Osteoarthritis is a common joint disease involving the breakdown of cartilage. It often affects weight-bearing joints like the knees and hips and risk factors include age, obesity, and joint injuries. Symptoms include pain, stiffness, and limited movement in the joints. Treatment focuses on pain management through medications, physical therapy, weight loss, and sometimes surgery like joint replacement for severe cases.

1. Osteoarthritis
Introduction
Background
Osteoarthritis )OA( is the most common articular
.disease worldwide
It also called degenerative joint disease, represents
failure of the diarthrodial )movable, synovial-lined(
.joint

2. Idiopathic )primary( OA:
The most common form of the disease, no •
.predisposing factor is apparent
: Secondary OA
pathologically indistinguishable from
idiopathic OA but is attributable to an
underlying cause

3. Pathophysiology
• It involves the entire joint organ, including the subchondral bone
and synovium.
• Inflammation occurs as cytokines and metalloproteinases are
released into the joint.
• Osteoarthritis predominantly involves the weight-bearing joints,
including the knees, hips, cervical and lumbosacral spine, and feet.
Other commonly affected joints include the distal interphalangeal
)DIP( and proximal interphalangeal )PIP( joints of the hands.
• Cartilage is grossly affected.
• Focal ulcerations eventually lead to cartilage loss and eburnation.
Subchondral bone formation also occurs, with development of bony
osteophytes.

6. The etiopathogenesis •
Stage 1:
Proteolytic breakdown of the cartilage matrix. Chondrocyte metabolism is
,
affected leading to an increased production of enzymes, which includes
metalloproteinases )eg, collagenase, stromelysin( that destroy the cartilage
.matrix
:Stage 2
fibrillation and erosion of the cartilage surface, with a subsequent release of
.proteoglycan and collagen fragments into the synovial fluid
:Stage 3
The breakdown products of cartilage induce a chronic inflammatory response in the
synovium. Synovial macrophage production of cytokines, interleukin 1 )IL-1(,
.tumor necrosis factor-alpha, and metalloproteinases, occurs
. Tissue destruction
these events alter the joint architecture, and compensatory bone overgrowth occurs

7. Frequency
International
Osteoarthritis is the most common articular
disease. Estimates vary among different
.populations

8. Mortality/Morbidity
The disease progression of osteoarthritis is
characteristically slow, occurring over
.several years or decades
. Pain
potential weight gain

9. Race
The prevalence of osteoarthritis differs
among different ethnic groups.Whether
these differences are genetic or due to
differences in joint usage related to life-
.style or occupation is unknown

10. Heredity
No mutation has been identified in the
common primary )i.e., idiopathic( form of
OA. Most of the mutations identified are
associated with relatively rare syndromes
afeature of which can be classified as
secondary OA

11. Sex
.The likelihood increases with age
The disease is equally common among men
.and women aged 45-55 years
After age 55 years, the disease becomes
.more common in women
DIP and PIP joint involvement that results in
Heberden and Bouchard nodes is more
common in women

12. Age
• occurs in 30% of affected individuals
aged 45-65 years and in more than 80%
by their eighth decade of life, although
most are asymptomatic.

13. Clinical
History
Pain
Initially, symptomatic patients incur pain during activity,
which can be relieved by rest and may respond to
.simple analgesics
Morning joint stiffness usually lasts for less than 30
.minutes
.Stiffness during rest )gelling( may develop
Joints may become unstable as the osteoarthritis
progresses; therefore, the pain may become more
prominent )even during rest( and may not respond to
.medications

14. Physical
.Signs limited to the affected joints
.Malalignment with a bony enlargement
Most cases of osteoarthritis do not involve
erythema or warmth over the affected
.joint)s(;an effusion may be present
Limitation of joint motion or muscle atrophy
.around a more severely affected joint

20. : Sources of pain
1. Joint effusion and stretching of the joint capsule
2. Increased vascular pressure in subchondral bone
3. Torn menisci
4. Inflammation of periarticular bursae
5. Periarticular muscle spasm
6. Psychological factors
7. Crepitus )a rough or crunchy sensation( may be
palpated during motion of an involved joint.

21. Causes
• Risk factors :
– Increasing age
– Obesity
– Female sex
– Trauma
– Infection
– Repetitive occupational trauma
– Genetic factors
– History of inflammatory arthritis
– Neuromuscular disorder
– Metabolic disorder

22. Differential Diagnoses
• other arthritides )eg, rheumatoid arthritis(.
• spondyloarthropathy .
• Reactive arthritis .

