What Is Osteoarthritis?
Osteoarthritis (OA) is the leading cause of disability in the USA. It is estimated that 1 out of 3 adults will suffer from arthritis. By definition osteoarthritis or degenerative joint disease (DJD) is a progressive disorder involving inflammation and degradation of the articular or hyaline cartilage on the ends of bones in various joints of the body. This type of cartilage has no nerve supply and is very resistant to friction making it perfect for weight bearing surfaces. When OA begins, the affected cartilage usually develops small tears in the joint surfaces that begin to progress into larger more substantial areas of wear. In normal joints, articular cartilage is capable of repairing minor wear in a limited capacity through chondrocyte production (cells that form new cartilage). When the damage rate becomes too significant and continuous, these cells can no longer repair the affected area. When this happens the process of degenerative joint disease begins. As this disease progresses, eventually the cartilage will wear out to a point where the underlying bone becomes exposed. This subchondral bone is rich in nerve supply and unlike hyaline cartilage is very prone to further wear from friction When this happens in a joint, the bones connecting the joint rub together resulting in pain and joint inflammation. This is where the term “bone on bone” comes from. As OA progresses, the affected joint will begin to form bone spurs around the joint margins and eventually lead to a noticable angular deformity at the joint. Although it is primarily found in weight bearing joints (knees and hips), it also occurs in non-weight bearing joints such as the shoulder.
DJD symptoms usually begin as stiffness (especially in the AM), pain with prolonged weight-bearing or immediately following activity, swelling, crepitus (audible grinding or ratcheting) and loss of motion. Symptoms vary from person to person and joint to joint.
The knee joint is one of the sites most commonly to be associated with OA. The knee joint is a hinge joint, which connects the large upper leg bone (femur) to the lower leg bone (tibia). In the knee, there are two unique structures called the menisci. One is on the inside weight bearing surface of the tibia (medial meniscus) and one is on the outside of the tibia. The meniscus is a spongy type of cartilage known as fibrocartilage which functions to cushion the knee much like the shocks on a car. These structures act as cushions for the ends of the bone and to protect the hyaline or articular cartilage on the ends of the bones. In addition, the meniscus is concave in shape to accommodate the convex shape of the femur. This shape allows the weight of the body to evenly be distributed to the femur and allow the amount of contact pressure of the femur to be diminished. When the meniscus is damaged, the contact pressures on the femur increase. In young and active individuals, meniscal injuries usually happen from trauma from sports or other high level activities. In older adults, the meniscus can begin to fray and degenerate without specific trauma. Over time, if the process continues the meniscus will fray, continue to tear and eventually fail exposing the articular cartilage to the increased contact pressures. This exposure can lead to an osteochondral defect (OCD) in the articular cartilage which resembles a “pothole” on the weight bearing surface of the joint. An OCD is uncapable of healing itself. Once an OCD is present it will expose the underlying bone. This bone has a rich nerve supply which unlike the articular cartilage is painful with compression such as weight bearing. Overtime, the OCD will continue to wear and begin to get larger and larger until the majority or all the articular cartilage is worn down to the bone. In end stage OA, a visible joint deformity is often noted. This is do to loss of space from the degradation of the meniscus. On X-rays, the bones will appear to be “kissing”.
A step-by-step approach is the common treatment for OA. This progression begins with conservative care and progresses to total joint replacement at end stage OA.
- Anti-inflammatory drugs: Your doctor will often prescribe a trial of NSAID’s (non-steroidal anti-flamatory drugs) such as Aleve, ibuprofen, Celebrex, Mobic, Advil, Naprosyn, etc.
- Physical Therapy: A trial of physical therapy is often prescribed at the same time as NSAIDS. Therapy will address joint restrictions, loss of strength, and flexibility as well as pain modulation. Many times, physical therapy will deter the progression of DJD. Generalized deconditioning is very common with arthritic joints. Skilled physical therapists will identify muscular imbalances and specific joint restrictions, which will improve joint function and overall strength and conditioning. Various therapeutic modalities in PT are helpful for pain modulation. Since OA is a progressive and chronic disorder, our clinic utilizes moist heat in conjunction with inferential electrical stimulation (IFC) or transcutaneus electrical nerve stimulation (TENS). Ice is only encouraged with an acute arthritic flare-up. The main-stay of conservative care for OA, are joint-sparing progressive resistive exercise as well as manual therapy for promotion of motion and joint lubrication. The phrase “Motion is Lotion” is the key for arthritic joints. The right exercise is essential to slow the progression of DJD and promote joint and overall health.
- Glucosamine and Chondroitin Supplementation: In theory, glucosamine helps to prevent the breakdown of cartilage as they produce cartilage-building proteins. Chondroitin is thought to aid in fighting inflammation and in inhibiting the production of cartilage destroying enzymes. Consumer Reports recommends Kirkland Signature (Costco), Spring Valley (Wal-Mart) and Target Triple Strength brands. Expensive brands bought at nutrition stores often add other supplements to their products that have little to no medical backing. Should not be taken with shellfish allergies or if you have a clotting disorder.
- Cortisone injections: Your doctor may recogmend a steroid injection which can decrease some of the inflammatory properties of OA. This has been a classic treatment option for management of OA.
- Viscosupplementation injections: Another option your doctor may discuss with you are a new type of injection which involves injecting hyaluronic acid (HA)in order to improve lubrication and to thereby reduce the inflammation of the joint. Hyaluronic acid is a nature substance in the fluid within the knee. As the OA progression occurs, the body stops producing HA in its normal amount. There are currently five different companies offering products for viscosupplementation. A series of three to five injections spaced one week apart are the current protocol at this time. Anywhere from 50 to 75% of patients express relief with this treatment.
- Surgical Intervention: The last and final treatment for end stage OA would be total joint arthroplasty. (TJA) This should be the last option to consider. Before considering a TJA, a patient should be in constant pain the significantly limits their capacity for activities of daily living or occupational duties.