Category Archives: cartilage

Does Acupuncture Work For Arthritis?

The ancient healing art, acupuncture, has been the topic of numerous scientific studies to determine its efficacy.  In particular, acupuncture has been examined as a treatment for osteoarthritis.  The most complete study of acupuncture was a meta-analysis of data from more than 29 randomized controlled trials of acupuncture for chronic pain. (Vickers AJ, et al. Arch Int Med.September 2012)acupuncture-knee

The study found that patients receiving acupuncture had less pain than controls and acupuncture was statistically superior to both sham and no acupuncture controls for the treatment of osteoarthritis.

The study concluded that acupuncture is a reasonable referral option for patients with pain due to OA.

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OA caused by defective pieces of DNA

Sophie Borland writing in the Daily Mail (and also reported in the BBC News) reported a breakthrough by British scientists that could lead to new treatments for osteoarthritis, the most common form of arthritis.osteoarthritis-knee-2

Researchers have discovered eight sections of DNA that are responsible for dnacausing this degenerative condition that causes cartilage to wear away prematurely. After comparing “the DNA of 7,400 UK osteoarthritis patients with that of 11,000 healthy volunteers,” then repeating their work in some 7,500 osteoarthritis patients and 43,000 people without the condition, researchers “confirmed the three previously reported gene variants and found a further eight linked to osteoarthritis.”

The team at Newcastle University found the common genes each increase the risk by between 11 per cent and 20 per cent,

Also, they think that at least two or three of these so-called ‘genetic regions’ could be used to treat the illness.

The research could lead to new treatment for thousands of arthritis sufferers

The scientists from the University of Newcastle believe that in future they could alter patients’ genes to make them produce stronger cartilage, helping to repair the damaged joints.

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What are the approaches to treatment of osteoarthritis of the knee?

There are multiple treatment approaches for osteoarthritis (OA) of the knee.

osteoarthritis-knee-2The most important to start with is weight loss and patient education.  Without these, other therapies won’t work.

Analgesics such as acetaminophen may work for mild disease and non-steroidal anti-inflammatory drugs(NSAIDS) can be used for more symptomatic disease. The use of the latter category of drug needs to be tempered with the knowledge that potential gastrointestinal and cardiovascular side-effects are associated with these medicines.  Topical NSAIDS may be safer.

Alternative therapies such ass glucosamine/chondroitin, acupuncture, and so on, serve a complementary role.

Exercise and physical therapy, and, if necessary, braces, orthotics, and other assistive devices may be helpful.

Injections of glucocorticoids and viscosupplements can provide significant palliative relief.

Guided mesenchymal stem cell layering is a technique that can provide symptomatic relief, potentially regrow cartilage, and delay the need for surgery.

Total knee replacement is to be considered for patients with end-stage disease.

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What can be done about osteoarthritis?

Osteoarthritis (OA) is the most common form of arthritis and affects approximately 28 million Americans.  While it has been viewed as a “wear and tear” phenomenon, it has become quite clear that it is a disease that is multifactorial in its development.

It is not a benign disease because, in addition to the pain, OA leads to functional disability.

The joint is a dynamic structure where anabolic (building) activities are counterbalanced by catabolic (destructive) activities.

With OA, the catabolic activities gradually overtake the anabolic ones. While there are attempts at repair, these attempts are dysfunctional , leading to the formation of bony spurs, called osteophytes.osteoarthritis-knee

There are three major risk factors for the development of osteoarthritis.  They are genetic (usually a family history is prominent), constitutional (obesity in the case of OA of the knee, and aging), and finally local components (injury and ligamentous laxity).

Cartilage consists of cells called chondrocytes that sit inside a “soup”, a matrix, which consists of collagen and proteoglycans.cartilage_1

The development of osteoarthritis starts with an initial injury to cartilage.

The injury may trigger an inflammatory response leading to the synthesis of cartilage matrix degrading enzymes, produced by chondrocytes. Over time, the catabolic activities override anabolic activities and abnormal repair mechanisms lead to the formation of osteophytes, while cartilage continues to degrade.

