FAQ Category: General

Blood injection, more formally known as platelet-rich plasma (PRP) is a fairly new treatment tool for a variety of musculoskeletal problems. Platelets taken from the person’s own blood are injected into the damaged or injured area. Special growth factors always present in platelets are released and stimulate tissue healing.

Using PRP to treat osteoarthritis is under investigation. In a recent study, scientists from the Netherlands took a look at the mechanism behind this healing process and see if it could be used for osteoarthritic joints. The study was conducted in a laboratory setting. They used human chondrocytes (joint cartilage cells) from older donor adults.

By working at the cellular level of investigation, they were able to see two things: 1) the cascade of events that occurs when a cartilage cell is exposed to platelet-rich plasma (PRP) and 2) the effect PRP has on joint cartilage cells.

The authors admit that what happens in a sterile lab may not mimic exactly what happens in the human body. But it is a place to start with the hope of finding better ways to stop the arthritic degenerative process in our joints as we age.

How does this study help the average person with joint osteoarthritis? It doesn’t quite yet. But it is an important step in understanding the processes by which joint destruction occurs. If scientists can identify specific mechanisms at the cellular level that lead to chondrocyte destruction AND turn those signals off (either by interrupting the domino cascade once it starts or stopping the first domino from tipping), then we may have some clinical applications.

The authors of this study say this is just one step of many needed to fully investigate the use of PRP for joint osteoarthritis. With so much variation in chondrocytes from person to person and many different ways to prepare the platelet-rich plasma, there is a need for further concentrated study in this area. The authors conclude if an effective, self-induced, low-cost treatment can be found from these studies, then it will be time and money well spent.

Platelet-rich plasma (PRP) is a fairly new treatment tool for a variety of musculoskeletal problems. Platelets taken from the person’s own blood are injected into the damaged or injured area. Platelets do have a role in clumping together to form blood clots when there is a wound or bleeding.

But platelets also contain growth factors that are released whenever there is a wound, injury, or damage to tissues. When stimulated, these growth factors are released and start the inflammatory process that ultimately results in tissue healing.

Scientists all over the world are trying to understand the mechanism behind this healing process and see if it could be used for osteoarthritic joints. One study in the Netherlands has really opened our understanding of what’s going on. The was conducted in a laboratory setting where they used human chondrocytes (joint cartilage cells) from older donor adults to assess the effects of platelet-rich plasma (PRP) on cartilage.

Here are a few things we already know about the inflammatory cycle that results in osteoarthritic changes in human joints. There are inflammatory factors that start the destructive process in the joints. For example, interleukin (IL)-1 beta is probably one of the most powerful of these inflammatory factors. It is part of a group of cells called cytokines.

This particular cytokine inhibits (stops or prevents) the formation of new, healthy cells. At the same time, IL-1 beta produces proteases. Proteases are enzymes that break down proteins. In the case of osteoarthritis, proteases contribute to the destructive process.

That sounds fairly simple and straightforward but the truth is that IL-1 beta has quite a few different ways to act in the body. These different pathways are called signaling cascades. A signaling cascade is exactly like a line of dominoes. When the first tile is pushed, it sets off a sequence of events that don’t stop until the last domino is down. It’s the same thing with a signaling cascade. When the first signal starts, every step in the reaction or process takes place until the final one.

One of the signaling cascades that has been identified in osteoarthritic destruction is the activation of a protein called Nuclear Factor kappa B or NFkB. This protein moves into the cell nucleus (center) and starts signaling (talking) with various regulatory genes. These regulatory genes decide when cells die (a process called apoptosis), when inflammatory cells are activated, and when other immune responses are initiated. NFkB actually regulates at least 150 genes, some of which are directly involved with inflammation and immune function.

Now, how does platelet-rich plasma (PRP) figure in here? PRP counteracts the effects of IL-1 beta on genes that are responsible for the building up of collagen and breakdown of cartilage cells. In this laboratory study, they took a look at the effect of PRP in this setting. They found that PRP actually reduced several different effects of the IL-1 beta. In particular, PRP was able to counteract the effects of NFkB on genes responsible for chondrocyte (cartilage cell) destruction.

This study shows that PRP has antiinflammatory abilities. Although there are many different pathways leading to joint destruction, at least one has to do with gene expression that either builds up or tears down the matrix (cells that group together) forming joint cartilage. At least in a petri dish in the lab, IL-1 beta can be stopped by PRP. The end result is protection of the chondrocytes in the same dish.

