Over 20 million Americans are currently affected by osteoarthritis, including more than half of the population over the age of 65. Osteoarthritis (OA) is a degenerative disease that involves the gradual breakdown of articular cartilage, as well as the synovium and subcondral bone of a joint (refer to anatomy). OA can be commonly seen in joints of the hip, knee, hands, feet, and spine. The purpose of this page is to focus on the effects of OA on the knee joint.1
The knee joint is a synovial joint, which consists of a joint capsule, synovial membrane, synovial fluid, subchondral bone, and articular cartilage. The joint capsule encases the whole knee. The synovial membrane provides nutrients to the surrounding structures. The smooth, hard articular cartilage plays a major role in reducing friction within the joint. It also provides protection to the subchondral bone within. Lastly, the synovial fluid acts as a lubricant to decrease friction as the knee moves. It also supplies nourishment to the avascular articular cartilage. 1
The four bones that make-up the knee are the femur (thigh), tibia (shin), fibula (outside border of shin), and patella (kneecap). The junction between the femur and tibia is where most movement occurs and the patella lies in a groove on the femur. The femur is a long bone that starts at the hip and travels down to the knee while the tibia and fibula travel down to the ankle. There are also two menisci (medial meniscus and lateral meniscus) over the surface of the tibia that play a vital role in shock absorption and weight distribution between the tibia and femur. The bones of the knee are important, but the stability of the knee is derived from ligaments.
The main ligaments of the knee include the anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), medial collateral ligament (MCL), and lateral collateral ligament (LCL). The ACL connects the anterior (front) of the tibia to the posterior (back) of the femur and prevents the tibia from excessively translating forward. The PCL attaches from the posterior femur to the anterior tibia and limits posterior translation of the tibia on the femur. The MCL restricts forces that stress the inside of the knee such as a blunt force that hits the outside of the knee. This ligament attaches on the inside aspect of the knee from the femur to the tibia. It also connects to the medial meniscus. The lateral meniscus travels from the outer aspect of the femur to the fibula and prevents forces from the inside of the knee.
The major blood supply to the knee joint is derived from branches of the genicular arteries. These branches are named according to which region of the knee they supply after all coming together (superior medial and lateral, the posterior, and the inferior medial and lateral).2
The major muscles and tendons of the knee include the quadriceps (rectus femoris, vastus lateralis, vastus medialis, vastus intermedius), hamstrings (biceps femoris, semimembranosis, semitendinosis ), patellar tendon/ligament, and the quadriceps tendon.
Image source: http://rmaeug.com/images/danceakpfig1.jpg
Osteoarthritis is the most common articular disease. At age 50, the prevalence of OA significantly increases due to natural age related wear-and-tear on the joint cartilage.1 Women typically have a higher prevalence than men in knee OA.3 At 45 years and older, it is reported that approximately 16% of Americans have symptoms of knee OA.4 Between 55-64 years old, 28% of men and women show signs of knee OA in the knee.1 Between the ages 65-74, 39% of men and women show signs of knee OA.1 Overall, most cases occur or are diagnosed between the 55-74 year range.5
There are many risk factors that contribute to the incidence of knee OA. Most of the main factors have to do with the loading of the knee joint. Degenerative processes of the articular cartilage can begin as a result of excessive loading to a healthy joint or normal loading to a previously hindered joint. Occupation can play a role in terms of repeated lifting or bending at the knee. Another major correlating factor is obesity.6 The knee joint can only provide so much shock absorption and excessive weight and mechanical loading wears down the cartilage very aggressively. The aging process contributes to natural breakdown of joint cartilage with joint space narrowing and a large occurrence of osteophytes. However, age alone is not considered a direct cause of knee OA. Other risk factors include genetics, muscular dysfunction, menopause, trauma that alters biomechanics, previous RA, infections, bone disorders (AVN, Paget disease), and previous orthopedic disorders (fractures, dislocations).1
The knee joint provides the movements of flexion (flexing), extension (extending), and tibial rotation (turning knee in/out). The main joint providing these movement is the tibio-femoral joint. The concave surface of the tibia articulates with the convex surface of the femur. To further understand the biomechanics of the knee, it is very important to understand the basic concepts of open vs. closed packed (chain) positions. Open chain means that the tibia is moving on a fixed femur where there are no forces acting from beneath the foot. In closed-chain however, the femur rotates on a fixed tibia. Here, the foot is fixed and stable on the ground and the femur is free to move over it. Below is a wonderful chart from Dr. Thompson of University of Oklahoma’s Dept. of Rehab Services, summarizing the biomechanics of the knee joint.7
