Osteoarthritis

Ehab AbusinnaOrth. Surgeon

OBJECTIVES TO DISCUSS

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

WHAT IS OA

&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

OSTEOARTHRITIS

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

RADIOGRAPHIC FEATURES

Joint space narrowing Subchondral sclerosis Marginal osteophytes Subchondral cyst

XRAYS

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

Obesity Heredity Gender Hypermobility Osteoporosis Trauma Congenital joint dysplasia Occupation Sport

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

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.

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.

Non pharmocologic Measures Education, Weight loss, Exercise, & Bracing

Pharmacologic Measures Analgesics, Glucosamine, Injectables

Alternative Therapies Acupuncture, Magnets, Balneotherapy, Thermotherapy

Surgery

TREATMENT OF OSTEOARTHRITIS

CONSERVATIVE CARE Weight control

Appropriate rest and Exercise

Physical therapies

Occupational therapies

Medial or lateral unloading

KNEE BRACING

DIETARY TREATMENT 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

GLUCOSAMINE/CHONDROITIN

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

OTHER EFFECTIVE THERAPIES

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

SURGERY

NO BENEFIT for unselected OA (mechanical or inflammatory causes)

ARTHROSCOPY

Universally recommended to improved pain, function, QOLUnicompartmentalTotal joint replacement

KNEE JOINT REPLACEMENT

OTHERS Implantation of chondrocytes Local injection of hyaluronic acid Topical treatment Surgical treatment Acupuncture