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Osteoarthritis
SMS3053
Dr . Mohanad R. Alwan
Osteoarthritis (OA)
 OA is a progressive irreversible disease characterized by
the degradation of articular cartilage.
 Cartilage becomes pitted and frayed at the surface and
becomes increasingly inelastic.
 As OA progresses, loss of cartilage increases and may wear
away completely leaving the bone ends exposed and able to
rub together.
 Pieces of cartilage and/or bone may break off into the
synovial fluid.
 Most common & most frequent of the disabling joint
disorders
 Classified as primary (idiopathic) or secondary, resulting
from previous joint injury or inflammatory disease
Classification of OAClassification of OA
• Primary OA
▫ Most common form
▫ Is rare before age 40 years,
prevalence increases
with age
▫ Knee joint most often affected
▫ Genetic predisposition,
particularly for hand arthritis
• Secondary OA
▫ Preceded by a predisposing
disorder such as joint trauma
▫ Occurs in any joint
Solomon L. 1997
 Primary OA has no single specific cause but is generally
associated with aging, normal mechanical stresses and
genetic factors.
 It usually occurs in weight-bearing joints that have undergone
abnormal stresses (e.g. from obesity or overuse), and is
frequently linked with increased age.
 Common sites of involvement include the hands, hips, knees
and feet. Primary OA is the most common form of OA.
 In contrast, secondary OA may occur in any joint at any age
and has an identifiable underlying cause (e.g. inflammatory
or metabolic disease).
 Secondary OA develops following any process that damages
the joint such as fractures, dislocations, sports injuries, joint
surgery or repetitive trauma (occupational trauma).
Risk Factors of OA
 Obesity,
 ↑ Age,
 Joint injury,
 stress on the joints from certain jobs and
playing sports
 Genetics (Legg-Calve-Perthes disease)
Risk factors for primary OARisk factors for primary OA
OA
Obesity
Occupation
Old age
Family history
Genetics
Trauma
Joint
dysplasia
Bone injury
Gender
Joint injury
Solomon L. 1997
Osteoarthritis
 Prevalence increases exponentially beyond
the age of 50 with about 80-90% of both
sexes having osteoarthritis by age 65.
 Age-related changes include: alterations in
proteoglycans & collagen, which decrease
tensile strength & shorten fatigue life but it is
not simply a disease of wear and tear
Gross appearance
Of OAK
Osteoarthritis
 Often leads to complete degeneration of
articular cartilage
Osteoarthritis (OA)
 Begins in the 3rd
decade of life and peaks
between the 5th
and 6th
 Direct correlation with age and the
degenerative process
Pathogenesis
• OA is a joint disease that mostly affects
cartilage.
• Cartilage is tissue that covers the bones in a
joint.
• Healthy cartilage allows bones to glide over
each other. It also helps absorb shock of
movement.
• In osteoarthritis, the top layer of cartilage breaks
down and wears away.
Pathophysiology
 This allows bones under the cartilage to rub
together.
 The rubbing causes pain, swelling, and loss of
motion of the joint. Over time, the joint lose its
normal shape.
 Also, bone spurs may grow on the edges of the
joint.
Bits of bone or cartilage can break off and float
inside the joint space, which causes more pain and
damage.
People with osteoarthritis often have joint pain and
reduced motion.
Unlike some other forms of arthritis, osteoarthritis
affects only joints and not internal organs.
Rheumatoid arthritis - the second most common
form of arthritis - affects other parts of the body
besides the joints.
Osteoarthritis
 Chondrocytes play a primary role and
constitute the cellular basis of the disease
 They produce IL-1 & TNF-alpha, which are
known to stimulate the production of
catabolic metalloproteinases and inhibit the
synthesis of both type 2 collagen and
proteoglycans; other mediators also have a
role in matrix degradation
QuickTime™ and a
Photo CD Decompressor
are needed to use this picture
 Natural history of OA: Progressive cartilage
loss, subchondral thickening, marginal
osteophytes
Modest, patchy
chronic synovitis
Bone ends thicken
Bony outgrowths
(osteophytes) form
Bone fragments may float
in the joint space
Fluid filled cysts may form
in the bone
OA jointNormal joint
Cartilage:
Pitted and frayed surface
Loss of elasticity
Cartilage may wear away
completely
Thickening
of capsule
Characteristics of OACharacteristics of OA
Dieppe P. 1998
Clinical Manifestations OA
 Stiffness in a joint after getting out of bed or
sitting for a long time
 Last <30 min. and ↓ with movement
 Swelling or tenderness in one or more joints
 A crunching feeling or the sound of bone
rubbing on bone.
