Testosterone selectively increases primary follicles in ovarian cortex grafted onto embryonic chick membranes: relevance to polycystic ovaries.

Histological studies have demonstrated that polycystic ovaries (PCO) contain increased numbers of preantral follicles with a specific increase in primary follicles. Polycystic ovary syndrome is associated with hyperandrogenism and pre- and postnatal androgenization of primates increases the pool of growing follicles producing changes resembling PCO. In vitro studies could test the hypothesis that androgens alter early folliculogenesis, but conventional culture techniques for small follicles are generally unsuitable in non-rodent species. Our objective was to develop and use a method to investigate the effects of testosterone on early folliculogenesis. We adapted an in ovo technique in which lamb cortical ovarian fragments were grafted onto the chorioallantoic membrane of fertilised chick eggs. Optimal experimental conditions for vascularisation and survival of tissue were determined and the model then used to investigate the effects of testosterone on follicle growth. Eggs were inoculated with testosterone at the time of implantation of the ovarian tissue, which was retrieved 5 days later. Tissue was sectioned and follicles staged and counted. There was no wholesale initiation of primordial follicle growth over the 5-day in ovo culture. Importantly, the proportion of primordial, primary and secondary follicles remained similar to those in unimplanted tissue. Testosterone increased the number of primary follicles by 50% compared with controls, an effect that was largely due to a reduction in atresia. In conclusion, incubation of ovarian cortex with testosterone reproduces the changes in early folliculogenesis reported in histological studies of PCO.

Dual effect of metformin on growth inhibition and oestradiol production in breast cancer cells.

Evidence has been accumulating for a role for metformin in reducing breast cancer risk in post-menopausal women. It inhibits growth of breast cancer cells via several mechanisms, primarily the AMPK/mTOR signalling pathway. Another possible protective mechanism may be the ability of metformin to inhibit aromatase activity. In the present study, we investigated the effects of metformin on the basal growth of MCF-7 cells, after oestradiol (E2) stimulation and after the inhibition of mTOR by rapamycin. Secondly, we investigated the effects of metformin on the activity of a number of steroidogenic enzymes and the mRNA expression of aromatase and steroid sulphatase (STS). High doses of metformin significantly inhibited both basal and oestrogen-stimulated cell division. Low-dose rapamycin (10-10 M) did not inhibit growth, but the addition of metformin induced a significant reduction in growth. High-dose rapamycin (10-8 M) inhibited growth, and this was further attenuated by the addition of metformin. Exposure to low (10-7 M) and high (10-4 M) doses of metformin for 7-10 days significantly reduced the conversion of androstenedione (ANDRO) and testosterone (TESTO) (both requiring aromatase), but not the conversion of oestrone or oestrone sulphate (ES) via 17ß-hydroxysteroid dehydrogenase/sulphatase to E2. This attenuation was via a downregulation in the expression of total aromatase mRNA and promoter II, whilst the expression of sulphatase was unaffected by metformin. In conclusion, plasma levels of metformin have a dual therapeutic action, first by directly inhibiting cell proliferation which can be augmented by rapamycin analogues, and secondly, by inhibiting aromatase activity and reducing the local conversion of androgens to E2.

A comparison of the effects of gonadal steroids on naloxone-induced LH secretion in gonadectomized rats.

The effects of the opiate antagonist naloxone on serum LH concentrations was investigated in gonadectomized rats given different regimes of steroid pretreatment. Two injections of testosterone given 48 and 24 h before naloxone treatment failed to reinstate LH responses to this drug in castrated rats while subcutaneous testosterone-filled silicone elastomer capsules implanted for a week were effective in this respect. Injections of oestrogen, oestrogen plus progesterone or progesterone alone all restored LH responses to naloxone in ovariectomized rats when given 48 and/or 24 h before drug treatment, although the magnitude of these responses varied according to the precise steroid treatments. The hypothalamic-pituitary axis was also responsive to naloxone just before the progesterone-induced LH surge in oestrogen-primed ovariectomized rats. Results show that gonadal steroids are permissive to the effects of opiate drugs, but they suggest that endogenous opioid systems do not necessarily mediate the negative feedback effects of steroids. Some other factor(s), as yet unidentified in the rat, may control the opioid modulation of gonadotrophin secretion or exert an independent inhibitory effect on gonadotrophin release.