The authors of this study say this is just one step of many needed to fully investigate the use of PRP for joint osteoarthritis. The research in this area is just getting started. That may be why the special you saw didn’t really say much more than to mention it. With so much variation in chondrocytes from person to person, with so many potential signaling pathways, and many different ways to prepare the platelet-rich plasma, there is a need for further concentrated study in this area.

But if blood injection turns out to be an effective, self-induced, low-cost treatment for joint arthritis, you can be sure we will hear a lot more about it in the years ahead! With the Baby Boomers “graduating” to senior status and remaining more active throughout the decades, joint osteoarthritis is taking center stage in the area of research and development.

Bone grafting is a process by which the surgeon takes bone cells from a donor bank or from the patient and uses them to fill in a hole, gap, or defect in bone. The lesion may be caused by failure of a fracture to heal, bone infection destroying bone cells, or surgery to remove bone for any reason.

Technically, the bone cells are no longer “alive” once they have been removed for use. But there is a small window (several hours to several days) when some bone cells are still biologically active. This means they can still promote bone formation.

Studies show that after implantation, the cells that do survive a bit longer release cytokines. Cytokines are part of the immune system response to injury. They help set up a new blood supply to the area and attract stem cells to the area that will eventually form into bone cells. In fact, researchers have shown that the graft may have a complete blood supply in as little as two days!

New bone takes a bit longer to develop (two weeks) but by the end of eight weeks remodeling efforts are clearly underway. Complete breakdown of the graft material and replacement with fresh, live, stable bone can take up to 12 months. That process is referred to as graft turnover. Graft turnover takes place one cell at a time as the old, dead cells are replaced by new, healthy cells. The cell-to-cell replacement is called creep substitution.

There is a newer graft process being used by some surgeons for large bone defects that are infected, where the bone is dying, or there has been a failure to heal for any reason. This technique is called induced membranes. It is a two-stage procedure, which means two separate operations four to six weeks apart.

In the first operation, the surgeon removes infected or necrotic (dead) bone. The hole or gap that remains is filled with a cement spacer to provide stability. The body starts to make its own tissue (called pseudomembrane) to fill in the hole.

The pseudomembrane doesn’t harden into bone so a graft is still needed. The graft placement is the second procedure. The defect or hole is filled in with autogenous bone graft. The pseudomembrane is left in place because it contains cells that will protect the graft and promote rapid integration of the graft material. It’s a win-win situation.

The time to recover varies from person-to-person depending on multiple factors. There’s the patient’s age and general health to consider. The size of the defect and type of procedure used are additional variables.

The surgeon may have a range of estimated times for each phase of recovery. It would be best to check with him or her but this information will help you gain a better big picture view of the potential complexity of the procedure. The simple term “bone graft” doesn’t begin to describe all that is involved!

You bring up a very good point. Complications around bone grafts may definitely seem like a major thing to the patient whereas the surgeon classifies them according to cost, need for a second hospitalization or repeat surgical procedure, and risk for long-term disability.

Donor bone comes from two sources: a bone bank (called allogeneic bone graft) or from the patient (autogenous bone graft). The most common problem with allogeneic bone bank graft material is rejection by the patient. The donor cells and the patient’s cells just aren’t compatible enough.

Autogenic bone grafts are preferred and can be taken from several areas such as the upper or lower part of the tibia (lower leg bone), radius (forearm bone) near the wrist, and the outer portion of the hip. But bone is taken most often from the pelvis because it is easy to access and it has different types of bone cells (e.g., osteoclasts, osteoblasts).

The bone collected there is biologically active and stays alive long enough to create more bone cells. That’s important in order to have fast bone remodeling. Having both types of bone cells also means the graft site will stable immediately.

With any autogenous bone grafts, there can be problems. Rejection isn’t usually one of them. The biggest complication is pain at the donor site. In fact, many patients say the donor graft site was the worst part of the entire procedure!

Other complications of bone grafting include deep infection (which can cause graft failure), nerve damage, hematoma (pocket of blood), and bone fracture at the donor site. The surgeon can prevent graft failure with proper handling of the graft material. It must be kept moist and used right away whenever possible.

For any of these problems, they are considered “minor” if you don’t need further medical treatment. Hematomas will eventually resolve on their own. Symptoms from nerve damage usually go away too as the nerve regenerates. But deep infection that requires another operation or permanent nerve damage that results in a limp would be considered a “major” complication.

