Conquering Osteoarthritis in Clinical Practice

by Dr. Greg Fors, DC – Board Certified Neurologist DIBCN Posted On: 04/15/2011

According to the World Health Organization, degenerative joint disease (DJD) is one of the top 10 global disease burdens in the world today. Approximately 1 in 3 adults in the US between 25 and 74 years of age have radiological evidence of Osteoarthritis (OA) in at least one joint. In the US, 25% of all visits to primary care physicians and half of all NSAIDs prescriptions are for Osteoarthritis.

However, degenerative joint disease is not an inevitable consequence of growing older. It develops when trauma, and/or biochemical changes trigger a shift between joint cartilage synthesis and degradation.(1) Primarily, when the cartilage synthesis of any joint cannot keep pace with the background degradation of the cartilage, the joint will degenerate. Two very important factors in the joint play a primary role in joint deterioration. The first factor is the reduction in proteoglycan production in the joint cartilage. The second factor is the rate of production of inflammatory catabolic cytokines in the chondrocytes and synovial cells.(2) The driving force behind these two factors is multifactorial of course, but genetics plays a primary role, which is influenced by the macro and micronutrient intake of the individual.

Low vitamin D levels are now linked to multiple health problems including degenerative disc disease of the spine.(3) A 2006 study showed that an inherited polymorphism of a vitamin D receptor in the spinal disc was associated with a high risk of degenerative disc disease and disc bulge developing, especially in individuals younger than 40 years.(4)

Early Assessment of Optimal Joint Health Even with today’s “modern medicine”, early diagnosis of degenerative joint disease is still based on keen clinical observation and radiographic changes. However, when you make the diagnosis at this point, your patient has already fully developed the disease. There has always been the hope of finding an inexpensive clinical lab test that would help indicate when a patient is heading for degenerative joint disease. From the previously cited studies, low Vitamin D3 levels may be indicative of spinal degeneration problems in the future. It may be prudent to keep your patients serum levels of Vitamin D, 25-hydroxycalciferol above the 50 ng per milliliter.

However, exciting work is now being done on the diagnostic relevance of high sensitivity C reactive protein to osteoarthritis. New ultra-sensitive methods for C-reactive protein (hsCRP) have improved the usefulness of this marker, especially in the assessment of systemic inflammation. One study found that patients with erosive OA averaged hsCRP levels of 4.7 mg/L, and individuals with non-erosive OA averaged 2.2 mg/L.(5) What is important to realize here is that both patient groups were well above the threshold for increased risk of systemic inflammation, that of 1 mg/L, and the erosive OA group was well above the significant risk level of 3 mg/L. What is indicated here is that patients well above ideal levels of hsCRP of 0.5 mg/L may be on the road to developing osteoarthritis. Fibrinogen is also an inexpensive clinical marker of low-grade systemic inflammation in the tissues and may be helpful in assessing the risk for the development of degenerative joint disease. Suspect systemic inflammation in patients with fibrinogen levels greater than 300 mg/L; in addition to the possibility that these patients are more prone to degenerative changes in their joints should their lifestyle circumstances remain constant.

Nutritional Support for Healthy Joints To properly treat the underlying metabolic causes of degenerative joint disease, it is vital to treat the underlying chronic catabolic inflammation, oxidative stress and poor cartilage repair. For the management of inflammatory catabolic cytokines of degenerative joint disease, concentrated standardized herbal extracts of Ginger, Curcumin, Nettle leaf, and Boswellia have been shown to help manage this inflammatory cascade. Specifically, standardized extracts of these herbs have been shown to manage the pro-inflammatory cytokines and prostaglandins involved in the pain, swelling, and cartilage destruction of OA. These herbs also reduce oxidative stress and support healthy muscle and joint tissue function. To help improve your management of inflammatory catabolic cytokines, combine these standardized herbal extracts with high levels of EPA/DHA fatty acids, at least 1.5 g of combined EPA and DHA.

Increase Cartilage Production and Support Healthy Cartilage To help improve proteoglycan production and cartilage synthesis in the joints, supplement 1.5 to 2 g of glucosamine sulfate. Glucosamine sulfate has been found to stimulate the synthesis of GAGs, proteoglycans, and collagen within the joint complex. It has also been shown to support healthy synovial fluid through the synthesis of hyaluronic acid, which may increase the mobility of joints and enhance their lubrication. It may also assist in the inhibiting of many enzymes that break down the cartilage matrix.

