News Category: General

Star Trek lovers are familiar with the “Vulcan nerve pinch”, a technique used by Dr. Spock to cause someone to lose consciousness. The technique was to pinch a pressure point at the base of the victim’s neck but in fact, it’s likely the pinch was in fact a trigger point (TrP) of the upper trapezius muscle. The upper trapezius muscle is the muscle along the top of the shoulder at the base of the neck (where the neck and shoulder meet).

Trigger points are defined as hyperirritable areas of tenderness in a muscle that when pressed or pinched can cause local and/or distant referred pain (e.g., someplace else down the arm). Trigger points can be active (currently already causing pain) or latent (only painful when pressed or pinched).

Physical therapists often treat this problem using a variety of techniques that may be noninvasive or invasive. Noninvasive approaches include massage, stretching, and ultrasound. Invasive treatments include dry needling and corticosteroid injections. Dry needling refers to using needles to stimulate the trigger point without actually injecting any medication or other substances.

In this study, physical therapists from Tehran University of Medical Sciences in Iran use three different treatments for latent trigger points of the upper trapezius muscle. There were four total groups all together (phonophoresis, pressure release, ultrasound therapy, control group). Participants in each group were all women who had a positive trigger point of the upper trapezius.

Phonophoresis is a way to use ultrasound to push a topical corticosteroid (antiinflammatory ointment applied over the skin) through the skin into the muscle. Pressure release is the application of sustained pressure to the trigger point until pain is reduced.

Ultrasound therapy is the same as phonophoresis but without the corticosteroid cream — just the sound waves applied over the surface of the skin but directed down toward the bone. The sound bounces back off the bone and creates heat to the muscle tissue. Of course, the control group received no treatment but was measured before and after just the same.

Before treatment, the physical therapist measured each woman’s pain level, pain pressure threshold (PPT), and neck range of motion. These same measurements were taken after treatment and compared for each group. Pain pressure threshold was measured using a special device called a dual inclinometer. Pressure was applied to the trigger point until pain was created. The amount of pressure required to elicit pain was recorded as the pain pressure threshold.

This was the first time phonophoresis with corticosteroids has been used for the treatment of trigger points. No study using this specific approach has ever been reported before. The results showed that the women in all three treatment groups had decreased pain, decreased pain pressure thresholds, and improved neck motion. The control group stayed the same without improvement in any area.

The phonophoresis and pressure release techniques yielded better results than the ultrasound. Phonophoresis outperformed pressure release. The mechanisms by which these treatments work to reduce the effects of trigger points aren’t entirely clear yet.

Some experts suggest the increase in blood flow to the area from phonophoresis helps clear out substances in the area that cause pain. Pressure release may help by lengthening the muscle fibers themselves. Once the pressure is removed, there is a release of antipain hormones (e.g., endorphins, enkephalins), thus blocking pain and making it possible to move once again. Ultrasound may not have been as effective as phonophoresis or pressure release because a pulsed form of ultrasound was used that does not generate any heat to improve circulation.

The authors concluded that phonophoresis and pressure release are both good treatment techniques to relieve the pain and loss of motion caused by trigger points of the upper trapezius muscle. This is the first study to suggest the use of phonophoresis for this problem.

Should you be the victim of the Vulcan nerve pinch or simply a neck pain sufferer from trigger points of the upper trapezius muscle, ask a physical therapist to apply either or both of these treatment techniques. Experience the safe and effective relief of painful symptoms without adverse effects that phonophoresis and/or pressure release have to offer.

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.

In this study, scientists from the Netherlands take 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 this is what happens in a sterile lab and 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.

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.

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.

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. 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. 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.

Orthopedic surgeons often find it necessary to use bone graft material to fill in holes, defects, and gaps in bone. The most common reasons bone grafting are needed include fractures that don’t heal and surgical procedures that require removal of bone. Most of the time, it’s best to use the patient’s own bone as the donor graft materials. That’s called an autogenous bone graft.

In this article, two surgeons from the University of Cincinnati College of Medicine offer other surgeons a complete review of autogenous bone grafts. They cover topics such as when to use them and why to use them. They also discuss how to perform a collection and graft and then what to watch out for in the way of complications or problems.

With almost a quarter of a million bone grafts performed each year in the United States, this information is timely and helpful. Autogenous bone grafts are preferred over bone from a bone bank. The patient’s own bone won’t be rejected so it is said to be histocompatible.

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.

Donor bone can be taken from other 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. With any autogenous bone grafts, there can be problems. The authors provide a detailed look at the pros and cons of each bone graft site.

The biggest disadvantage for any bone graft site 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 grafts 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.

There are new ways now to prepare the graft site to make it “graft-friendly.” A special kind of cement is used to help foster bone growth once the graft in place. When the area of bone needing a graft is already infected, the donor graft can be mixed with antibiotic. Studies show this method can get rid of the infection in up to 96 per cent of patients.

Sometimes where and how bone is harvested depends on the volume (how much) of bone is needed. For smaller amounts of bone collection, the surgeon can scrape enough bone to use. This technique is called curettage. When larger amounts of bone graft material are needed, the surgeon may have to harvest bone from more than one place. Special tools have been developed for this procedure. For example, a reamer-aspirator-inspirator or IRA can get to deeper bone.

This is a fairly new technique so the authors describe when and how to use it in detail for other surgeons. The reamer is faster making operative time (and cost) less. In addition to the other types of complications already mentioned, the use of this tool adds its own potential problems.

