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Prospective controlled study reveals lower serum GPER-1 levels in children with cleft palate, suggesting estrogen signaling contributes to embryonic palatal development.
Objective Cleft palate is one of the most common congenital craniofacial anomalies. Both genetic and environmental factors contribute to its aetiology. G protein-coupled estrogen receptor-1 (GPER-1) is a membrane receptor involved in cellular proliferation, migration, and embryonic development. This study aimed to compare serum GPER-1 levels between children with cleft palate and healthy controls. Materials and Methods This prospective controlled study included 20 children aged 0 to 3 years. The cleft palate group consisted of 10 patients with complete or incomplete cleft palate, while the control group included 10 healthy children without cleft palate, craniofacial anomalies, or known systemic disease. Venous blood samples were collected, centrifuged, and stored at −20°C until analysis. Serum GPER-1 levels were measured using a commercial enzyme-linked immunosorbent assay (ELISA) kit. Statistical analyses were performed using SPSS 20.0. Normality was assessed with the Shapiro-Wilk test. Group comparisons were conducted using the independent samples t -test and Mann-Whitney U test. Statistical significance was set at P < .05. Results Serum GPER-1 levels were significantly lower in the cleft palate group than in the control group (10.38 ± 2.66 ng/mL vs. 14.13 ± 1.99 ng/mL, respectively; P = .038). The observed reduction suggests a possible association between GPER-1-mediated signalling and biological processes involved in palatal development. Conclusion Children with cleft palate exhibited significantly lower serum GPER-1 levels than healthy controls. These findings suggest that GPER-1-mediated estrogen signalling may contribute to palatal development. Further studies with larger sample sizes are required to clarify the role of GPER-1 in the pathogenesis of cleft palate.
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Bilgen et al. (2026) studied this question.
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