Background: Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with osteoporosis. There have been very few data on the use of peripheral quantitative computed tomography (QCT) in anti-TNF-treated patients.

Objectives: We wished to assess volumetric bone mineral density (BMD) by forearm QCT in conjunction with dual-energy X-ray absorptiometry (DXA) and bone biomarkers in RA and AS.

Methods: Forty RA and AS patients treated with etanercept (ETN) or certolizumab pegol (CZP) were included in a 12-month follow-up study. Peripheral QCT and DXA BMD were determined. Bone biomarkers, such as PTH, osteocalcin, RANKL, 25-hydroxyvitamin D (VITD), P1NP, CTX, sclerostin, DKK-1 and cathepsin K (CATHK) were assessed by ELISA.

Results: There was no further bone loss during anti-TNF treatment. Volumetric and areal BMD showed significant correlations with each other (p<0.05). Total QCT BMD after 12 months was inversely determined by disease activity at baseline in the full cohort (p=0.030). Cortical BMD was negatively determined by baseline disease activity (p=0.005) and CATHK (p=0.025). In RA, VITD-0 determined QTRABBMD-12 (p=0.005). In the full cohort, the one-year change in QTRABBMD was related to TNF inhibition together with higher VITD-0 (p=0.031). Therapy and lower CATHK determined QCORTBMD changes (p=0.006). In RA, treatment together with VITD-0 (p<0.01) or CATHK-0 (p=0.002), while in AS, treatment together with RANKL-0 (p<0.05) determined QCT BMD changes.

Conclusion: QCT confirmed that biologics may attenuate bone loss. Disease activity, CATHK, RANKL and VITD may predict the effects of anti-TNF treatment on volumetric BMD changes. There may be differences between RA and AS in this respect.

Acknowledgements: This research was supported by Hungarian National Scientific Research Fund (OTKA) grant No. K 105073 (H.P.B. and Z.S.); by the European Union and the State of Hungary and co-financed by the European Social Fund in the framework of TAMOP-4.2.4.A/2-11/1-2012-0001 ‘National Excellence Program ’(Z.S.); by the European Union grant GINOP-2.3.2-15-2016-00050 (Z.S.); and by the Pfizer Investigator Initiated Research Grants no. WS1695414 and WS1695450 (Z.S.).

Disclosure of Interests: Balázs Juhász: None declared, Katalin Gulyás: None declared, Ágnes Horváth: None declared, Edit Végh: None declared, Anita Pusztai: None declared, Agnes Szentpetery: None declared, Zsófia Pethö: None declared, Nóra Bodnár: None declared, Attila Hamar: None declared, Levente Bodoki: None declared, Harjit Pal Bhattoa: None declared, Éva Szekanecz: None declared, Katalin Hodosi: None declared, Andrea Domjan: None declared, Szilvia Szamosi Speakers bureau: Roche, Csaba Horváth: None declared, Sándor Szántó Speakers bureau: Abbvie, MSD, Novartis, Consultant of: Abbvie, Novartis, Gabriella Szücs Speakers bureau: Roche, Boehringer, Actelion, Sager, Consultant of: Actelion, Boehringer, Hennie Raterman: None declared, WIllem Lems Speakers bureau: Pfizer, Amgen, Lilly, UCB, Galapagos, Consultant of: Pfizer, Amgen, Lilly, UCB, Galapagos, Oliver FitzGerald Speakers bureau: AbbVie, Janssen, Pfizer, Consultant of: BMS, Celgene, Eli Lilly, Janssen, Pfizer, Grant/research support from: AbbVie, BMS, Eli Lilly, Novartis, Pfizer, Zoltán Szekanecz Speakers bureau: Pfizer, Roche, Abbvie, Novartis, Lilly, Sanofi, Consultant of: Pfizer, Abbvie, Novartis, Grant/research support from: Pfizer, UCB.