The amount of blood lost during this procedure can be excessive, too. The reamer itself can malfunction during the procedure or get stuck in the bone canal. Failure to control the tool can also result in bone fracture. The surgeon can use fluoroscopy (real-time X-rays) to observe the path of the reamer and see where there are places of bone too thin to harvest.

One final bone graft technique is presented in this article called induced membranes. This is a two-stage procedure, which means two separate operations four to six weeks apart. It is used for large bone defects where there is infection or a complete failure to heal.

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 first study published on the induced membrane technique was in 2010 so more research will be needed before this becomes a standard bone graft procedure. Surgeons will find this article full of information about old (standard) ways of doing bone grafts as well as an update on the newer approaches. The authors of this review conclude that surgeons must remain familiar with when to use bone grafts, how to perform each technique, and the possible complications of each type.

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.

Scientists are taking a new and fresh look at this potential problem. In this report, surgeons from the University of California – San Francisco provide an update on current findings related to toxic effects of local anesthetics on joint cartilage.

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.

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.

With this new information about the potential destructive effect of local anesthetics, the next area of concern was pain pumps with their more continuous exposure. It turns out that damage done by pain pumps after surgery is similar to changes seen with early osteoarthritis.

The last and final step in new research was a search 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).

In summary, the use of postoperative pain pumps is 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. The use of anesthetics delivered by pain pump may be something to be reconsidered if not discouraged or even discontinued.

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.

The things orthopedic surgeons do to help heal damaged soft tissue and bone aren’t magical and they don’t come out of a hat somewhere. Treatment techniques applied to the human body (especially bones and the surrounding soft tissues) come from basic science research.

Some of the newer ideas (e.g., using stem cells and growth factors in healing) appear to have clinical application. But they have not produced the kind of positive results expected. The reason for this disconnect isn’t clear yet but it is something scientists are paying attention to and exploring further.

Here’s what we know so far. First, when it comes to using stem cell therapy during surgery to reattach a torn tendon to the bone, it looks like more research is needed. Before this treatment can be successful, scientists must find ways to signal stem cells to form the different cells needed at the insertion site. The goal is to find ways to use the patient’s own stem cells (rather than injecting donor stem cells from someone else) to form what is needed at the specific site of injury.

The results of studies so far suggest that this transition site from tendon to bone is very complex. In normal anatomy, joint stability, and movement, there is a load transfer from tendon to bone. Tendon and bone are two uniquely different types of tissue. One type of stem cell may not be enough to accomplish the task of restoring normal anatomy and function. Some cells must be formed of stiffer collagen fibers for bone while other cells remain soft and flexible to form tendons.

Efforts to use platelet-rich plasma (PRP) with its concentrated growth factors in tendon healing have not been as successful as was first predicted. When studies have compared patient healing, pain relief, function, and return-to-sports (with and without platelet-rich plasma (PRP)), there have not been consistently better results with the PRP.

Let’s turn our attention to research into gene technology. One application of spine deformity genetics is to treat idiopathic scoliosis (curvature of the spine of unknown cause). These studies have begun with fish. The goal is to develop a genetic test that could predict which children will develop this condition. The intended final outcome is to find ways to prevent idiopathic scoliosis or minimize its effects.

In the area of osteoarthritis research, researchers continue to focus on understanding what happens to the joint cartilage in the formation of osteoarthritis. Scientists have been able to identify key molecules involved in the process. Applying this information to mice has resulted in decreased osteoarthritis.

Right now, various types of growth factors are being tested in the treatment of joint pain from early osteoarthritic changes. It has been discovered that when osteogenic (bone) protein is combined with insulin-like growth factor joint regeneration is possible.

Other biologic therapies for the regeneration of tissue such as joint cartilage currently under investigation include autologous conditioned (blood) serum and bone marrow concentrate. Autologous refers to the body’s own cells. Any time autologous sources of cells can be used, it is considered an advantage both in terms of (lower) cost and (easy) administration.

What’s new in the area of joint replacements? Implant design continues to change and improve in an effort to get bone to stick to and form around the implant. For example, titanium mesh is being replaced by a product called tantalum.

The surface of a tantalum implant is more porous and seems to stimulate faster and more bone cells to form around the implant. Tantalum implants stand up better to high levels of friction and load. The focus of future studies will be to see if this formation and incorporation of bone (called oseointegration) will last over the long-term (10 to 20 plus years).

One other area of research of interest relates to damaged menisci (the C-shaped thick cartilage inside the knee). Right now a mild-to-moderate tear of the meniscus is repaired by stitching it back together and reattaching it to the bone.

Severely torn, frayed, or destroyed meniscus may have to be removed. Knee joints without the natural meniscus are at increased risk for early osteoarthritic changes. Even removal of part of the meniscus puts the knee at a biomechanical disadvantage.

There are two new ideas on the horizon for regenerating or replacing the meniscus. The first is called non-cell-seeded scaffolds. The idea is to encourage tissue regrowth by implanting an absorbable collagen mesh. Early studies show a definite advantage of using these scaffolds over removing the meniscus (a procedure called meniscectomy.

A second regenerative or biologic therapy being studied for repair of damaged menisci (plural form of meniscus) is called nondegradable synthetic menisci. This is like a meniscus replacement. A composite material that has been reinforced with lightweight polyethylene (plastic) fiber is being tried. It acts like a replacement for the meniscus that is removed. There is even a free-floating type of synthetic meniscus being tried.

In summary, a review of the new tissue regenerating options currently available or under study in orthopedics is provided in this article. This update covers a wide range of treatment options including stem cells, growth factors, platelet-rich plasma, meniscus repairs and replacements, joint replacements, and spine healing.

