Effects of estrogen deficiency during puberty on maxillary and mandibular growth and associated gene expression – an μCT study on rats

Abstract

Background Estrogen is a well-known and important hormone involved in skeletal homeostasis, which regulates genes involved in bone biology. Some studies support that estrogen is important for craniofacial growth and development. Therefore this in vivo animal study aimed to investigate, whether and in which way low estrogen levels in the prepubertal period affect craniofacial development in the postpubertal stage and to quantify the gene expression of RANK, RANKL and OPG in cranial growth sites in ovariectomized estrogen-deficient rats during puberty. Methods Control (sham-operated, n = 18) and ovariectomy (OVX, n = 18) surgeries were performed on 21-days-old female Wistar rats. Animals euthanized at an age of 45 days (pubertal stage) were used for gene expression analyses (n = 6 per group) and immunohistochemistry of RANK, RANKL and OPG. Animals euthanized at 63 days of age (post-pubertal stage) were used for craniofacial two-dimensional and three-dimensional craniofacial measurements using μCT imaging (n = 12 per group). Results In the μCT analysis of the mandible and maxilla many statistically significant differences between sham-operated and OVX groups were observed, such as increased maxillary and mandibular bone length in OVX animals (p < 0.05). Condylar volume was also significantly different between groups (p < 0.05). The sham-operated group showed a higher level of RANK expression in the midpalatal suture (p = 0.036) and the RANKL:OPG ratio levels were higher in the OVX group (p = 0.015). Conclusions Our results suggest that estrogen deficiency during the prepubertal period is associated with alterations in the maxillary and mandibular bone length and condylar growth.

Estrogen deficiency influences SEC23A gene expression in the odontogenic region of incisors – a murine model study

“…80% to 90% of serum levels of vitamin D are synthesized endogenously under UVB irradiation, the remainder, 10% to 20%, come from the diet, the main dietary sources being cholecalciferol (D 3 ) and ergosterol (D 2 ). Estrogen deficiency and vitamin D deficiency share several adverse health outcomes, including bone resorption itself, mood disorders, increased risk of cardiovascular disease and cancers [24][25][26][27][28] affect growth and development [2][3][4][29][30][31].…”

Glycyrrhizae radix et Rhizoma-Derived Carbon Dots and Their Effect on Menopause Syndrome in Ovariectomized Mice

“…Low levels of estrogen could cause various problems during different periods of women’s lifetime. Experimental evidence has confirmed that estrogen deficiency during the prepubertal period affects craniofacial growth and development [ 25 ]. Some researchers considered that the absence of estrogen may cause obesity among menopausal women [ 26 ].…”

Transcriptomic analysis reveals the molecular mechanisms underlying osteoclast differentiation in the estrogen-deficient pullets

“…High estradiol concentrations in late adolescence led to growth plate closure ( Börjesson et al, 2012 ). In prepubertal ovariectomy mice, E2 deficiency can promote both maxilla and mandible growth, accompanied by an increase in RANKL/OPG ratio ( Omori et al, 2020 ; Küchler et al, 2021 ). The loss of E2 during sexual maturity leads to reduced medullary bone formation ( Figure 1 ).…”

“…According to a reported study on Japanese quails, E2-induced osteoclastogenesis can be regulated in the bone marrow cells via the RANK/RANKL/OPG (RANK/RANK Ligand/Osteoprotegerin) system during medullary bone formation ( Hiyama et al, 2019 ). Moreover, in prepubertal ovariectomy mice, E2 deficiency can promote both maxilla and mandible growth, accompanied by an increase in RANKL/OPG ratio ( Omori et al, 2020 ; Küchler et al, 2021 ). A low bone turnover in 20-day-old rats treated with E2 for 14 d was due to decreased bone remodeling ( Zhang et al, 2012 ).…”