Oesteoarthritis

Osteoarthritis

SMS3053Dr . 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 historyGenetics

TraumaJoint

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 appearanceOf 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

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Natural history of OA: Progressive cartilage loss, subchondral thickening, marginal osteophytes

Modest, patchychronic 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

Thickeningof 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 nodulesin 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

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