Studies show that most of the bone graft complications are “minor” (as defined medically). Major complications are much less common. There are single cases reported sometimes for problems like joint instability or ureteral injury (the ureter is the tube that goes from the kidney to the bladder). Such complicatons would be considered major by both patient and surgeon.

Efforts are underway by the surgical community to find improved safe, but effective ways to conduct all bone graft procedures. The goal is to enhance bone formation with the fewest side effects or problems. Certainly, long-term pain and disability is to be avoided.

Blood injection, also known as platelet-rich plasma (PRP) refers to a sample of serum (blood) plasma that has as much as four times more than the normal amount of platelets and their associated growth factors. This treatment enhances the body’s natural ability to heal itself. It is used to improve healing and shorten recovery time from acute and chronic soft tissue injuries.

It has been used for years after plastic surgery and surgery on the mouth, jaw, and neck. It seems to promote bone graft healing. Researchers have found a way to combine this substance with other chemicals to make it into a putty or gel that can be painted on a surgical site to speed up healing.

Blood injection therapy of this type has been used for knee osteoarthritis, degenerative cartilage, spinal fusion, bone fractures that don’t heal, and poor wound healing. This treatment technique is fairly new in the sports medicine treatment of tendon, cartilage, and ligament problems, but gaining popularity quickly.

According to a recent review and update on platelet-rich plasma (PRP), there are now 1000s of articles published on the topic. Yet for all that research, we still don’t know if platelet-rich plasma treatment is really the way to go for tendon (or other soft tissue and bone) healing. And its use for degenerative disc disease remains uncharted territory (in other words, research is needed in this area).

We know that platelet-rich plasma does stimulate cells to reproduce and clear out dead cells. Whether or not PRP could stimulate cells to build new disc tissue is unknown. Tissue engineering of this type is a very popular area of research right now. So let’s hope a break through comes soon for everyone with this condition!

Platelet-rich plasma (PRP) is a product that contains a high concentration of platelets from the person’s own blood serum (the clear part of the blood). The normal amount of platelets in a person’s blood is anywhere from 150,000 to 350,000 per microliter. PRP has many more platelets with their unique growth factors aimed at restoring normal blood flow to and healing of damaged tissue.

The question of dosage (how much, how often, what concentration) has been debated and studied by many different people. Finding the optimal treatment protocol has been quite a challenge. For one thing, platelet-rich plasma is being used for a wide number of problems and injected into different tissue types (e.g., tendons, ligaments, cartilage, bone).

This treatment approach is also being tried for acute (early) injuries as well as chronic (long-term) problems. It’s very likely that what works for one problem won’t necessarily be as successful as another condition affecting the musculoskeletal system.

Whether to use low, moderate, or high concentrations of PRP remains a point of debate. It is difficult to actually measure how many platelets are activated and delivered to damaged tissue. There is a concern that too much concentration would oversaturate the area and cause problems. And there is some evidence that high platelet levels create a threshold effect. This means that after a certain number of platelets (PRP concentration level), the effect is actually negative rather than positive.

Of course, too little concentration may not have the desired healing response. Studies comparing the effects of low to moderate to high concentrations of PRP remain at the stage of animal studies. Future studies with humans are still needed in this area.

As for the number of injections that work best, research results are limited because in most animal and human studies, only one injection has been used. The focus has been more on the timing of the injection. Some reports published showed better results when PRP injections were given during the first seven days after injury. So the chase has been on to find the ideal window for treatment by PRP injection. It may turn out that the timing is different for acute versus chronic tissue damage.

Experts suggest (based on evidence presented so far) that too high a concentration of PRP can lead to delayed wound healing and more scar tissue. Using two to three times the normal amount of platelets is a good place to start until further studies are done. It seems likely that maintaining a steady elevated level of platelets is a good idea. Waiting three to seven days between injections is advised right now.

The ideal or maximum number of injections may differ depending on the problem and the person. For now, it is suggested that acute ligamentous and tendinous injuries be treated with one to three injections. More chronic problems (arthritis) may benefit more from three to five injections.

There are no reported ill effects from platelet-rich plasma treatments but until more is known about the long-term effects, these guidelines are recommended.

This is an excellent question and we applaud you for not only asking it but also for considering donating your physical body for the sake of study. When properly written, your advance directive and will can reflect your intentions to support research efforts to improve medical procedures.