OA: Symptoms and Signs
• Pain is related to
use
• Pain gets worse
during the day
• Minimal morning
stiffness (<20 min)
and after inactivity
(gelling)
• Range of motion
decreases
• Joint instability
• Bony enlargement
• Restricted
movement
• Crepitus
• Variable swelling
and/or instability
Osteoarthritis
 Is an insidious disease
 Characteristic symptoms include: deep,
achy pain that worsens with use.
 Impingement on spinal foramina by
osteophytes results in cervical & lumbar
nerve root compression with pain.
 muscle spasms & atrophy & neurologic
deficits
Osteoarthritis
 Typically, only one or a few joints are
involved
 Joints commonly involved are: hips, knees,
lower lumbar & cervical vertebrae, proximal
& distal interphalangeal joints of fingers,
etc.
 Heberden nodes: which common in
women, represent prominent osteophytes
in distal interphalangeal joints
Finger deformities in OAFinger deformities in OA
• Deformities occur at:
• The base of the thumb
(Bouchard’s nodes)
• The middle joint of a finger
(Bouchard’s nodes)
• The finger tip
(Heberden’s nodules)
Heberden’s nodules
in a patient with OA
Sciencephoto.com
Osteoarthritis: Clinical Features
Joint involvement in OAJoint involvement in OA
Common
Knee
Hip
Fingers
Spine
Less common
Elbow
Shoulder
Wrist
Ankle
Knee deformity in OAKnee deformity in OA
Sciencephoto.com
 The various changes in bone structure
associated with OA lead to a number of classical
deformities.
 Muscle weakness and joint instability can result
in a shift in the parts of the joints that bear the
load.
 This can lead to alterations in the joint shape,
as shown above, where the bones of the joint
are no longer correctly aligned.
Assessment and Diagnosis
 Difficult to diagnose
 Physical assessment
 Tender enlarged joints
 Inflammation
 Progressive loss of cartilage appears on xray
 Blood test are not useful
Medical Management Goals
 Osteoarthritis treatment has four main goals:
 Improve joint function
 Keep a healthy body weight
 Control pain
 Achieve a healthy lifestyle
Medical Management of OA
 Conservative treatment
 Education
 Use of heat
 Weight reduction
 Joint rest and avoidance of joint overuse
 Orthotic devices
 Isometric and aerobic exercises
 Massage, yoga,
 Occupational and physical therapy
Medical Management of OA
 Alternative therapy
 Herbal and dietary supplements
 Acupuncture, acupressure
 Copper bracelets or magnets
Pharmacologic Therapy
 Symptom management and pain control
 Medication selection
 Patients needs
 Stage of disease
 Risk of side effects
 Medications and other treatments
Pharmacologic Therapy Cont’
 Initial therapy
 Acetaminophen
 Nonselective NSAID’s
 diclofenac (voltaren) ibuprofen (Advil, Motrin)
 COX-2 inhibitors
 celecoxib (Celebrex) valdecoxib (Bextra)
 Associated with risk CVD
Pharmacologic Therapy Cont’
 Opioids
 Codiene, oxycodone (Percocet)
 Intra-articular corticosteroids
 Topical analgesic
 capsaicin (Capsin, Zostrix)
 Methylsalicylate
Surgical Management
 Osteotomy- alter the distribution of weight
within the joint
 Arthroplasty- disease joint components are
replaced with artificial products
 Tidal irrigation- lavage (provides pain relief
for up to 6 months)
Nursing Management
 Pain management
 Optimal function
 Patient’s understanding of disease
 Lifestyle changes
 Weight loss
 Referrals
 Assistive devices
Case: Carpometacarpal Joint
 Radiograph shows
severe changes
 Most common
location in hand
 May cause
significant loss of
function
Osteoarthritis
 Often leads to complete degeneration of
articular cartilage
Finish
and
any
question???

