{'fraction_non_alphanumeric': 0.03561643835616438, 'fraction_numerical': 0.006392694063926941, 'mean_word_length': 5.692464358452138, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
AB0767 PATIENTS WITH RHEUMATOID ARTHRITIS HAVE A LOWER BONE DENSITY THAN PATIENTS WITH PSORIATIC ARTHRITIS

Background: Osteoporosis is a skeletal disease characterized by the loss of bone density resulting in an increased fracture risk. Female sex, advanced age, Caucasian ancestry, previous history of fractures, menopause and certain genetic factors predispose for osteoporosis. In addition, recent studies could prove that chronic inflammatory diseases such as Rheumatoid Arthritis (RA) and long-term treatment with higher doses of glucocorticoids (GCs) represent independent risk factors for the development of osteoporosis. On the other hand, the intake of vitamin D, a calcium-rich diet and physical exercise can be protective. Data describing the prevalence of osteoporosis in patients with other rheumatic diseases like psoriatic arthritis (PsA) are lacking. Objectives: We compared the prevalence of osteopenia and osteoporosis in patients with RA and PsA, respectively, based on data obtained from our ongoing prospective monocentric study Rh-GIOP investigating glucocorticoid (GC)-induced osteoporosis in patients with different rheumatic diseases (NCT02719314). Methods: Bone mineral density data measured by dual x-ray absorptiometry (DXA) in patients with PsA (n=92) were compared with data measured in 92 age- and gender-matched patients with RA. The results were analysed with respect to clinical and laboratory parameters such as data on GC treatment (frequency, duration defined as start of treatment until timepoint of measurement, actual and cumulative dose), csDMARD and bDMARD (including as well tsDMARDs) therapy, serological parameters (Vitamin D, alkaline phosphatase, calcium, inflammatory markers and rheumatoid factor) and functional status (e.g. Health Assessment Questionnaire (HAQ), sporting activities). Statistical analyses were performed descriptively using mean and standard deviation, t-tests for metric variables, and chi-square tests for nominal variables. For subgroup analyses with less than 30 patients per group, tests for non-normally distributed data were used due to the lower test power. Results: RA patients showed significantly lower means of bone density values (minimal T-score, p=0.03) than PsA patients leading to a higher frequency of osteopenic bone densities (p Conclusion: The lower bone density in RA patients seems not to be fully explained by higher GCCD, disease duration or higher levels of inflammation. However, RA patients had a higher frequency of current GC intake. Additionally, differences in bone density between the two groups could be related to the higher number of bDMARD therapies in PsA patients, but further investigations like multivariate analyses with higher numbers of patients are necessary. Furthermore there is more need for research on possible molecular and genetic factors in PsA, which are protecting from low bone density. Disclosure of Interests: Desiree Freier: None declared, Edgar Wiebe: None declared, Robert Biesen: None declared, Thomas Buttgereit: None declared, Sandra Hermann: None declared, Timo Gaber: None declared, Frank Buttgereit Grant/research support from: Amgen, BMS, Celgene, Generic Assays, GSK, Hexal, Horizon, Lilly, medac, Mundipharma, Novartis, Pfizer, Roche, and Sanofi.