definite osteophyte, no loss of joint space
• Grade 3: Some diminution of joint space
• Grade 4: Advanced joint space loss and sclerosis of bone

30. X-rays

33. Blood Tests
• Raised CRP ( in some cases)
• Normal ESR
• Rheumatoid factor and Antinuclear antibodies are negative
MRI
• Early cartilage and subchondral bone changes, although it is not routinely used due to
cost
Arthroscopy
• Reveal early fissuring and surface erosions
Synovial Fluid Analysis
• Viscous with low turbidity
• Can be used to exclude gout, CPPD or septic arthritis if diagnosis is in doubt

34. Outerbridge classification
Grade 0 : Normal cartilage
Grade I : Softening and swelling of cartilage
Grade II: Fragmentation and fissuring of the cartilage in an area less
than ½ inch in diameter
Grade III: Fragmentation and fissuring of the cartilage in an area more than ½ inch in
diameter
Grade IV: Exposure of underlying bone

35. Modified Outerbridge Classification
Grade 0 : Intact cartilage
Grade I : Chondral softening or blistering with intact surface
Grade II : Superficial ulceration,fibrillation, or fissuring less than 50% of depth of
cartilage
Grade III : Deep ulceration, fibrillation, fissuring, or chondral flap more than 50% of
cartilage without exposed bone
Grade IV : Full thickness wear with exposed subchondral bone

36. Secondary OA: Special Tests
• Ochronosis: Presence of homogenistic acid in urine which turns black in
exposure to air
• Wilson’s disease: Reduced serum ceruloplasmin, increased urinary excretion of
copper
• Hemochromatosis: Raised serum iron and ferritin
• Gout: Raised serum urate
• Hypothyroidism: Low T3 ,T4 and raised TSH
• Hyperparathyroidism: Raised PTH,calcium and low phosphate
• Tabes dorsalis: Positive VDRL
• DM: Abnormal glucose tolerance test

37. Management
Basic principles of symptomatic management of OA
Pyramid of treatment for symptomatic OA ( From Dieppe and Lohmander,2005)

38. Based on the UK National Institute for Health and Care Excellence
(NICE) 2014 guideline.
Step 1: Take a holistic approach and encourage self-management
• Assessing the impact of OA on the individual’s quality of life, function, mood ,
relationships and activities
• Self-management strategies include
Alterations of diet (lose weight)
Alteration in activities
Changing footwear

39. Step 2: Introduce the “core treatments” appropriate for most people
with OA
• These includes
Provision of information about the condition and its management
To increase their exercise level
Footwear advice
To do specific exercises to strengthen muscles around affected joints

40. Step 3: Introduce specific non-surgical interventions
These may be pharmacological or non-pharmacological
Non-pharmacological
• Supervised courses of physical therapy
• Use of aids and devices
Braces and splints
Walking aids such as sticks or crutches
Electrotherapy such as TENS

41. PHYSIOTHERAPY
• Hamstring stretching
exercises

42. • Quadriceps strengthening
exercises

43. • Calf muscle
strengthening

44. Knee Brace
Advantages
• Enhanced stability
• Reduced swelling
• Reduced pressure
• Increased confidence

45. Knee adduction moment (KAM) during gait is known to indicate disease severity and prognosis of
varus knee Thus, to reduce KAM is a key strategy in treatment of knee OA.
KAM is primarily calculated as the product of the resultant ground reaction force (GRF) in the frontal
plane and the perpendicular distance from the GRF to the knee joint center (frontal plane lever arm).

46. Pharmacological
 NSAIDs
• Non-selective NSAID
• COX-2 selective
 Tramadol, opioids
Intra-articular injection
• Local anaesthetic
• Corticosteroids
Supplements
• Glucosamine
• Chondroitin sulfate etc

47. Step 4: Consider surgical options
Arthroscopic procedures
• Joint debridement
• Removal of mechanical obstructions
• Joint lavage
• Drilling of sclerotic lesions
• Abrasion chondroplasty
• Autologous chondrocyte transplantation

48. Proximal Tibial Osteotomy
• Indications for proximal tibial osteotomy are
Pain and disability resulting from osteoarthritis that significantly interfere with
high-demand employment or recreation
Evidence on weight-bearing radiographs of degenerative arthritis that is confined
to one compartment with a corresponding varus or valgus deformity

49. Contraindications to a proximal tibial osteotomy
• Narrowing of lateral compartment cartilage space
• Lateral tibial subluxation of more than 1 cm
• Medial compartment tibial bone loss of more than 2 or 3 mm
• Flexion contracture of more than 15 degrees
• Knee flexion of less than 90 degrees
• More than 20 degrees of correction needed
• Inflammatory arthritis
• Significant peripheral vascular disease.

51. LATERAL CLOSING WEDGE OSTEOTOMY
Advantages
• It is made near the deformity, that is, the knee joint
• Made through cancellous bone, which heals rapidly
• Permits the fragments to be held firmly in position by staples or a rigid fixation
device, such as a plate-and-screw construct
• Permits exploration of the knee through the same incision.

52. Disadvantages
• Fibular osteotomy or release of
proximal TF joint
• Peroneal nerve injury
• Shortening of leg
• Muscle detachment
• Difficult to correct in 2 plans

53. MEDIAL OPENING WEDGE OSTEOTOMY

55. Proximal Fibular Osteotomy
Proximal fibular osteotomy is an alternative treatment to high tibial osteotomy.
It is a surgical procedure for medial compartment knee osteoarthritis

57. Total Knee Arthroplasty After PTO
• At 10 to 15 years after proximal tibial osteotomy, 40% of patients require
conversion to total knee arthroplasty
• Studies have shown that the outcome of total knee arthroplasty in patients with
previous high tibial osteotomies was not significantly different from outcomes
after primary total knee arthroplasty
• Although total knee arthroplasty after high tibial osteotomy is technically
demanding and is a longer operative procedure.
• Unicompartmental arthroplasty has poor results after high tibial osteotomy (28%
failure at 5 years).

58. • Indications of TKA
Relieve pain caused by severe
arthritis, with or without deformity
Failed high tibial osteotomy
Kellgren and Lawrence grade IV

60. Arthrodesis Of Knee
• Most frequent indication for knee arthrodesis is failed total knee arthrodesis,
secondary to infection
• Salvage procedure after failed TKA, expected to have some inferior results
compared with primary knee arthrodesis including
Lower fusion rates
Higher infection rates
Shortening of leg

61. Techniques
• Compression arthrodesis with external fixation
• Arthrodesis with intramedullary rod fixation
• Arthrodesis with plate fixation

65. Hip Joint : Total Hip Arthroplasty
Indication
• Alleviation of incapacitating arthritic pain in patients older than age 65 years whose pain
could not be relieved sufficiently by non surgical means and for whom the only surgical
alternative was resection of hip joint or arthrodesis

66. Ankle joint
Surgical Treatment
• Arthroscopic debridement
• Arthrodesis
• Total ankle replacement

67. Foot
Arthrodesis
• Subtalar arthrodesis
• Calcaneocuboid arthrodesis
• Talonavicular arthrodesis
• Double arthrodesis
• Triple arthrodesis

68. First MTP Joint OA
Surgical Treatment
• Cheilectomy
• Osteotomy -Dorsiflexion phalangeal
osteotomy
-Metatarsal osteotomy
• Arthrodesis
• Arthroplasty -Hemiarthroplasty
-Total joint arthroplasty

69. References
• Apley’s system of orthopedics and fractures, 9th edition
• Robbins and cotran pathologic basis of disease,9th edition
• Campbell’s operative orthopedics, 13th edition