Nonsurgical management of osteoarthritis of the knee

Osteoarthritis (OA) is the most common type of arthritis. It is associated with a breakdown of cartilage in the joints and can occur in almost any joint in the body. The fingers, hips, spine, and knees are particularly vulnerable. Although some risk factors for OA—such as age and race—cannot be changed, others—including obesity and repetitive joint trauma—can be modified. Table 1 lists the most common risk factors for OA.¹

More than 80% of people older than 55 years have radiographic findings of OA, and of these, 10% to 20% have symptomatic complaints and limitations of daily activity. Knee OA is the leading cause of chronic disability in elderly persons in the United States. With more than 76 million baby boomers now in their 50s and the first of this generation approaching 60, a significant number of them will develop this condition. This review can help PAs be prepared.

Pathophysiology

Articular cartilage is a hypocellular, avascular, alymphatic tissue with a dense collagen and proteoglycan matrix that provides a low-friction and highly durable wear-resistant surface. Chondrocytes, important components within this matrix, maintain the makeup of the articular cartilage.² Type II collagen is the primary type of fibrillar collagen within articular cartilage.

The structure develops a high hydrostatic pressure that resists the compressive forces of normal daily activities, providing a type of “water shock absorber” for the body. Synovial fluid, a highly viscous lubricant within the joint capsule, enables and assists with smooth articulation within the joint. The primary active component of synovial fluid is hyaluronic acid. Because of this dense matrix complex, the knee is able to withstand a significant amount of repetitive strain over a lifetime.^2-4

As damage occurs to the articular cartilage, surface integrity and collagen matrix interconnectivity are lost. Matrix damage results in increased osmotic pressure, causing swelling to occur within the articular cartilage. The elevated osmotic pressure further damages the collagen matrix and the mechanical properties of the cartilage; additionally, inflammatory cytokines present at high levels within the synovial fluid lead to direct degradation of the articular cartilage.^2,4 While this cycle can be delayed, currently there are no known ways to reverse this trend and renew intact articular cartilage.

History and physical examination

When the patient presents with knee pain, the medical, social, and surgical history can provide information about risk factors and prior treatments.

Pain is the most common presenting symptom in patients with knee OA. It might be localized to one compartment initially; however, with long-standing OA, pain often occurs throughout the entire knee. Swelling, decreased range of motion (ROM), and mechanical abnormalities accompany the pain. Symptoms are intermittent in the beginning but increase in duration and severity as the disease progresses. Exercise, increased physical activity, or changes in the weather will often exacerbate symptoms, as will prolonged sitting, stair-climbing, or squatting. With advanced disease, the patient will often report a catching or locking within the knee joint, typically produced by osteophytes or meniscal abnormalities. Weakness and instability should be assessed in order to determine if symptoms are due to patient inhibition or if some mechanical defect or insufficiency is present. The patient should be asked about any previous attempts at intervention, including lifestyle modification, medications, and surgery, along with response to the treatment.

The physical examination begins with an overall evaluation of body habitus and a gait analysis. Antalgic gait patterns may be due to either a static limb or functional abnormality. Examine static limb alignment for varus or valgus deformities that could lead to the development of unicompartmental OA. Common sites of pain include the patellofemoral joint and the medial joint-line, with pain being either focal or diffuse.

Diagnostic imaging

Plain radiography is performed first in patients with knee OA. Anteroposterior (AP), lateral, and sunrise views that evaluate the patella are most commonly ordered. When obtaining the AP view, the technician should place the patient in a standing (or lying) position with knees bent at a 45-degree angle. This positioning enables the joint spaces to be accurately viewed and any spurring, narrowing, or osteophyte formation to be evaluated. Films taken during weight-bearing allow better evaluation of the knee in a position of function (see Figure 1).

Destruction of the articular cartilage or previous meniscectomy cause joint space narrowing and the varus/ valgus deformities noted on plain films. The chondral surface may become flattened as cartilage destruction occurs. Subchondral cysts may arise from increases in joint pressures. Osteophytes, bony outgrowths that develop at the joint margins or ligamentous attachments, progressively enlarge as the disease progresses. Radiographs should be focused on the knee joints, or include the hips and ankle joints, to evaluate the mechanical and anatomic axes of the lower extremities.

MRI is useful in evaluating the knee when radiographs reveal minimal bony change even though soft tissue pathology is present clinically. Bone scans will be abnormal with a variety of conditions including OA, meniscal injuries, stress fractures, and osteochondral defects. Special studies are not generally needed when imaging shows joint space narrowing and/or osteophyte formation.

Classification

There are two classifications of OA. Primary OA is the term used for the progressive degeneration of the articular cartilage and joints that increases in prevalence with age (see Figure 2). Secondary OA comprises degenerative changes to the articular cartilage and joints that occur after a significant injury, resulting in ligamentous/meniscal deficiency, intra-articular fracture, or varus/valgus deformity (see Figure 3). Table 2 lists diagnostic criteria for OA.