The treatment for osteoarthritis is primarily symptomatic.  Analgesics (pain nsaidsrelievers), non-steroidal-anti-inflammatory drugs (NSAIDS), weight loss, exercise, assistive devices such as wedge insoles, braces, canes, walkers, and such. Injection of glucocorticoids and viscosupplements (lubricants viscosupplementderived either from rooster combs or from bacteria) may also be helpful.

knee-joint-replacement-surgeryEventually patients will require surgery in the form of joint replacement. Joint replacement surgery has come a long way, but there are still concerns about them.  The first is the possibility of a surgical complication such as blood clot or infection.  The second issue is the finite lifespan of the prosthesis.  They usually last 10 to 15 years but this is a function of activity and joint replacement patients do have restrictions on their activity level.  Persistent pain due to particle induced inflammation can also be a problem.

Finally, the chance of faulty prosthetic devices such as the recent  Johnson & Johnson metal-on-metal hip debacle, makes the choice of total joint replacement less attractive.

Recent developments in stem cell technology may provide an alternative to joint replacement.

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Antibiotics for arthritis?

Research has pointed to a possible benefit of using antibiotics for the treatment of some types of arthritis. This article discusses some of the data.

The role of antibiotic therapy for the treatment of arthritis is controversial. However there is at least some evidence for effectiveness in two examples. Minocycline, a member of the tetracycline family, appears to suppress enzymes involved in the inflammatory process. Doxycycline is an antibiotic that also belongs to the tetracycline group and has shown to have positive benefits in osteoarthritis.


In 1949, at the International Congress on Rheumatic Diseases, a possible relationship between mycoplasmas and joint disease was described.

Thomas McPherson Brown, M.D. and his colleagues at the National Institutes of Health reported the following year that rheumatoid arthritis may be caused by an immunologic reaction of antigen and antibody (with mycoplasma as the suspected antigen).

In 1955, Brown reported that mycoplasmas, unlike bacteria and viruses, could live in tissue cell cultures without destroying the tissue cells. In 1964 a high incidence of mycoplasma antibodies in the blood of rheumatoid arthritis patients was found, indicating current or previous infection. Also noted was a four-fold higher incidence of mycoplasma antibodies in females suggesting a correlation with the higher incidence of rheumatoid arthritis in females.

Efforts to demonstrate the effectiveness of tetracycline therapy were initiated and first reported by Dr. Brown shortly thereafter. In 1989, NIH initiated controlled clinical trials of tetracycline therapy for rheumatoid arthritis. The preliminary results of the clinical trials, known now as MIRA or Minocycline in Rheumatoid Arthritis, were promising.

The result of the MIRA clinical trial were: “Patients who suffer from mild to moderate RA now have the choice of another therapeutic agent. Not only did the antibiotic significantly reduce symptoms, but side effects were minimal and less severe than observed for most other common rheumatoid treatments”.

Despite these findings, many rheumatologists remain skeptical. Other studies have failed to demonstrate clinically significant improvement.

According to the American College of Rheumatology, “Minocycline is prescribed for patients with symptoms of mild rheumatoid arthritis. It is sometimes combined with other medications to treat patients with persistent symptoms of this form of arthritis.”

Their formal position is stated in this fact sheet for patients:

…There is evidence minocycline may slow the progression of joint damage in arthritis and prevent disability like other drugs in the class known as DMARDs (disease-modifying antirheumatic drugs).

Minocycline is prescribed for patients with symptoms of mild rheumatoid arthritis, sometimes in combination with other medications to treat patients with persistent symptoms of this form of arthritis.

…Minocycline decreases the production of substances causing inflammation, such as prostaglandins and leukotrienes, while increasing production of interleukin-10, a substance that reduces inflammation.

Minocycline usually is given as a 100 milligram (mg) capsule twice a day. It may be taken with food, although it should not be taken with other medications such as antacids or iron tablets.

It may take 2 to 3 months before any improvement in arthritis symptoms is experienced and up to a year before maximum benefits are realized.

The most common side effects from this medicine are gastrointestinal symptoms, dizziness and skin rash. Some women who take minocycline develop vaginal yeast infections. While this can occur with other antibiotics, it seems more prevalent with minocycline and other tetracyclines. It is thought minocycline kills bacteria normally present in the body which protect against yeast infections.

Minocycline increases sensitivity to sunlight, resulting in more frequent sunburns or the development of rashes following sun exposure. It is recommended patients apply sunscreen (SPF 15 or greater) before outdoor activities or avoid prolonged exposure to the sun while taking minocycline.

More rarely, minocycline can affect the kidneys or liver. Doctors may recommend periodic blood tests for long-term users to check liver and kidney function. In equally rare cases, minocycline can induce lupus, but this condition usually improves after stopping the medication.

