documentoa
TRANSCRIPT
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Osteoarthritis
Ehab AbusinnaOrth. Surgeon
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OBJECTIVES TO DISCUSS
Diagnosis of Osteoarthritis
Risk factors for Osteoarthritis
Treating active persons with Osteoarthritis
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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
WHAT IS OA
&PAIN!
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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
OSTEOARTHRITIS
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DEFINITION 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
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RADIOGRAPHIC FEATURES
Joint space narrowing Subchondral sclerosis Marginal osteophytes Subchondral cyst
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XRAYS
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RISK FACTORS FOR OA
Systemic Risk Factors
Age 10-fold increase from 3065
Genetics (generalized) Gender
Men <50: higher risk Women >50: higher risk
Nutritional Low vitamin C and D intake
Joint Biomechanical Risk Factors
Joint trauma Obesity (knee, hip, hand) Occupation Abnormal joint
biomechanics Dysplasia, malalignment,
instability, abnormal innervation
Knee extensor wkness Sports w/ joint risk
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Obesity Heredity Gender Hypermobility Osteoporosis Trauma Congenital joint dysplasia Occupation Sport
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Primary OA: No known causeSecondary 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
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CLINICAL PICTURE
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.
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TREATMENT 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.
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Non pharmocologic Measures Education, Weight loss, Exercise, & Bracing
Pharmacologic Measures Analgesics, Glucosamine, Injectables
Alternative Therapies Acupuncture, Magnets, Balneotherapy, Thermotherapy
Surgery
TREATMENT OF OSTEOARTHRITIS
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CONSERVATIVE CARE Weight control
Appropriate rest and Exercise
Physical therapies
Occupational therapies
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Medial or lateral unloading
KNEE BRACING
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DIETARY TREATMENT Glucoseamine, chondroitin sulphate, antioxidants,
others…
SPECIFIC MEDICATIONS Paracetamol NSAIDs COX-2 selective inhibitors Corticosteroids
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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
GLUCOSAMINE/CHONDROITIN
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HYALURONIDASE MECHANISMSBased 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
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OTHER EFFECTIVE THERAPIES
TENS effective in some with knee or hip OA Short-term, 2-4 weeks
Acupuncture relieves pain Heat/Ice thermotherapy Balneotherapy
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Arthroscopy Cartilage transplantation Joint replacement
SURGERY
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NO BENEFIT for unselected OA (mechanical or inflammatory causes)
ARTHROSCOPY
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Universally recommended to improved pain, function, QOLUnicompartmentalTotal joint replacement
KNEE JOINT REPLACEMENT
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OTHERS Implantation of chondrocytes Local injection of hyaluronic acid Topical treatment Surgical treatment Acupuncture
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