You may want to consider becoming an organ donor as well — this is the gift of life for some people waiting for critical organs needed just to stay alive. There are many studies published in medical journals based on the use of cadavers (human bodies preserved after death for study). Here’s one that crossed our desks this week. The question was asked:

When is surgery indicated for a rotator cuff tear? That is the focus of a cadaver study from the Orthopaedic Biomechanics Laboratory in California. They started with the hypothesis that there is a critical point at which a rotator cuff tear is large enough to cause abnormal joint biomechanics.

Usually surgery is scheduled when the patient has completed a rehab program and is still experiencing significant pain and loss of motion. If loss of motion (and therefore function) depends on the size of the tear, then what is the critical tear stage that just won’t respond to rehab and requires surgery?

This study was done in order to identify the critical stage when rotator cuff tears will progress to the point of needing surgery. The researchers used a custom-built shoulder testing system to measure the effects of varying loads placed on the muscles of the rotator cuff and parascapular muscles.

They loaded the muscles of eight cadavers under three separate conditions: 1) rotator cuff only, 2) rotator cuff muscles with deltoid muscle, and 3) rotator cuff, deltoid, pectoralis major, and latissimus dorsi muscles. They used the traditional staging for rotator cuff tears based on footprint anatomy (that’s where the muscle inserts on the bone).

Stage I was a tear of the front or anterior portion of the supraspinatus tendon (one of the four tendons of the rotator cuff). Stage II represented a complete tear of the supraspinatus tendon insertion. Stage III was a complete tear of the supraspinatus and half of the infraspinatus (another of the four tendons of the rotator cuff). And finally, Stage IV was defined as a complete tear of both the supraspinatus and infraspinatus tendons.

What did the researchers conclude from this information about the critical stage when surgery is needed for rotator cuff tears? Stage II tears signal a change in shoulder external rotation and abduction. Progression to Stage III and Stage IV result in biomechanical changes in the humeral head in relation to the shoulder socket (also affecting motion).

Rehab early on is still recommended as the first line of treatment. The goal is to prevent progression of the tear while restoring normal shoulder joint kinematics. Strengthening the suprascapular muscles is equally important during conservative care (rehab). By strengthening the pectoralis major, latissimus dorsi, and deltoid muscles, it may be possible to restore normal joint movement, reduce pain, and eliminate the need for surgery.

And with the many active athletes (traumatic tears) and older adults (degenerative tears) with this problem, a study such as this is very important to help direct and guide treatment (conservative versus surgical). Of course, this is only one example but a useful one as it is estimated that 17 million people in the United States alone are affected by rotator cuff disorders. One cadaver can make a difference!

Injections into joints of anesthetics (numbing agents) and pain relieving medications have been used for a long time. They were considered “safe” based on clinical research in the mid-1980s. The use of single injection anesthetics such as lidocaine and bupivacaine gradually expanded to include modern day use of pain pumps.

A pain pump delivers a continuous, steady low-dose of anesthetic to the joint. With maximum pain control (for example after joint replacement surgery), patients are able to reduce the amount of narcotics used with each surgical episode. With less pain, they are able to get up, move, and enter into a rehab program sooner. And that is a huge benefit of pain pumps.

Locally injected medications do have some systemic effects (e.g., heart attack, depression, seizures) but these are rare. There is new evidence that delivery of anesthetics into joints may have some local toxic effects previously unrecognized. Whereas the joint can quickly clear the effects of a single (local) injection of anesthetics, there isn’t a similar ability with continuous exposure.

Scientists are taking a new and fresh look at this potential problem. The use of postoperative pain pumps is getting a second look. The use of anesthetics delivered by pain pump may be something to be reconsidered if not discouraged or even discontinued. In a recent report, surgeons from the University of California – San Francisco provided an update on current findings related to toxic effects of local anesthetics on joint cartilage. Here’s a quick summary.

Basic science studies have shown that numbing agents (bupivacaine, lidocaine, ropivacaine) do indeed kill cartilage cells called chondrocytes. Even brief exposure can decrease cell metabolism and cause cellular disruption. The end result is chondrocyte breakdown and self-destruction. This effect of anesthetics on cartilage cells is called chondrotoxicity.

Once the thin protective layer is destroyed, the number of dead cells increases. More time and further exposure to anesthetic agents are the two main risk factors for chondrotoxicity. The damage to chondrocytes after contact with anesthetics is permanent. Damage done by pain pumps after surgery is similar to changes seen with early osteoarthritis.

