osteoarthritis
Although they may have similarities, these two forms also have differences. Primary OA is not associated with any known risk factors, but this is not so with secondary OA (see more below). Men are more likely to suffer from OA than women -- up to the age of 45. From 45-55, both men and women have an equal likelihood of suffering from the disease; but, after that, it is more women than men who develop the condition. Not only is it more frequent in women after the age of 55, but also more severe.
OA usually affects just a few joints, mainly the knees, hips, hands, neck, and lower spine. It can appear anywhere in the body, in no particular order, and initially, does not strike symmetrically, that is, both hips or both knees. It may also appear in the joint of the big toe as a bunion or bony spurs on the end joints of the fingers (Herberden's nodes) or on the middle joints (Bouchard's nodes). These are most prevalent among women between the ages of 40 and 60 and thought to be an inherited form since they often occur in members of the same family. There may also be cysts, gross bony overgrowths, bowed legs, knock knees, and fluid retention associated with the condition.
Certain foods have proven to have the ability to accelerate arthritic symptoms or help ease them. For instance, arachidonic acid found in animal products, increases inflammation, while the essential fatty acids (linolenic acid and linoleic acid) help reduce inflammation. Nightshade vegetables have proven to aggravate arthritic symptoms in some people.
Primary OA occurs more often than secondary. It is a slow, progressive condition that affects mainly the weight-bearing joints of the knees and hips; but it can also affect the lower back, neck, and fingers. Obesity and family history are thought to be the main contributing factors. There are several theories as to the cause of primary OA, including the following:
- Possible changes in the cartilage matrix. Chondrocytes (responsible for maintaining a normal blend of collagen), proteoglycans, and water, sometimes mix the balanced formula. The body tries to compensate by making more chondrocytes which, in turn, causes greater amounts of collagen and proteoglycans to be manufactured. At the same time, there is also an excess fluid build-up which washes away these newly synthesized molecules (as well as some older ones) leaving fewer than before.
- An out-of-control enzyme. While chondrocytes make collagen and proteoglycans, they also produce enzymes that break down these ageing molecules. Consequently, when more chondrocytes are manufactured to try and rectify a possible change in the matrix, more enzymes are also produced. The result is the opposite of the intended purpose, with more cartilage being destroyed than created. When a joint is flooded with these enzymes, the collagen fibers in the cartilage become smaller and the dense netting that they provide begins to relax. As a result, the proteoglycans, normally held in place by the collagen, now begin to drift off and disappear. Without enough proteoglycans to attract and hold water, the cartilage begins to dry out, becoming more susceptible to cracking, fissuring, and wearing through.
- Trauma to the subchondral bone. This portion of the bone, located directly under the cartilage, may be damaged by an injury or by repeated stress to the joint, which can lead to a cycle of bony overgrowth and joint damage.
- Bone disease. A problem with the blood supply can weaken the bone, which ultimately leads to tiny fractures and osteonecrosis (bone death). Alcoholism, infection, and acute trauma are among the possible primary causes.
- Abnormal liver function. The liver is a source of many hormones, growth factors, and substances that aid cartilage and bone formation. If there is any chronic abnormality in its function, bony overgrowths and cartilage destruction result.
Secondary OA is quite different from the primary form. It often appears before the age of 40 and has a clearly defined cause. All of the following risk factors alter cartilage in some way and accelerate the rate of cartilage loss:
- Trauma, as sprains, strains, joint dislocations, and fractures.
- Long-term mechanical stress associated with athletics, ballet dancing, or such repetitive physical tasks as tennis, gardening, typing, or even knitting.
- The presence of inflammation in joint structures where inflamed cells release enzymes capable of digesting cartilage cells.
- Joint instability caused by damage to supporting structures, usually of the joint capsule, ligaments, or tendons.
- Neurologic disorders, as diabetic neruopathy or Charcot's disease, where pain and reflexes are diminished or lost, increases the tendency for abnormal movement, positioning, or weight-bearing.
- Congenital or acquired skeletal deformities.
- Blood or endocrine disorders, as hemophilia, which causes chronic bleeding into the joints, or hyperparathyroidism, which causes bone to lose calcium.
- Drugs, as colchicine, indomethacin, and steroids which stimulate the activity of collagen-digesting enzymes in the synovial membrane.
Pathophysiology of Osteoarthritis:
Normally, when a synovial joint is at rest, cartilage soaks up liquid (synovial fluid); but when the joint is in motion, the liquid is squeezed out. This continual in and out "squishing" happens hundreds of times during the course of a day. Over time, the protective barriers begin to erode. Since most of the body weight rests on the knees, they are usually the first to become affected. This often begins with stiffness or the occasional pain which becomes progressively worse. However, actual deterioration begins long before these symptoms are felt.
The problem begins in the cartilage matrix, the birthplace of cartilage. The cartilage matrix is made up of proteoglycans, glycosaminoglycans (carbohydrates that contain amino sugars found in proteoglycans), chondrocytes, and collagen (a fibrous structural protein). Normally, all four elements -- collagen, proteoglycans, chondrocytes, and water -- work together to ensure smooth, pain-free movement. This part is essential in understanding why the supplements glucosamine and chondroitin sulfates are a popular and effective treatment for arthritis.
