Methotrexate and osteoarthritis
by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Methotrexate is used in rheumatoid arthritis. Methotrexate is an inhibitor of folate metabolism and is the cornerstone of treatment in rheumatoid arthritis.
It is considered a disease-modifying-anti-rheumatic drug (DMARD) reserved for use in patients with inflammatory autoimmune forms of arthritis.
However, there is a subset of patients with a severe condition called “inflammatory erosive osteoarthritis.” This is a rapidly debilitating condition for which the standard OA treatments are ineffective. Many of these patients have significant inflammatory and erosive disease.
Anecdotal reports of methotrexate efficacy in these patients indicates that this type of OA probably shares biologic characteristics with RA.
Findings indicating a significant role for pro-inflammatory cytokines (especially interleukin 1), further supports the notion that the final common pathway appears to be chronic inflammation. This would explain why some patients with inflammatory erosive OA might respond to methotrexate.
This study outline below is further reminder of the complexity of the inflammatory process.
Br J Nutr 2001 Mar;85(3):251-69
Antioxidants and fatty acids in the amelioration of rheumatoid arthritis and related disorders.
Darlington LG, Stone TW
Epsom General Hospital, Dorking Rd., Epsom, Surrey KT18 7EG, UK.
The generation of reactive oxygen species (free radicals) is an important factor in the development and maintenance of rheumatoid arthritis in humans and animal models. One source of free radicals is nitric oxide produced within the synoviocytes and chondrocytes and giving rise to the highly toxic radical peroxynitrite. Several cytokines, including tumour necrosis factor-alpha (TNFalpha) are involved in the formation of free radicals, partly by increasing the activity of nitric oxide synthase. Indeed, nitric oxide may mediate some of the deleterious effects of cytokines on bone resorption. Aspirin, tetracyclines, steroids and methotrexate can suppress nitric oxide synthase. Dietary antioxidants include ascorbate and the tocopherols and beneficial effects of high doses have been reported especially in osteoarthritis. There is also evidence for beneficial effects of beta-carotene and selenium, the latter being a component of the antioxidant enzyme glutathione peroxidase. The polyunsaturated fatty acids (PUFA) include the n-3 compounds, some of which are precursors of eicosanoid synthesis, and the n-6 group which can increase formation of the pro-inflammatory cytokines TNFalpha and interleukin-6, and of reactive oxygen species. Some prostaglandins, however, suppress cytokine formation, so that n-3 PUFA often oppose the inflammatory effects of some n-6-PUFA. gamma-linolenic acid (GLA) is a precursor of prostaglandin E1, a fact which may account for its reported ability to ameliorate arthritic symptoms. Fish oil supplements, rich in n-3 PUFA such as eicosapentaenoic acid have been claimed as beneficial in rheumatoid arthritis, possibly by suppression of the immune system and its cytokine repertoire. Some other oils of marine origin (e.g. from the green-lipped mussel) and a range of vegetable oils (e.g. olive oil and evening primrose oil) have indirect anti-inflammatory actions, probably mediated via prostaglandin E1. Overall, there is a growing scientific rationale for the use of dietary supplements as adjuncts in the treatment of inflammatory disorders such as rheumatoid arthritis and osteoarthritis.
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