Effects of chronic treatment with oestrogen, an oestrogen antagonist and a potent luteinizing hormone releasing hormone agonist analogue on pituitary responsiveness to luteinizing hormone releasing hormone in the rat.

The rise in gonadotrophin release which occurs after ovariectomy is caused by steroid withdrawal resulting in an enhanced pituitary responsiveness to LH releasing hormone (LHRH) associated with increased LHRH release and pituitary LHRH binding. The effects of oestrogen replacement after ovariectomy and chronic treatment of intact rats with an oestrogen antagonist, tamoxifen, on LH release and in-vitro pituitary responses to LHRH have been investigated. Capsules containing crystalline oestradiol, implanted at the time of ovariectomy, completely inhibited the rise in LH release although pituitary responsiveness was greater after 10 days in the oestrogen-treated rats than in untreated ovariectomized controls. On day 4 after ovariectomy pituitary responses to LHRH were comparable in both treated and untreated groups although in both groups the responses were greater than those measured in intact dioestrous rats. Treatment with tamoxifen over a 4-day period also augmented pituitary responsiveness but only at the lowest dose (0.5 mg/kg); no effect on serum LH concentrations was observed. Higher doses of the antagonist (1 and 2 mg/kg) did not affect pituitary responses, although the highest dose did cause a significant rise in serum LH. Treatment with a daily dose of 50 ng [D-Ser(But)6]LHRH(1-9)nonapeptide-ethylamide, starting on the day of ovariectomy, markedly attenuated the LH responses to LHRH ex vivo at days 2, 4 and 10 after ovariectomy. In contrast, the analogue treatment did not abolish the rise in LH release but this was proportionately less than in controls.

Pituitary sensitivity to gonadotrophin releasing hormone after hyperprolactinaemia induced with neuroleptics and domperidone in the rat.

The effect of hyperprolactinaemia induced by dopamine-antagonist drugs on pituitary responsiveness to gonadotrophin releasing hormone (Gn-RH) and on plasma LH levels has been investigated in intact and ovariectomized rats. The animals were pretreated with haloperidol, pimozide or domperidone and the sensitivity of isolated pituitary glands to pulses of Gn-RH were tested using a perifusion system. Trunk blood, collected at the time of killing, was assayed for plasma LH and prolactin. In addition, a direct effect of the drugs on pituitary responsiveness to Gn-RH was investigated by perfusing pituitary glands taken from untreated, pro-oestrous rats in medium containing the dopamine antagonists. The pituitary responsiveness was significantly impaired in intact rats after treatment with each of the drugs whereas no effect was observed in pretreated ovariectomized rats. None of the drug treatments altered levels of circulating LH. High concentrations of the drugs present in the perifusion medium also inhibited pituitary responsiveness although it is not known whether the concentrations of the drugs present in the pretreated animals would exert a similar effect. The results suggest that short-term hyperprolactinaemia impairs pituitary responsiveness through a modulation of ovarian steroid secretion and that Gn-RH release is not altered. Treatment with domperidone exhibited similar effects on the parameters measured here to those caused by the two neuroleptics, indicating that this novel anti-dopaminergic drug is acting in a similar manner.

Feedback effects of steroids on gonadotrophin release in hyperprolactinaemic, ovariectomized rats.