Approaches to treatment

Total knee arthroplasty (TKA) is the most aggressive treatment for OA of the knee, but there are a number of reasons to try to avoid it:

In younger, more active patients, the procedure will often have to be redone. The implant prosthesis can be expected to last 10 to 20 years in patients undergoing a first TKA, but replacement may be required within 10 years in subsequent surgeries.^5,6
The morbidity risk is significant. Infection rates are 2% to 5% in the acute setting, and rates for late infection secondary to comorbid disease are higher. Even with treatment of infection, successful retention of the prosthesis varies from 18% to 70%. Deep vein thrombosis (DVT) can be potentially catastrophic, with consequences ranging from local necrosis to pulmonary embolism, stroke, and even sudden cardiac death. Without prophylaxis, occurrence rates for DVT are as high as 70% to 80%, but even with adequate prophylaxis, DVT develops in 5.9% to 49% of cases.^7-11 The peroneal nerve is not directly in line during the surgical approach; however, injury from compression, traction, or ischemia occurs in 0.002% to 1.8% of cases after primary TKA. Hardware can fail for various reasons, including infection, patient selection, choice and design of implant, surgical technique, and functional sequelae.^5,12,13
The costs are significant. The price of the hardware set is $2,000 to $3,500, and the procedure—including the hospital stay and postoperative rehabilitation—can be more than $16,000.^14,15

When a patient with OA of the knee presents for treatment, here are some options you can give before referring the patient to an orthopedic surgeon.

Activity modifications

Altering activity is the first action patients must take when dealing with OA. Advise them to reduce or eliminate high-impact activities to diminish the progressive wear these activities cause to the joint surface. Running on concrete and jumping onto hard surfaces (in basketball, for example) are examples of the kind of high-impact activities that should be avoided. If the patient must run for exercise, soft surfaces are recommended. Patients should continue activities that maintain ROM, make changes to their footwear as needed, and reduce body weight if they are overweight or obese.

Physical therapy that teaches active/passive ROM exercises, along with flexibility exercises, can help the patient to maintain or improve the ROM of the knee. Exercises to strengthen the quadriceps and hamstrings aid in maintaining joint alignment as well as diminish the bone-on-bone pounding that can occur in the arthritic knee. Heat or cold therapy loosens up stiffened joints and reduces joint inflammation. Proprioceptive training helps reduce potential jarring to the joints due to loss of balance.

Footwear is important in the nonoperative management of knee OA. Wedge inserts or modifications to the shoe sole can correct alignment deformities up to 5 to 10 degrees in patients with pronation or supination. One study noted a statistically significant reduction of pain scores (greater than 75% over 12 months) in patients treated with a lateral wedge insole for medial compartmental OA.¹⁶ Cushioned shoes can diminish pain from prolonged periods of standing or walking.

Obesity is a well-documented risk factor for OA. The American College of Rheumatology (ACR) reports that a decrease in total body mass will reduce the joint reactive forces and decrease the physical manifestations of OA.¹⁷ This is especially important for women, who have a higher incidence of knee OA than do men in the same age group. One study showed that a weight loss of 5 kg over 10 years reduced the risk of degenerative arthritis by more than 50%.¹⁸ All clinicians should encourage weight reduction, because even a loss of 5 lb can decrease the stressors to the knee up to 25 lb.¹⁸

Assistive devices such as neoprene (elastic) knee braces minimize swelling, offer gentle support, and warm the knee without changing alignment. They may also aid balance by giving proprioceptive feedback to the patient. Neoprene braces provide no structural support for the knee, however, and they may compromise circulation.

Support braces typically are hinged to assist with stability within various planes of movement. They do not unload joint compressive forces and may be too restrictive for some patients. Unloading braces distract the compressive joint forces by applying varus/ valgus forces to the knee. Valgus bracing increases joint space and reduces focal joint pain up to 50% of the time in patients with medial compartment OA.¹⁹ However, obesity and certain body types limit the widespread use of the device. All of these braces are expensive, large, and uncomfortable when worn for extended periods of time.^20,21

Pharmacologic therapies

Medication is a mainstay of the nonsurgical treatment of OA. The drugs most often used include acetaminophen, NSAIDs, and chondroprotective oral supplements.

