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Ross A Hauser, MD et al recently published an article on the use of Platelet rich plasma (PRP) Prolotherapy for the torn meniscus.

Abstract:

Meniscus injuries are a common cause of knee pain, accounting for a large number of surgeries in the U.S. annually. While surgical treatments range from total to partial meniscectomy, meniscal repair and even meniscus transplantation, all have a high long-term failure rate with the recurrence of symptoms. The most serious of the long-term post-surgical consequences is an acceleration of joint degeneration. The poor healing potential of meniscus tears, along with the consequence of post-surgical joint degeneration, has led to the investigation of methods to stimulate non-surgical, biological meniscal repair. While platelet rich plasma prolotherapy (PRPP) has been studied for many types of connective tissue injuries, no study has focused specifically on its use for meniscus tears.

Dr Ross Hauser et al give a very comprehensive review of the anatomy and pathophysiology of meniscus tears, with five case reports of MRI-documented meniscus tears successfully treated with PRPP. While further study under more controlled circumstances is needed, the logic of the authors’ discussion and the results reported clearly validate the use of platelet rich plasma prolotherapy as a first-line treatment for meniscus tears.

— Donna Alderman, DO

Practical Pain Management. July/August 2010.

Click here to read the full article from Practical Pain Management!  If you have a question about this article for Dr. Ross Hauser or would like to discuss your torn meniscus, please email at drhauser@caringmedical.com.

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Prolotherapy for rugby and soccer injuries

On June 15, 2010, in News, by JOP Blog Admin

World Cup Soccer is all the rage right now! Everyone is following their favorite team, hoping for victory. Have you ever watched those guys play? Wow – talk about an injury waiting to happen! With so much stopping and starting, kicking, running, and sliding, it’s no wonder that the sport produces all sorts of injury to the groin, knees, feet, and other body parts.  Prolotherapy is a great treatment for these athletes to get back to their sport quickly and not have to prolong their rehab or let alone lose a whole season due to surgery.

A study done by Dr’s Topol, Reeves, and Hassanein that was published in the Archives of Physical Medicine in 2005  examined the use of Prolotherapy in elite male kicking-sport athletes with chronic groin pain.  The study was done in an orthopedic and trauma center in Argentina. Twenty two rugby and two soccer players with chronic groin pain that prevented them from fully participating in their sports participated in the study. VAS scores for pain with sports and Nirschl Pain Phase scales were used to measure pain. After treatment results were as follows: mean of 2.8 treatments were given, the NPPS score improved from 5.3+/-0.7 to +0.8/-1.9 (P<.001). Twenty of the 24 patients had no pain and 22 of 24 were able to play their sports unrestricted at the time of final data collection.

The conclusion of the study was that dextrose Prolotherapy showed marked efficacy for chronic groin pain in this group of elite rugby and soccer players.

Efficacy of dextrose prolotherapy in elite male kicking-sport athletes with chronic groin pain. Topol, G., Reeves, k, and Hassanein, K. Archives of Physical Medicine; 2005; 86(4): 697-702

Author: Ross A Hauser, MD

Medical Director, Caring Medical and Rehabilitation Services, Oak Park, IL

A B S T R A C T
Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world for the treatment of osteoarthritis (OA) symptoms, and are taken by 20-30% of elderly people in developed countries. Because of the potential for significant side effects of these medications on the liver, stomach, gastrointestinal tract and heart, including death, treatment guidelines advise against their long term use to treat OA. One of the best documented but lesser known long-term side effects of NSAIDs is their negative impact on articular cartilage.

In the normal joint, there is a balance between the continuous process of cartilage matrix degradation and repair. In OA, there is a disruption of the homeostatic state and the catabolic (breakdown) processes of chondrocytes. It is clear from the scientific literature that NSAIDs from in vitro and in vivo studies in both animals and humans have a significantly negative effect on cartilage matrix which causes an acceleration of the deterioration of articular cartilage in osteoarthritic joints. The preponderance of evidence shows that NSAIDs have no beneficial effect on articular cartilage in OA and accelerate the very disease for which they are most often used and prescribed. Some of the effects of NSAIDs on the articular cartilage in OA include inhibition of chondrocyte proliferation, synthesis of cellular matrix components, glycosaminoglycan synthesis, collagen synthesis and proteoglycan synthesis.  The net effect of all or some of the above is an acceleration of articular cartilage breakdown.

In human studies, NSAIDs have been shown to accelerate the radiographic progression of OA of the knee and hip. For those using NSAIDs compared to the patients who do not use them, joint replacements occur earlier and more quickly and frequently. The author notes that massive NSAID use in osteoarthritic patients since their introduction over the past forty years is one of the main causes of the rapid rise in the need for hip and knee replacements, both now and in the future.

