OSTEOARTHRITIS

Prof. Abdel-Azim Alhefny

Prof. of Internal Medicine, Rheumatology & Immunology

Ain Shams University

Synovium

Secretes the

synovial fluid

Capsule

Ligaments hold the

bones together

Synovial fluid

Lubricates the

joint capsule

Bone

Cartilage

Protects the

end of the bone

Anatomy of a normal synovial joint

Muscle

Tendon

Dieppe P. 1998

Osteoarthritis

OA is a slowly progressive

degenerative disease

leading to gradual loss of

articular cartilage.

It is characterized by focal

degeneration and new bone

formation.

OA is not a disease of a single tissue (articular cartilage );

but a disease of an organ (the synovial joints) in which all

the tissues are affected

including:-

Subchondral bone.

Ligaments.

Capsules.

Synovial membrane.

Peri-articular muscles.

As there is heart failure , kidney

failure also we have joint Failure.

Osteoarthritis

Classification Of OA

A- Primary : (Localized, Generalized & erosive) Most common form of OA Commonly occurs in weight-bearing joints Is rare before age of 40 , prevalence increases with age Genetic predisposition, particularly for

hand arthritis

1-Localised: Hands: Heberdens and Bushard`s nodes Feet: Hallux valgus Hip : Spine Apophyseal joints

2-Generalised (3 areas or more).3- Erosive: hand DIP/PIP (OA) associated with synovitis and

radiographic central erosions of the articular surface.

B-Secondary: Preceded by a predisposing disorder such as joint trauma

Occurs in any joint at any age

1. Traumatic : Acute – Chronic - occupational (Sports).

2. Cogenital or Developmental

3. Mechanical Factors

4. Metabolic

5. Endocrinal

6. Calcium Deposition Disease

7. Neuropathic

8. Endemic

9. Miscellanous

Classification Of OA

Risk factors for primary OA

OA

Obesity

Occupation

Old age

Family history

Genetics

Joint

dysplasia

Bone injury

Ƒ Gender

Joint injury

Bad Prognostic Factors for OA

1. Older age.

2. Female sex.

3. Heberden`s nodes.

4. Low dietary intake of

vitamin C.

5. Low dietary intake of vitamin D.

Knee osteoarthritis

Most common form of arthritis .

10 % of people over 55 have disabling knee

symptoms (1/4 of them are severely disabled).

30 % of subjects over 65yrs have radiographic

evidence of OA (1/3 is symptomatic).

Risk of disability same for knee OA as for cardiac

disease.

WHO –considers OA the 4th cause of disability in

women, & the 8th cause in men.

OA RA

Type of Arth. Degenerative Inflammatory

Site Mostly weight

bearing joints,

affects DIP,

1st CMC

Small joints of the

hands and feet,

bil. Symmetrical,

DIP are spared,

Stiffness Morning stiffness

< 15 M.

Morning stiffness

>30 m.

Extra-

articular

manifestations

not present Present (cardiac, lung,

kidney, skin, S.c.

nodule, eye, vasculitis )

Laboratory

Tests

-ve, unremarkable +ve ( ESR, RF, Anti CCP,

CRP, occasionally ANA)

Pattern of joint involvement in OA

Commonly occurs in weight-bearing joints

Common Signs & Symptoms in OA

Symptoms

Joint pain (usage)

Joint stiffness < 15min

Crepitus

Alteration in joint shape

Deformity, swelling

Functional impairment

Limited mov., instability

Common Signs & Symptoms in OA

Signs

Crepitus

Restricted movement

Tenderness

Bony & soft tissue swelling

Limp

Deformity: Hand Heberden's or

Bouchard's nodes, Knee: varus or valgus

Muscle atrophy / weakness

Cool effusion

Instability

Heberden’s nodules

in a patient with OA

Heberden’s and Bouchard’s Nodes

Sciops-Medical Division

Heberden’s nodes :Hard or bony swellings which develop in the DIP.

Bouchard's nodes: bony growths in the proximal interphalangeal (PIP) joints

Hallux valgus and cock-up toe

deformities, characteristic of

osteoarthritis in the foot.

Deformities

Knee deformity in OA

Sciencephoto.com

Deformities

Deformity

INVESTIGATIONS

Routine Lab. work usually normal.

ESR usually normal.

RF, CCP, ANA, dsDNA are negative.

