OA (
osteoarthritis) and RA (
rheumatoid arthritis) lead to deterioration of the joints. Early OA is associated with loss of bone due to increased bone remodelling. A role for
inflammation is thought to be integral to the pathology. RA is a chronic inflammatory disease of the synovium, a membrane lining the non-weight-bearing surfaces of the joint. The mainstay of RA diagnostic testing is for
autoantibodies.
Rheumatoid factor has been a primary diagnostic test; however, sensitivity is approximately 75%, but specificity is limited. Recently, detection of
antibodies against
cyclic citrullinated peptide, identified as a screening marker and marker of
disease progression, has been proposed. Studies of glycation in
arthritis have focused mostly on levels of AGEs (
advanced glycation end-products), Nε-
carboxymethyl-lysine and
pentosidine. There was a weak correlation of skin and urinary
pentosidine with joint damage in early-stage OA. RAGE (receptor for AGEs) is a
cell-surface receptor in the synovial tissue of patients with OA and RA. The RAGE agonist
S100A12 is increased in RA and OA. Activation of RAGE may decrease expression of Glo1 (
glyoxalase I). Conflict between RAGE-activated inflammatory signalling and Nrf2 (nuclear factor-erythroid 2-related factor 2) regulation of basal and inducible expression of Glo1 may be involved. Thereby
glyoxal- and
methylglyoxal-derived AGEs may be increased in OA and RA. Further studies are now required to investigate the role of glyoxalase and dicarbonyl glycation in OA and RA for early-stage diagnosis and potential novel preventive
therapy.