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Oesteoarthritis

  • 2. Osteoarthritis (OA)  OA is a progressive irreversible disease characterized by the degradation of articular cartilage.  Cartilage becomes pitted and frayed at the surface and becomes increasingly inelastic.  As OA progresses, loss of cartilage increases and may wear away completely leaving the bone ends exposed and able to rub together.  Pieces of cartilage and/or bone may break off into the synovial fluid.  Most common & most frequent of the disabling joint disorders  Classified as primary (idiopathic) or secondary, resulting from previous joint injury or inflammatory disease
  • 3. Classification of OAClassification of OA • Primary OA ▫ Most common form ▫ Is rare before age 40 years, prevalence increases with age ▫ Knee joint most often affected ▫ Genetic predisposition, particularly for hand arthritis • Secondary OA ▫ Preceded by a predisposing disorder such as joint trauma ▫ Occurs in any joint Solomon L. 1997
  • 4.  Primary OA has no single specific cause but is generally associated with aging, normal mechanical stresses and genetic factors.  It usually occurs in weight-bearing joints that have undergone abnormal stresses (e.g. from obesity or overuse), and is frequently linked with increased age.  Common sites of involvement include the hands, hips, knees and feet. Primary OA is the most common form of OA.  In contrast, secondary OA may occur in any joint at any age and has an identifiable underlying cause (e.g. inflammatory or metabolic disease).  Secondary OA develops following any process that damages the joint such as fractures, dislocations, sports injuries, joint surgery or repetitive trauma (occupational trauma).
  • 5. Risk Factors of OA  Obesity,  ↑ Age,  Joint injury,  stress on the joints from certain jobs and playing sports  Genetics (Legg-Calve-Perthes disease)
  • 6. Risk factors for primary OARisk factors for primary OA OA Obesity Occupation Old age Family history Genetics Trauma Joint dysplasia Bone injury Gender Joint injury Solomon L. 1997
  • 7. Osteoarthritis  Prevalence increases exponentially beyond the age of 50 with about 80-90% of both sexes having osteoarthritis by age 65.  Age-related changes include: alterations in proteoglycans & collagen, which decrease tensile strength & shorten fatigue life but it is not simply a disease of wear and tear
  • 9. Osteoarthritis  Often leads to complete degeneration of articular cartilage
  • 10. Osteoarthritis (OA)  Begins in the 3rd decade of life and peaks between the 5th and 6th  Direct correlation with age and the degenerative process
  • 11. Pathogenesis • OA is a joint disease that mostly affects cartilage. • Cartilage is tissue that covers the bones in a joint. • Healthy cartilage allows bones to glide over each other. It also helps absorb shock of movement. • In osteoarthritis, the top layer of cartilage breaks down and wears away.
  • 12. Pathophysiology  This allows bones under the cartilage to rub together.  The rubbing causes pain, swelling, and loss of motion of the joint. Over time, the joint lose its normal shape.  Also, bone spurs may grow on the edges of the joint.
  • 13. Bits of bone or cartilage can break off and float inside the joint space, which causes more pain and damage. People with osteoarthritis often have joint pain and reduced motion. Unlike some other forms of arthritis, osteoarthritis affects only joints and not internal organs. Rheumatoid arthritis - the second most common form of arthritis - affects other parts of the body besides the joints.
  • 14. Osteoarthritis  Chondrocytes play a primary role and constitute the cellular basis of the disease  They produce IL-1 & TNF-alpha, which are known to stimulate the production of catabolic metalloproteinases and inhibit the synthesis of both type 2 collagen and proteoglycans; other mediators also have a role in matrix degradation
  • 15. QuickTime™ and a Photo CD Decompressor are needed to use this picture  Natural history of OA: Progressive cartilage loss, subchondral thickening, marginal osteophytes
  • 16. Modest, patchy chronic synovitis Bone ends thicken Bony outgrowths (osteophytes) form Bone fragments may float in the joint space Fluid filled cysts may form in the bone OA jointNormal joint Cartilage: Pitted and frayed surface Loss of elasticity Cartilage may wear away completely Thickening of capsule Characteristics of OACharacteristics of OA Dieppe P. 1998
  • 17. Clinical Manifestations OA  Stiffness in a joint after getting out of bed or sitting for a long time  Last <30 min. and ↓ with movement  Swelling or tenderness in one or more joints  A crunching feeling or the sound of bone rubbing on bone.