|DURING KNEE EXTENSION||DURING KNEE FLEXION|
|OPEN CHAIN||CLOSED CHAIN||OPEN CHAIN||CLOSED CHAIN|
|TIBIA GLIDES ANTERIORLY ON FEMUR||FEMUR GLIDES POSTERIORLY ON TIBIA||TIBIA GLIDES POSTERIORLY ON FEMUR||FEMUR GLIDES ANTERIORLY ON TIBIA|
Patients with knee OA will typically present with deep, achy, localized knee pain that becomes worse upon activity and is reduced with rest. More severe cases will have pain at rest. Stiffness is also extremely common following periods of inactivity (sitting, sleeping, etc.). Examination findings may demonstrate crepitus, decreased ROM, effusion, bony enlargement, and tenderness upon palpation of the joint line. Radiographic findings may show joint effusion and synovial thickening, bone marrow edema, osteophytes, small cartilaginous lesions, changes in patellar cartilage, and periarticular lesions, which can include bursitis and iliotibial band syndrome.8,9,10,11
Radiographic testing (X-Ray) is typically the method of choice in diagnosing knee OA, although clinical evidence contributes as well. Radiographs can illustrate joint-space loss, as well as subchondral bony sclerosis and cyst formation.1 An MRI can depict many of the same characteristics of osteoarthritis as those displayed on radiographs, including joint narrowing, subchondral osseous changes, and osteophytes.12 However, only the MRI can depict articular cartilage directly.1 Diagnosis is typically based on the presence of knee pain and osteophytosis along with stiffness lasting shorter than 30 minutes and/or crepitus.12,13 Blood tests and bone scans are used occasionally to rule out other forms of arthritis or similar conditions (RA, Chondrocalcinosis, Charcot’s Joint, Osteomyelitis).14 The Kellegren-Lawrence Grading scale is sometimes used to classify the degree or severity of degeneration.15
KELLGREN-LAWRENCE GRADING SCALE:
Conservative approaches to knee OA should be prioritized before considering surgical intervention. Treatment should be based around reducing pain and improving functional status.16 Lifestyle modification should be strongly considered as a conservative treatment approach. Reducing the amount of load in weight bearing may be achieved by modifications with weight reduction, mechanics in ADL’s/work (bending, squatting, carrying), or using an assistive device. Patient education is also crucial in the management of knee OA. Patients should engage in discussions with a physical therapist about ways to lose weight, improve body mechanics and posture, and how to properly use an assistive device.1 Despite the assumption that unloading the joint means to not use the joint, participation in certain forms of exercise are proven to be beneficial. Research has found that non-weightbearing activity can provide equal benefits to exercise in weight-bearing in terms of improving knee function.17 Low impact activities like water aerobics and riding a stationary bike are great. While further research is indicated, tai chi has also been shown to be effective by some research to improve physical function scores as well as pain scores.18 Physical Therapy establishes a specific stretching program to increase ROM and strengthening program with a focus on quadriceps. Improving ROM and increasing strength has been found to reduce pain and enhance quality of life.19 A therapist may also choose to incorporate balance/proprioception training. In an article looking at a variety of evidence based research on treatments, Ringdahl et al. 2011, evidence shows that engaging in aquatic or land-based exercise, aerobic walking, quadriceps strengthening, resistance exercise, and tai chi are most effective for pain reduction and decreasing disability from knee osteoarthritis.20,21,22,23,24,25,26,27 Medications such as NSAIDS should be taken for pain relief and physicians may also recommend acetaminophen, muscle relaxants, or glucocorticoids for slowing the progression of knee OA.1,28 In addition, corticosteroid injections have been shown to give a beneficial amount of short-term relief.29,30
An osteotomy is considered for patients who wish to remain active and are typically under the age of 60. The surgery is a realignment of the joint in an effort to move the stress of the damaged medial knee to the healthier lateral side of the knee. An osteotomy can potentially decrease pain and potentially prolong the need for a joint replacement. It is most often indicated for bony deformations or postural deviations of the knee.31
An arthroplasty should be considered as a last resort following an unsuccessful attempt with physical therapy. Assuming no complications, approximately 8-15 years of viability are expected with an arthroplasty. The arthroplasty involves removal of the damaged joint surface and the insertion of a prosthetic device that is stabilized by cement or by bone growth.1
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