23. Workup
• Laboratory Studies
• No specific laboratory abnormalities are
associated with osteoarthritis )OA(.
– Levels of acute-phase reactants and
erythrocyte sedimentation rate are within the
reference range.
– Synovial fluid analysis usually indicates a WBC
count below 2000/µL with a mononuclear
predominance.

24. Imaging Studies
• Radiography .
– The presence of osteophytes )ie, spurs at the
joint margins( is the most characteristic
findings.
– Other findings in osteoarthritis include
asymmetric joint-space narrowing,
subchondral sclerosis, and subchondral cyst
formation.

25. Procedures
• Arthrocentesis of the affected joint can
help exclude inflammatory arthritis,
infection, and/or crystal arthropathy.

26. Treatment
• Medical Care
• Nonpharmacologic interventions are the cornerstones of
osteoarthritis )OA( therapy and include:
• patient education
• temperature modalities
• weight loss
• exercise
• physical therapy
• occupational therapy
• joint unloading in certain joints )eg, knee, hip(.

27. Physical therapy
– Aerobic and muscle-strengthening exercises.
– Hydrotherapy.
– Heat and capsaicin cream
– Ice.

28. Pharmacologic therapy
The goals :
– pain alleviation
– improvement of functional status.
no practical medication-based disease or
structure-modifying intervention has been
proven.

29. : Treatment
– Acetaminophen for mild or moderate pain without apparent
inflammation.
– Nonsteroidal anti-inflammatory drug )NSAIDs(.
– Tramadol.
– Muscle relaxants .
– Contemplate intra-articular injections of glucocorticoids
– Systemic glucocorticoids have no role
– Intra-articular injections of hyaluronic acid )HA( are approved
as symptomatic therapy of osteoarthritis in the knee
– Judicious use of narcotics )eg, acetaminophen with codeine( is
reserved for patients with severe osteoarthritis.

30. Surgical Care
• Joint lavage:
• Arthroscopy: for repairing meniscal tears, removing fragments of
torn menisci that are producing symptoms(.
• Osteotomy
– malaligned hip or knee joint.
– younger patients .
– Osteotomy can lessen the pain, although it can lead to more
challenging surgery later if the patient requires arthroplasty.
• Arthroplasty
– if all other modalities are ineffective and osteotomy is not viable or if a
patient cannot perform his or her daily activities despite maximal
therapy.

31. Follow-up
• Overweight patients who have early signs
of osteoarthritis )OA( or who are at high
risk should be encouraged to lose weight.
• Recommend quadriceps-strengthening
exercises in patients with osteoarthritis of
the knees.

32. Prognosis
• The prognosis of osteoarthritis depends on
joints involved and severity

33. Patient Education
• Educate the patient on the natural history
of and management options for
osteoarthritis.
• Explain the differences between
osteoarthritis and other more rapidly
progressive arthritides such as rheumatoid
arthritis.

34. ?Osteoarthritis: What Is It
Also called "wear and tear" arthritis

35. Osteoarthritis: Symptoms
slowly. pain or soreness ,stiff or creaky. In •
the hands: bony enlargements in the
fingers, which may or may not cause pain

36. Osteoarthritis: Where Does It
? Hurt

37. Osteoarthritis: What Causes
?It

38. Risk Factors You Can't Control

39. Risk Factors You Can Control
• sports ,jobs , Obesity .

40. Impact on Daily Life
.

41. Diagnosing Osteoarthritis
• symptoms and signs
• X-rays &blood tests

42. Long-Term Complications
• Deformities.
• Bow-legged appearance
• Irritate nerves

43. Treatment: Physical Therapy
• No treatment
• Ways to improve joint function)physical ,
hot or cold therapies (

44. Supportive Devices
• Finger splints or knee braces, canes,
crutches, or walkers .
• Back brace or neck
collar.

45. Medication for OA
• over-the-counter pain and
anTinflammatory medication, Pain-
relieving creams . injection of steroids or
hyaluronans .

46. Supplements
• no benefits of glucosamine and
chondroitin.

47. Osteoarthritis and Weight
• Losing weight not only cuts down on pain,
but may also reduce long-term joint
damage.

48. Osteoarthritis and Exercise
• low-impact activities such as swimming,
walking, or bicycling can improve mobility
and increase strength.

49. ?Is Surgery for You
• If : interferes , and the symptoms don't
improve = joint replacement surgery is an
option.

50. Preventing Osteoarthritis
.keep your weight in check •
Preventing injuries.