Minocyline use during pregnancy can slow the growth of teeth or bones in infants after birth as well as cause discoloration of the newborn’s teeth when taken during the last half of pregnancy. Minocycline may decrease the effectiveness of some birth control pills.

Minocycline is passed into breast milk, so mothers should avoid breast-feeding to prevent delayed development of teeth and bones in their infants. Minocycline can increase a nursing infant’s risk of fungal infections or dizziness in the newborn. Because minocycline may cause discoloration of teeth and problems with bone growth in young children, it is recommended that those younger than 8 years old not take this medication. This is not a problem in older children and adults.

Possible interactions with minocycline may occur when taking warfarin (Coumadin), antacids containing calcium, aluminum or magnesium (such as Tums, Rolaids, Maalox, or Mylanta), iron tablets and oral contraceptives (birth control pills).

To highlight one of the potential side effects of minocycline, a small study reported in the June 2006 issue of the Journal of Rheumatology indicated that skin discoloration (hyperpigmentation) appears to be a very common side effect of minocycline use. The study involved 27 patients. Forty-one percent (11 patients) reported developing skin discoloration after using minocycline for approximately one year. Four of the 11 patients stopped using minocycline because of hyperpigmentation (two had skin discoloration on their face and two had skin discoloration on their arms).

The use of minocycline for rheumatoid arthritis is rare nowadays because of the development of newer biologic therapies. Nonetheless, it remains a viable option for the rare person with extremely mild disease.


Doxycycline, another tetracycline derivative, has been used to treat osteoarthritis. Study results reported in Arthritis & Rheumatism (July 2005 issue) suggest that treatment with the antibiotic doxycycline may slow the progression of this disease.

Researchers compared the use of doxycycline to placebo, using about 400 obese women with knee arthritis as study participants. Researchers analyzed the impact of doxycycline on the joint space of the affected knee.

The study participants were randomized into two groups, receiving either 100 mgs of doxycycline two times a day or placebo for up to two and a half years.

Following 16 months of treatment, results indicated that the average loss of joint space in the affected knee was 40% less among participants taking doxycycline than those who took placebo.

At the end of the two and a half year period, the loss of joint space was 33% less in the group who took doxycyline than in the group who took placebo.

Doxycycline treated patients also reported having marginally less joint pain.

Researchers said that this was the first major study of doxycycline as a potential treatment for osteoarthritis. More studies will be needed to confirm these results.

While the study did not clearly show that oral doxycycline was effective in reducing pain, there was evidence that there was less progression of osteoarthritis (i.e. less cartilage loss) in patients on the antibiotic. The authors felt doxycycline works through anti-inflammatory effect and not due to an anti-bacterial effect.

Based on this study, it is difficult to recommend long term doxycyline for relief of symptoms. (Although I admit, I’m a closet doxycycline user on occasion). On the other hand, it is possible that patients taking the antibiotic may be less likely to require joint replacement in the future due to a decrease in joint damage on x-ray.  Obviously, longer term studies are required. The problem, as it exists today, is that we have no other drugs with significant disease-modifying effects for osteoarthritis.

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The four types of stem cells that could be used for osteoarthritis treatment

stem-cellThere are four types of stem cells undergoing current study. They are embryonic SCs, allogeneic (donor) SCs, induced pluripotential adult SCs, and finally autologous SCs. Of these four, only two, donor SCs and autologous SCs have been used to treat arthritis so far.

However, this discussion would be incomplete without mentioning the other types as well.

Embryonic SCs (ESCs) are derived from embryos and are pluripotential, meaning they can easily differentiate into any body tissue.

stem-cell-differentiationSelf-renewing cells were first extensively studied in mouse cancer models. These cells showed the ability to not only self-duplicate but to also differentiate into multiple types of tissue. Obviously, though, cells that are capable of self-duplication are also capable of becoming malignant.

Potential pitfalls associated with embryonic stem cells are the following:

• The ethical dilemma which has restricted the amount of government spending towards ESC research.

• The risk of malignancy associated with cells that have not completely differentiated yet and are as potent as ESCs.

• The theoretical problem with a graft versus host reaction. While immunosuppressive drugs can be used to mitigate the effects of this, these drugs are not without significant side effects.