While it is admirable for the various consensus and rheumatology organizations to educate doctors and the lay public about the necessity to limit NSAID use in OA, the author recommends that the following warning label be on each NSAID bottle:

The use of this nonsteroidal anti-inflammatory medication has been shown in scientific studies to accelerate the articular cartilage breakdown in osteoarthritis. Use of this product poses a significant risk in accelerating osteoarthritis joint breakdown. Anyone using this product for the pain of osteoarthritis should be under a doctor’s care and the use of this product should be with the very lowest dosage and for the shortest duration of time.

If NSAID use continues, then most likely the exponential rise in degenerative arthritis and subsequent musculoskeletal surgeries, including knee and hip replacements as well as spine surgeries, will continue to rise as well.

Journal of Prolotherapy. 2010;(2)1:305-322.

KEYWORDS: accelerating articular cartilage degeneration, articular cartilage, cox-2 inhibition, non-steroidal anti-inflammatory medication, NSAID, osteoarthritis, prostaglandin.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world for the treatment of osteoarthritis (OA) symptoms,1 and are taken by 20-30% of elderly people (defined as people over the age of 64 years) in developed countries.2 The worldwide pain management prescription drug market totaled approximately $24 billion in 2002 and passed $30 billion by 2006. Celebrex (celecoxib) led the pack with nearly $4 billion in sales in 2002.3 Each year, over 70 million prescriptions for NSAIDs are dispensed in the United States, 20 million in Great Britain and 10 million in Canada.4-6 These numbers do not include the 30 billion over-the-counter tablets sold each year in the United States alone.7, 8 The most common over-the-counter and prescription nonsteroidal anti-inflammatory drugs are seen in Figure 1.

Treatment guidelines in the United States, Great Britain, and Canada recommend NSAIDs as second-line treatment (after acetaminophen) for mild OA and as first-line treatment for moderate to severe OA.9-11 As baby boomers age, it is estimated that the number of NSAID users will continue to climb, despite the fact that over 100,000 people are hospitalized for gastrointestinal bleeding and of those 16,500 people die from NSAID toxicity each year.12, 13 In 2006, the Osteoarthritis Research Society International formed an international committee to review all guidelines and evidence available on OA. Based on the evidence of potentially serious adverse reactions to NSAIDs, the committee has advised against the long-term use of NSAIDs to treat OA.14 One of the most serious adverse reactions to NSAIDs, that is little appreciated, is that as a class of compounds they cause the breakdown of articular cartilage, thereby accelerating OA, the very disease for which they are most commonly prescribed.

In the normal joint, there is a balance between the continuous process of cartilage matrix degradation and repair. In OA, disruption of the homeostatic state occurs and the catabolic (breakdown) processes of chondrocytes are increased.

Chondrocytes – the only cells in cartilage tissue responsible for the synthesis of collagen and proteoglycans that makeup the cartilage matrix
Cytokines are signaling molecules used extensively in cellular communications.

The principal cytokines linked to the catabolism of cartilage and to the OA process are interleukin (IL)-1, tumor necrosis factor (TNF)-a, and IL-6. IL-1 is the prototypic inducer of catabolic responses in chondrocytes. This substance causes the increased secretion of proteinases (which breakdown cartilage matrix) including collagenase, the suppression of proteoglycan synthesis leading to the suppression of matrix synthesis, and ultimately the reduction of the number of chondrocytes.15, 16 (See Figure 2.) IL-1 is a potent inducer of prostaglandin (PG) synthesis by inducing PGE2 synthesis in human chondrocytes. The rate-limiting step for the synthesis of PGE2 and other prostaglandins is the conversion of arachidonic acid to prostaglandin endoperoxide by cyclooxygenase (COX), which exists in two isoforms, COX-1 and COX-2. All NSAIDs inhibit both COX 1 and 2 enzymes but most of the NSAIDs that have been developed in recent years show greater activity of COX 2 in order to decrease gastrointestinal side effects. (See Figure 3.) PGs act (among other things) as messenger molecules in the process of inflammation. It was hoped that the use of NSAIDs would decrease the catabolic program in OA, thereby having a disease-modifying effect. Research, unfortunately is showing PGs, like PGE2, stimulate chondrocyte proliferation and subsequent synthesis of cellular matrix components.17 The net result of their blockade and other NSAID effects is the acceleration of articular cartilage degeneration. To show how this occurs and to what extent, a basic understanding of articular cartilage anatomy is needed.

Figure 1. Common over-the-counter and prescription nonsteroidal anti-inflammatory drugs (NSAIDs).
Figure 2. The catabolic physiology leading to articular cartilage breakdown. Interleukin-1 is one of the principle cytokines that initiates a cascade that leads to chondrocyte cell death and extracellular matrix breakdown. NSAIDs inhibit prostaglandins, such as PGE2, from stimulating chondrocyte DNA matrix synthesis thereby contributing to articular cartilage degeneration.
Figure 3. Inhibition of cyclooxygenase 1 and 2 by NSAIDs. Studies have shown that, although most NSAIDs inhibit both COX-1 and COX-2, it is the inhibition of COX-2 that is responsible for the anti-inflammatory effects of NSAIDS. On the other hand, inhibition of COX-1 by these agents causes damage to the GI tract. This has led to the development of a new generation of NSAIDs that specifically inhibit COX-2.
To read the full article by Dr. Hauser, please click here.

