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   Diagnosis of Osteoarthritis
   Risk factors for Osteoarthritis
   Treating active persons with Osteoarthritis
Disease of the joints
  characterized by:
–   Progressive articular
    cartilage loss
–   New subchondral bone
    formation
–   New bone and cartilage
    formation at joint
    margins
–   Low level synovitis
                             & PAIN!
 OA is a group of diseases and mechanical
  abnormalities entailing degradation of joints,
  including articular cartilage and the subchondral bone
  next to it

 OA is derived from the Greek word ‘ostoe’, meaning
  ‘of the bone’, ‘arthro’, meaning ‘joint’, and ‘itis’,
  meaning inflammation
  Also known as degenerative
  joint disease or “wear and
  tear arthritis”.
 Progressive loss of cartilage
  with remodeling of
  subchondral bone and
  progressive deformity of the
  joint (s).
 Cartilage destruction may be
  a result of a variety of
  etiologies
 Joint space narrowing
 Subchondral sclerosis
 Marginal osteophytes
 Subchondral cyst
 Joint trauma
   Age                                Obesity (knee, hip,

       10-fold increase from 3065
                                        hand)
                                       Occupation
 Genetics (generalized)
                                       Abnormal joint
 Gender
                                        biomechanics
       Men <50: higher risk                 Dysplasia, malalignment,
       Women >50: higher risk                instability, abnormal
                                              innervation
   Nutritional
       Low vitamin C and D intake
                                       Knee extensor wkness
                                       Sports w/ joint risk

           Systemic Risk Factors       Joint Biomechanical Risk Factors
 Obesity
 Heredity
 Gender
 Hypermobility
 Osteoporosis
 Trauma
 Congenitaljoint dysplasia
 Occupation
 Sport
Primary OA: No known cause
Secondary OA
 Pre-existing joint damage:
  RA, Gout, Seronegative spondyloarthropathy, Septic
 arthritis, Paget's disease, Avascular necrosis, e.g.
 corticosteroid therapy
 Metabolic   disease: Chondrocalcinosis, Hereditary
  haemochromatosis, Acromegaly
 Systemic diseases: Haemophilia- recurrent
  haemarthrosis, Haemoglobinopathies, e.g. sickle
  cell disease, Neuropathies
Signs
   Joint tenderness
   Crepitus on movement
   Limitation of range of movement
   Joint instability
   Joint effusion and variable levels of
    inflammation
   Bony swelling
   Wasting of muscles.
Generally speaking, the process of
  clinically detectable osteoarthritis is
           IRREVERSIBLE
and typical treatment consists of
 medication or other interventions
 that can reduce the pain of OA and
 thereby improve the function of the
 joint
 Non    pharmocologic Measures
     Education, Weight loss, Exercise, & Bracing
 Pharmacologic      Measures
     Analgesics, Glucosamine, Injectables
 Alternative Therapies
     Acupuncture, Magnets, Balneotherapy, Thermotherapy
 Surgery
 Weight   control
 Appropriate   rest and Exercise
 Physical   therapies
 Occupational    therapies
   Medial or lateral unloading
 Glucoseamine,     chondroitin sulphate, antioxidants,
 others…

SPECIFIC MEDICATIONS
 Paracetamol
 NSAIDs
 COX-2 selective   inhibitors
 Corticosteroids
 I recommend in    ALL patients with knee and hip OA
     GS 1500 mg/ CS 800 mg
 3 month    trial, evaluate efficacy; continue if
  helping
 Consider indefinite use even if no pain relief for
  joint space preservation
Based on research dating back to the 1980’s
 Increases the viscosity and elasticity of OA
 synovial fluid
 Stimulates endogenous hyaluronic acid
 production
 Inhibits induction and activity of degradative
 enzymes
 Reduces inflammatory response
 Analgesic effect
   TENS effective in some with knee or hip OA
       Short-term, 2-4 weeks
 Acupuncture relieves pain
 Heat/Ice thermotherapy
 Balneotherapy
 Arthroscopy
 Cartilage transplantation
 Joint replacement
 NOBENEFIT for unselected OA
 (mechanical or inflammatory
 causes)
 Universally
           recommended to
 improved pain, function, QOL
     Unicompartmental
     Total joint replacement
 Implantation of  chondrocytes
 Local injection of hyaluronic acid
 Topical treatment
 Surgical treatment
 Acupuncture
Oa