Developing orthopedic therapies are aimed at finding practical (clinical) ways to use discoveries made in the lab. Not all of the techniques described are available for use yet. The goal remains to translate or transfer basic science into the most effective clinical practice with the fewest side effects possible.

According to the authors of this 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.

Let’s take a look at what this review was able to uncover about platelet-rich plasma. Here’s a quick review for those who don’t know what it is. 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. This treatment enhances the body’s natural ability to heal itself and 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.

Despite the many publications on the topic of PRP, it’s still unclear if it works, why it works, or how to prepare the product for use with any of these problems. That’s where this article comes in. The authors ask and answer these questions:

After going through all the fuss to replace a joint, you want the best results, right? Well, here are a few tips to help you along the way. The focus is on physical activity (how much is too much?) and ways to prevent complications and revision (second) surgeries.

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 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.

Osteoporosis (decreased bone density) is a common problem for “older” adults — and for many who don’t consider themselves “older”. For example, some people over age 50 who have risk factors for osteoporosis may find themselves facing this brittle bone disease much sooner than expected.

Who should be screened? How can osteoporosis be prevented? Who should be treated and how? These are the questions addressed by the authors of this review article. The rise in numbers of older adults at risk has captured our attention. The sheer number of Baby Boomers (born between 1946 and 1964) makes the information presented in this special focus feature all the more important.

First, who should be screened and why? The ‘why’ question is easier to answer: because osteoporosis increases the risk of bone fractures. Hip fractures are especially common. And such injuries often require surgery and puts the affected adult at increased risk for a move from home into a long-term care facility (nursing home).

Now comes the trickier part: who should be screened? Despite all the research, debate, and discussion on this point, we still don’t have agreement among major groups. The National Osteoporosis Foundation, American College of Physicians, U.S. Preventative Task Force, and the Canadian Medical Association have all made recommendations. But they differ in their proposed guidelines.

Everyone agrees that risk assessment is a huge part of osteoporosis screening. Anyone with known risk factors (poor diet, inactivity, postmenopausal women, advancing age, use of certain medications) should be evaluated.

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).

So what’s the hold up in making straightforward recommendations on who should be screened for osteoporosis? Simply stated: 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. And there are really several different groups to be considered: postmenopausal women, older men, and younger men and women who have risk factors for osteoporosis.

What can be done if you are at increased risk for osteoporosis-related fractures? First, reduce your risk of falls because unexpected loss of balance, falls, and the force of a fall are what lead to bone fractures. How can you do this?

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.

And finally, there are certain medications (e.g., bisphosphonates, Denosumab, Estrogen, parathyroid hormone, nitroglycerin) that may be beneficial for some people. Each of these groups of medications is under investigation.

What we know so far is that each of these chemicals works in different ways. For example, bisphosphonates prevent bone resorption and prevent fractures. Denosumab (a human monoclonal antibody) decreases bone resorption AND increases bone density. Estrogen may help prevent osteoporosis but doesn’t treat decreased bone mineral density. Nitroglycerin inhibits the breakdown of bone while also stimulating bone growth.

All of these medications have potential adverse side effects, which can increase the risk for other kinds of problems. That’s why scientists are continuing their search for the ideal way to prevent and treat osteoporosis.

In the meantime, hospital staff are lending their efforts to help patients with hip fractures get the right care early on. The goal is to reduce the risk of mortality (death) and morbidity (loss of function, increased disability) during hospitalization for hip fracture. This is done by approaching the problem as a team, getting the patient evaluated quickly, and into surgery as soon as possible when that treatment approach is warranted. Improved quality of care in this fashion has been shown to create better outcomes with fewer long-term problems.

Wouldn’t it be nice if all you had to do to find out if you have osteoporosis is answer a few simple questions? No testing required. No special X-rays. Well, thanks to the work of some German researchers, it’s easier than ever to predict who might be at risk for osteoporosis.

What could be better than a simple, safe screening tool that doesn’t cost a lot of money? Can something that good be true? Let’s take a look at the study and see what they had to say.

A 21-item questionnaire was developed by 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.

There are possible explanations for each of these risk factors being linked to osteoporosis. For example, drinking excessive amounts of alcohol (more than one drink per day for women and more than two drinks each day for men) has the effect of taking calcium out of the body through the kidneys.

With menopause, there is a natural reduction of the hormone estrogen. Estrogen has the effect of holding bone in place. Without it, bone cells are destroyed faster without being replaced. Poor nutrition associated with alcohol intake and increasing age may play a role in bone loss as well.

Osteoporosis is a big problem for men and women all around the world. In fact, it is listed as one of the top 10 major diseases with serious consequences. A fracture may seem like a simple thing but it can result in the eventual decline and death in older adults.

In many places there is limited availability of health care. The rising costs of medical testing add another dimension to help explain why people aren’t getting tested or identified early as having osteoporosis.

This new questionnaire focuses on the most important risk factors and may help identify people at risk earlier. There is a potential for preventing disabling fractures. Once an individual is recognized as being at risk for osteoporosis then additional testing may be needed. But at least with this new survey, those who need to be evaluated and treated can be directed accordingly.

If you are a gout sufferer or know someone who is…this information may be of interest to you. The data comes from many studies around the world on gout and was presented at a special meeting. The meeting was the 2011 Annual Congress of the European League Against Rheumatism, also known as EULAR.

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.

This combination of problems can happen with drinking alcohol, especially beer. The more alcohol the patient drinks, the worse the problem is. Alcohol both raises uric acid levels in the body and impairs the kidneys’ ability to excrete the buildup.

