Osteoarthritis of the Spine
Osteoarthritis of the spine is commonly seen in the chiropractic and medical office setting. Half of the world’s population, aged 65 and older, suffers from osteoarthritis (OA).1 Although spinal OA aka degenerative disc disease (DDD) aka degenerative joint disease (DJD) can be located at various, random levels of the human spine, it is frequently observed at the C4/5/6 vertebral levels in the cervical spine and at the L4/5/S1 levels in the lumbar spine/pelvis. Typically, patients will present with neck pain or low back pain that may or may not be directly attributed to spinal OA. In other words, the patients’ signs and symptoms can be directly related to OA, they can be caused by other factors, or they can be a combination of both OA and a random injury or repetitive strain. Signs and symptoms of a patient presenting with OA may include mild, moderate or severe neck, upper back, and lower back or gluteal/pelvic pain, stiffness and pain without movement, usually without radiating arm or leg pain. Oftentimes, symptoms are worse in the morning. X-ray images of the area of chief complaint are routinely obtained for those patients 50 years of age or older. Regardless of age, if relevant trauma is involved, or there are any red flags, such as suspicion of instability or malignancy, x-rays would be warranted. The x-ray helps confirm the diagnosis of spinal OA with degenerative changes seen at the intervertebral disc and/or facet joints. The point of this article is to discuss the causes, and provide treatment recommendations, for spinal OA that is often detected in patients with neck or low back pain. Oftentimes, patients are unaware of the fact that OA exists in their spine. This article will provide rationale supporting the premise that several of the causes of the neck or low back pain, as well as the cause of the spinal OA, have a common thread.
The causes of neck pain and low back pain may be due to repetitive stress, irritation or injury to the body from a car accident, work or sports injury, improper lifting, poor posture, lack of exercise, extended sitting or standing, inadequate rest, poor diet and emotional stress.
“For several decades, OA was considered a wear and tear disease, leading to joint tissue destruction and disability. The widely held view was that increased pressure or overload on weight-bearing joints, anatomical joint incongruence and fragility of articular cartilage tissue were the key predisposing factors. Nowadays, thanks to the advent of molecular biology and key discoveries in the field, OA is being redefined as a very complex and multifactorial disease.
OA may broadly be classified in two different forms, primary and secondary. Primary or idiopathic OA is a gene-dependent disease. Secondary OA, also called post-traumatic OA, frequently occurs sometime after a traumatic event. Although primary and secondary OA are caused by different factors, the resulting pathology is the same: a degenerative phenomenon, complicated by inflammatory reactions.” 1
This article will focus on secondary OA in the scenario of an adult with neck or low back pain that works full time at a computer, has a poor diet and does not exercise. In this situation, patients often ignore the pain and discomfort associated with these types of stresses or injuries, and their condition becomes chronic. This is the classic scenario wherein the person experiences “wear and tear, without proper repair.” In this case, the postural stress and musculoskeletal strain associated with long-term computer usage, triggers the inflammatory response in the body. Coincidentally, extended sitting with poor posture will tend to stress the spine most significantly at the mid cervical region, upper back and lumbosacral region. Postural stress irritates nociceptors, which are found in muscles, ligaments, joints and blood vessels, and when stimulated, drive nociceptive pathways that trigger the inflammatory response and pain. Also, muscle stress/strain drives spinal joint stiffness and restriction via the nociceptive pathways. As the postural stress and musculoskeletal strain process continues over an unspecified period of time, repeatedly triggering the inflammatory response, coupled with lack of exercise and poor diet, a chronic inflammatory cascade ensues, setting the foundation for spinal disc and facet joint degradation and degeneration, quite possibly at the segmental level experiencing the most biomechanical stress.
The primary dietary driver of chronic inflammation includes consumption of processed food containing refined sugar, refined flour and refined seed oils (corn, safflower, sunflower, peanut, soybeans). The majority of calories consumed by Americans is a combination of refined sugar, flour and seed oils. Refined carbohydrates lack nutrients and when consumed produce an excess of free radicals and cause hyperglycemia, which leads to an immediate inflammatory response that is proportional to the blood sugar elevation. Free radicals are supposed to be held in check by antioxidants found in healthy foods. When refined carbohydrates are consumed, they do not deliver antioxidant polyphenols, carotenoids, or other nutrients to the cells to control free radical production, so an excess of free radicals is produced, which leads inflammation. All cells, including connective tissue cells found in joints, intervertebral discs, tendon and cartilage, respond to stimulation of an inflammatory trigger such as hyperglycemia or excess free radical production. This scenario leads to the release of nuclear factor-kappa B (NF-κB), which stimulates the production of interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF), matrix metalloproteinase (MMP), and vascular endothelial growth factor (VEGF) further driving inflammation. Seeds oils from corn, sunflower seeds, safflower seeds, cottonseeds, peanuts, and soybeans used most commonly in forms that include salad dressings, cooking oils, shortening, and margarine, are high in omega-6 fatty acids. We also get omega-6 fatty acids from grain-fed beef, chicken and fish. Excess omega-6 fatty acids are pro inflammatory, as they ultimately drive NF-κB release and increase the amount of arachidonic acid (AA) within cells, which stimulates phospholipase A2 (PLA2), cyclooxygenase (COX), and lipoxygenase (LOX) to overproduce prostaglandin E2 (PGE-2) and leukotriene B4 (LTB4), which perpetuates inflammation and disease. 2(61-82)
The typical Western or American diet lacks the food and nutrients that we are genetically designed to metabolize and absorb. The typical American diet lacks organic, pesticide-free fresh fruits and vegetables, grass-fed beef, pork and poultry, wild game, wild caught fish/seafood, raw nuts and adequate amounts of clean water. A plant-based diet with clean sources of protein and healthy fats is anti-inflammatory, and therefore, necessary for proper repair of injured tissues and in the prevention of developing chronic inflammation, and ultimately spinal OA.