Proteoglycans, also called chondroitin sulfates, are huge molecules made up of protein and sugars that are woven around and through collagen fibers forming a dense netting inside the cartilage. These molecules make cartilage so resilient that it can stretch and then bounce back when moved. They also trap water molecules much like a sponge. In a Harvard health letter from 1992, proteoglycans were described like this: "Healthy proteoglycans look like fresh Christmas trees; in osteoarthritis, they are as scraggly as cast-offs in February."
Chondrocytes are special cells sprinkled throughout the matrix. They are the only cells found within the matrix and are continually producing new collagen and proteoglycan molecules. They are also responsible for releasing enzymes that dispose of ageing collagen and proteoglycan molecules that have surpassed their usefulness.
Collagen is found in many different parts of the body, taking different forms to fulfill various functions. Collagen can be altered into strong ropes to form tendons, thin sheets to make skin, clear membranes for corneas, and strong, weight-bearing structures called bones. Collagen is a vital part of cartilage providing it with elasticity and the ability to absorb shock. It also creates a framework to hold the proteoglycans in place and can be referred to as the "glue" that holds the cartilage matrix together.
Enzymes are released to break down the large molecules of these components into diffusable fragments which are then taken up by the chondrocytes and digested by the cell's own lysosomal enzymes. Scientists are not certain where or how these enzymes are formed, but they have several theories:
- Some may be lie dormant in the matrix or in the cartilage itself.
- Others might originate in the synovial membrane, blood plasma, or leukocytes and migrate into the synovial cavity.
- Possible activation of these enzymes may be the result of injury, dietary allergies, inflammation, or other conditions that trigger an excessive release of enzymes in the joint.
Any changes in the structure of proteoglycans disrupts the pumping action that regulates the movement of synovial fluid into and out of the cartilage. Without this regulatory action, the cartilage accumulates too much fluid and becomes less able to withstand the stresses of weight bearing. The lining (synovium) often becomes inflamed and, since it has many nerve endings and pain receptors, any inflammation sends pain messages rocketing to the brain. In response, the brain screams back "fix it" and the synovium tries to solve the problem by producing more fluid. This results in a flooding of the area, which causes more pain and swelling. The synovium itself may also swell and exude a puslike material.
As the disease progresses, the cartilage begins to soften and crack, resulting in longitudinal fissures (fibrillation). In advanced cases, bone spurs (osteophytes), abnormal bone hardening (eburnation), and fluid-filled pockets in the bone (subchondral cysts) can form. Pressure builds in the cysts until its contents are forced into the synovial cavity, breaking through the articular cartilage on the way. As the articular cartilage erodes, cartilage-coated osteophytes may grow outward from the underlying bone. These spur-like bony projections enlarge until small pieces, called "joint mice," break off into the synovial cavity. These fragments can cause irritation, resulting in inflammation and an accumulation of unwanted fluid (joint effusion) and the cycle begins again.
As the cartilage degenerates, more stress is placed on the joints which, in turn, speeds up the destruction of even more cartilage. The bones then become damaged and, as the body's regulatory mechanisms fail, the afflicted joint may become deformed. The bones thicken or change shape, narrowing the space within a joint. Bone spurs twist the joints contours, making it difficult for the bones to move. Heberden's or Bouchard's nodes can disfigure the joints of the fingers.
On an x-ray, the joint will appear narrowed and no longer held wide apart with the even contours of healthy cartilage. Inside the arthritic joint, the cartilage will be pitted and irregular and may have holes. New cartilage and new bone are continually being laid down in an attempt to compensate, but this cannot completely replace what is being lost.
Symptoms of OA
- Pain usually begins as a minor ache that appears after the joint has been used and disappears with rest. But, as the disease progresses, a sharp pain may strike if the joint is used even a little. Eventually, the joint aches even when in a resting position and may disrupt sleep.
- Stiffness will begin as a bothersome condition, appearing only after long periods of rest; but as the disease progresses, it will become chronic, affecting permanent range of motion.
- Crepitus, the crunching sound that emanates from affected joints, begins most often in the knees and occurs in advanced stages of OA.
Differences between osteoarthritis and rheumatoid arthritis
- OA usually begins after age 40, while RA initially strikes between the ages of 25 and 50.
- OA develops gradually, while RA comes and goes without warning.
- OA usually begins in joints on one side of the body, while RA attacks the joints on both sides simultaneously.
- OA does not usually produce redness, warmth, or swelling but feel cool and hard to the touch; while in RA, the joints feel warm and spongy.
- OA affects mainly the joints of knees, hands, hips, feet, and spine and only occasionally attacks the knuckles, wrists, elbows, or shoulders; while RA affects many or most joints.
- OA does not cause an overall feeling of sickness; while RA does as well as fatigue, weight loss, and fever.
- OA joints have a popping, clicking, or banging sound; while those of RA tend to make a sound like crinkling cellophane.
Differences between OA and simple aging joints
- OA deterioration occurs on weight-bearing cartilage surfaces, while deterioration in ageing occurs on non-weight-bearing cartilage surfaces.
- OA joints show significant physical, chemical, and degrading changes in the cartilage matrix, while ageing joints show minimal physical and chemical changes.
- OA joints increase in tissue volume, but not in ageing joints.
- OA joints show early and dramatic increases in the liquid content of the cartilage -- which may be the first physical change; while there is no liquid content change in ageing joints.
- OA joints display no pigment in the cartilage, while there is pigment in the cartilage of ageing joints.
- OA joints show excess bone density or overgrowth (eburnation), while there is none in ageing joints.
- OA joints display obvious bone changes, including new bone formation (osteophytes), while there is no obvious bone changes in the ageing joint.