Sometimes the increase in uric acid is caused by certain kinds of drugs, such as diuretics, cyclosporine, and low-dose aspirin. Other medical conditions, such as obesity, hypertension, and diabetes, can also make some people more likely to develop gout.

Gout cannot be cured, but it can be very successfully treated. The main goal of treating gout is to reduce the amount of urate in the blood. During the acute or early phase of a gouty attack, doctors prescribe medicines called colchicine, certain nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids to decrease swelling and relieve pain.

All of these drugs work quickly and are considered very effective. But that’s where the results of this report come in. Studies show that 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.

For patients taking the newer medications (e.g., pegloticase), there is good news. In a study in the United States, 42 per cent had normal serum uric acid levels after six months. They could stop taking the drug for periods of time while still maintaining normal levels of uric acid.

These new treatments called uricase therapy are used for patients who don’t respond to other forms of treatment. Uricase therapy involves the use pig and baboon enzymes that can break down uric acid easily. The use of these therapies is still in the study phase in the U.S..

There were two other major findings reported at the EULAR meeting. One was that combining two medications (lesinurad and allopurinol) seems to be much more effective than just taking allopurinol. Allopurinol is another group of medications available to lower urate levels in the body. Zyloprim is the brand name for allopurinol. Other allopurinol drugs on the market include Allohexal, Allosig, Progout, and Zyloric.

And one final tidbit of information. Sugar-sweetened drinks are recognized now as a risk factor for developing gout in some people. Drinking four or more beverages each day containing high levels of corn sweetener (corn syrup) or other sugar compounds significantly increases the risk of gout.

The main take-away point from the EULAR gout studies is this. Even with more modern drug treatments, gout can still be a chronic disease with a significant daily burden for many people. Continued research is needed to find better ways to control the disease, the disease process, and the effects of the disease.

Tuberculosis (also known as TB) is a bacterial infection affecting the lungs and other parts of the body. It was almost completely gone from the United States but is now on the rise again. And patients being treated for rheumatoid arthritis may be at increased risk.

Before the development of anti-TB drugs in the late 1940s, TB was the leading cause of death in the United States. Drug therapy, along with improvements in public health and general living standards, resulted in a marked decline in the number of new cases of tuberculosis.

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. The new trend was first noticed in the mid-1980s, after a 40-year period of decline.

How does having rheumatoid arthritis (RA) figure in here? This particular group of patients when 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?

A group of experts got together to discuss these diagnostic issues. They offered a series of what they refer to as clinical pearls to help guide patients and physicians in this matter. Here’s a quick summary of the most important points:

One way to prevent baseball injuries is to understand how they happen. A good way to do that is to create a computerized database where information on injuries can be downloaded, stored, studied, and analyzed. We are one step closer to having such a tool.

In this study, a group of researchers took a look at the disabled list kept on all players by the two major league baseball organizations: the American League and the National League. Data was extracted from the 2002 season through the 2008 season.

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.

Data collected was broken up into different categories for ease of comparison. Area injured (by anatomical parts or zones) and injury type were recorded. Pitchers and fielders (nonpitchers) were analyzed separately. Players were assessed to see if they had more than one injury. Number of games played and number of seasons played were also noted.

After analyzing all the data there were no surprises. They discovered that pitchers are more likely to injure their shoulders/arms compared with outfielders who have more leg injuries. Practice injuries were highest during the preseason, probably due to deconditioning and overload. Rookies were more likely to injure themselves and take longer to recover (three weeks compared with three days for high-level players).

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

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.

The overall rate of injury climbed 37 per cent from year-to-year starting in 2005 and ending with 2008 (when the study ended). The reason for this last finding is unknown but there is some speculation that it may have to do with the change in drug testing. Just before the 2006 season, drug surveillance increased and was more strictly enforced.

In summary, studies show that the number and severity of sports-related injuries is on the rise especially in baseball. Time lost from participation in the preseason and season games is significant at the collegial and professional levels.

Creating a national database to track injuries and results may help direct future studies. The authors suggest a tool for collecting data that includes injuries that are not severe enough to bench the player on the disability list. 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.

If you haven’t heard about Pilates, you’re not alone. But for the millions of people who have discovered and now use of this specialized exercise for core stabilization, you will find the results of this study of interest. And if you are looking for some help with exercise, fitness, or rehabilitation from an injury, Pilates may be something to consider.

Pilates is actually the name of the German born man (Joseph Pilates) who first developed this technique back in the mid-1900s. It was almost a lost art until about 10 years ago. And then the momentum behind the Pilates movement seemed to snowball. The word spread and now it is a technique that is offered in classes at the local YMCA, health club, fitness center and even physical therapy clinics.

For physical therapists, two questions arise: 1) is there any scientific basis for the Pilates technique and 2) is there any evidence to support its use in a rehabilitation program? According to this review of 90 articles published since 1995, there is a scientific foundation but limited evidence for Pilates.

Actually, only nine of the 90 published studies were high enough quality to be considered in the review. But those studies did show that some of the Pilates techniques designed to align, lengthen, and protect the spine are effective in developing strength of the abdominal and trunk muscles.

As it turns out, the combined use of focus, breathing, rhythmical movement, and precision results in total body strengthening (not just the core or central muscles of the abdomen and trunk).

Weaker muscles start to contract and participate in the movement when stronger muscles are engaged. With improved muscle control comes better alignment and protection of the spine. The end result is the ability to perform even more advanced skilled movements with perfect balance and coordination.

You can see why this approach appeals to dancers, martial artists, and athletes of all kinds who need strength, balance, coordination, and endurance all at the same time. And physical therapists quickly saw the advantage of these techniques for patients suffering from chronic back pain or recovering from injuries.

