The word arthritis literally means inflammation of the joint. Joints can become inflamed for many reasons, but most of us think of arthritis usually as one of two kinds: osteoarthritis or rheumatoid arthritis. These are two very distinct entities, and they are both a huge source of discomfort and disability. A significant amount of new research provides an understanding of both kinds of arthritis so that those who are afflicted may find relief.
Inflammation is a living tissue response to mechanical, chemical, and immunological challenge. Normal aging often results in the excessive production of autoimmune factors that destroy joint cartilage and other tissues in the body. Suppressing these inflammatory factors is a critical component of an effective arthritis treatment program.
Inflammation is partially characterized by high levels of arachidonic acid products which are metabolized along two different enzymatic pathways: cyclooxygenase (COX) and lipoxygenase, leading to prostaglandin (PGE-2) and leukotriene (LTB4). Some physicians believe these are the most important mediators of inflammation (Srivastava et al. 1992). PGE2 and LTB4 play a crucial role in arthritis by causing resorption of bone, stimulating the secretion of collagen breakdown enzymes, and inhibiting the formation of proteoglycans--the building blocks of cartilage.
The destruction of cartilage and bone in both osteoarthritis (OA) and rheumatoid arthritis (RA) is related to the action of matrix enzymes (metalloproteinases), which include collagenases and stromelysins (Birkedal-Hansen et al. 1993; Hill et al. 1994). Some of these enzymes have proinflammatory characteristics and some have anti-inflammatory properties. The varying balance between these forces probably accounts for the variation in disease activity as it flares up and subsides. These enzymes are under the control of cytokines, such as interleuken 1 (IL-1b) and tumor necrosis factor-alpha (TNF-alpha), which are highly activated in RA and are elevated in the synovial membrane, the synovial fluid, and the cartilage of OA patients (Saklatvala 1986). Cytokines are proteins that carry messages between cells and regulate immunity and inflammation. In animal models, inhibition of TNF-alpha results in decreased inflammation, while inhibition of IL-1b effectively prevents cartilage destruction (Plows et al. 1995; Frye et al. 1996).
As noted, TNF-alpha and IL-1b have been identified as factors in the destruction of cartilage in both OA and RA. Studies show that the blockade of these aberrant immune factors can produce therapeutic results. Nettle leaf has been shown to reduce TNF-alpha levels and IL-1b. Nettle leaf also inhibits the genetic transcription factor that activates TNF-alpha in synovial tissue.