The authors who reviewed this new information suggest further study is needed in this area. There is a need to verify these findings and to uncover any long-term effects of pain pumps on joints. Surgeons won’t be quick to stop the use of pain pumps because of the positive benefits. But given these new findings, it may be something to discuss with the surgeon before proceeding ahead.

A pain pump delivers a continuous, steady low-dose of anesthetic (numbing agent) to the joint. With maximum pain control (for example after joint replacement surgery), patients are able to reduce the amount of narcotics used with each surgical episode. With less pain, they are able to get up, move, and enter into a rehab program sooner. And that is a huge benefit of pain pumps.

There is some new evidence that numbing agents (bupivacaine, lidocaine, ropivacaine) do indeed kill cartilage cells called chondrocytes. Even brief exposure can decrease cell metabolism and cause cellular disruption. The end result is chondrocyte breakdown and self-destruction. This effect of anesthetics on cartilage cells is called chondrotoxicity.

Further study showed scientists that once the thin protective layer of cartilage is destroyed, the number of dead cells increases. More time and further exposure to anesthetic agents are the two main risk factors for chondrotoxicity. And they found that the damage to chondrocytes after contact with anesthetics is permanent. The chondrocytes do not regenerate or replace themselves.

In fact, there is some evidence that the damage done by pain pumps after surgery is similar to changes seen with early osteoarthritis. Scientists are now looking for the reason why anesthetics delivered by pain pumps cause joint cartilage destruction.

Current theories include chemical effects, pH (acid-base balance), and preservatives in the solution used to deliver the agents. There may also be an effect of anesthetics on potassium and calcium that damages the cartilage cell DNA. There’s enough destruction to turn on cell apoptosis (the cell’s suicide cycle).

As you have discovered, the use of postoperative pain pumps is indeed getting a second look. Whereas the joint can quickly clear the effects of a single (local) injection of anesthetics, there isn’t a similar ability with continuous exposure. This new information suggest further study is needed in this area. There is a need to verify these findings and to uncover any long-term effects of pain pumps on joints.

This is a great question! We always encourage self-care for everyone. And it’s never too early to get started. After all, building up the “bone bank” so-to-speak begins in childhood and continues throughout the young adult years.

At any age, balance training and exercise are still the number one tool for falls and fracture prevention. Strength training and weight-bearing exercises are the key to osteoporosis prevention. Studies show that simple movements taught in gentle yoga, tai chi, and Qi Gong can be very effective in reducing the risk of falls and fractures.

Second, pay attention to your diet and supplementation. It’s important to get the right amount of calcium (based on age and gender), vitamin D, and protein. Your primary care physician is the best one to advise you about your risk and individual needs as well as the best way to get those needs met.

Getting screened for bone density isn’t a bad idea. Depending on your age, a baseline is advised for older adults. Exactly what age screening should begin remains a controversial subject. The National Osteoporosis and the Canadiam Medical Association recommend bone mineral density screening beginning at at 50 if there are significant risk factors present (e.g., previous history of hip fracture, tobacco and alcohol use, use of high-risk medications).

There is general agreement among various organizations concerned about osteoporosis that screening for all women should take place after age 65 for women and 70 for men. If you are interested in knowing your risk for osteoporosis-related fractures, a simple place to start is with the Fracture Risk Assessment Calculator known as FRAX.

Anyone can assess their risk at any time with this tool. It is available at the World Health Organization’s website (www.shef.ac.uk/FRAX/tool.jsp). A nice feature of this test is its ability to take into account your individual risk fracture for fracture (not just bone mineral density).

Just be aware that there is an absence of evidence showing that screening via bone mineral density testing is effective in reducing fractures. Being at increased risk of a fracture doesn’t mean you’ll actually break a bone. For example, some studies show that the FRAX only predicted 43 per cent of fractures that did occur. And half the people who did fracture a bone were considered at low risk for fracture.

The best person to advise you is a health care professional who can take into account all aspects of your life and health. This could be a primary care provider, nurse practitioner, or other expert who focuses on self-care, prevention, and aging issues.

After going through all the fuss to replace a joint, you do want the best results, right? Well, here are a few tips to help you along the way. Knowing how much activity is too much and ways to prevent complications are important.

The information comes from a systematic review of 30 years’ worth of research results (over a period from 1980 to 2010). All English-language studies of total joint replacements were gathered and reviewed. A special search was done to find studies that reported on sports or recreational activities after total joint surgery. Most of the surgeries were to replace the hip, knee, or shoulder.

