Knee osteoarthritis (OA), also known as degenerative joint disease, is typically the result of wear and tear and progressive loss of articular cartilage. It is most common in elderly women and men. Knee osteoarthritis can be divided into two types, primary and secondary. Primary osteoarthritis is articular degeneration without any apparent underlying reason. Secondary osteoarthritis is the consequence of either an abnormal concentration of force across the joint as with post-traumatic causes or abnormal articular cartilage, such as rheumatoid arthritis (RA). Osteoarthritis is typically a progressive disease that may eventually lead to disability. The intensity of the clinical symptoms may vary from each individual. However, they typically become more severe, more frequent, and more debilitating over time. The rate of progression also varies for each individual. Common clinical symptoms include knee pain that is gradual in onset and worse with activity, knee stiffness and swelling, pain after prolonged sitting or resting, and pain that worsens over time. Treatment for knee osteoarthritis begins with conservative methods and progresses to surgical treatment options when conservative treatment fails. While medications can help slow the progression of RA and other inflammatory conditions, no proven disease-modifying agents for the treatment of knee osteoarthritis currently exist.
Knee osteoarthritis is classified as either primary or secondary, depending on its cause. Primary knee osteoarthritis is the result of articular cartilage degeneration without any known reason. This is typically thought of as degeneration due to age as well as wear and tear. Secondary knee osteoarthritis is the result of articular cartilage degeneration due to a known reason.
Possible Causes of Secondary Knee OA
Risk Factors for Knee OA
Knee osteoarthritis is the most common type of arthritis diagnosed, and its prevalence will continue to increase as life expectancy and obesity rises. Depending on the source, roughly 13% of women and 10% of men 60 years and older have symptomatic knee osteoarthritis. Among those older than 70 years of age, the prevalence rises to as high as 40%. The prevalence of knee osteoarthritis in males is also lower than in females. Interestingly, not everyone who demonstrates radiographic findings of knee osteoarthritis will be symptomatic. One study found that only 15% of patients with radiographic findings of knee OA were symptomatic. Not factoring in age, the incidence of symptomatic knee osteoarthritis is roughly 240 cases per 100,000 people per year.
Articular cartilage is composed primarily of type II collagen, proteoglycans, chondrocytes, and water. Healthy articular cartilage constantly maintains an equilibrium between each of the components so that any degradation of cartilage is matched by synthesis. Healthy articular cartilage is thus maintained. In the process of osteoarthritis, matrix metalloproteases (MMPs), or degradative enzymes, are overexpressed, disrupting the equilibrium and resulting in an overall loss of collagen and proteoglycans. In the early stages of osteoarthritis, chondrocytes secrete tissue inhibitors of MMPs (TIMPs) and attempt to increase synthesis of proteoglycans to match the degradative process. However, this reparative process is not enough. The loss in equilibrium results in a decreased amount of proteoglycans despite increased synthesis, increase in water content, the disorganized pattern of collagen, and ultimately loss of articular cartilage elasticity. Macroscopically these changes result in cracking and fissuring of the cartilage and ultimately erosion of the articular surface.
Although knee osteoarthritis is closely correlated with aging, it is important to note that knee osteoarthritis is not simply a consequence of aging, but rather its own disease. This is supported by the differences seen in cartilage with both osteoarthritis and aging. Furthermore, it the enzymes responsible for cartilage degradation are expressed in higher amounts in knee osteoarthritis, whereas they are at normal levels in the normal aging cartilage.
Cartilage Changes in Aging
Cartilage Changes in OA
Responsible for cartilage matrix degradation
Tissue inhibitors of MMPs
Control MMP activity preventing excess degradation
Patients typically present to their healthcare provider with the chief complaint of knee pain. It is essential to obtain a detailed history of their symptoms. Pay careful attention to the history as knee pain can be referred from the lumbar spine or the hip joint. It is equally important to obtain a detailed medical and surgical history to identify any risk factors associated with secondary knee OA.
The history of the present illness should include the following:
Clinical Symptoms of Knee OA
Physical examination of the knee should begin with a visual inspection. With the patient standing, look for periarticular erythema and swelling, quadriceps muscle atrophy, and varus or valgus deformities. Observe gait for signs of pain or abnormal motion of the knee joint that can be indicative of ligamentous instability. Inspect the surrounding skin for the presence and location of any scars from previous surgical procedures, overlying evidence of trauma, or any soft tissue lesions.
