SFEBES2026 Poster Presentations Bone and Calcium (28 abstracts)
1Department of Metabolism, Digestion and Reproduction, Imperial College, London, United Kingdom; 2Department of Endocrinology, Imperial College Healthcare NHS Trust, London, United Kingdom
Background: Reproductive-endocrine disorders influence bone homeostasis through complex, not fully understood hormonal mechanisms. Here, we compared bone turnover markers (BTMs) across distinct reproductive-endocrine states to investigate hormonal determinants of bone metabolism.
Methods: Fasting BTMs (P1NP, CTx) were assessed in women aged 20-36yrs, not receiving hormonal therapy: eugonadal controls (n = 26), hypothalamic amenorrhoea (HA;n = 29), congenital hypogonadotrophic hypogonadism (CHH;n = 9), and polycystic ovary syndrome (PCOS;n = 56). Groups were compared using Kruskal-Wallis test. Hormone-BTM correlations were assessed using Spearman-r.
Results: BTMs were highest in CHH: CTx - 0.61ng/ml vs controls (0.38ng/ml; P = 0.01), HA (0.39ng/ml; P = 0.02), and PCOS (0.34ng/m P = 0.002); P1NP - 86.7ng/ml vs controls (57.3ng/ml; P = 0.01), HA (58.1ng/ml; P = 0.02), and PCOS (53.1ng/ml; P = 0.005). Notably, bone turnover was higher in CHH than HA despite comparable oestradiol (HA:86pmol/l; CHH:85pmol/l), indicating additional modulators. Indeed, in HA, P1NP correlated with hypogonadism severity-indices (LH:r = 0.51, P = 0.01; oestradiol:r = 0.53, P = 0.008), and hormones of other endocrine axes characteristically disrupted in HA (IGF-1:r = 0.44, P = 0.03; fT3:r = 0.49, P = 0.02). Androgens consistently and positively correlated with bone turnover across groups: CTx correlated with androstenedione in controls (r = 0.44, P = 0.04) and HA (r = 0.46, P = 0.03), dihydrotestosterone in controls (r = 0.44, P = 0.04), and DHEAS in PCOS (r = 0.29, P = 0.04). P1NP correlated with dihydrotestosterone and androstenedione in controls (r = 0.53, P = 0.01;r = 0.45, P = 0.03) and HA (r = 0.49, P = 0.02;r = 0.46, P = 0.03), and testosterone in PCOS (r = 0.36, P = 0.01). P1NP also correlated with DHEAS in CHH (r = 0.82, P = 0.03) and PCOS (r = 0.32, P = 0.02). Finally, CTx correlated inversely with BMI in PCOS (r=-0.31, P = 0.02).
Discussion: Androgens emerged as consistent positive correlates of bone turnover across reproductive-endocrine states, underscoring potential mechanistic roles for androgens in female bone metabolism beyond oestrogen. Additionally, the strong DHEAS-bone association in CHH suggests adrenal androgen compensation for hypoestrogenism. In HA, our data identify multi-hormonal impacts on bone turnover, while in PCOS we identified BMI-dependent suppression of resorption. Together, these findings offer novel insights into the hormonal influences on bone metabolism across diverse reproductive-endocrine states.