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Oa

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  • 3. Diagnosis of Osteoarthritis  Risk factors for Osteoarthritis  Treating active persons with Osteoarthritis
  • 4. Disease of the joints characterized by: – Progressive articular cartilage loss – New subchondral bone formation – New bone and cartilage formation at joint margins – Low level synovitis & PAIN!
  • 5.  OA is a group of diseases and mechanical abnormalities entailing degradation of joints, including articular cartilage and the subchondral bone next to it  OA is derived from the Greek word ‘ostoe’, meaning ‘of the bone’, ‘arthro’, meaning ‘joint’, and ‘itis’, meaning inflammation
  • 6.  Also known as degenerative joint disease or “wear and tear arthritis”.  Progressive loss of cartilage with remodeling of subchondral bone and progressive deformity of the joint (s).  Cartilage destruction may be a result of a variety of etiologies
  • 7.  Joint space narrowing  Subchondral sclerosis  Marginal osteophytes  Subchondral cyst
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  • 12.  Joint trauma  Age  Obesity (knee, hip,  10-fold increase from 3065 hand)  Occupation  Genetics (generalized)  Abnormal joint  Gender biomechanics  Men <50: higher risk  Dysplasia, malalignment,  Women >50: higher risk instability, abnormal innervation  Nutritional  Low vitamin C and D intake  Knee extensor wkness  Sports w/ joint risk Systemic Risk Factors Joint Biomechanical Risk Factors
  • 13.  Obesity  Heredity  Gender  Hypermobility  Osteoporosis  Trauma  Congenitaljoint dysplasia  Occupation  Sport
  • 14. Primary OA: No known cause Secondary OA  Pre-existing joint damage: RA, Gout, Seronegative spondyloarthropathy, Septic arthritis, Paget's disease, Avascular necrosis, e.g. corticosteroid therapy  Metabolic disease: Chondrocalcinosis, Hereditary haemochromatosis, Acromegaly  Systemic diseases: Haemophilia- recurrent haemarthrosis, Haemoglobinopathies, e.g. sickle cell disease, Neuropathies
  • 15. Signs  Joint tenderness  Crepitus on movement  Limitation of range of movement  Joint instability  Joint effusion and variable levels of inflammation  Bony swelling  Wasting of muscles.
  • 16. Generally speaking, the process of clinically detectable osteoarthritis is IRREVERSIBLE and typical treatment consists of medication or other interventions that can reduce the pain of OA and thereby improve the function of the joint
  • 17.  Non pharmocologic Measures  Education, Weight loss, Exercise, & Bracing  Pharmacologic Measures  Analgesics, Glucosamine, Injectables  Alternative Therapies  Acupuncture, Magnets, Balneotherapy, Thermotherapy  Surgery
  • 18.  Weight control  Appropriate rest and Exercise  Physical therapies  Occupational therapies
  • 19. Medial or lateral unloading
  • 20.  Glucoseamine, chondroitin sulphate, antioxidants, others… SPECIFIC MEDICATIONS  Paracetamol  NSAIDs  COX-2 selective inhibitors  Corticosteroids
  • 21.  I recommend in ALL patients with knee and hip OA  GS 1500 mg/ CS 800 mg  3 month trial, evaluate efficacy; continue if helping  Consider indefinite use even if no pain relief for joint space preservation
  • 22. Based on research dating back to the 1980’s  Increases the viscosity and elasticity of OA synovial fluid  Stimulates endogenous hyaluronic acid production  Inhibits induction and activity of degradative enzymes  Reduces inflammatory response  Analgesic effect
  • 23. TENS effective in some with knee or hip OA  Short-term, 2-4 weeks  Acupuncture relieves pain  Heat/Ice thermotherapy  Balneotherapy
  • 24.  Arthroscopy  Cartilage transplantation  Joint replacement
  • 25.  NOBENEFIT for unselected OA (mechanical or inflammatory causes)
  • 26.  Universally recommended to improved pain, function, QOL  Unicompartmental  Total joint replacement
  • 27.  Implantation of chondrocytes  Local injection of hyaluronic acid  Topical treatment  Surgical treatment  Acupuncture