Osteoarthritis

• Typically affects the fingers, spine, hips and knees

BYBY

INT. KAMOLWANINT. KAMOLWAN

OA KNEE

• Chronic, degenerative disorder of multifactorial aetiology, characterised by loss of articular cartilage and periarticular bone remodelling, particularly large weight-bearing joints

• Common in older patients but can occur in younger patients ( genetic mechanism , previous joint trauma )

Pathophysiology

• Degenerative alterations primarily begin in the articular cartilage

• External forces accelerate the catabolic effects of the chondrocytes and disrupt the cartilaginous matrix

• Enzymatic destruction increases cartilage degradation ↓ proteoglycans and collagen synthesis

• Decreased strength of the cartilage is compounded by adverse alterations of the collagen

• Reduced contact area of the cartilage

Pathophysiology

• Loss of cartilage results in the loss of the joint space

• Progressive erosion of the damaged cartilage occurs until the underlying bone is exposed

• Subchondral bone responds with vascular invasion and increased cellularity, at areas of pressure

Pathophysiology

• The traumatized subchondral bone may undergo cystic degeneration

• At nonpressure areas along the articular margin → irregular outgrowth of new bone (osteophytes)

• Normal joint• hinge joint formed

• Surface layer of cartilage break down and wears away,causes the bones under the cartilage to rub together

• Pain, swelling, and loss of motion result

• formation of bone spurs

Incidence

• Incidence increases with age

• USA approximately 80-90% of individuals older than 65 years have evidence of primary osteoarthritis

• After age 55 years, the prevalence increases in women in comparison with men

Incidence

• Equivalent prevalence occurs in men and women aged 45-55 years (↑dramatically after the age of 50 years)

• Most adults older than 55 years show radiographic evidence of osteoarthritis

• No significant correlation exists between incidence of OA and race

Causes

Primary OA

• Idiopathic

• Defective gene

Causes

Secondary OA – Obesity – Repetitive use (ie, jobs requiring heavy labor

and bending)– Previous trauma (ie, posttraumatic OA)– Infection

Causes

– Crystal deposition– Acromegaly– Previous rheumatoid arthritis (ie, burnt-out

rheumatoid arthritis)– Heritable metabolic causes (eg, alkaptonuria,

hemochromatosis, Wilson disease)

Causes

– Hemoglobinopathies (eg, sickle cell disease, thalassemia)

– Underlying orthopedic disorders (eg, congenital hip dislocation, slipped femoral capital epiphysis)

– Disorders of bone (eg, Paget disease, avascular necrosis)

History

• Insidious throbbing arthralgias with activity

• Initially, resting relieves the pain

• Eventually, the pain occurs even at rest

• Morning stiffness ≥ 30 minutes

• Intermittent joint swelling

Symptoms

• Pain

• Stiffness

• Gelling

• Instability

Signs

• Pain

• Tenderness

• Swelling

• Effusion

• Crepitus

• Limitation of movement and muscle wasting

Physical

• Early– Joints may appear normal– Gait may be antalgic if weight-bearing joints

are involved

Physical

• Later – Visible osteophytes may be noted– Joints may be warm to palpation– Palpable osteophytes frequently are noted– Joint effusion frequently is evidenced in

superficial joints

Physical

– Range-of-motion limitations, because of bony restrictions and/or soft tissue contractures, are characteristic

– Crepitus with range of motion is not uncommon

Imaging

• Plain radiographs

• Bone scans may be helpful in early diagnosis of OA of the hand

• The space between the bones of the upper and lower leg is smaller

• Bony spurs (osteophytes)

• Increase bone density at the margin of the joint

- x ray findings

– Joint space narrowing

– Osteophytes– Subchondral sclerosis : ↑ bone density, fre

quently found adjacent to joint space

– Subchondral cysts : fluid-filled sacs which extrude from the joint

Diagnosis

• On the basis of the initial history and examination

• X-rays

PROGRESS

• Osteoarthritis begins when the joint cartilage starts to become worn down → decreases the ability of the cartilage to work as a shock-absorber to reduce the impact of stress on the joints

• The remaining cartilage wears down faster→ bones to grind against one another

• Bone spurs may form

Treatment

Goals of managing OA

• Controlling pain

• Maintaining and improving the range of movement and stability of affected joints

• Limiting functional impairment

Treatment

• Education and behavioural intervention- Aim is to provide patients with an

understanding of the disease process, its prognosis and the rationale and implications of managing their condition

• Weight loss - Weight loss (< 5 kg) has significant short-

term and long-term reduction in symptoms of OA

Treatment

• Mechanical aids

- Wear shock-absorbing footwear with good mediolateral support, adequate arch support and calcaneal cushion

• Exercise - Aim of exercise is to reduce pain and disability

by strengthening muscle, improving joint stability, increasing the range of movement and improving aerobic fitness

Treatment

• Medication

- Acetaminophen (Tylenol®) is a mild pain reliever with few side effects

- Anti-inflammatory medication, such as ibuprofen and aspirin

- COX-2 inhibitors

- Glucosamine and Chondroitin sulfate

Treatment

• Intra-articular injection

- Glucocorticoids injection

- Hyaluronic Acid (HA) and similar

hyaluronan preparations (eg, Synvisc)

Treatment

• Surgery

- Arthroscopy (including debridement,and lavage/irrigation)

- Proximal Tibial Osteotomy

- Artificial Knee Replacement

- Osteotomy

- Arthroplasty or Joint Replacement