The effect of hyperprolactinaemia on the progesterone-induced LH surge which occurs in oestrogen-primed, ovariectomized rats has been investigated. Hyperprolactinaemia was produced by implanting pituitary glands under the kidney capsule and levels of LH and prolactin in the circulation were measured at appropriate times during the steroid treatment. Twenty-four hours after oestrogen administration plasma LH levels were significantly reduced in both hyperprolactinaemic and sham-operated control rats. Progesterone induced a surge of LH which peaked 5 h after injection in both groups of rats. However, the peak LH level in the hyperprolactinaemic rats was less than 50% of that observed in the controls. Differences were also found in the effect of oestrogen on prolactin release in the hyperprolactinaemic rats. It is suggested that prolactin reduces the sensitivity to progesterone by a direct action on the hypothalamic-pituitary axis.

Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose-response study.

The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls.

Dynamic changes in pituitary responses to luteinizing hormone releasing hormone after ovariectomy in the rat.

Changes in pituitary responses to pulses of LH releasing hormone (LH-RH) after ovariectomy in the rat have been investigated with an in-vitro perifusion system. On the third day after ovariectomy there was a large increase in the responsiveness of the pituitary gland to LH-RH compared with days 1 and 2 and this preceded the first significant rise in circulating concentrations of LH. Exaggerated responses were observed on all subsequent days tested (days 4, 6, 10, 18 and 28) although the size of the response on day 10 was significantly lower compared with days 6, 18 or 28. It is suggested that the early phase of increased pituitary responsiveness to LH-RH results from a rise in pituitary LH-RH receptors, which increases both the synthesis of LH and the response to exogenous LH-RH. The reduced LH response, measured on day 10, may correlate with an increase in the endogenous secretion of LH-RH and an imbalance between LH synthesis and secretion at this time.

Pituitary receptors for LH-releasing hormone (LHRH) and responsiveness to LHRH in adult female rats after neonatal monosodium L-glutamate treatment.

The effects of neonatal monosodium L-glutamate (MSG) treatment on pituitary responsiveness to LH-releasing hormone (LHRH) and on pituitary LHRH receptors have been investigated in the intact adult female rat. Three- to four-month-old rats treated with MSG (4 mg/g body wt) on days 2, 4, 6, 8 and 10 after birth had significantly reduced ovarian and pituitary weights, showed an absence or disruption of ovarian cyclicity after puberty, and had significantly higher concentrations of serum prolactin despite normal levels of LH. In-vitro pituitary LH responses to LHRH were in the normal range for one group of treated animals whilst in a second group the LH responses were markedly enhanced. In contrast, the total number of pituitary LHRH receptors were significantly reduced in all MSG-treated animals showing that the increased pituitary responsiveness of MSG-treated animals is not attributable to an increase in pituitary LHRH receptors.

Evidence for an increased opioid inhibition of LH secretion in hyperprolactinaemic ovariectomized rats.

The effects of acute and sub-chronic hyperprolactinaemia on the positive feedback action of progesterone in oestrogen-primed ovariectomized rats have been compared. A single injection of ovine prolactin administered with progesterone had no effect on the LH surge measured 5 h later although hyperprolactinaemia induced by 5-day treatment with the dopamine antagonist, domperidone, markedly attenuated the surge. Repeated injections of naloxone (5 mg/kg) during the development of the progesterone-stimulated LH surge completely reversed this inhibitory effect of hyperprolactinaemia, but had no apparent effect on the positive feedback action in control animals. In oestrogen-primed animals similar treatment with naloxone (0.4 and 5 mg/kg) stimulated LH secretion but the increase was significantly smaller than that observed after injecting progesterone. It is suggested that hyperprolactinaemia increases the inhibitory opioid modulation of LH release and that this effect is responsible for the impairment of the positive feedback action of progesterone.

Interactions between interleukin-1 beta, nitric oxide and prostaglandin E2 in the rat ovary: effects on steroidogenesis.