Research to better understand the effects of Pilates has fostered the growth of Pilates technique in rehab. It has been shown to help reduce stress and chronic back pain, improve flexibility, and promote better posture and relaxation. Although it is believed that anyone of any age in any condition can benefit from Pilates exercises, research to support this with evidence is still lacking.

Future studies are also needed to investigate the effects of using the traditional classical approach as taught by Joseph Pilates versus the modified forms of Pilates currently in use.

For example, his program has been varied and changed for the more physically challenged individual who cannot perform the advanced or technical Pilates techniques. Are these altered movements just as effective? Perhaps even more effective? Is there any benefit at all in doing Pilates when there are any physical limitations? These are all questions that must be addressed before physical therapists incorporate Pilates as a mainstream rehabilitation technique.

Platelet-rich plasma (PRP) (also known as blood injection therapy) is a medical treatment being used for a wide range of musculoskeletal problems. Platelet-rich plasma refers to a sample of serum (blood) plasma that has as much as four times more than the normal amount of platelets.

In some conditions, this treatment has been shown to enhance 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. 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 musculoskeletal problems, but gaining popularity quickly.

One area where the use of PRP has been questioned is in the treatment of chronic musculoskeletal problems like chronic tendinopathy. Some of the other uses (e.g., spinal fusion, tendon-to-bone grafts, bone fractures) have come under closer investigation. So what do we know about the effectiveness of PRP in treating these various problems?

To answer this question, a group of 50 experts in the area of PRP therapy met and discussed their findings from clinical use (with patients) and from research efforts. They made the following key observations:

Bursitis may be a word you only heard spoken by the elderly but, in fact, this condition can affect people of all ages. Older adults are the most likely to develop pain, swelling, and tenderness around a joint from bursitis. But younger folks can be affected, too.

What exactly is this problem? Bursitis is the inflammation of a bursa. A bursa is a sac made of thin, slippery tissue. Bursae (plural) occur in the body wherever skin, muscles, or tendons need to slide over bone. Bursae are lubricated with a small amount of fluid inside that helps reduce friction from the sliding parts. They can also be found between muscle and fibrous bands of connective tissue.

Four main areas of bursitis are the focus of this article: the knee, elbow, hip, and heel. Causes of bursitis include trauma, inflammation, and infection.

The diagnosis is made based on patient history, symptoms, and special tests. The problem must always be sorted out carefully as the same symptoms can occur with tumors, arthritis, fractures, tendinitis, and nerve damage. Sometimes bursitis is a secondary problem caused by some other disease process such as gout or sarcoidosis.

When trauma is the cause, it may be the result of a direct blow or a fall onto the knee, elbow, hip, or heel that damages the bursa. This usually causes bleeding into the bursa sac, because the blood vessels in the tissues that make up the bursa are damaged and torn. In the skin, this would simply form a bruise, but in a bursa blood may actually fill the bursa sac. This causes the bursa to swell up like a rubber balloon filled with water.

The blood in the bursa is thought to cause an inflammatory reaction. The walls of the bursa may thicken and remain thickened and tender even after the blood has been absorbed by the body. This thickening and swelling of the bursa is what we refer to as bursitis.

The bursae can become irritated and inflamed in other ways. For example, in the case of prepatellar (knee) bursitis, repeated injury can lead to irritation and thickening of the bursa over time. For example, people who work on their knees, such as carpet layers and plumbers, can repeatedly injure the prepatellar bursa (pad in front of and behind the patellar tendon just below the knee cap). This repeated injury can lead to irritation and thickening of the bursa over time.

When infection is the cause of bursitis, it is usually from a staph or strep infection. The bacteria enter the body close to the affected joint through a cut or small opening in the skin. A minor skin infection of the skin over the bursa can spread down into the bursa. In this case, instead of blood or inflammatory fluid in the bursa, pus fills it. The area around the bursa becomes hot, red, and very tender.

Bacteria can travel to the joint via the bloodstream but it’s not thought that this is the way infectious bursitis develops. Why not? Because there isn’t much of a blood supply to the bursa.

As mentioned, the patient’s history and symptoms are often a clear indication of the problem. The real challenge is in determining whether or not there is an infectious process going on. Sometimes the physician has to aspirate the bursa. Aspiration is a way to remove some of the fluid for analysis. A very thin needle is inserted into the bursa to suction out the fluid.

Imaging studies such as MRIs are also helpful. X-rays may be taken first to rule out arthritis and fractures. And for each location (elbow, knee, hip, heel), there are special tests the examiner (e.g., physician, physical therapist) can apply to confirm the presence of a bursitis. Most of these tests involve some type of movement or position that compresses (pushes on) the bursa, thus reproducing the symptoms.

Treatment is usually conservative (nonoperative) care. Rest, activity modification, and medications such as antiinflammatories (for pain and swelling) or antibiotics (for infection) are the main management tools. Stretching the soft tissues around the bursa may help. In the case of a heel bursitis, a change in shoe wear may be recommended. The idea is to find a shoe that doesn’t rub against the heel over the bursa.

Surgery to remove the bursa (called bursectomy) is usually reserved for patients who do not respond to nonsurgical care. There is always a risk of additional problems or complications with any surgery, so this is not the first step in treatment. But it has its place when all else fails.

Other surgical techniques depend on the location of the bursa. For example, in the hip area, it may be necessary to remove a portion of bone or release some of the involved soft tissues (e.g., the iliotibial band).