Why is this information important? Because like you, more and more young adults and active older adults are turning to joint replacement to alleviate pain from degenerative joint disease. And they intend to stay active after the surgery.

It is in their best interest to receive advice about level of activity and exercise. What’s reasonable? What’s too much? What’s allowed? What’s prohibited? How will the final results of the joint replacement be affected by physical activity and exercise? These are some of the issues addressed by this study.

Here’s a list of the current guidelines available. Keep in mind, these are NOT the result of direct research studies comparing one patient group to another. They are the answers provided by surgeons filling out surveys and from consensus statements (agreements) made by groups of surgeons.

You are correct — what is being reported by the news media and health care experts does seem confusing. Just as you say, too much alcohol consumption can lead to some serious health consequences and even death. But how much is too much?

Right now, the medical definition of an alcoholic is a male who drinks more than 14 alcoholic drinks/week or more than 4 drinks on any day. For women (who don’t metabolize alcohol as easily as men do), more than seven alcoholic drinks/week or more than 3 drinks on any day constitutes alcoholism. One drink is equal to one 12 oz. beer, one 5 oz. glass of wine, or 1.5 oz. of hard liquor.

Using these definitions, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) reports that two to 10 percent of individuals aged 65 years or older are alcoholics. That percentage translates into about three million older Americans and 14 million total number of adults in the United States.

When is a little alcohol good for you and why? Recommendations for one drink a day as being healthy started with awareness that tannins and antioxidants (present in the grape skins used to make wine) are beneficial to the heart. A glass of wine may also benefit the bones. But the sugar and alcohol content in wine may not be as helpful. And the recommendation to drink daily certainly does not extend to hard liquor.

Most experts suggest if you don’t drink, don’t start. If you do drink and you drink more than the recommended amount, it’s likely time to stop. This is especially true for anyone who cannot go a day without a drink and suffer some ill side effects when trying to stop.

But for those who can sip a glass of red wine once a day or even every other day, the benefits may outweight the empty calories. Of course many people have turned to nutritional supplements that contain all the healthful ingredients of wine to support heart and bone health without putting the liver and other organs at risk.

Nothing like an over-the-counter test kit to look for osteoporosis is available at this time. But that is a great idea! We can suggest a 21-item questionnaire developed by a group of German researchers.

This simple questionnaire was developed by first analyzing a group of patients who had a broken bone caused by osteoporosis. The presence of osteoporosis was verified in each of these patients using the special dual energy X-ray absorptiometry (DXA) available for testing bone density.

The group ranged in age from 40 to 80 years old. Decreased bone mineral density was observed in 80 per cent of the patients. Half were diagnosed with a clear case of osteoporosis. By studying common factors among the group, they were able to identify the most important risks. The first was age over 70 followed by a history of smoking or heavy alcohol use.

Early menopause (women younger than 45 years old) and a loss of more than four centimeters (one inch) in height (for men and women) also correlated with increased risk of bone fracture linked to osteoporosis. There was one other important risk factor and that was a long period of being immobile (e.g., bed bound or in a wheelchair) or inactive.

If your mother has a cluster of these risk factors (two or more) then it’s probably time to insist on a closer inspection. More formal testing can be done through the use of dual energy X-ray absorptiometry (DXA), a special way to measure bone density.

You can also get some great information from the National Osteoporosis Foundation website to help you convince your mother of the need to seek medical help sooner than later. Prevention is the key but short of that step, then early recognition and treatment of the condition can help prevent disabling and even life-threatening fractures.

You may be referring to the meeting that was the 2011 Annual Congress of the European League Against Rheumatism, also known as EULAR. Results of many gout studies from around the world are reported at this meeting.

One significant finding is the one you heard: the condition is not being controlled adequately for the majority of patients. In fact, only about one-third of all patients in Europe who get these medications have normal serum uric acid levels.

Not too surprising, quality of life is lower when gout is not under good control. Swollen, tender, and painful joints can be very debilitating. Patients say the pain is so bad the joint can’t even stand the slightest touch. Even the weight of a sheet in bed at night causes excruciating pain.

Walking and standing are almost impossible during an acute flare-up if the legs or feet are affected. Many patients have flu-like symptoms, including fever and chills. The pain may go away on its own in a few hours, or it may take a few weeks. Understandably, work and social life suffer.

