Osteoarthritis Typically affects the fingers, spine, hips and knees

BY INT. KAMOLWAN INT. 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 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, frequently 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