Joint fluid is straw-colored with good viscosity, fluid WBCs < 2000/ml; (of value in ruling out crystal induced arthritis or infective arthritis).

Radiogtaphs may show:- Joint space narrowing

Marginal osteophyte.

subchondral bone sclerosis

subchondral cysts

Osteophytes

Muskuloskeletal Ultrasonography:

MRI: early cartilage changes.

Arthroscopy: showed surface erosion and fissuring

Cool effusion

Joint Effusion

Synovial fluid

should aspirated & sent for

1.Cell count.

2.Gram stain.

3.Culture & Sensitivity.

Plain radiograph showing advanced OA

Non-weight

bearing

Weight-bearing

Radiographic features

1st CMC

(thumb base)

Subchondral sclerosis

Osteoarthritis: Narrowing Sclerosis Osteophyte

formation

Kissing Osteophytes: Lumbar Spine

Differential Diagnosis

Crystal-induced arthritides

Osteonecrosis

Charcot joint

Rheumatoid arthritis

Psoriatic arthritis

TREATMENT

Goals of The Treatment

Relief pain, swelling and inflammation.

Inhibit joint damage, to.

• Prevent or retard Disease Progression

• Improve function and Minimize Disability

Improve quality of life.

Osteoarthritis and Cartilage (2008) 16, 624e630

Modalities Of OA Management

1-Nonpharmacological:

Educational strategies

Physical treatment

2-Pharmacological

Drugs

Nutritional approaches.

3-Surgical intervention

Components of Multimodal OA Treatment

Opioid Analgesics

Intra Articular Injections (corticosteroids & hyaluronic

acid)

Pharmacologic Therapy Acetaminophen

NSAIDS / COX2

Topical agents / Nutritional supplements

DMOADs

Non Pharmacological Education/ Exercise / Weight control / Physical therapy /

Occupational therapy / Assistive devices

Surgery

Pharmacological Therapy

Drug Interventions Has been

Classified Into

Symptoms modifying

drugs

Structures modifying

drugs

Pharmacological Therapy

List of

Drugs

Analgesics

NSAIDs

Myorelaxants

Vit. C, D and E.

Oligoeliment Supplementation (Sel, Cu)

Symptom modifying drugs

Paracetamol

COX-2 specific

inhibitors

Nonselective NSAIDs

(plus misoprostol or a

pump inhibitor)

Nonacetylated

salicylates

1-Analgesics and NSAIDs 2-Pure Analgesics

Tramadol

Opioid

3-IA injection

• Glucocorticoids

• Hylauronan

4-Topical

• Capsaicin

• Methylsalicylate

Structures Modifying Drugs

Glucosamine & chondroitin Supplements. Used as

complementary and alternative therapies to relieve the chronic pain of OA.

These supplements are not medications and are not regulated by the U.S. Food and drug (FDA).

IL-1ß inhibitor (diacerine):Inhibition of the

production and activity of IL-1

With repoted side effects

Drugs

Glucocorticoids

• Psychosis

• Acute Addisonian crisis due to

withdrawal

Nonsteroidal anti-inflammatory

drugs

• Acute gastritis

• Perforated / bleeding peptic ulcer

• Acute enteritis

• Analgesic nephropathy

• Acute interstitial nephritis

• Hypersensitivity reactions

• Thrombocytopenia

• Pancytopenia

• Steven Johnson syndrome

• Erythema multiforme

• Toxic epidermal necrolysis

• Acute interstitial nephritis

Disease- modifying

antirheumatic drugs

• Hypersensitivity reactions

• Thrombocytopenia

• Aplastic anaemia

• Exfoliative dermatitis

• Steven Johnson syndrome

Surgical Treatment

Surgery may be considered in patients with

intractable pain, loss of function who are not

responding to other measures.

Surgical Intervention

Patellar taping

Osteotomy

Arthrodesis

Arthroplasty

Tidal knee Irrigation

Arthroscopic lavage with or

without debridement

Total knee replacement.

American College of Rheumatology

2000 Guidelines for OA of the Knee

Nonpharmacologic Modalities

Acetaminophen

Viscosupplements

COX-2–specific inhibitor

NSAID and GI-protective agent

Glucocorticoid injection

At increased risk

for an upper GI adverse event

Not at risk

for an upper GI adverse event

Viscosupplements

COX-2–specific inhibitor

Low-dose NSAID

Glucocorticoid injection

Surgery