A simple blood test will tell you what your serum (blood level) uric acid is at the time of the test. There may be some daily fluctuations (periodic ups and downs) in your uric acid level. But the goal is to have a consistent level that is less than six milligrams per deciliter.

Studies like the ones presented at the EULAR meeting are important to keep us all up-to-date on this condition. Trends like this one where patients really aren’t getting the kind of control they need is a good one to bring forward for consideration and change.

See your primary care physician or rheumatologist for an evaluation. Let your physician know anytime you experience an increase in painful, tender, swollen joints. Staying on top of the disease and its symptoms with adequate medical treatment is important.

There is some new evidence that sugar-sweetened beverages is linked with gout. The study that was done was in New Zealand. They found an increase of four times the normal rate of gout in people who drank four or more sugar-sweetened drinks each day.

Gout is a disease that involves the build-up of uric acid in the body. Uric acid is a normal chemical in the blood that comes from the breakdown of other chemicals in the body tissues. Everyone has some uric acid in his blood.

As your immune system tries to get rid of the crystals, inflammation develops. For the person with too much uric acid, this inflammation can cause painful arthritis. In fact, gout was the first disease in which researchers recognized that crystals in the synovial (joint) fluid could be the cause of joint pain.

Many gout patients have a combination of overproduction and under-excretion of uric acid. Their bodies create too much uric acid and have problems getting rid of it. More than 90 percent of people with gout have kidneys that don’t effectively get rid of uric acid.

The link between sugar and uric acid isn’t clear yet. But scientists suggest fructose (sugar) increases the production of adenosine monophosphate, which is converted into uric acid. Adenosine monophosphate is a sugar molecule that is part of your DNA and has to do with energy production.

Sugar is an essential part of what keeps us going but sugared beverages have no nutritional values. They provide empty calories and a quick burst of energy. That’s okay in small quantities occasionally. But as a daily diet, it can lead to chronic problems like obesity, diabetes, and gout. So your mother is correct as usual and even more so if she is encouraging you to get your sugar from natural fruits and vegetables!

You may be experiencing something that has been recently recognized as a potential problem. Patients with rheumatoid arthritis who are treated with some of the newer immune modifying drugs are experiencing a reactivation of latent (inactive or silent) tuberculosis. The same thing is happening to organ transplant recipients and patients with other immune-based problems who are being treated with these kinds of medications.

People with latent tuberculosis have the live tuberculosis bacteria in their bodies. But you aren’t contagious and can’t spread TB. With latent tuberculosis, there aren’t any symptoms of TB but treatment is needed to prevent the TB from becoming active (full-blown disease).

Studies show the latent form of TB becomes active in about 10 per cent of all cases. A reactivated case of TB can have some serious consequences. Treating latent tuberculosis can reduce the risk of active infection by 60 per cent. That statistic supports the recommendation to screen regularly and treat rheumatoid arthritis patients who test positive for latent tubercular disease.

It sounds like your job requirements including a TB test was a blessing in disguise. Getting treatment is the most likely next step. If your physician hasn’t already discussed treatment with you, ask what are her recommendations and go from there.

Tuberculosis is on the rise again in the United States. After almost 40 years of almost no new active cases, there has been a steady increase in reports of this disease. There are several reasons for the increased number of people developing this disease.

Immigrants coming to the U.S. from developing Third World nations, rising homeless populations, and the emergence of HIV have led to an increase in reported cases. How does having rheumatoid arthritis (RA) figure in here?

Patients with rheumatoid arthritis who are being treated with some of the newer immune modifying drugs are experiencing a reactivation of latent (inactive or silent) tuberculosis. The same thing is happening to organ transplant recipients and patients with other immune-based problems who are being treated with these kinds of medications.

What does this mean for people with rheumatoid arthritis (RA)? Should they stop taking the helpful medications for the sake of avoiding tuberculosis? Should they be tested more often for TB?

Experts recommend anyone with rheumatoid arthritis should be screened for TB regularly — even if they are not being treated with the newer disease-modifying anti-rheumatic medications (DMARDs).

That’s because for some (as yet unknown) reason, people with rheumatoid arthritis (RA) get TB four times more often than folks who don’t have RA. Patients with RA should be tested for tuberculosis before being put on the disease modifying antirheumatic medications.

The experts recommend yearly tests for TB. That means an updated medical history, tuberculin skin test, chest X-ray, and physical examination. Each physician will decide exactly which tests are needed for individual patients. There are a couple of additional tests that may be required (e.g., sputum analysis, Interferon-Gamma Release Assay or IGRA).

