| Contact Us | Physician Requests | Doctor Locator | |||||||||||
 |
Metabolic Processes of OA |  |
 |
||||||||
|
For many years, osteoarthritis (OA) has primarily been associated with aging (1). Osteoarthritis is usually initiated by damage as a result of injury or continued chronic overuse and mechanical strain on the joints (2). Young adults suffering acute trauma from sports or acute injuries that cause ligament or meniscal tears also have a high incidence of osteoarthritis (3). Muscle weakness also leads to a high incidence of osteoarthritis, suggesting that the muscular structure stabilizes the joint to support proper alignment and lessening of load on articular cartilage (4). Initial damage to a joint leads to generalized pain which restricts range of motion and may or may not be seen by radiographic examination in the early stages of the disease (5). Though injury or overuse may cause initial joint pain, other factors such as genetics, obesity, and diet all contribute to the development of osteoarthritis. New insights, in fact, have shown that after the initial damage, there is an essential change in the joint which causes a chronic increase in arachidonic acid (AA) metabolism that increases inflammation and can also destroy cartilage. The Western diet has changed dramatically in recent times with increased consumption of omega-6 oils, including AA, and decreased consumption of omega-3 oils. Arachidonic acid is derived from the dietary essential fatty acid (EFA), linoleic acid and a-linolenic acid, respectively, by sequential desaturation and elongation (6), and also by dietary intake. An overabundance of AA in the diet and elevated production in the body has shifted the balance of fatty acid metabolism toward an increase in pro-inflammatory metabolite generation, via the LOX (5-lipoxygenase) and COX (cyclooxygenase) enzymatic pathways (see below). These pro-inflammatory, AA metabolites have been found to play an integral role in the pathophysiology of osteoarthritis (7). Fatty acid imbalances are commonly seen in patients with chronic inflammatory conditions such as arthritis. Fatty acid levels in bone have been shown to be 50-90% higher in osteoarthritis patients compared to controls (8). In addition, depending on the severity of osteoarthritis, there is an associated accumulation of total fatty acids and EFA in the chondrocytes in osteoarthritis patients suggesting a strong involvement of fatty acid metabolism in the etiology of the disease. Clinical studies have also shown a strong linkage between metabolic defects in EFA metabolism or an overabundance of fatty acids that lead to osteoarthritis through key metabolic mediators (9). These metabolic mediators include cytokines and eicosanoids, whose production is greatly impacted by levels of fatty acids in the body and the underlying metabolic processes making osteoarthritis primarily a metabolic disease (10). Recent evidence has suggested that certain key nutrients known as flavonoids (found in fruits, vegetables, nuts, grains, tea, and even red wine) are effective at restoring the proper metabolic balance of inflammatory metabolites at the cellular level. They have naturally effective anti-inflammatory and antioxidant properties which, in sufficient quantities, can help in the dietary management of the metabolic aspects of osteoarthritis (11-14). Flavonoids exhibit their beneficial effects on two key metabolic processes affecting osteoarthritis on COX and LOX: 1.) Arachidonic Acid Metabolism on COX & LOX Pathways 2.) Oxidative Activity |
| ||||||||||
