Evaluation of mandibular growth in a prepubertal Class I and Class II population: a longitudinal analysis.

OBJECTIVE: This study aims to identify the presence, timing, and magnitude of a prepubertal mandibular growth spurt in a Class I and Class II population. METHODS: From the Burlington and Iowa Growth study of the AAOF Craniofacial Growth Legacy Collection, 83 Class I subjects (37 females and 46 males) and 32 Class II subjects (18 males and 14 females) were identified, as having at least seven consecutive annual lateral cephalograms taken from 5 to 11 years of age. Only subjects with a normodivergent facial pattern were considered. A customized cephalometric analysis was performed, and total mandibular length, defined as the distance between Condylion (Co) and Gnathion (Gn), was calculated. RESULTS: Overall, a significant early peak of mandibular growth was present in all the subjects analysed both in Class I (4.69 mm for males and 4.18 mm for females; P < .05) and in Class II (5.85 mm for males and 4.05 mm for females; P < .05). No differences between males and females were found for the timing of this peak (7 years for Class I and Class II females and 7 years for Class I and 6.5 years for Class II males). In males, a significantly larger peak was observed in Class II than Class I subjects (P = .007). LIMITATIONS: The main limitations of this study were the impossibility of using a suitable growth indicator to identify the timing of the early mandibular growth peak and the limited Class II records retrievable. CONCLUSION: This investigation suggests that a prepubertal mandibular growth peak is consistently present in both Class I and Class II males and females of clinically significant magnitude. Despite that, chronological age confirms to be unsuitable to identify this peak.

Normalization of puberty and adult height in girls with Turner syndrome: results of the Swedish Growth Hormone trials initiating transition into adulthood.

Objective: To study the impact of GH dose and age at GH start in girls with Turner syndrome (TS), aiming for normal height and age at pubertal onset (PO) and at adult height (AH). However, age at diagnosis will limit treatment possibilities. Methods: National multicenter investigator-initiated studies (TNR 87-052-01 and TNR 88-072) in girls with TS, age 3-16 years at GH start during year 1987-1998, with AH in 2003-2011. Of the 144 prepubertal girls with TS, 132 girls were followed to AH (intention to treat), while 43 girls reduced dose or stopped treatment prematurely, making n=89 for Per Protocol population. Age at GH start was 3-9 years (young; n=79) or 9-16 years (old; n=53). Treatment given were recombinant human (rh)GH (Genotropin® Kabi Peptide Hormones, Sweden) 33 or 67 µg/kg/day, oral ethinyl-estradiol (2/3) or transdermal 17ß-estradiol (1/3), and, after age 11 years, mostly oxandrolone. Gain in heightSDS, AHSDS, and age at PO and at AH were evaluated. Results: At GH start, heightSDS was -2.8 (versus non-TS girls) for all subgroups and mean age for young was 5.7 years and that of old was 11.6 years. There was a clear dose-response in both young and old TS girls; the mean difference was (95%CI) 0.66 (-0.91 to -0.26) and 0.57 (-1.0 to -0.13), respectively. The prepubertal gainSDS (1.3-2.1) was partly lost during puberty (-0.4 to -2.1). Age/heightSDS at PO ranged from 13 years/-0.42 for GH67young to 15.2 years/-1.47 for GH33old. At AH, GH67old group became tallest (17.2 years; 159.9 cm; -1.27 SDS; total gainSDS, 1.55) compared to GH67young group being least delayed (16.1 years; 157.1 cm; -1.73 SDS; total, 1.08). The shortest was the GH33young group (17.3 years; 153.7 cm: -2.28 SDS; total gainSDS, 0.53), and the most delayed was the GH33old group, (18.5 years; 156.5 cm; -1.82 SDS; total gainSDS, 0.98). Conclusion: For both young and old TS girls, there was a GH-dose growth response, and for the young, there was less delayed age at PO and at AH. All four groups reached an AH within normal range, despite partly losing the prepubertal gain during puberty. Depending on age at diagnosis, low age at start with higher GH dose resulted in greater prepubertal height gain, permitting estrogen to start earlier at normal age and attaining normal AH at normal age, favoring physiological treatment and possibly also bone health, hearing, uterine growth and fertility, psychosocial wellbeing during adolescence, and the transition to adulthood.

Twice Daily Compared to Three Times Daily Hydrocortisone in Prepubertal Children with Congenital Adrenal Hyperplasia.

INTRODUCTION: Glucocorticoid therapy in children with congenital adrenal hyperplasia (CAH) must be finely balanced between optimizing adrenal control and minimizing side effects. Twice (BID) rather than three times daily (TID) hydrocortisone may provide similar adrenal control and reduce metabolic risk. We compared BID and TID regimens with respect to adrenal control, growth, and metabolic effects. METHODS: A retrospective chart review (n = 128 visits, 36 individual patients) of prepubertal children with classical CAH was conducted at a tertiary care center between March 2007 and February 2020. Adrenal control, growth, and metabolic data were extracted in those taking hydrocortisone BID versus TID. Univariate generalized estimating equations models were performed to analyze the effect of dose frequency on outcomes of interest. RESULTS: Overall, we found no difference in adrenal control (8% vs. 18% poor control) or testosterone levels (9.65 ng/dL vs. 7.62 ng/dL) between the BID versus TID groups. We detected no difference in growth velocity (6.86 vs. 6.32 cm/year) or bone age advancement (11.3 vs. 5.91 months) between the groups. There was no difference in daily steroid dose (12.1 vs. 11.7 mg/m2/day), BMI Z-score (0.43 vs. 0.31), or systolic blood pressure percentile (65.5 vs. 61.7). CONCLUSION: BID dosing provides similar adrenal control and does not appear to impact growth or bone age advancement. On the other hand, TID dosing does not appear to increase the metabolic side effect profile in this age-group. Dosing should be patient-centered with individualized consideration.

