No abstract

Background: Modifying the balance between resorption and apposition through selectively injuring the cortical plate of the alveolus has been an approach to speed tooth movement and is referred to as periodontally accelerated osteogenic orthodontics. The aim of this study was to investigate the alveolar response to corticotomy as a function of time and proximity to the surgical injury in a rat model.

Within the limitations of our study (number of animals, duration in time, and limited data on the anabolic activity), our preliminary results suggest that Piezocision-facilitated orthodontic tooth movement increases the rate of movement of the teeth undergoing orthodontic treatment through the coupled remodelling of the alveolar bone. This process is initiated by the osteoclastic activity following surgery and extended via the synergistic relationship between Piezocision and tooth movement.

Avec un nombre croissant d’adultes se présentant en consultation orthodontique, la demande d’un traitement de courte durée revient de manière récurrente de la part des patients. Afin de répondre à ces attentes, plusieurs techniques ortho-chirurgicales visant à accélérer les mouvements dentaires ont été publiées mais se sont révélées relativement invasives. Nous introduisons ici une technique ortho-chirurgicale novatrice, minimalement invasive, sans lambeau muco-periosté, combinant micro-incisions, incisions corticales piézoélectriques et tunnelisation sélective permettant des greffes osseuses et gingivales. En associant plan de traitement consciencieux et compréhension des phénomènes biologiques impliqués, le métabolisme osseux alvéolaire peut ainsi être localement manipulé par cette nouvelle technique afin d’obtenir des résultats orthodontiques stables et rapides. La piézocision permet la correction rapide de malocclusions sévères sans présenter les inconvénients des approches chirurgicales extensives et traumatiques des corticotomies alvéolaires classiques.

SUMMARY A study of hypothalamo‐pituitary function was carried out in chronic alcoholic women aged 29–66 years, with chronic pancreatitis or cirrhosis of the liver. Amenorrhoea was present in most of them (67%). The hormonal investigation included assessment of basal plasma steroids, gonadotrophin and prolactin values, followed by an anterior pituitary function test. Clomiphene stimulation and/or hCG tests were performed. The subjects were divided into four groups according to their oestrogen status on the one hand, and the baseline gonadotrophin concentration on the other. Results were compared with two control groups composed of twelve healthy post‐menopausal women and ten normal women of reproductive age. Five different patterns of hypothalamo‐pituitary ovarian activity could be distinguished: post‐menopausal women (eight), perimenopausal women (eight), hypothalamic amenorrhoea (five), anovulation (four) and inadequate luteal phase (six). A normal peri‐ or post‐menopausal hormonal profile was found in most (77%) chronic alcoholics of more than 45 years of age. In contrast, 84% of patients of reproductive age had functional hypothalamic disorders. These observations suggest that chronic alcoholism affects sexual function at the hypothalamo‐pituitary level chiefly during the reproductive period. The pathogenesis of these endocrine changes is not clear. The relative importance of ethanol consumption, liver damage and non‐specific factors such as nutritional status and chronic illness are discussed.

No abstract

The role of somatostatin (SRIF) on adenohypophysial hormone secretion in starved rats was reassessed by passive immunization. Because of the absence of pulsatile GH secretion in starved rats, the effects of the injection of SRIF antiserum on GH levels can be clearly demonstrated. To determine whether starvation modifies the sensitivity of the adenohypophysis to SRIF, we measured 125I-labelled iodo-N-Tyr-SRIF binding. There was no difference in the dissociation constant (Kd) nor in the maximal binding capacity (Bmax) in fed (n = 15) and starved (n = 15) animals (Kd = 0.38 +/- 0.09 (S.E.M.) and 0.45 +/- 0.09 nmol; Bmax = 204 +/- 39 and 205 +/- 30 fmol/mg protein respectively). Administration of SRIF antiserum resulted in a dose-dependent increase in plasma concentrations of GH, TSH and prolactin. The minimal effective dose of SRIF antiserum was 50 microliters for GH, 100 microliters TSH and 200 microliter for prolactin. Our results show that: starvation does not modify adenohypophysial SRIF-binding sites, in starved male rats endogenous SRIF exerts a negative control on prolactin secretion in vivo and sensitivity to endogenous SRIF seems to be different for each hypophysial cell type.

After 3 days of starvation, refeeding with carbohydrate (CHO) leads to a rapid increase in plasma T4 and T3, suggesting increased TSH secretion. The aim of the present study was to describe the time course of plasma TSH changes during refeeding with CHO and fat. Repetitive blood samples were obtained from freely moving animals by indwelling jugular venous catheters. Refeeding was performed on the fourth day of starvation at either 1100 or 1900 h, and blood was sampled during the preceding hour and during the following 3 h. In control experiments, blood was sampled over 4 h without refeeding. Refeeding with CHO and fat induced a significant increase in plasma TSH in the first hour. This increase could be abolished by a previous injection of an anti-TRH serum, while normal rabbit serum was without effect. Plasma corticosterone, measured hourly, also showed a tendency to increase with refeeding. It is concluded that refeeding of starved rats represents a reproducible stimulus for TSH secretion.