Acetaminophen is recommended by the ACR as a first-line therapy for symptomatic OA. It is very effective in pain reduction and has a limited side-effect profile. Recommended dosages are up to 4,000 mg daily taken in 4 divided doses. Studies show that NSAIDs and acetaminophen provide equivalent relief, even in patients with clinical symptoms of synovitis.²² The number of documented cases of hepatoxicity or nephrotoxicity in patients taking acetaminophen is dwarfed by the number of deaths from GI bleeding in patients taking NSAIDs.^23,24

NSAIDs are utilized for their anti-inflammatory as well as their analgesic properties. They work by reversibly inhibiting COX-1 and COX-2 acid metabolism, which blocks the production of inflammatory agents such as prostaglandins and leukotrienes. Studies have shown that no one NSAID is superior to the others. Also, research has shown that both short-term and long-term pain control from NSAIDs is not superior to acetaminophen’s.^22,25 Although effective, NSAIDs have adverse effects such as inhibiting the beneficial character of gastric mucosal lining production, reducing renal blood flow, and causing abnormalities in sodium balance. There is also a reversible antiplatelet effect that usually corrects itself within 24 hours after NSAID use is stopped.

More serious effects of NSAIDs include dyspepsia, GI ulceration, renal toxicity, hepatotoxicity, electrolyte imbalances, hypertension, and cardiac failure. Contraindications to NSAID use include GI, renal, and hepatic disease and the simultaneous administration of anticoagulation therapy. While NSAIDs are effective for long-term pain control in OA, the ACR and others recommend ordering a CBC, liver function tests, a stool guaiac test, and tests of renal function annually to monitor for possible side effects.

Chondroprotective oral supplements act on the articular cartilage. This is the dense tissue matrix primarily composed of chondrocytes, type II collagen, and proteoglycans. It holds abnormally large amounts of water, thus deflecting the compressive forces upon the joint. When the cartilage is damaged, however, it has limited ability to repair itself. ^2,26,27

Glucosamine and chondroitin sulfate are integral parts of the articular cartilage matrix. Numerous studies have shown that supplements containing both have reduced the progression of articular destruction of joints, reduced joint pain, and improved mobility.^26,28-30 The recommended dosage of glucosamine sulfate is 1,500 mg daily. Chondroitin sulfate is effective at daily dosages of 800-1,200 mg. Patients must take the supplements daily for a minimum of 3 months before the beneficial effects appear. Higher dosages are recommended for obese persons, those taking diuretics, and those who have peptic ulcer disease. Side effects, which are usually infrequent and stop with discontinuance of the drug, may include GI upset, headache, nausea, vomiting, heartburn, dyspepsia, constipation, and skin reactions.²⁶

Intra-articular injections

Both corticosteroids and viscosupplementation can be injected to treat OA. The corticosteroids used include prednisolone, methylprednisolone, triamcinolone hexacetonide, and betamethasone. The most common viscosupplementation agent is hyaluronic acid, which is usually given as a series of 2-mL injections.

Corticosteroids are administered in a single intra-articular dose, usually to treat acute exacerbations of pain. To reduce the risk of complications, the injection is not repeated for 3 to 6 months.³¹ The corticosteroid is typically combined with lidocaine and/or bupivacaine and injected after aspiration. When combined with aspiration of the knee effusion, corticosteroid injection provides 60%-87% of patients with relief for a variable period of days to months.^32,33

One controversy surrounding corticosteroid injection into the knee is whether it is the medication or the effusion aspiration that relieves the pain. The authors are not aware of studies evaluating this question. While corticosteroids have generalized anti-inflammatory effects, various studies have demonstrated deterioration of articular cartilage with long-term use.^2,34,35

Viscosupplementation is intended to replace hyaluronic acid, levels of which are reduced in the arthritic knee (see Figure 4).³ Hyaluronic acid is a critical component in the composition of synovial fluid, functioning as a joint lubricant and aiding in the absorption of joint loading forces. Synthetic viscosupplementation is comprised of either cross-linked or noncross-linked hyaluronic acid. A variety of synthetic viscosupplements are available, each with essentially the same chemical make-up. Injections, which are administered once a week over 3 to 6 weeks and can be repeated as frequently as every 3 months, reduce intra-articular bradykinins and inflammatory mediators and inhibit nociceptors.³Adverse reactions becomes more likely with successive injections. Beneficial effects can last longer more than 6 months.

One study evaluated whether viscosupplementation was more effective than corticosteroid injections.³⁶Over 6 months, 100 patients received a series of injections with either Synvisc (hylan G-F 20) or betamethasone. Both supplements were effective to a moderate degree, but women, interestingly, received less benefit than men from both treatments.

Conclusion

OA of the knee is a problem for the primary care provider as well as for the orthopedic surgeon. Treatment options that actively involve the patient include weight loss, exercise, flexibility and strength training, and the use of assistive devices, pharmacologic therapies, and intra-articular injections—all of which can delay the need for surgical intervention. Given the high cost of surgery and its possible complications, primary care providers should be prepared to try these options first to reduce the burdens of this condition on the patient and society.