Osteoarthritis (OA) of the knee and hip is a debilitating disease and the risk increases precipitously with aging. The severity of OA varies from person to person, but the consonant clinical signs include pain, reduced range of motion, inflammation and deformity (1
). OA and other rheumatic diseases currently affect >43 million Americans with the number expected to increase to an estimated 60 million by the year 2020 (3
). The high prevalence of OA with its associated loss of joint function results in expensive and long-term conventional therapies that poses a significant socioeconomic burden. This fact alone makes OA a significant health and economic challenge. When clinically evident, OA is characterized by joint pain, tenderness, limitation of movement, crepitus, occasional effusion and variable degrees of inflammation without systemic effects. Although not a traditional inflammatory disease, symptoms of local inflammation and synovitis are present in many patients of OA and also seen in animal models of OA [reviewed in (5
)]. The presence of elevated levels of proinflammatory cytokines IL-1 and TNF-α has been demonstrated in OA synovial fluid and it has been shown that proinflammatory cytokines can stimulate the expression of inflammatory mediators and matrix degrading metalloproteinases in an arthritic joint [(6
) and references therein]. Pharmacological management of OA includes the administration of analgesics and non-steroidal anti-inflammatory drugs (NSAIDs), but their use does not provide adequate pain relief in some patients.
Inflammatory joint diseases, of which rheumatoid arthritis (RA) represents the most common form, is a chronic and systemic inflammatory disease of unknown etiology and is marked by synovial hyperplasia with local invasion of bone and cartilage leading to joint destruction (8
). RA affects ~1% of the adult population with more women being afflicted than men [(3
) and references therein]. Recent reports suggest that patients with RA not only have a higher chronic disease burden [(11
) and references therein] but may also have increased morbidity and mortality from cardiovascular disease compared with persons without RA (13
). RA pathogenesis is regulated by proinflammatory cytokines such as IL-1 and TNF-α that activate a broad array of intracellular signal transduction mechanisms (14
). In RA, migration of leukocytes into the synovial tissue (ST) occurs. These leukocytes and other cells in the ST, particularly RA ST fibroblasts, produce several mediators of inflammation, including chemokines—chemotactic cytokines that recruit leukocytes to the inflamed joint and also play a role in angiogenesis [(17
) and references therein].
Like OA, current treatment modalities for RA are mostly symptomatic although recently it has been suggested that use of disease-modifying antirheumatic drugs (DMARDs) has led to important gains in our overall ability to treat RA patients, resulting in a better health status for patients with RA (18
). The value of DMARDs for treating OA or RA is also limited by their side effects and the fact that they are more expensive to use than traditional NSAIDs. The major side effects of NSAIDs are their propensity to cause stomach ulcers, GI bleeding and perforations. Although a new class of NSAIDs—the specific inhibitors of COX-2—was developed, these drugs have similar efficacy as the general NSAIDs but are safer with respect to gastrointestinal toxicity. However, some of these COX-2 inhibitors were recently withdrawn from the market or ordered by the United States Food and Drug Administration (FDA) to have a black box warning on the label because of concerns that their long-term use may increase the risk of stroke and heart attack.
However, despite optimal use of currently available antirheumatic agents, most RA patients live with chronic pain and severe functional decline because these therapies focus primarily on preventing joint inflammation and soft tissue swelling, but are not effective in preventing cartilage breakdown and the joint destruction associated with RA.
Recently, efforts have been focused on using the class of drugs called biologics (antibodies or soluble receptors for IL-1, IL-6 and TNF-α) for the treatment of OA and RA. Although these agents reduce inflammation and joint destruction, their long-term risks and benefits are not yet clear. Additionally, higher costs and the findings that they are not effective universally and severe side effects such as life-threatening infections and increased risk of malignancies limit the use of such agents in many populations (19
). Thus, a final assessment on the use of biologics for the treatment of RA or OA, particularly with regard to risk of infections, malignancies and autoantibody production has to be carefully monitored.
Because of these and other limitations, the use of complementary and alternative medicine (CAM) therapies, such as acupuncture and extracts of medicinal herbs, is on the rise and according to reports ~60–90% of dissatisfied arthritis patients are likely to seek the option of CAM therapy (24
). While most of the rheumatologists and other clinicians are skeptical of CAM therapies, patients who use CAM appear to be satisfied with the self-care approach. This self-satisfaction is mostly based on the notion that since these herbs and plants are found in nature, remedies derived from them must be safe. However, the long-term safety and efficacy of most of the herbal preparations commonly promoted as antiarthritic have not been established by placebo-controlled randomized trials either in OA or RA patients and indeed some of these may even interfere with the ongoing treatments. Therefore, it is imperative that scientific evidence regarding the safety and efficacy of herbal preparations commonly used by arthritis patients be presented to both the physicians and the patients helping them in making informed decisions. The objective of this review is to summarize the currently available information on selective herbal preparations that are commonly consumed by arthritis patients.