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Reproductive Endocrinology

SAT-137 - Endocrine Determinants of Bone Turnover Across Reproductive-Endocrine Disorders Reveal Condition-Specific Skeletal Regulation Beyond Estrogen

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT
Location: ENDOExpo; Poster Floor
Disclosure(s):
JOVANNA TSOUTSOUKI, MBBS BSc(Hons) PhD(Phil) PgCert(MedEd) FHEA: No financial relationships to disclose
Background
Bone turnover disturbances in reproductive disorders are often attributed to alterations in estrogen exposure. However, reproductive-endocrine conditions are characterised by broader perturbations across metabolic, adrenal, and hypothalamic axes. Whether bone turnover reflects shared or condition-specific endocrine regulation across states remains unclear.

Methods
Using a comparative approach, fasting bone turnover markers (BTMs; P1NP, CTX) were measured in women aged 20-36 years not receiving hormonal therapy: healthy controls (n=26), hypothalamic amenorrhea (HA; n=29), congenital hypogonadotropic hypogonadism (CHH; n=9), and polycystic ovary syndrome (PCOS; n=56). Group differences were assessed using Kruskal-Wallis tests, and within-group endocrine associations using Spearman correlations.

Results
Bone turnover was highest in CHH, with median CTX 0.61 ng/mL and P1NP 86.7 ng/mL, compared with controls (CTX 0.38; P1NP 57.3), HA (CTX 0.39; P1NP 58.1), and PCOS (CTX 0.34; P1NP 53.1; all p≤0.02 compared with CHH). Despite comparable estradiol concentrations in CHH and HA, both resorption and formation markers were significantly higher in CHH, suggesting mechanisms beyond current sex steroid exposure.

Across reproductive-endocrine states, androgens emerged as consistent positive correlates of bone turnover. CTX correlated with androstenedione and dihydrotestosterone in controls (r=0.44, p=0.04) and HA (r=0.46, p=0.03), and with DHEAS in PCOS (r=0.29, p=0.04). P1NP correlated with dihydrotestosterone and androstenedione in controls (r=0.45-0.53, p< 0.03) and HA (r=0.46-0.49, p< 0.03), testosterone in PCOS (r=0.36, p=0.01) and strongly with DHEAS in CHH (r=0.82, p=0.03).

Condition-specific regulatory patterns were evident. In HA, P1NP correlated with indices of hypothalamic suppression (LH: r=0.51, p=0.01; estradiol: r=0.53, p=0.008) and with hormones of additional endocrine axes disrupted in HA (IGF1: r=0.44, p=0.03; fT3: r=0.49, p=0.02). In PCOS, CTX correlated inversely with BMI (r=−0.31, p=0.02), identifying suppression of resorption with increasing adiposity.

Conclusion
Taken together, androgens consistently correlate with bone turnover across reproductive-endocrine states, challenging purely estrogen-centric models of female bone metabolism. Elevated bone turnover in CHH, despite profound estrogen deficiency comparable to HA, highlights the contribution of non-estrogenic steroid influences in skeletal regulation. In HA, bone formation is associated with disruption across multiple endocrine axes rather than isolated gonadal suppression, while in PCOS metabolic context modulates bone resorption. These findings reveal androgens as underappreciated determinants of skeletal metabolism in women and support condition-specific, phenotypic approaches to skeletal risk assessment beyond estrogen alone.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*