Along with changing the diet, patients with spinal OA also need to develop sound ergonomic habits to reduce spinal stress/strain. For example, a proper computer work station should include the ability to stand or sit with the monitor at eye level. In the sitting position, the lower back/lumbar spine should be supported. The elbows and wrists should be supported while utilizing the keyboard. Frequent micro breaks (3 per hour), should be a habit to minimize eye strain and postural stress. A moderate exercise program that includes aerobic and anaerobic activities at least three times per week for a minimum of 30 minutes is helpful in reducing chronic inflammation. Moderate exercise stimulates Interleukin-10 (IL-10), which is an anti-inflammatory cytokine.3,4
Lastly, poor eating habits and a sedentary lifestyle predisposes these patients to becoming overweight or obese, which drives inflammatory pathways that are responsible for the metabolically destroying processes affecting connective tissue cells found in joints, intervertebral discs, tendon and cartilage. In 2015, Giuseppe Musumeci and colleagues explained that the systemic factors that could influence the onset of OA may be due to adipokines, such as leptin, adiponectin, resistin, and visfatin, which are present in adipose tissue. These adipokines mediate lipid and glucose metabolism and insulin sensitivity. It appears that the most important of the adipokines involved in the onset of OA, is represented by leptin. Leptin may influence both growth factor synthesis and chondrocyte anabolism and catabolism. Excess leptin may reduce the extracellular matrix synthesis leading to increased susceptibility of the joints to lesions. The cartilage destroying mechanism of leptin could also be explained by its association with IL-1, which results in increased nitric oxide (NO) production. NO interferes with chondrocyte function causing loss of cartilage matrix by apoptosis induction, MMP activation, and type II collagen synthesis inhibition.1
In the clinical setting, a specific treatment plan would include the following: 1. Spinal manipulation to address areas of spinal joint stiffness/restriction that developed as a result of muscle stress/strain and the nociceptive pathways. 2. Ergonomic advice including workstation modifications and micro breaks. 3. Physical therapy/rehabilitation to address muscle weakness and lack of flexibility. 4. Dietary changes that embrace an anti-inflammatory diet. 5. Vitamins/supplements to include the following: Vitamin D3: 5,000 IU/day, Omega 3 Fatty Acids/Fish Oil: 1,000 to 3,000 mg/day, Magnesium: 400 mg/day, Turmeric: 500 to 1,000 mg/day, Alpha Lipoic Acid: 300 mg/day, Acetyl-L-Carnitine: 500/mg/day and Coenzyme Q10: 100 mg/day.
In general, the dietary and supplement recommendations suggested are anti-inflammatory via the following mechanisms: 1. Direct inhibition of nuclear factor-kappa B (NF-κB). 2. Inhibition of free radicals, which reduces NF-kB activation. 3. Reduction of NF-kB activation. 4. Inhibition of PLA-2, COX, and LOX enzymes that promote inflammation. 2(p.75)
In our opinion, long term prevention of spinal OA would include periodic spinal manipulation, moderate exercise 3 to 5 times per week, continuation of an anti-inflammatory diet and supplementation, proper ergonomic workstation modifications and frequent micro breaks.
This article outlines the causes and treatment recommendations for patients with neck or low back pain and concomitant spinal OA that are routinely seen by health care providers.
A comprehensive approach that incorporates spinal manipulation, moderate exercise, an organic/plant-based anti-inflammatory diet including organic/free range/grass-fed beef/poultry/chicken, wild caught fish/seafood, raw nuts and adequate amounts of clean water, supplementation, including vitamin D3, omega-3 fatty acids/fish oil, magnesium, alpha lipoic acid, acetyl-L-carnitine, turmeric and CoQ10 and ergonomic workstation modifications is suggested as the best care approach for the prevention of advancing spinal OA, or to slow the progression of spinal OA.
1. Musumeci G, Aiello F, Szychlinska M. Osteoarthritis in the XXIst century: risk factors and behaviours that influence disease onset and progression. Int J Mol Sci. 2015 Mar 16; 16(3):6093-112.
2. Seaman, David R. The DeFlame Diet: DeFlame your diet, body, and mind. Shadow Panther Press. Kindle Edition.
3. Mosser DM, Zhang X. Interleukin-10: new perspectives on an old cytokine. Immunol Rev. 2008;226: 205-18.
4. Uceyler N, Valenza R, Stock M, Schedel R, Sprotte G, Sommer C. Reduced levels of anti-inflammatory cytokines in patients with chronic widespread pain. Arth Rheum. 2006;54: 2656-64.