Joints inflammatory diseases

The efficient removal of O2 and H2O2 vvill diminish OH formation and therefore antioxidant defence systems have evolved to limit their accumulation. Enzymic and low molecular weight antioxidants exist to scavenge free radicals as self-protection mechanisms. Some proteins exhibit antioxidant properties because they chelate transition-metal catalysts. The significance of antioxidants in relation to inflammatory joint disease is discussed below. 

Fairburn, K., Grootveld, M., Ward, R.J., Abiuka, C., Kus, M., Williams, R.B., Winyard, P.G. and Blake, D.R. (1992). Tocopherol, lipids and lipoproteins in knee-joint synovial fluid and serum from patients with inflammatory joint disease. Clin. Sci. 83, 657-664. 

Bruhl H, Wagner K, Kellner H, Schattenkirchner M., Schlondorff D, Mack M. Surface expression of CC- and CXC-chemokine receptors on leucocyte subsets in inflammatory joint diseases. Clin Exp Immunol 2001 126 551-559. 

Robinson, J. J., Watson, F., Bucknall, R. C., Edwards, S. W. (1992). Activation of neutrophil reactive-oxidant production by synovial fluid from patients with inflammatory joint disease Soluble and insoluble immunoglobulin aggregates activate different pathways in primed and unprimed cells. Biochem. J. 286,345-51. 

Roshak AK, CaUahan JF, Blake SM. Small-molecule inhibitors of NF-kB for the treatment of inflammatory joint disease. Curr Opin Pharmacol 2002 2 316-21. 

Buckley CD, Filer A, Haworth O, Parsonage G, Salmon M. Defining a role for fibroblasts in the persistence of chronic inflammatory joint disease. Ann Rheum Dis 2004 63 Suppl 11 92-5. 

Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory joint disease. It is a progressive symmetrical, destructive and deforming polyarthritis affecting proxi-... 

NSAIDs provide s/mptom relief by their analgesic and anti-inflammatory effects but do not modify the course of inflammatory joint disease,... 

Gelenkerkrankungen met D-penicillamin und Wundheilungsstdrungen bei rheumaorthopadischen Eingriffen. [Basic therapy of chronic inflammatory joint diseases with D-penicillamine and disorders of wound healing in rheumatoid orthopedic interventions.] Z Rheumatol 1988 47(Suppl l) 41-3. 

AA protein is often deposited in chronic inflammatory diseases such as rheumatoid arthritis (incidence up to 20%) and other inflammatory joint diseases, and in chronic suppurative and granulomatous infections such as tuberculosis and osteomyelitis. Deposits of AA protein are also observed in nonlymphoid tumors such as renal and gastric carcinomas and in Hodgkin s disease. Deposits of AA protein are most often found in the kidneys, liver, and spleen, usually resulting in nephrotic syndrome and hepatosplenomegaly. 

Parkes and co-workers have also conducted H NMR studies on s5movial fluid from patients with rheumatoid arthritis. Tbe nature of the nontransferrin-bound iron in the synovial fluid of patients with inflammatory joint disease was investigated. Transferrin is an iron ion transport protein. In these patients the synovial fluid contains non-transferrin-bound iron which appears to be in low-molecular-mass, redox-active complexes of unknown type. This form of iron has the adverse effect of stimulating free-radical lipid peroxidations involving oxygen. 500 MHz spin-echo H NMR spectroscopy was used to show that the incubation of patient synovial fluid with the powerful Fe(III)... 

Ralph, J.A., McEvoy, A.N., Kane, D., Bresnihan, B., FitzGerald, O. and Murphy, E.P. (2005) Modulation of orphan nuclear receptor NURR1 expression by methotrexate in human inflammatory joint disease involves adenosine A2A receptor-mediated responses. Journal of Immunology (Baltimore, Md 1950), 175, 555-565. 

Rheumatoid arthritis (RA). An episodic inflammatory systemic disease with autoimmune pathogenetic mechanisms. It primarily affects the joints, causing symmetrical lesions and severe damage to the affected joints. Rheumatoid arthritis is the most common form of inflammatory joint disease (prevalence about 0.5-1%). 

Rheumatic diseases are chronic inflammatory diseases primarily affecting the joints, but with involvement of other tissues and organs. Gout is included as a chronic inflammatory joint disease and osteoarthritis as a chronic degenerative joint disease. 

In use DMARDs reduce the symptoms and signs of inflammatory joint disease and also improve systemic effects such as vasculitis. In addition, serum markers of disease progression (erythrocyte sedimentation rate and rheumatoid factor concentration) are reduced. 

Gout is an inflammatory joint disease caused by deposition of uric acid crystals in the joints. Treatment of gout aims to control acute attacks with analgesics and colchicine and in the longer term to reduce circulating uric acid levels either by inhibiting its production with allopurinol or by encouraging its excretion by the kidneys with probenecid or sulfinpyrazone. 

Propionic acids, such as ibuprofen. fenbufen and naproxen, have been widely regarded as the drugs of first choice for the treatment of inflammatory joint disease, because they had the lowest incidence of side-effects. However, the selective COX-2 inhibitors celecuxib and rofccoxib have the lowest toxicity and are believed by many to be the drugs of choice in inflammatory joint disease,... 

Kunkel SL, Lukacs N, Kasama T et al. The role of chemokines in inflammatory joint disease. J... 

S Fraseri, et al, Microwave Thermogr hy - an index of inflammatory joint disease , British Journal of Rheumatology, 1987 261 37-39. 

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