We hope our readers have been enjoying the latest issue of JOP and passing it along to colleagues, patients, and loved ones. The goal of the Journal is to help spread the word about the life-changing effects that Prolotherapy can have on a person’s life. We are constantly reviewing the literature, blogs, articles, and research that is out regarding Prolotherapy and the word is DEFINITELY getting out there. With more doctors using the technique and more athletes receiving the treatment (especially high profile professional athletes), acceptance continues to grow. Our goal is to see Prolotherapy become the first-line treatment for conditions such as back pain, knee pain, meniscus tears, carpal tunnel, headaches, arthritis, plantar fasciitis, shin splints, hip pain, pelvic pain, shoulder injuries, and much more.

Prolotherapy just makes sense. It stimulates your own body to heal the injured area. Ligaments are often the source of the pain and the only treatment we know of that can heal ligaments is Prolotherapy. Exercise, massage, chiropractic, ultrasound, supplements, etc. do not heal the injured area. These may help the muscles get stronger, but the underlying ligament weakness remains unless something is used to stimulate healing.

Dr. Hauser is one of the leading proponents of Prolotherapy and is leading the team at Journal of Prolotherapy in getting the word out there. We are thankful that he continues to dedicate so much time and effort to this cause.

People need to know that there is a better way to heal their chronic pain and/or sports injuries. NSAIDs, rest, ice, cortisone shots, MRIs etc. all result in long term degeneration, leading to surgery.  The end result is often that the patient still has pain, weakness, and cannot do the things he/she loves to do.

Most patients are turning to Prolotherapy because they want a cure. Often insurance companies are not covering the treatment because it is not “the norm.” Well, the norm is covered, but it causes further degeneration? When you look at the patient’s out of pocket expenses for “covered procedures” often they would have been better off getting Prolotherapy (financially speaking) because their co-pay is actually higher than the cost of Prolotherapy.  One word of caution to our readers or those of you contemplating Prolotherapy vs traditional treatments – do not let your insurance company decide what is best for you!

The good news is that Prolotherapy is gaining acceptance and many people are jumping on the band wagon and getting the help that they need! GO FOR IT!

If you are looking for a physician who does Prolotherapy, please check out www.getprolo.com.

Feb 2010 the CDC and the Arthritis Foundation announced a major initiative to dramatically reduce the impact of osteoarthritis on Americans.  Arthritis is already one of the nation’s most common cause of disability. The article states that 46 million people have arthritis and an estimated 67 million will be affected by 2030. The article goes on toe state that the prevalence is escalating and the average annual costs are around $5700/person/year.  Dr. John Klippel, MD, president of the Arthritis Foundation is quoted as saying, “Now is the time that we as a nation must invest our resources in the prevention of osteoarthritis…This national public health agenda with the CDC and the new public awareness campaign with the Ad Council will dispel the myth that osteoarthritis is an inevitable part of aging and will call on the nation and individuals to take proven steps to prevent and decrease the pain and disability of arthritis.”

The article goes on the discuss the agenda – which includes self management education, physical activity, injury prevention, and weight management.

Unfortunately, what this article fails to mention is the ligament injury connection to osteoarthritis. Osteoarthritis (OA) or degenerative joint disease (DJD) is more common than all the other types of arthritis combined. It is well-established that injury to a joint increases the chances that the joint will develop osteoarthritis over time. Precipitating causes include sudden impact or trauma, overuse or repetitive motion injuries, biomechanical abnormalities (congenital or acquired), ligamentous injury, joint hypermobility, obesity, intra-articular or systemic corticosteroids, avascular necrosis, and hereditary factors. Osteoarthritis, though the accepted term used to describe degenerative joint disease, is misleading because it primarily relates to cartilage, not bone, and involves degeneration, not inflammation. A lack of understanding about the development of osteoarthritis has resulted in a broad array of symptom-based treatment options such as rest, ice, heat, analgesics, anti-inflammatories, narcotics, braces and wraps, physical therapy and exercise, chiropractic, viscosupplementation, corticosteroid injections, and surgery. While advances have been made in joint replacement, cartilage repair, cartilage replacement, and spinal procedures, treatments to limit or even reverse articular cartilage breakdown have been lacking. Being that ligament injury, excess laxity, joint hypermobility, and clinical instability are known to be major causes of osteoarthritis, any treatment which can address restoration of ligament function would help reduce the incidence, pain, and dysfunction of osteoarthritis.

The Feb 2010 Journal of Prolotherapy issue contains a full article on the ligament injury connection to osteoarthritis.