The best thing you can do for your mother is make sure she asks her regular physician and/or her rheumatologist about her risk for tuberculosis. Just asking the question will likely help set into motion a review of her situation and any testing she needs.

You are indeed right in your observation that reportable injuries (those that put a player on the disability list) have increased in the last few years. To be on the disabled list, players must have a specific diagnosis made by the team doctor.

The physician must certify that the player cannot play for a minimum of 15 days. Players can certainly stay on the disabled list for more than 15 days if necessary. The extended time is often needed when there is a severe injury or more than one problem at the same time.

According to a recent review of the Major League Baseball disabled list, injuries went up 37 per cent between 2005 and 2008. The reason for this finding is unknown but there is some speculation it may have to do with the change in drug testing. Just before the 2006 season, drug surveillance increased and was more strictly enforced.

There are some definite patterns to when injuries occur and what type of injuries are most common. For example, pitchers are more likely to injure their shoulders/arms compared with outfielders who have more leg injuries.

Practice injuries are highest during the preseason, probably due to deconditioning and overload. Rookies are more likely to injure themselves and take longer to recover (three weeks compared with three days for high-level players).

Injuries during games are far more likely during the first month of the season (April being the highest month of injuries). Injuries decline as the season goes on with the lowest month being the last month of the season (September).

In the most recent analysis of data from the disabled list, there was no difference in number or type of injuries based on whether the player was in the National or American League. In both groups, half of all injuries involved the upper extremity (arm). One-third affected the lower extremity (leg). And the remaining were injuries to the trunk and/or spine.

There is certainly room for injury prevention among all athletes including the American and National Leagues. Creating a national database to track injuries and results may help direct future studies. Less severe and even minor injuries among league ball players can still have a significant effect. The goal is to prevent injuries and develop better, faster rehab programs to foster recovery when injuries do occur.

A rookie in baseball is defined as someone with fewer than 130 at bats, 50 innings pitched or 45 days on the active roster of a Major League club (excluding time in military service or on the disabled list) before September 1.

According to data collected for the disability list, rookies are more likely to injure themselves and take longer to recover (three weeks compared with three days for high-level players).

You won’t be surprised to hear that pitchers are more likely to injure their shoulders/arms compared with outfielders who have more leg injuries. Half of all injuries involve the upper extremity (arm). One-third affect the lower extremity (leg). And the remaining injuries are to the trunk and/or spine.

Practice injuries are highest during the preseason, probably due to deconditioning and overload. As the name suggests, rookies are “beginners” in a sense. With time, training, good common sense, and a little luck, more experienced players tend to have fewer and less severe injuries. They still spend their fair share of time on the disability list but they seem better able to bounce back into the game. Hopefully, the same thing will happen to your brother with a little time and a few more seasons.

Bone cysts are spaces within a bone that are filled with some type of fluid. Two common benign bone cysts are unicameral and aneurysmal. Unicameral bone cysts are often close to the growth plate next to a joint. They tend to fill up with synovial (joint) fluid.

Aneurysmal bone cysts are more likely to be filled with blood. They affect the long bones (upper arm, thigh, ribs) and back of the spine most often. Aneurysmal bone cysts are considered “benign” meaning they aren’t cancerous and don’t spread. But they can do plenty of damage even causing the bone to break.

The cause of bone cysts remains unknown but there are some theories. Sluggish flow and congestion of fluids, trauma, and local disturbances in blood circulation are some of the more likely causes. There is evidence to support each one of these ideas. Molecular and genetic theories exist as well.

Knowing how bone cysts develop may help with prevention but once they appear, treatment is based more on the natural history and prognosis. Bone cysts don’t usually go away by themselves without some type of treatment. Usually that treatment is surgical removal.

Left alone, they will just get bigger and increase the risk of another bone fracture. If the cyst is large enough, it may be necessary to fill in the empty space (after removal) with a bone graft.

Aneurysmal bone cysts tend to come back even after surgical removal. Efforts are being made to find effective ways to kill any unseen cells left behind. Liquid nitrogen, phenol, and argon beam coagulation are three examples of treatments used to prevent recurrence.

Only a very wide resection (cutting around the edges) of aneurysmal bone cysts has a zero per cent chance of recurrence. Other methods under investigation include arterial embolization. This is a way of injecting blood clots into the blood vessel to close it down and prevent further bleeding.