It has been reported that interleukin (IL)-1 beta induces the synthesis of both nitric oxide (NO) and prostaglandin (PG)E2 in cultures of dispersed ovarian cells and exerts cytotoxic effects on these cells. Since PGE2, NO and IL-1 beta have been implicated as modulators of steroidogenesis, experiments have been undertaken to determine how IL-1 beta-induced NO and PGE2 production may affect steroidogenesis in cultures of ovarian dispersates obtained from untreated adult oestrous rats and to compare the action of IL-1 beta in cultures of granulosa/luteal (GL) cell-only cultures and GL cells co-cultured with peritoneal macrophages. IL-1 beta significantly increased the production of NO (assessed by nitrite measured in the culture medium) and PGE2 in cultures of ovarian dispersates but had no effect on cultures of GL cells in which NO production was typically very low and PGE2 production was undetectable. In contrast both NO and PGE2 were high in co-cultures and were not significantly altered by the addition of IL-1 beta. The NO donor sodium nitroprusside inhibited steroidogenesis in cultures of ovarian cells in a dose-dependent manner while PGE2 had a stimulatory effect. Concomitant inhibition of NO production with aminoguanidine and PG production with indomethacin resulted in a significant enhancement of basal progesterone production in these cultures. Finally, IL-1 beta inhibited progesterone responses to forskolin and PGE2 in ovarian dispersates: an effect not observed in GL cell-only cultures nor in co-cultures in which forskolin-induced progesterone production is always inhibited. No cytotoxic effects of IL-1 beta during the 48 h period of culture were observed. A comparison of the steroidogenic NO and PGE2 responses to IL-1 beta in the three culture models suggests that (i) the response to IL-1 beta observed in ovarian dispersates could be due to cytokine activation of resident and infiltrating macrophages or that the action of IL-1 beta requires some other heterologous cell-cell contact, and (ii) IL-1 beta acts indirectly on signal transduction pathways which stimulate steroidogenesis.

Effect of ovariectomy and steroid hormone replacement on the recovery of arterial blood pressure following haemorrhage in anaesthetized Brattleboro rats.

There is increasing evidence that ovarian steroids inhibit vascular responsiveness to the neurohypophysial hormone vasopressin. The present study examined the recovery of the arterial blood pressure following a single (2 ml/100 g body weight) haemorrhage in ovariectomized (OVX) Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) and rats of the parent Long Evans (LE) strain. Some groups of OVX rats received subcutaneous implants of either 17 beta-oestradiol (E2) or progesterone 7 days prior to haemorrhage. The arterial blood pressure recovery immediately following haemorrhage was significantly impaired in both groups of steroid-treated OVX LE rats compared with the OVX controls (both comparisons P < 0.05). The impairment in blood pressure recovery seen in the steroid-replaced OVX LE rats was similar to that seen in pro-oestrous rats (when ovarian steroid levels are raised) compared with male rats of this strain (P < 0.05). In contrast, ovariectomy with or without steroid replacement in BDI rats had no further effect on the already attenuated recovery of arterial blood pressure after haemorrhage in this strain. Heart rate responses to haemorrhage also showed strain differences, which were dependent on steroid treatment. Pro-oestrous female LE rats showed a small decrease in heart rate after haemorrhage, followed by a recovery process, and this initial bradycardia was markedly enhanced in the OVX steroid-treated animals. In contrast, untreated OVX LE rats showed an initial and sustained increase in heart rate which was significantly higher than in the steroid-treated OVX animals (P < 0.05). All BDI rats, irrespective of treatment, consistently showed an increased heart rate after haemorrhage. In conclusion, ovarian steroid replacement in OVX LE, but not vasopressin-deficient BDI, rats was associated with an attenuated pressor recovery after haemorrhage. This provides further evidence for the existence of an important inhibitory interaction between ovarian steroids and vasopressin. The initial decrease in heart rate observed in pro-oestrous and steroid-treated OVX LE rats after haemorrhage also appears to be related to an ovarian steroid-vasopressin interaction.

Influence of oestrous cycle on the pressor recovery following haemorrhage in anaesthetized Brattleboro rats.

