Osteoarthritis

Hoveda Mufti M.D. 9/6/06

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

Prevalence and epidemiology

Over 20 million affected in U.S. About 60-90% of people over age 65 60Under 45 yrs it is equally common in men and women Over 55 yrs its more common in women Nodal OA involving DIP and PIP joints is more common in women and their first degree female relatives

Premature OA associated with gene mutations that encode collagen types 2, 9, 10 OA of knee is more common in African American women Commonest cause of long-term disability longLarge economic impact as a result of medical costs OA cost the U.S. economy nearly $125 billion per year in direct expenses and lost wages and production.

It is not an inevitable part of aging, some people are more susceptible than others A combination of different factors are involved. Both mechanical and biologic destructive processes play a role in OA.

Risk factors Metabolic (hemachromatosis) Inflammatory (RA, infection) age gender genetic factors trauma weight

Classification
Primary Idopathic Localized or generalized Local: knee, hip, spine, hands Generalized: large joints and spine Small peripheral joints and spine Mixed and spine Secondary PostPost-traumataic Congenital or developmental Localized or generalized Calcium deposition disease Other: Inflammatory Avascular necrosis

Inflammatory OA
OA is generally a non-inflammtory arthritis. nonIncreasing evidence for inflammatory type: caused by cytokines, metalloproteinase release. This erosive inflammatory type may have flares but later acts like typical OA. Primarily in women May be suspected from evidence of active synovitis, chondrocalcinosis on x-rays, morning xstiffness greater than 30 mins, history of swelling and night pain.

Overview of the process

Articular cartilage gets disrupted Damage progresses deeper to subchondral bone

Fragments of cartilage released into joint Matrix degenerates Eventually there is complete loss of cartilage Bone is exposed

Normal knee anatomy

left: Normal x-ray xRight: worn away cartilage reflected by decreased joint space

The process

at a cellular level Cartilage matrix has increased water content and decreased proteoglycan This is different from the changes that occur with aging cartilage dries up. Increased activity of proteinases compared to inhibitors of proteinases. Breakdown products of cartilage cause inflammatory reaction of synovium Cytokines cause matrix degeneration. Where do they come from? chondrocytes Cycle of destruction starts Compensatory bone overgrowth occurs - subchondral bone increases in density

Left: View of normal elbow cartilage through an arthroscope - white, glistening, smooth Right: severe elbow osteoarthritis - cartilage is lost and the bone underneath is exposed

The process cont d

Bony proliferations at joint margins form, what are they called? osteophytes Thought to be new bone formation in response to degenerating cartilage They cause joint motion restriction

What to look for in an x-ray xRadiographic changes visible relatively late in the disease Subchondral sclerosis Joint space narrowing esp where there is stress Subchondral cysts Osteophytes Bone mineralization should be normal

Joint space narrowing where there is more stress Subchondral bone has thickened bony overgrowth

significant joint space narrowing as well as proliferative bone formation around the femoral neck (arrows)

Left: normal hip Right: There is some joint space medially but the superior portion is completely destroyed. Supralateral aspects affected most because the weight is transfered through the roof of the acetabulum. Note the sclerosis and oseophyte formation (arrow).

painful bone on bone contact at the CMC joint and the large bone spurs -- osteophytes.

X-ray shows lateral osteophytes, varus deformity, narrow joint space in a 70 yr old female with OA

Are crystals found in osteoarthritic joints? Yes Calcium pyrophosphate dihydrate and apatite. Are of unknown significance and asymptomatic

Clinical features and diagnosis

Pain Sources
Joint effusion and stretching of the joint capsule Torn menisci Inflammation of periarticular bursae Periarticular muscle spasm Psychological factors

Deep, aching localized to the joint Slow in onset Worsened with activity in initial stages Occurs at rest with advanced disease

May be referred eg hip pain referred to the thigh, groin, knee. Pain may be aggravated with weather changes

Exam
Joint line tenderness Bony enlargement of joint +/+/- effusion Crepitus Decreased range of motion

Joint exam
Joint line pain can indicate tear of the lining of the capsule or the meniscus. Where is the patella?

Joint exam
In the evaluation of joint line pain, perform a varus or valgus stress test. test. Apply stress across the joint, place fingers directly over the joint line to assess for pain, a clunk may indicate a meniscal tear, tear, or crepitus may indicate cartilage damage.