There is actually a variant of embryonic stem cells, the fetal stem cell.  For more about this, here’s a video:

The second type of SC is the induced pluripotential SC. In 2006, Japanese researchers used retroviruses to insert genes into mouse cells. They were able to take these adult mouse cells and cause them to revert back to a pluripotential embryonic state.

The identical technique was then applied to human skin cells. These “adult turned baby cells” are known as induced pluripotential stem cells (IPSCs). Therefore, it is technically possible to take any adult cell and make it function like an embryonic stem cell.

As one might expect, the primary concern is malignancy. How can these cells get controlled off once they start to multiply?

The third type of SC and one which has been used to treat arthritis in both animals as well as humans is the allogeneic or donor SC. These cells come from healthy donors. Advantages are that a tremendous number of SCs can be cultured. Downsides include the potential transmission of unknown genetic disorders as well as the possibility of infection.

The fourth and most commonly used type of SC in arthritis treatment are the autologous SCs or adult SCs. There are various techniques used to harvest these cells from the adult. Typically, they are obtained from bone marrow, fat, or blood, which is then concentrated to provide a maximum number of cells in the smallest possible volume.

Autologous SCs have the advantage of coming from the host – the patient. This helps avoid the consequences of rejection or graft versus host reaction which may occur with SCs that come from either embryos or donors.
These are multipotent, meaning they can be coaxed into becoming a limited number of different tissue types. This is one of the major differences between adult SCs and embryonic SCs (and induced pluripotential SCs).

For a great video about this topic:

Embryonic SCs and induced pluripotential SCs are pluripotent, meaning they can be converted into any type of tissue.

Nonetheless, the multipotent property of autologous (also known as “mesenchymal” SCs) is sufficient for them to be used to treat disorders involving connective tissue, such as blood, tendon, ligament, cartilage, bone, nerve, muscle, and liver.

These cells are programmed to zero in on areas of tissue injury to help with repair. While it is still not clear what the homing mechanism is, it is suspected that different types of chemical messengers are involved in “calling” mesenchymal SCs. These cells are capable of contributing to both repair as well as regeneration.

One danger is that some techniques using adult SCs involve the use of cell culture ex vivo, meaning outside the body. The possibility of contamination and infection is a concern. Also, when cultured for a lengthy period of time, these SCs may become unstable and the possibility of malignancy developing arises.

Finally, a major weakness of adult SCs is that they are restricted in their capacity to replicate and differentiate. In other words, they go through an aging process and have a limited life span. This is unlike embryonic SCs which have the capacity to multiply and divide forever.

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Seven tips about stem cells for arthritis


A feature article appearing on ABC News (Newcomb “Stem Cell Treatments for Zoo Animals Hold Promise for Humans) underscored the interest that both scientists as well as lay people have in the new technology of using stem cells to repair and treat degenerative conditions.

“We just extract them, concentrate them, wash them and in the same setting readminster them. Inject them in your heart or your knees, wherever you need them,” Dr. Eckhard Alt told ABC Station KTRK-TV in Houston after treating an arthritic pig at the Houston Zoo.”

So… can this technology be applied to humans?

Here are seven tips about stem cells (SCs) for arthritis treatment you might want to know…

1. There are four types of SCs currently being studied. They are embryonic SCs, allogeneic (donor) SCs, induced pluripotential adult SCs, and finally autologous SCs. Of these four, only two, donor SCs and autologous SCs have been used in either animals or humans to treat arthritis. Here’s a video that gives the basics on stem cells :

2. The SC that appears to generate the most interest is the autologous SC. This is the SC that is present in the patient and can be found in bone marrow, periosteum of bone, fat, and peripheral blood. Autologous SCs are referred to as “repair SCs” because these are the SCs that help with the healing process.

3. Arthritis occurs as a result of cartilage degeneration. Various attempts at inducing cartilage healing with SCs have met with mixed results. The results appear to be highly dependent upon the following factors: age of the patient, body mass index (BMI), extent of cartilage loss, and the technical expertise of the center performing the procedure.

4. The processing and administering of SCs for an arthritis problem is more than just getting SCs out and injecting them. There appears to be a need for some type of acute injury to help stimulate the stem cells to multiply and divide.

5. Possible complications of SC treatment can vary. They include the following: infection, rejection, graft versus host reaction, malignancy, and transmission of genetic disease.

6. The need for a cartilage restorative procedure is very evident since the only treatments available currently for osteoarthritis are palliative, meaning pain control only. This is not satisfactory.