A Body Weight Sensor Regulates Prepubertal Growth via the Somatotropic Axis in Male Rats.

In healthy conditions, prepubertal growth follows an individual specific growth channel. Growth hormone (GH) is undoubtedly the major regulator of growth. However, the homeostatic regulation to maintain the individual specific growth channel during growth is unclear. We recently hypothesized a body weight sensing homeostatic regulation of body weight during adulthood, the gravitostat. We now investigated if sensing of body weight also contributes to the strict homeostatic regulation to maintain the individual specific growth channel during prepubertal growth. To evaluate the effect of increased artificial loading on prepubertal growth, we implanted heavy (20% of body weight) or light (2% of the body weight) capsules into the abdomen of 26-day-old male rats. The body growth, as determined by change in biological body weight and growth of the long bones and the axial skeleton, was reduced in rats bearing a heavy load compared with light load. Removal of the increased load resulted in a catch-up growth and a normalization of body weight. Loading decreased hypothalamic growth hormone releasing hormone mRNA, liver insulin-like growth factor (IGF)-1 mRNA, and serum IGF-1, suggesting that the reduced body growth was caused by a negative feedback regulation on the somatotropic axis and this notion was supported by the fact that increased loading did not reduce body growth in GH-treated rats. Based on these data, we propose the gravitostat hypothesis for the regulation of prepubertal growth. This states that there is a homeostatic regulation to maintain the individual specific growth channel via body weight sensing, regulating the somatotropic axis and explaining catch-up growth.

Prepubertal growth and single nucleotide polymorphism analysis of the growth hormone gene of low birth weight Holstein calves.

Holstein calves weighing less than 20 kg at birth have been noted in Korea. Due to insufficient information, we raised small calves with age-matched normal birth weight Holstein calves and determined body weights before puberty. In addition, 3 single nucleotide polymorphisms (SNPs) of the growth hormone (GH) gene were analyzed. Up to 10 months of age, low birth weight calves were smaller than normal weight calves. In exon 5 of the GH gene, SNP genotype variation was detected in some small calves; however, this did not appear to be the only factor inducing low birth weight and slow growth.

Prepubertal growth and single nucleotide polymorphism analysis of the growth hormone gene of low birth weight Holstein calves

Holstein calves weighing less than 20 kg at birth have been noted in Korea. Due to insufficient information, we raised small calves with age-matched normal birth weight Holstein calves and determined body weights before puberty. In addition, 3 single nucleotide polymorphisms (SNPs) of the growth hormone (GH) gene were analyzed. Up to 10 months of age, low birth weight calves were smaller than normal weight calves. In exon 5 of the GH gene, SNP genotype variation was detected in some small calves; however, this did not appear to be the only factor inducing low birth weight and slow growth.

The relationship between Norwegian Red heifer growth and their first-lactation test-day milk yield: A field study.

Today's Norwegian Red (NR) is markedly different from the one that existed 25 yr ago due to the continuous genetic improvement of economically important traits. Still, current national recommendations on replacement heifer rearing largely are based on results from Danish studies from the late 1980s to the mid 1990s. The objectives of the present study were to gain information on (1) growth and growth profiles of modern NR replacement heifers in commercial dairy herds and (2) how growth during the rearing period affects the heifers' milk yield during their first lactation. To this end, we conducted a field study on 5 high-producing and 5 low-producing commercial dairy farms from each of 3 geographical regions in Norway. On these 30 farms, we combined repeated onsite registrations of growth on all available females from newborn to calving with registrations deriving from the Norwegian Dairy Herd Recording System. Each herd was visited 6 to 8 times over a period of 2 yr. At each visit, heart girth circumference on all available young females was measured. Registrations were made on a total of 3,110 heifers. After imposing restrictions on the data, growth parameters were estimated based on information from 536 animals, whereas 350 of these animals had the required information needed to estimate the relationship between growth and test-day milk yield. Our findings pointed toward an optimal ADG of 830 g/d from 10 to 15 mo of age that would optimize first-lactation yield of heifers in an average Norwegian dairy herd. The optimum will likely increase from selection over time. Utilizing simple proportionality, the ADG between 5 and 10 mo of age ideally should be 879 g/d, taking into account the fact that animal growth rate is higher at low ages and that a high prepubertal growth rate had no negative effect on first-lactation yield. When such a rearing practice is used to meet the requirements of today's genetically improved NR heifer, heifers can both optimize production in their first lactation and enter the milking herd earlier than the current average age of 24.8 mo.