In the heel, an osteotomy of the bone may help change the alignment and take pressure off the bursa. An osteotomy is the removal of a tiny wedge-shaped piece of bone. Collapsing the remaining edges of bone together (called a closing wedge osteotomy) rotates the calcaneus (heel) bone just enough to remove pressure from the bone and stop the bursitis.

For anyone with bursitis at one of these four main areas (elbow, knee, hip, or heel), this is a good review article. The authors provide a nice summary of the condition, drawings to explain the problem, and photos of MRIs to give a visual description. The diagnosis and management for each type (infectious, traumatic, inflammatory) and each location are also included.

If you haven’t heard of platelet-rich plasma as a treatment for various musculoskeletal problems, let us fill you in! Platelet-rich plasma or PRP is the clear portion of blood (plasma) with the blood clotting platelets.

It is taken from the patient so doesn’t require blood donors. The growth factors contained within the platelets enhance the body’s natural ability to heal itself. PRP 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 musculoskeletal problems, but gaining popularity quickly.

In fact, there have been over 5,000 studies already published on this treatment technique. Recently, a group of 50 medical experts got together to discuss platelet-rich plasma (PRP) therapy. The goal was to review what is known about the use of PRP and what type of future research is needed.

One concern raised by the group is the lack of quality control over platelet-rich plasma. There is no way to standardize the product because the body simply doesn’t produce the same amount of platelets every hour of every day in every person. What you eat, how well you sleep, medications you take, and even the exercise you get can all affect platelet levels in the blood.

There’s more than one way to extract (remove) the platelet-rich plasma (PRP) and that can also affect the quality of the product. Other components of the blood (such as white blood cells) may get in the sample used and alter the body’s healing response (not always favorably).

A closer look at the different studies highlighted some of the difficulties in comparing one study to another. That may explain why results can be opposite from study to study. One common theme seems to be that platelet-rich plasma may be most effective for chronic musculoskeletal injuries. It’s not a given that the results obtained in one condition will be the same for another type of soft tissue injury.

Another problem is the wide range of tissue types being treated (e.g., cartilage, bone, tendons, ligaments, muscles). Results seem to differ within the tissue types so that how platelet-rich plasma affects a ligament in the knee may not be the same as the effects on a similar ligament in the ankle.

And a third major stumbling block in the research that’s being done on platelet-rich plasma (PRP) is the way results are recorded. Some studies look at patient response in terms of pain levels and activities of living. Others are measuring strength after treatment or speed of wound healing during recovery.

The panel of researchers express concern over the fact that high-profile athletes are being treated with this tool in order to get them back into action as soon as possible. That’s the case regardless of whether the athlete is a good candidate for the treatment and without knowing how soon it’s safe to jump back into the game.

There may be a risk of graft rupture or reinjury if tissue repair isn’t yet complete. Likewise, the tissue under repair may not be strong enough to withstand forces during full sports participation. But we don’t know what those limits are yet based on any scientific evidence.

All that is to say, despite 5,000 studies on the topic of platelet-rich plasma, there is plenty of room and a real need for further studies to answer many questions. Who’s a good candidate for this treatment? What kind of conditions can be treated effectively with platelet-rich plasma? How long should we wait after having platelet-rich plasma before resuming normal activities?

Engineering healing with platelet-rich plasma is an exciting area of research and study. If successful, it could result in fast, effective healing of all types of soft tissue injuries. Panels like the one that met to review this topic are important to keep research on track. We’re not quite ready for any real treatment guidelines yet but we are a step closer to organizing and directing future studies.

This is the second article in a two-part series to bring us up-to-date on psoriatic arthritis (PsA). The first part focused on the diagnosis of this condition using biomarkers and advanced imaging studies. In this second half, the use of medications to treat the problem is highlighted.

Psoriasis is a disease that most people think of as primarily a skin disease because the condition causes a persistent rash in various areas of the body. Psoriatic arthritis is a type of joint disease that occurs in roughly seven percent of people who have psoriasis.

Psoriatic arthritis affects people of all ages, but most get it between the ages of 30 and 50. Usually a patient has psoriasis (the skin rash) for many years before the arthritis develops, and the arthritis comes on slowly. Patients with psoriatic arthritis must manage both the outbreaks of itchy, scaly skin and the pain and stiffness of arthritis.

One of the most commonly used medications for the treatment of psoriatic arthritis (PsA) is a disease-modifying antirheumatic drug (DMARD) called methotrexate. DMARDs like methotrexate not only control symptoms, they also slow the progression of disease. That’s what makes them “disease-modifying”.

Methotrexate may not be as effective with psoriatic arthritis as it is for patients with rheumatoid arthritis but without the psoriasis. Some patients don’t respond at all while others have an adverse reaction to the medication. And in some cases, it may be necessary to combine methotrexate with another drug (e.g., infliximab) to get the desired results (decreased joint pain, swelling, and stiffness).

Infliximab is a type of disease-modifying medication in a class called anti-tumor necrosis factor (TNF) agents. The anti-TNF agents are a special type of antibody referred to as human monoclonal antibodies. They specifically target (and inhibit) tumor necrosis factor.

Tumor necrosis factor (TNF) promotes the inflammatory response, which in turn causes many of the clinical problems associated with autoimmune disorders such as rheumatoid arthritis. Golimumab is another new TNF-inhibitor that has been approved by the FDA for use with patients who have active moderate-to-severe psoriatic arthritis (PsA).

Not everyone with psoriatic arthritis (PsA) responds well to TNF inhibitors (and not everyone can afford them). What can be done for these patients? Well, that’s a problem scientists are trying to solve. Right now, there aren’t very many options left for these patients.

