Prevention and Treatment of Osteoarthritis

Osteoarthritis (OA) is a progressive degenerative disease of the diarthrodial joints especially those that are weight bearing (Danning, 2013), including the knees, hips, shoulders and spine, but can occur at any joint.  Figure 1 contains the diarthrodial joints.  OA is characterized by the degeneration of articular cartilage and formation of subchondral bone and new bone at the joint margins (Danning, 2013). Increasing age correlates with the progressive nature of the disease (but does not cause the disease) finding the highest incidence in populations over 70 years.  Postmenopausal woman are greatly affected in the knee and hand joints. 

The etiology of osteoarthritis results from mechanical and/or biochemical factors.   Mechanical causes include misalignment of the joint, wear and tear of joints due to obesity, previous joint trauma/injury including surgeries and congenital disorders.  Biochemical causes include dehydration, mineral and nutritional deficiencies, hormonal imbalances and genetic predisposition (Danning, 2013).  We will briefly describe the pathophysiology of OA and present complementary and alternative medical (CAM) nutritional therapies for the prevention and treatment of osteoarthritis induced by biochemical causes. 

Biochemical pathophysiologic factors leading to degeneration of articular cartilage result from alterations in numerous biological systems including pH, bone remodeling and protein activities that influence the health of synovial fluids and articular cartilage.    The synovial fluids bathe the joint capsule reducing friction between cartilages and protecting joint tissues.  Movement is essential for healthy joint function as fluid is forced from the cartilages when a join is compressed from pressure and movement (Marieb, 2013).  The presence of calcium phosphate crystals in joint fluid has been shown by some studies to suggest hydroxyapatite formation (Yavorskyy & Santana & McCarthy 2008).  Chronic synovial inflammation induced by calcium crystal deposits could result in chronic polyarthritis (Yavorskyy et al. 2008). Calcification of hydroxyapatite and calcium crystals accentuates the degeneration process by cutting off nutrient supply of glucose and oxygen and interfering with the removal of metabolic waste (Paesold & Nerlich & Boos, 2007). 

The pH of synovial fluids is essential for healthy joint function.  Hyaluronic acid which lubricates surfaces between synovium and cartilage is more stable in conditions of a pH of 7.2-7.4 (Yavorskyy et al. 2008).  Measurements in spinal vertebrae demonstrate low oxygen concentration and elevation in lactic acid which lowers the pH inside the disc.  Low oxygen concentrations and acidic pH affect proteoglycan synthesis rates of vertebral disc cells which may lead to reduction of proteoglycan content and disc degeneration (Paesold, et al. 2007).  CAM nutritional strategies are to upregulate the microenvironment of the joint capsule by prevention and treatment of bone loss, hydroxyapatite formation and to optimize pH of body fluids

Water Hydration of the articular cartilage is essential for joint lubrication and cushioning of weight bearing joints to protect from wear and tear.  Articular cartilage is composed of proteoglycan, collagen fibril and water, the most abundant component.  Water allows the swelling of the collagen–PG matrix providing stability and cushioning.  Hydration is essential for cartilage to maintain normal function, structural integrity and prevent rupture. Dehydrated cartilage is more easily ruptured than hydrated cartilage (Wang & Yang & Niu et al. 2013).  Sixty percent of bodyweight in water is recommended, with an additional 24 oz per hour of exercise.

Glucosamine Sulfate Glucosamine Sulfate (GS), composed of glucose and an amine, promotes targeted support for joints and connective tissue.  Production of GS abates with age resulting in degeneration of cartilage (Murray, 2013). GS is a component of glycoproteins, proteoglycans and glycosaminoglycan’s (Dalirfarouei & Karimi & Jamialahmadi, 2016) and promotes the incorporation of sulfur into cartilage (Murray, 2013). GS also has antioxidant and anti-inflammatory properties (Dalirfarouei et al. 2016).  GS and a mud bath treatment were shown to improve pain, function and quality of life in patients with osteoarthritis (Peluso & Caso & Costa et al. 2016).

Vitamin K  Fat soluble vitamin K is a cofactor for calcium binding proteins and an inhibitor of bone demineralization and calcium crystal growth (Shea & Kritchevsky & Hsu et al. 2015).   Cartilage and meniscal calcification are implicated in the pathogenesis of OA and Vitamin K cofactor for matrix gla proteins inhibits ectopic mineralization by binding calcium crystals and inhibiting calcium crystal growth (Shea et al. 2015).   Vitamin K2 helps prevent bone resorption through stimulation of the gene expression of osteoblasts and the upregulation of osteocalcin activity (Marshall, 2016). 

Aquamin Red Algae (lithothamnion sp) Mineralized Red Algae is rich in calcium, magnesium and 72 other trace minerals (Marshall, 2016).  It reduces the symptoms of osteoarthritis and aids in the mineralization and maturation of osteoblasts (Marshall, 2016).  Red Algae also regulate the pro-inflammatory activity of NFkB (Marshall, 2016).

