Background Rheumatoid arthritis (RA) is an independent risk factor for osteoporosis which influences bone remodeling processes via increased production of proinflammatory cytokines, especially tumor necrosis factor-α (TNF-α), or through hormone-mediated mechanisms. The presence of other classical risk factors for osteoporosis additionally raises the risk of changes in bone tissue. Some of the most commonly used biological drugs in the osteoporosis treatment are those that inhibit TNF-α action. Apart from reducing inflammation, these TNF-inhibitors suppress osteoclast activity. Objectives To determine the impact of osteoporosis risk factors on the bone turnover marker levels in RA patients treated with TNF-inhibitors. Methods This 12-month-long study included 50 patients with RA who received a drug from the TNF-inhibitor group. In order to enter the study, patients had to fulfill certain inclusion/exclusion criteria considering the RA duration, the RA treatment method, the degree of joint damage, and the presence of other diseases affecting bone tissue. Data regarding traditional risk factors for osteoporosis and fractures were collected, such as menopause length, body mass index (BMI), previous fractures due to minor trauma, family history of osteoporosis and osteoporotic fractures, reduced physical activity, cigarette smoking, and alcohol consumption. Serum levels of the bone synthesis marker procollagen type I N propeptide (P1NP), and the bone resorption marker beta C-terminal telopeptide of type I collagen (b-CTX) were assessed via ECLIA method at the baseline and upon TNF-inhibitor therapy completion. Results The mean age in this cohort was 51.6 years. A higher percentage increase in P1NP and b-CTX was recorded in patients aged below 50 years, as well as those of normal weight (BMI = 18.50−24.99 kg/m², P1NP: Wilk’s lambda =0.83, F = 9.56, p = 0.003; b-CTKS: Wilk’s lambda = 0.77, F = 14.16, p = 0.000). A greater increase in the P1NP and b-CTX levels was also observed in non-smokers (28.70% and 27.50%) relative to smokers (27.50% and 7.75%). Menopause length had a statistically significant effect on both P1NP (Wilk’s lambda = 0.84, F = 8.18, p = 0.006) and b-CTX (Wilk’s lambda = 0.77, F = 13.31, p = 0.001) concentrations, whereby the highest percentage increase in P1NP (29.85%) was related to menopause duration below 2 years. On the other hand, the greatest b-CTX increase (10.2%) was recorded in patients that had entered menopause 2−3 years ago. Physical activity had a significant effect on changes in P1NP (Wilk’s lambda = 0.84, F = 8.57, p = 0.005) as well as b-CTX (Wilk’s lambda = 0.78, F = 13.30, p = 0.001) values. Further, P1NP percentage increase was higher in patients without family history of osteoporosis, while the opposite was true for the b-CTX levels. Finally, number of previous fractures was inversely correlated with the P1NP and b-CTX percentage increase. Conclusion After 12-month TNF-inhibitor treatment, although a significant increase in both bone turnover markers was achieved, it was greater in the bone synthesis marker P1NP. Younger age, normal body weight, shorter menopause duration, greater physical activity, negative osteoporosis family history, and non-smoking emerged as the most important factors associated with the P1NP percentage increase. Reference [1]Llorente I, et al. Osteoporosis in rheumatoid arthritis: dangerous liaisons. Front Med (Lausanne) 2020;7:601618. doi: 10.3389/fmed.2020.60161 Disclosure of Interests None declared. Changes in bone biochemical markers due to the influence of osteoporosis risk factors in patients with rheumatoid arthritis treated with tumor necrosis factor inhibitors. Disclosure of Interests None Declared.
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