Oral medications (pills taken by mouth) under investigation that might be available in the future for the treatment of psoriatic arthritis include ustekinumab, apremilast, and tofacitinib. Each of these medications works in a slightly different way to regulate the immune system.

Ustekinumab (Stelara, Centocor) is a human monoclonal antibody. It is directed against two specific interleukins (interleukin 12 and 23). Interleukins are naturally occurring proteins that regulate the immune system and inflammatory disorders like rheumatoid arthritis. In Phase III trials for moderate-to-severe psoriasis, ustekinumab was safe and effective, especially for patients who failed to respond to other standard medications.

Apremilast works as an anti-inflammatory by suppressing more than one pro-inflammatory cells including, TNF-alpha, interleukins 6, 17 & 23, and interferon-gamma (among others). It is currently in Phase III clinical trials for the treatment of psoriasis, psoriatic arthritis, and other chronic inflammatory diseases. Early stage studies found this medication to be safe and well-tolerated with few side effects.

Tofacitinib inhibits Janus kinase, an enzyme that acts as a special signaling messenger in the immune system. Tofacitinib is currently in phase two trials with psoriasis and will be tested next with psoriatic arthritis. Tests are scheduled to run until January 2015. So it may be a while before we see this one on the market for psoriatic arthritis.

In summary, the use of disease-modifying antirheumatic drugs (DMARDs) has changed the quality of life for many patients suffering from the effects of psoriatic arthritis. For those individuals who do not do well with these drugs, there aren’t very many other choices. But scientists point to a “therapeutic pipeline” of drugs that may be available in the near future.

If you have a condition called lupus (short for systemic lupus erythematosus or SLE, this report may be of interest to you. For the first time in over 50 years, the Food and Drug Administration (FDA) has given the nod for a new drug to treat this condition.

Lupus is a chronic inflammatory autoimmune disorder that can affect just the skin (face, neck, scalp) or target organs and any system in the body. Autoimmune means that the immune system mistakenly attacks body parts in an effort to get rid of them. Why a person’s immune system sees your own body as foreign or something to attack remains a mystery.

According to the Lupus Foundation of America about 1.5 million Americans have some form of lupus. Systemic lupus erythematosus (SLE) rarely develops in older people. It is primarily a disease of young women in their childbearing years. Men and children can develop lupus but this happens much less often than in women.

Lupus (SLE) is three times more common in African American women than in Caucasian women and is also more common in women of Hispanic, Asian, and Native American descent. It is believed that both genetic and environmental factors play a role in the development of the disease.

Other risk factors include physical or mental stress, which can provoke neuroendocrine changes affecting immune cell function; streptococcal or viral infections; exposure to sunlight or ultraviolet light, which can cause inflammation and tissue damage; immunization; pregnancy; and abnormal estrogen metabolism.

The main immunologic disturbance in SLE is something called auto-antibody production. The body produces antibodies against its own cells and antigens.
In fact, one significant feature of SLE is the ability to produce antibodies against many different tissue components. Almost any organ or tissue in the body including blood cells can be targeted.

Symptoms vary depending on the body part, cells, or systems affected. There can be a skin rash, severe joint pain, extreme fatigue, inflammation of blood vessels, and hair loss. Headaches, irritability, and depression signal autoantibodies reacting with the nervous system.

Some patients report problems with shortness of breath, seizures, strokes, and/or difficulty with memory. Anemia, hepatitis, nausea, vomiting, diarrhea, and abdominal pain are among the many other symptoms possible.

The standard means of treatment has been with corticosteroids (antiinflammatory drugs) and medications that suppress the overactive immune system. Drugs to treat malaria have also been helpful. But now with the introduction ofBenlysta (belimumab), patients have a new treatment option.

The drug is administered intravenously (through a vein) once a month. It is designed to target B-lymphocyte stimulator protein. The goal is to reduce the number of abnormal B-cells. The effect is to turn down the immune system response.

Benlysta is the first drug to be developed specifically to treat lupus. It is considered safe, effective, and provides tolerable treatments. Not everyone can benefit from this drug and there are some potential side effects.

In drug trials before Benlysta was approved for public use, only one in three patients experienced relief from their symptoms. Because Benlysta weakens the immune system, patients taking the drug are at an increased risk for infections, cancers, depression, and suicide. The drug was not specifically studied in African-Americans, the group affected by lupus most often.

The drug may allow patients to reduce the amount of corticosteroids they are currently using to manage the inflammatory symptoms of lupus. And that’s important because these drugs can do more organ damage over the long term than the disease itself.

Lupus sufferers may find Benlysta helpful in reducing flare-ups, providing less fatigue, and resuming a more normal lifestyle. Patients who have had success using this drug for their lupus say their quality of life is much improved. With no cure for lupus and treatment only able to target the symptoms, Benlysta may give some patients a new lease on life.

Did you know that caffeine in its various forms is considered a psychoactive agent? Psychoactive means it has a stimulating effect on the central nervous system. Given its effects on the nervous system, some even consider this substance a drug.

Did you know that surveys show that almost all adults (up to 95 per cent) ingest some form of caffeine everyday? Many people have a total caffeine intake up to 400 mg/day (that’s considered a high level). That may not be surprising when you consider caffeine is a substance in a variety of beverages as well as some foods and medications.

You probably know about caffeine in coffee and tea, but don’t forget soft drinks, energy drinks, and chocolate. There is caffeine in many over-the-counter drugs (for cold symptoms, headache pain relievers) and some prescription medications. Some people even take caffeine pills to stay awake and alert.