Vitamin D Insufficient vitamin D levels are implicated in an increased risk of OA.  Bassiouni & Aly & Zaky et al. (2016) found the mean values of Vitamin D were statistically lower in knee OA patients.  Significant deterioration of the medial menisci was also observed in vitamin D deficient OA patients (Bassiouni et al 2016).  Low D levels predict loss of cartilage as shown by reduced joint space and osteophyte growth (Murray, 2013). Live source vitamin D3 from sheep’s lanolin is an ideal source from PRLabs.  Recommended dose is at least 2,000 IU daily.  Individuals over the age of 40 and those with gallbladder malfunction can take 12,000 IU with food grade organic limonene oil (Marshall, 2015)

Calcium Adequate levels of calcium are essential for healthy bones, electrolyte balance and the prevention of bone loss. Low calcium intake will increase bone resorption, decrease bone mineralization (Carmeliet et al. 2015) and can lead to formation of  hydroxyapatite crystals which are often found in synovial fluids of OA  patients.( Yavorskyy et al. 2008).

 Natural occurring calcium from greens and marine coral are the ideal options.  Oat Grass, Avena sativa contains a rich array of essential minerals including calcium, potassium, phosphorus, magnesium, chromium, iron and selenium (Marshall, 2015).  Studies show Oat Grass stimulates cell growth including osteoblasts (Marshall, 2015).  Sango marine coral from Okinawa is 90 % ionized, highly absorbed and an ideal 2:1 ratio of calcium and magnesium. (Marshall, 2015).

References

Bassiouni, H., Aly, H., Zaky, K., Abaza, N., & Bardin, T. (2016). Probing tThe relation between Vitamin D deficiency and progression of medial femoro -tibial osteoarthitis of the knee. Current Rheumatology Reviews. Abstract retrieved from PMID:

Carmeliet, G., Dermauw, V., & Bouillon, R. (2015). Vitamin D signaling in calcium and bone homeostasis: A delicate balance [Abstract]. Best Practice and Research: Clinical Endocrinology Metabolism, 621-31. doi:10.1016/j.beem.2015.06.001

Dalirfardouei, R., Karimi, G., & Jamialahmadi, K. (2016). Molecular mechanisms and biomedical applications of glucosamine as a potential multifunctional therapeutic agent. [Abstract]. Life Sciences, 179-85. doi:10.1016/j.lfs.2016.03.028.

Danning, C. (2013). Alterations in musculoskeletal function: rheumatic disorders. In L. E. Copstead & J. Banasik (Eds.), Pathophysiology (5th, pp. 1039-1042). St. Louis, Missouri: Elsevier Saunders.

Marieb, E., & Hoehn, K. (2013). Joints. In S. Beuparlant (Ed.), Human Anatomy & Physiology (9th, pp. 249-270). Glenview, IL: Pearson Education, Inc.

Marshall, B. (2015, June 9). No Bones About it, Nutrition is Vital for Bone Health [Webinar]. Retrieved from www.PRLabs.com

Murray, M. (2013). Osteoarthritis. In J. Pizzorno & M. Murray (Eds.), Textbook of Natural Medicine (4th, pp. 1651-1661). St. Louis, Missouri: Elsevier, Churchill Livingstone.

Paesold, G., Nerlich, A. G., & Boos, N. (2007). Biological treatment strategies for disc degeneration: potentials and shortcomings. European Spine Journal, 447-468. doi:10.1007/s00586-006-0220-y

Peluso, R., Caso, F., Costa, L., Sorbo, D., Carraturo, N., Di Minno, M. N., . . . Scarpa, R. (2016). Mud-bath therapy and oral glucosamine sulfate in patients with knee osteoarthritis: a randomized, controlled, crossover study. Clinical and Experimental Rheumatology. Abstract retrieved from PMID: 27050908

Shea, M., Kritchevsky, S., Hsu, F. C., Nevitt, M., Booth, S., Kwoh, C. K., . . . Loeser, R. F. (2015). The association between vitamin K status and knee osteoarthritis features in older adults: The Health, Aging and Body Composition Study [Abstract]. Osteoarthritis Cartilage, 370-378. doi:10.1016/j.joca.2014.12.008

Wang, Q., Yang, Y. Y., Niu, H. J., Zhang, W. J., Feng, Q. J., & Chen, W. F. (2013). An ultrasound study of altered hydration behaviour of proteoglycan-degraded articular cartilage. BMC Musculoskeletal Disorders. doi:10.1186/1471-2474-14-289

Yavorskyy, A., Hernandez-Santana, A., McCarthy, G., & McMahon, G. (2008). Detection of calcium phosphate crystals in the joint fluid of patients with osteoarthritis – analytical approaches and challenges. Analyst, 302-318. doi:10.1039/b716791a