A sexual dimorphism in the pressor responsiveness to the neurohypophysial hormone vasopressin may be associated with a peripheral interaction between ovarian steroids and the neurohypophysial hormone. Indeed, the ovarian steroids may inhibit the vasopressin-dependent component of the pressor response to haemorrhage. The present study examined the recovery of the arterial blood pressure following it single large (2% v/w) haemorrhage in anaesthetized male Long Evans (LE) rats and females of the same strain during either pro-oestrous or di-oestrous phases of the reproductive cycle. In addition the same recovery process was examined in Brattleboro rats with diabetes insipidus (BDI) lacking circulating vasopressin. All BDI rats had an impaired blood pressure recovery following haemorrhage compared with male rats of the parent LE strain, and this was irrespective of sex or stage of the oestrous cycle. While the blood pressure recovery was more impaired in both groups of BDI female rats than in the males of the same strain during the first 20 min after haemorrhage (both comparisons p < 0.001; ANOVA), there was no difference between the recoveries of the female rats in pro-oestrus or di-oestrus. In contrast a significantly impaired blood pressure recovery was observed in female LE rats at pro-oestrus, when circulating ovarian steroid concentrations are raised, compared with male (p < 0.001: ANOVA) and di-oestrous (p < 0.02: ANOVA) rats of the same strain. Heart rate responses to haemorrhage showed strain differences, with LE rats having initial decreased heart rates followed by a recovery process, while the heart rate responses of BDI rats increased immediately. The novel use of the female Brattleboro rat in this study provides evidence for the existence of an important inhibitory interaction between ovarian steroids and vasopressin during the blood pressure recovery phase following haemorrhage, and indicates a possible direct influence of gonadal steroids on the recovery process.

The effect of chronic neuroleptic treatment on gonadotrophin release.

Although neuroleptic-induced hyperprolactinaemia is a common cause of amenorrhoea in women, the mechanism by which ovarian function is disturbed is unknown. Previous studies on both hyperprolactinaemic women and rats have indicated that an impairment of the pituitary response to LH-RH may be involved. We have investigated this possibility in female psychiatric patients undergoing chronic treatment with depot neuroleptics. The patients and a group of healthy controls were subjected to a standard LH-RH provocation test. Basal and post-stimulation serum levels of gonadotrophins, prolactin and oestradiol were determined. We have found that the LH responses of the patients fell into three groups: exaggerated, normal and impaired. Differences in the basal levels of gonadotrophins were also observed. The abnormal basal hormone levels and LH-RH responses appear to be related to neuroleptic dose and/or serum prolactin concentration, but no well-defined relationship was found. The results suggest that an action of the neuroleptics which is independent of high serum prolactin levels may be involved in the disruption of pituitary function. Thus the amenorrhoea caused by neuroleptic drug treatment may be etiologically different from that of other forms of hyperprolactinaemic amenorrhoea.

Stimulation of luteinizing hormone-Beta messenger ribonucleic Acid and post-translational modification of luteinizing hormone isoforms by second messengers mediating the action of gonadotrophin-releasing hormone.

Abstract Several second messenger systems have been implicated in mediating the action of gonadotrophin-releasing hormone on the pituitary gonadotrophs and numerous studies have shown that activation of these systems induces luteinizing hormone (LH) secretion. However, it is not known how gonadotrophin-releasing hormone or the second messenger systems induce de novo LH biosynthesis and post-translational modification of the hormone. In these experiments hemipituitary glands have been perifused with drugs which activate second messengers or stimulate protein kinase C directly. The LH secretory responses have been correlated with measurements of common a and LHbeta mRNA and the molecular species of LH which were present in the pituitary perifusate after exposure to the drugs. Gonadotrophin-releasing hormone (50 ng/ml, 42 nM), with and without the presence of extracellular Ca(2+), the Ca(2+) ionophore, A23187 (10 muM), and phorbol 12-myristate (1 muM) all stimulated an increase in LHbeta mRNA compared with controls and the appearance of a different isoform of LH to that found stored in and released from the unstimulated pituitary gland. Phospholipase C was without effect on LHbeta mRNA levels and showed minimal efficacy in inducing the appearance of the different LH isoform.

Protein tyrosine kinase activity of lavendustin A and the phytoestrogen genistein on progesterone synthesis in cultured rat ovarian cells.