Range of motion (ROM) testing is a very important aspect of the knee exam. Active and passive ROM with regard to flexion and extension should be assessed and documented.
Palpation along the bony and soft tissue structures is an essential part of any knee exam. The palpatory exam can be broken down into the medial, midline, and lateral structures of the knee.
Areas of focus for the medial aspect of the knee
Areas of focus for the midline of the knee
Areas of focus for the lateral aspect of the knee
A thorough neurovascular exam should be performed and documented. It is important to assess the strength of the quadriceps and hamstring muscles as these often times will become atrophied in the presence of knee pain. A sensory exam of the femoral, peroneal, and tibial nerve should be assessed as there may be concomitant neurogenic symptoms associated. Palpation of a popliteal, dorsalis pedis, and posterior tibial pulse is important as any abnormalities may raise the concern for vascular problems.
Other knee tests may be performed, depending on the clinical suspicion based on the history.
Special knee tests
In addition to a thorough history and physical, radiographic imaging is required. The recommend views include standing anteroposterior (AP), standing lateral in extension, and a skyline view of the patella. A standing 45-degree posteroanterior (PA) view of the knee may be obtained which gives a better assessment of the weight-bearing surface of the knee. Occasionally, long leg standing films will be obtained to view the degree of deformity and overall alignment of the lower extremity. It is important to understand that radiographs of the knee must be obtained with the patient standing. This gives an accurate representation of the joint space narrowing present. Often, films will be taken with the patient supine which gives a false sense of joint space and alignment and therefore should not be used is the evaluation of suspected knee OA.
Radiographic Findings of OA
Treatment for knee osteoarthritis can be broken down into non-surgical and surgical management. Initial treatment begins with non-surgical modalities and moves to surgical treatment once the non-surgical methods are no longer effective. A wide range of non-surgical modalities is available for the treatment of knee osteoarthritis. These interventions do not alter the underlying disease process, but they may substantially diminish pain and disability.
Non-Surgical Treatment Options
The first-line treatment for all patients with symptomatic knee osteoarthritis includes patient education and physical therapy. A combination of supervised exercises and a home exercise program have been shown to have the best results. These benefits are lost after 6 months if the exercises are stopped. The American Academy of Orthopedic Surgeons (AAOS) recommends this treatment.
Weight loss is valuable in all stages of knee osteoarthritis. It is indicated in patients with symptomatic arthritis with a body mass index greater than 25. The best recommendation to achieve weight loss is with diet control and low-impact aerobic exercise. There is moderate evidence for weight loss based on the AAOS guidelines.
Knee bracing in the setting of osteoarthritis includes unloader-type braces which shift the load away from the involved knee compartment. This may be useful in the setting where either the lateral or medial compartment of the knee is involved such as in a valgus or varus deformity.
Drug therapy is also the first-line treatment for patients with symptomatic osteoarthritis. There are a wide variety of NSAIDs available, and the choice should be based on physician preference, patient acceptability, and cost. The duration of treatment with NSAIDs should be based on effectiveness, adverse effects, and past medical history. There is strong evidence for NSAID use based on the AAOS guidelines.
Glucosamine and chondroitin sulfate are available as dietary supplements. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage. No strong evidence exists that these supplements are beneficial in knee OA; in fact, there is strong evidence against the use according to the AAOS guidelines. There are no major downsides to taking the supplement. If the patient understands the evidence behind these supplements and is willing to try the supplement, it is a relatively safe option. Any benefit gained from supplementation is likely due to a placebo effect.
Intra-articular corticosteroid injections may be useful for symptomatic knee osteoarthritis, especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with osteoarthritis and minimize the systemic effects of the steroid.
Intra-articular hyaluronic acid injections (HA) injections are another injectable option for knee osteoarthritis. HA is a glycosaminoglycan that is found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of osteoarthritis and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint. Depending on the brand of HA, it can either be produced from avian cells or bacterial cells in the laboratory and therefore must be used with caution in those with avian allergies. While this is a prevalent treatment option, it is not highly supported in the literature, and there is strong evidence against its use based on the AAOS guidelines.