Have the patient to lie supine on the exam table with leg muscles relaxed Press the patella downward and quickly release it. the patella visibly rebounds. What does this mean? a large knee effusion Ballotable patella

Have the patient lie supine with leg muscles relaxed Compress the suprapatellar pouch with your thumb, palm, and index finger. "Milk" downward and laterally so that any excess fluid collects on the medial side. Tap gently over the collected fluid and observe the effect on the lateral side A fullness on the lateral side indicates the presence small knee effusion

Involved joints
DIP, PIP 1st carpometacarpal cervical/lumbar facet joints 1st metatarsophalangeal Hips Knees

Uncommon Wrist, elbows, shoulders, ankles

1st metatarso-phalangeal most commonly metatarsoaffected in OA of the foot.

Typical findings
Heberden s nodes Bouchard s nodes

Rt: varus deformity of the knee

Treatment
NonNon-pharmacokinetic No proven medication-based disease modifying medicationintervention exists. Analgesics (acetominophen) NSAIDS Help pain symptoms but controversial for long term use in non-inflammatory OA because of nonrisks vs benefits Narcotics IntraIntra-articular steroids Chondroprotective agents AntiAnti-depressants

NonNon-pharmacokinetic rx Reasonable evidence for efficacy Exercise prevent disuse atrophy of muscles Physical therapy: Hydrotherapy/heat/cold, paraffin baths Weight loss Education Wedges shoe insoles/braces Refer to physiatrist for management plan.

Analgesics
Acetominophen at doses of upto 4g per day 2004 meta analysis of 10 trials showed that acetominophen superior to placebo but less efficacious in relieving pain than NSAIDS Do you worry about hepatotoxicity? Only seen in pts who are taking excessive amounts of alcohol, underlying disease.

Opioid analgesics
Generally should be avoided for long term use For short term rx they may be effective. A study showed oxycodone to be synergistic with NSAIDS. In older pts use caution because of side effects such as confusion, constipation, sedation. Can use tramadol with acetominophen, in addition to NSAID/COX-2 inhibitor NSAID/COX-

A controlled study showed codeine and acetominophen combination to be equivalent to to tramadol and acetominophen Consider opiates if pt is not a candidate for surgery, or is at high risk for side effects from NSAIDS

NSAIDS
Useful in non-inflammatory OA when pain nonis moderate to severe Topical preparations available PGE2 may contribute to local inflammation and so there is a role for NSAIDS in inflammatory OA

There is variability amongst patients in terms of side effects and efficacy of NSAIDS NonNon-acetylated salicylates have less renal toxicity: Sulindac, salsalate Indomethacin has been associated with accelerated joint destruction, so avoid it for long term use in pts with hip OA

Selective COX-2 inhibitors COXThey have 200-300 times selectivity for 200COXCOX-2 over COX-1. COXLess gastroduodenal toxicity But if used with ASA pts may be at increased risk for GI bleeding. Use GI prophylaxis Avoid in pts with atherosclerotic CAD - use traditional NSAIDS with a PPI/sucralfate/misoprostol

Side effects
Rash/hypersensitivity GI bleeding CNS dysfunction in elderly Impairment of renal/hepatic/platelet function. How can NSAIDS lead to renal dysfunction? By interfering with vasodilator renal PG and causing renal ischemia.

IntraIntra-articular corticosteroids
May be used if NSAIDS are contraindicated, persistent pain despite use of other medications. (not > 4 injections per year per joint) 2004 meta-analysis of controlled trials (w/ metaplacebo) showed short term improvement in knee pain, but efficacy in other joints is uncertain. saline vs steroid injection? A study comparing the two in knee OA showed no effect on joint space narrowing or significant difference in pain at the end of the study, but over a 2 yr period saline injections has less pain relief.

IntraIntra-articular hyaluronans
Evidence shows they have a small advantage in terms of pain control, compared to intra-articular placebos or intraNSAIDS. No evidence for improvement in function Two studies comparing intra-articular intrasteroids to hyaluronans have come to opposite conclusions-more trials are conclusionsneeded.

Surgical: arthroscopy
arthroscopy is not recommended for nonspecific "cleaning of the knee . Used to fix specific structural damage on imaging (repairing meniscal tears, removing fragments of torn menisci that are producing symptoms).

Joint replacement
If all other rx ineffective, and pain is severe Loss of joint function Joints last 8-15 years 8without complications

The end