Glucosamine Sulfate and Chondroitin Sulfate have been shown in multiple studies to support healthy cartilage and increase cartilage regeneration. These nutraceuticals accomplish this by stimulating the synthesis of the building blocks of cartilage, such as GAGs, proteoglycans and collagen. Furthermore, in two studies it was found that they enhance the synthesis of hyaluronic acid supporting healthy synovial fluid and improving the lubrication of joints, thereby increasing joint mobility.(6), (7)

A meta-analysis of rigorous studies on methylsulfonylmethane (MSM) in the treatment of OA found that MSM is superior to placebo in the treatment of mild to moderate OA of the knee.(8) Further, studies have found that combining glucosamine sulfate with MSM provides superior results compared to utilizing them individually. One randomized double-blind placebo-controlled study concluded: “Combination therapy of oral Glucosamine and MSM showed better efficacy in reducing pain and swelling and in improving the functional ability of joints than the individual agents.”(9)

The Importance of Avocado/Soybean Unsaponifiables Three randomized placebo-controlled double-blind trials found efficacy of Avocado/Soybean Unsaponifiables (ASU) for improving the symptoms of knee and hip OA. The dosage of ASU in these trials was 300 mg/day.(10) Another meta-analysis of four different randomized placebo controlled trials using ASU on osteoarthritis found significant benefits in utilizing this nutraceutical in DJD. The study concluded that “Based on the available evidence, patients may be recommended to give ASU a chance for e.g., 3 months.”(11)

For best results always combine nutraceuticals that manage inflammatory catabolic cytokines with those that promote proteoglycan production and cartilage synthesis. To increase chances of success make sure these nutraceuticals have sufficient quantities of quality ingredients. As found in Inflam-Rx, standardized extracts of Ginger Root should reach 2 g per day, and Curcumin a minimum of 1 g per day to achieve good clinical results. Additionally, research shows that glucosamine should reach levels of 1 to 1.5 g daily to be effective, chondroitin should reach a minimum of 800 mg, and ASU should reach 300 mg/day to achieve good clinical results. These levels can be found in BIOSPEC’s Maximum G-C-M. Both Inflam-Rx and Maximum G-C-M should be supplemented for a minimum of 12 weeks before the therapeutic effect can be evaluated.

1. Silver FH, Bradica G, Tria A. Relationship among biomechanical, biochemical, and cellular changes associated with osteoarthritis. Crit Rev Biomed Eng. 2001; 29(4):373-91.

2. Notoya K, Jovanovic DV, Reboul P, Martel-Pelletier J, Mineau F, Pelletier JP. The induction of cell death in human osteoarthritis chondrocytes by nitric oxide is related to the production of prostaglandin E2 via the induction of cyclooxygenase-2. J Immunol. 2000 Sep 15; 165(6):3402-10.

3. Videman T, Gibbons LE, Battie MC, et al. The relative roles of iatrogenic polymorphisms of the vitamin d receptor gene in lumbar spine degeneration and bone density. Spine. 2001 Feb 1.

4. Cheung KM, Chan D, Karppinen J, ET. Al. Association of the Taq I allele in vitamin D receptor with degenerative disc disease and disc bulge in a Chinese population. Spine. 2006 May 1; 31(10):1143-8.

5. Punzi L, Ramonda R, Oliviero F et al. Value of C reactive protein in the assessment of erosive osteoarthritis of the hand Ann Rheum Dis. 2005 Jun; 64(6):955-7.

6. Reginster JY, ET. Al, Rheumatology (Oxford). 2007 May; 46(5):731-5.

7. McAlindon TE, ET. Al, JAMA. 2000 Mar 15; 283(11):1469-75.

8. Review. Brien S, ET. Al. Osteoarthritis Cartilage. 2008 Nov; 16(11):1277-88.

9. Usha PR, Naidu MU Clin Drug Investig. 2004; 24(6):353-63.

10. Ernst E. Clin Rheumatol. 2003 Oct; 22(4-5):285-8.

11. Christensen R, ET. al. Osteoarthritis Cartilage. 2008 Apr; 16(4):399-408.