Why is caffeine added to other pain relievers such as acetaminophen (Tylenol) or ibuprofen? Adding caffeine to an analgesic (pain reliever) seems to boost its ability to decrease pain. This effect is called adjuvant analgesia and its most noticeable with headache pain. Caffeine as an adjuvant analgesic doesn’t seem to be as good for postsurgical pain.

Why does caffeine reduce headache pain? Caffeine is a vasoconstrictor — that means it closes down or narrows the blood vessels. The effect is to reduce the amount of blood flow to an area.

If you have a “throbbing” headache, it’s often because there is too much blood flow to the brain. Caffeine reduces the blood flow and thus decreases the pain. You could get the same effect (vasoconstriction of blood vessels in the head) by putting your feet in a bucket of ice cold water because blood would be diverted from the head to warm the feet. But you can see why an over-the-counter headache medication containing caffeine would be easier and less uncomfortable to use.

But as anyone knows who uses caffeine in any form on a daily basis, there are withdrawal symptoms. Headache is the number one withdrawal symptom experienced by most people. Fatigue is another common effect of caffeine withdrawal. In fact, anyone getting ready for surgery or fasting for blood tests who consumes caffeine on a regular basis can expect to have a headache from the caffeine withdrawal.

How does caffeine work that it can reduce pain and/or help other pain relievers provide pain relief? The mechanisms aren’t clearly understood but in simple terms, caffeine blocks pain receptors.

Newer studies show that low doses of caffeine may actually have the opposite effect: it inhibits blocking pain receptors. What does this new information mean for us? It’s possible that a cup of coffee or tea (or small amounts of other foods and beverages containing less than 100 mg of caffeine) could prevent other pain relievers from working. This same inhibitory effect of low doses of caffeine has been observed with acupuncture and electrical stimulation.

Researchers aren’t quite ready yet to say we should avoid caffeine before acupuncture treatment or when using electrical stimulation to control pain. Further studies on the effects of varying doses of caffeine are needed before any specific guidelines on caffeine use can be determined.

Arthritis comes in many forms including one called psoriatic arthritis (PsA). Psoriasis is a disease that most people think of as primarily a skin disease because the condition causes a persistent rash in various areas of the body. Psoriatic arthritis is a type of joint disease that occurs in roughly seven percent of people who have psoriasis.

Psoriatic arthritis affects people of all ages, but most get it between the ages of 30 and 50. Usually a patient has psoriasis (the skin rash) for many years before the arthritis develops, and the arthritis comes on slowly. But this is not always the case. No matter what, patients with psoriatic arthritis must manage both the outbreaks of itchy, scaly skin and the pain and stiffness of arthritis.

Psoriatic arthritis (PsA) can be a very aggressive disease. Based on the evidence we have so far, it is believed that early recognition and treatment of this problem yields better results.

Scientists are looking for faster, more reliable ways to tell if someone is developing PsA. Until such tests are available, physicians must rely on screening tools currently available such as the Psoriatic Arthritis Screening and Evaluation (PACE), Toronto Psoriatic Arthritis Screen (ToPAS), and the Psoriasis Epidemiology Screening Tool (PEST).

These screening tools are not enough by themselves because psoriatic arthritis is more than just a skin and joint disease. There is often a wide range of signs and symptoms involving many different body parts. One screening tool can’t possibly assess everything equally at the same time.

Physicians must also use other diagnostic tools such as X-rays, ultrasonography, and MRIs. Each one of these tests provides a little different information. For example, X-rays show early signs of bone erosion but do not reveal anything about the condition of tendons, ligaments, or other soft tissues often affected by psoriatic arthritis.

Ultrasonography, the use of sound waves to create a picture of what’s going on inside, provides a better look at the whole package: bones, joints, and soft tissues. This diagnostic test is also noninvasive and does not expose the patient to any radiation. Ultrasound also has the ability to show small changes in the nails and early signs of inflammation in tendons and small joints.

MRIs are slowly being replaced by ultrasound studies. MRIs can show bone marrow edema, tenosynovitis, and early joint erosion. Tenosynovitis is the inflammation of the fluid-filled sheath (called the synovium) that surrounds a tendon.

But reliability is a problem with MRIs because what one examiner sees may not be the same as another observer. Changes in the small joints of the hands and feet don’t show up well on MRIs like they do with ultrasonography.

One advantage MRIs do have over ultrasonography is the availability of whole body MRI. By scanning the entire body, it is possible to identify areas of inflammation undetected by clinical exam. And whole-body ultrasonography just isn’t reasonable.

Until blood studies are able to find biomarkers (biologic evidence of disease) indicating the presence of psoriatic arthritis, physicians will probably have to use a combination of different tests to diagnose the problem. The information these tests provide is important in determining treatment.

Research in the area of psoriatic arthritis is on the brink of making some major discoveries that will improve the diagnosis and management of this disabling disease. Besides serum biomarkers (in the blood), better tools are being developed to assess the progression of this disease.

Likewise, drugs to specifically target the problem called biologic agents will eventually replace current medications that help with symptoms but either have adverse side effects or affect more than just the targeted tissues. Better screening tools would be helpful, too — or at least knowing which screening tool to use for each clinical setting and/or patient would be a step in the right direction.

This article is the first of two parts bringing us up-to-date on the condition known as psoriatic arthritis (PsA). The second part will cover treatment, including changes in treatment based on imaging findings described here.

Knowing that the management of this condition depends on early detection of bone, joint, and soft tissue pathology helps us understand the need for both improved diagnostic and treatment approaches. The potential for severe progression of disease may be halted (or at least slowed) with a management approach that includes (repeated or serial) diagnostic imaging throughout the course of treatment.