  • 18. OA: Symptoms and Signs • Pain is related to use • Pain gets worse during the day • Minimal morning stiffness (<20 min) and after inactivity (gelling) • Range of motion decreases • Joint instability • Bony enlargement • Restricted movement • Crepitus • Variable swelling and/or instability
  • 19. Osteoarthritis  Is an insidious disease  Characteristic symptoms include: deep, achy pain that worsens with use.  Impingement on spinal foramina by osteophytes results in cervical & lumbar nerve root compression with pain.  muscle spasms & atrophy & neurologic deficits
  • 20. Osteoarthritis  Typically, only one or a few joints are involved  Joints commonly involved are: hips, knees, lower lumbar & cervical vertebrae, proximal & distal interphalangeal joints of fingers, etc.  Heberden nodes: which common in women, represent prominent osteophytes in distal interphalangeal joints
  • 21. Finger deformities in OAFinger deformities in OA • Deformities occur at: • The base of the thumb (Bouchard’s nodes) • The middle joint of a finger (Bouchard’s nodes) • The finger tip (Heberden’s nodules) Heberden’s nodules in a patient with OA Sciencephoto.com
  • 23. Joint involvement in OAJoint involvement in OA Common Knee Hip Fingers Spine Less common Elbow Shoulder Wrist Ankle
  • 24. Knee deformity in OAKnee deformity in OA Sciencephoto.com
  • 25.  The various changes in bone structure associated with OA lead to a number of classical deformities.  Muscle weakness and joint instability can result in a shift in the parts of the joints that bear the load.  This can lead to alterations in the joint shape, as shown above, where the bones of the joint are no longer correctly aligned.
  • 26. Assessment and Diagnosis  Difficult to diagnose  Physical assessment  Tender enlarged joints  Inflammation  Progressive loss of cartilage appears on xray  Blood test are not useful
  • 27. Medical Management Goals  Osteoarthritis treatment has four main goals:  Improve joint function  Keep a healthy body weight  Control pain  Achieve a healthy lifestyle
  • 28. Medical Management of OA  Conservative treatment  Education  Use of heat  Weight reduction  Joint rest and avoidance of joint overuse  Orthotic devices  Isometric and aerobic exercises  Massage, yoga,  Occupational and physical therapy
  • 29. Medical Management of OA  Alternative therapy  Herbal and dietary supplements  Acupuncture, acupressure  Copper bracelets or magnets
  • 30. Pharmacologic Therapy  Symptom management and pain control  Medication selection  Patients needs  Stage of disease  Risk of side effects  Medications and other treatments
  • 31. Pharmacologic Therapy Cont’  Initial therapy  Acetaminophen  Nonselective NSAID’s  diclofenac (voltaren) ibuprofen (Advil, Motrin)  COX-2 inhibitors  celecoxib (Celebrex) valdecoxib (Bextra)  Associated with risk CVD
  • 32. Pharmacologic Therapy Cont’  Opioids  Codiene, oxycodone (Percocet)  Intra-articular corticosteroids  Topical analgesic  capsaicin (Capsin, Zostrix)  Methylsalicylate
  • 33. Surgical Management  Osteotomy- alter the distribution of weight within the joint  Arthroplasty- disease joint components are replaced with artificial products  Tidal irrigation- lavage (provides pain relief for up to 6 months)
  • 34. Nursing Management  Pain management  Optimal function  Patient’s understanding of disease  Lifestyle changes  Weight loss  Referrals  Assistive devices
  • 35. Case: Carpometacarpal Joint  Radiograph shows severe changes  Most common location in hand  May cause significant loss of function
  • 36. Osteoarthritis  Often leads to complete degeneration of articular cartilage

Hinweis der Redaktion

  1. The prevalence of OA increases with age, rising from about 1% in those under 30 years to more than 70% in those over 70 years of age. Men and women are equally prone to OA, but more joints are affected in women. Obesity is a significant risk factor for the development and progression of OA, particularly OA of the knee. Joint injuries due to trauma, or as a result of repetitive occupational activities, are also strongly associated with OA. Frequently, patients with OA will have a family history of the disease and there is often a similarity in the type of OA that develops among family members. Reference Solomon L. Clinical features of osteoarthritis. Textbook Rheum 1997;2:1383–1393.
  2. Reference Dieppe P, Lim K. Osteoarthritis and related disorders. Clinical features and diagnostic problems. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;3.1–3.16.
  3. OA most commonly affects the knee, hip, fingers or spine. Less frequently, it may affect the joints of the elbow, shoulder, wrist or ankle. Reference Solomon L. Clinical features of osteoarthritis. Textbook Rheum 1997;2:1383–1393.
  4. The various changes in bone structure associated with OA lead to a number of classical deformities. Muscle weakness and joint instability can result in a shift in the parts of the joints that bear the load. This can lead to alterations in the joint shape, as shown above, where the bones of the joint are no longer correctly aligned. Reference Dieppe P, Lim K. Osteoarthritis and related disorders. Clinical features and diagnostic problems. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;3.1–3.16.