7. In the proper hands autologous SC treatment can be successful. Early data indicating an improvement in cartilage thickness in the treatment of osteoarthritis of the knee has been published.

(Wei N, Beard S, Delauter S, Bitner C, Gillis R, Rau L, Miller C, Clark T. Guided Mesenchymal Stem Cell Layering Technique for Treatment of Osteoarthritis of the Knee. J Applied Res. 2011; 11: 44-48)

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Osteoarthritis… what is it?

Osteoarthritis (OA) is the most common joint disease.  It affects approximately 28 million Americans and tends to become more common with increasing age. It is a universal condition in people past the age of 70 although not everyone is symptomatic. It is a disease that affects articular cartilage, the gristle that caps the ends of long bones.cartilage_0

There are risk factors for the disease.  Increasing age, as mentioned earlier is one.  In addition, female gender, genetic predisposition, obesity, and trauma are the other important items.

The most frequent targets for OA to strike are the neck, low back, fingers, base of the thumb, knees, and hips.

Less commonly the ankles, shoulders, and elbows are involved.  In these areas, antecedent trauma appears to be the primary cause.

knee-arthritisOA is what is called, a focal disease.  What that means is that it doesn’t affect the whole joint.  It preferentially attacks certain areas within the joint.  An example would be the knee where the medial (inside) part of the joint cartilage-defectis affected far more often than the lateral (outside) part.

In the hip, the top part of the joint tends to become involved while the rest of the joint is relatively spared.  The same is true for other joints affected by OA.

Symptoms of the condition consist of pain that is aggravated by use and relieved by rest.  Also, there is short term stiffness with inactivity. This is called “gelling.” Night time pain is also a common feature. Another common lament is crunching of the joint with movement.  This is called “crepitus.”

On exam the rheumatologist will often spot swelling due to the formation of bone spurs, called “osteophytes.”  There can be tenderness of the joint, pain with movement, swelling due to fluid accumulation, and muscle wasting around the joint.

In advanced cases, there is clear deformity and sometimes evidence of instability.

Laboratory tests are usually normal.  Imaging studies can help with the diagnosis.  Magnetic resonance imaging will pick up early changes.  X-ray findings also can help with the diagnosis.  The problem is that if x-ray changes are evident, then the disease has progressed substantially.  The primary changes seen on x-ray are narrowing of the joint, bone spurs, and changes in the bone underlying the cartilage.

Joint fluid, if present, should be aspirated.  The joint fluid is typically viscous, translucent, and has fewer than 200 white blood cells per cubic milliliter.  Occasionally the white blood cell count will be higher if a patient has a particularly inflammatory form of osteoarthritis. This is the conundrum of OA.  While the old thinking was that the condition was primarily a mechanical disease, it has become quite clear that OA has a significant inflammatory component as well.

What has been a perplexing question is, “What causes pain in OA of the knee?”  Cartilage has no blood vessels nor does it have nerves.  So the topic of pain mechanism in osteoarthritis has been the subject of intense interest.knee

There are a number of potential suspects.  For example, when osteophytes (bone spurs) develop, they can lift the periosteum (the thin top layer of the bone).  Periosteum is rich in nerve fibers and certainly can be a source of pain.

It has been noted that blood vessels in bone underlying osteoarthritic cartilage can become engorged and this may elevate the pressure inside the bone which could also, theoretically, cause pain.

The lining of the joint (synovium) becomes inflamed in OA.  Pain fibers are located within the joint capsule and these inflammatory processes could irritate them.

The joint capsule can contract or shrink leading to irritation of nerve fibers located within the capsule.

By the same token, if fluid builds up within the joint, it can stretch the joint capsule again leading to stimulation of pain fibers.

As mentioned earlier, there are two small pieces of fibrocartilage located within the knee.  These pieces of fibrocartilage (menisci) have a rich blood and nerve supply where they attach to the joint capsule.  OA often leads to tearing of these menisci. This can cause damage to the capsular attachment leading to pain.

Spasm of the muscles surrounding the knee can also lead to pain.

Finally, there is increasing interest in the role of the central nervous system- the brain- in causing the pain of knee OA.  Recent studies showing the effectiveness of drugs like Cymbalta, a drug originally prescribed for depression, but also showing beneficial effects on pain relief in patients with OA, led to FDA approval for this indication in 2011.

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