Surgical Treatment Options
A high tibial osteotomy (HTO) may be indicated for unicompartmental knee osteoarthritis associated with malalignment. Typically an HTO is done for varus deformities where the medial compartment of the knee is worn and arthritic. The ideal patient for an HTO would be a young, active patient in whom arthroplasty would fail due to excessive component wear. An HTO preserves the actual knee joint, including the cruciate ligaments, and allows the patient to return to high-impact activities once healed. It does require additional healing time compared to an arthroplasty, is more prone to complications, depends on bone and fracture healing, is less reliable for pain relief, and ultimately does not replace cartilage that is already lost or repair any remaining cartilage. An osteotomy will delay the need for an arthroplasty for up to 10 years.
Indications for HTO
Contraindications for HTO
A UKA also is indicated in unicompartmental knee osteoarthritis. It is an alternative to an HTO and a TKA. It is indicated for older patients, typically 60 years or older, and relatively thin patients; although, with newer surgical techniques the indications are being pushed.
Indications for UKA
Contraindications for UKA
A TKA is the surgical treatment option for patients failing conservative management and those with osteoarthritis in more than one compartment. It is regarded as a valuable intervention for patients who have severe daily pain along with radiographic evidence of knee osteoarthritis.
Indications for TKA
Contraindications for TKA
Advantages of UKA vs TKA
Advantages of UKA vs HTO
Any potential cause of local or diffuse knee pain should be considered in the differential diagnosis of knee osteoarthritis.
Complications associated with non-surgical treatment are largely associated with NSAID use.
Common Adverse Effects of NSAID Use
Common Adverse Effects of Intra-Articular Corticosteroid Injection
Common Adverse Effects of Intra-Articular HA Injection
Complications Associated with HTO
Complications Associated with UKA
Complications Associated with TKA
Postoperative and rehabilitation care after a TKA is aimed at restoring the highest possible range of mobility in and full muscular control of the operated knee. Adequate rehabilitation is an important requirement for successful TKA. The specific rehabilitation program following a TKA is somewhat controversial and varies from surgeon to surgeon. Bed mobility, transfer training, and bedside exercises begin the same day as surgery. Full weight-bearing, typically with a walker, under the supervision of a therapist, is also allowed. Active range of motion (ROM), terminal knee extensions, straight leg raises, and muscle strengthening exercises begin on postoperative day one. Gait training and transfers continue as well. In general, the patient must demonstrate safe ambulation with an assistive walking device on flat ground and stairs, the ability to safely transfer from bed to seated and standing positions, and adequate pain control prior to being discharged from the hospital. Patients are typically discharged to home or a skilled nursing facility. This is based on individual need in consultation with social work. Discharge to home is greatly preferred if possible. The typical hospital stays for a TKA is 1 to 2 nights depending on the patient. The first postoperative visit is at the two-week mark where a wound check is performed and surgical staples are removed if present. Outpatient physical therapy will begin at this time if not begun already. The patient increases their ambulation, independence in their activities of daily living, works on their ROM, and works on their quadriceps strength. Patients can resume driving when they can operate the pedals safely and rapidly. This usually takes 4 to 6 weeks. Return to work usually takes 4 to 10 weeks, depending on the work obligations. Patient follow up is routinely at 6 weeks, 3 months, and one year after surgery. Once strength, mobility, and balance are regained, patients can resume low-impact sporting activities. High-impact activities are discouraged.
The best predictor of final postoperative ROM following TKA is preoperative ROM, and patients should be aware of this before TKA.
Knee osteoarthritis (OA) is best managed by an interprofessional team that consists of an orthopedic surgeon, rheumatologist, physical therapist, dietitian, a pain specialist, and internist. The disorder has no cure and thus attempts should be made to prevent progression of the disorder. The patient should be referred to a dietitian for weight loss and to physical therapy to regain joint function and muscle strength. Treatment for knee osteoarthritis begins with conservative methods and progresses to surgical treatment options when conservative treatment fails. The pharmacist should look at the patient's medications to ensure there are no interactions and that the dosing and indications are all correct. While medications can help slow the progression of RA and other inflammatory conditions, no proven disease-modifying agents for the treatment of knee osteoarthritis currently exist. (level II)
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