142 A UNIQUE DEAMIDATED CARTILAGE OLIGOMERIC MATRIX PROTEIN (COMP) BIOMARKER PREFERENTIALLY IDENTIFIES HIP OSTEOARTHRITIS

Abstract

Results: Cartilage pentosidine (a marker of AGE) levels were ~5 fold enhanced (p =0.001 vs. PBS injected joints). The macroscopic and microscopic damage was similar for the AGEd and PBS injected joints (macroscopic score of 1 of a max score of 4 and histological OARSI score of 3–5 of a max score of 36, respectively). For the PG synthesis (5.09±0.29 vs 4.64±0.32) % total and newly formed PG (23.29±1.88 vs 23.66±2.02 and 43.02±2.23 vs 43.75±2.4), as well as the PG content (31.20±1.17 vs 30.83±0.98) no statistically difference could be found between both groups. This was not expected and therefore no control (untouched) and OA (experimentally induced according to the classic Groove model) joint were included in the study. Therefore, the biochemical data were compared to historical controls of the most recent study using the Groove model. Comparing these results, it demonstrates that the AGEd joints are in general in between the PBS injected joints and the experimental early OA joints (for example PG content 31.20±1.17 vs 30.83±0.98 vs 30.44±1.52). The PBS injected joints are in between the normal healthy joints and the AGEd joints. Assuming a stepwise increase in severity of damage there was a clear correlation between severity of damage and the different conditions from healthy control joints, via PBS injected joints with minimally surgically damage, AGEd joints with minimal surgical damage, to experimentally induced OA joints according to the Groove model (PG synthesis r = −0.873, % total and newly formed PG release r = 0.971, p = 0.029 and r = 0.954, p = 0.046, and PG content r = 0.836). Conclusions: Despite the fact that enhanced cross-linking of macromolecules by the AGEs restrains loss of proteoglycans, corroborating the diminished turnover of old cartilage, and a tendency toward enhanced cartilage damage in the artificially aged joints, the present data do not clearly support a role for enhanced cartilage AGE levels in development of joint degeneration.