OBJECTIVE: To compare the effects of two protein tyrosine kinase inhibitors, lavendustin A and the phytoestrogen genistein, on progesterone synthesis in cultured rat ovarian cells. DESIGN: Experimental animal study. SETTING: Medical school laboratory. ANIMAL(S): Porton Wistar rats. INTERVENTION(S): Ovaries from estrous rats were used to establish cell cultures of granulosa-luteal cells from freshly ruptured follicles, granulosa-luteal cells cocultured with peritoneal macrophages, and whole ovarian dispersates. MAIN OUTCOME MEASURE(S): Progesterone and nitrite concentrations in the culture medium. RESULT(S): The protein tyrosine kinase inhibitors suppressed steroid synthesis in a dose-dependent manner and completely inhibited the steroidogenic response to both FSH and the adenyl cyclase stimulator forskolin. The inhibitory action of cocultured macrophages on basal and forskolin-stimulated progesterone production in granulosa-luteal cells was not reversed by genistein, nor was the inhibitory effect of interleukin-1beta in cultures of ovarian dispersates. CONCLUSION(S): Genistein and the nonestrogenic protein tyrosine kinase inhibitor lavendustin A exert potent inhibitory effects on steroidogenesis that are independent of cytokines. The toxic effects of genistein on sexual development and reproduction may be attributed not only to its estrogenic action but also to its action as a protein tyrosine kinase inhibitor.

Endometriosis and polycystic ovary syndrome: enhanced stimulatory effect of peritoneal fluid on progesterone release from human granulosa-lutein cells.

OBJECTIVE: To compare the activity of peritoneal fluid (PF) from women with and without endometriosis or polycystic ovary syndrome (PCOS) on P release from cultured human granulosa-lutein cells. DESIGN: Case-control study. SETTING: Medical school and hospital. PATIENTS: Women with mild to moderate endometriosis or PCOS and controls undergoing laparoscopic sterilizations. MAIN OUTCOME MEASURES: Human granulosa-lutein cells, obtained from the IVF clinic, were cultured with increasing volumes of steroid-extracted PF samples with and without hCG. Progesterone concentrations in the media after 72 hours culture were measured by RIA. RESULTS: Peritoneal fluid stimulated P release in a dose-dependent manner and, at the highest dose, the response was enhanced significantly by PF from women with endometriosis and PCOS compared with control samples. The effects of PF plus hCG were not simply additive. There was a large potentiation of the response, which was greater in women with endometriosis and PCOS. CONCLUSIONS: Peritoneal fluid contains factors that stimulate P release and potentiate the response to hCG. The increased activity of PF associated with endometriosis and PCOS in part may have some significance in abnormal ovarian function associated with these syndromes.

Differing effects of endocrine-disrupting chemicals on basal and FSH-stimulated progesterone production in rat granulosa-luteal cells.

Previous studies have shown that the phytoestrogen, genistein, inhibits basal and forskolin-stimulated progesterone synthesis in rat granulosa-luteal cells. Genistein, however, not only binds and activates the estrogen receptor (ER), but is also a potent inhibitor of tyrosine kinase. In these studies we have compared the effects of estradiol, two other phytoestrogens, apigenin and coumarin, the pesticide, [2-(chlorphenyl)-2-(4-chlorphenyl)-1,1,1-trichlorethan] (2,4'DDT), and the industrial chemical, 4-octyl-phenol, on basal and follicle stimulating hormone (FSH)-stimulated progesterone production in the same experimental system. Only a supraphysiological dose of estradiol (10(-5) M) significantly inhibited basal and forskolin-stimulated progesterone production in granulosa-luteal cells, but had no effect on FSH-stimulated production. In contrast, apigenin, DDT, and octyl-phenol stimulated basal progesterone production at doses around 10(-8) to 10(-7) M, but this effect was reversed at higher doses. Coumarin was without effect. Like basal production, the two phytoestrogens had opposing effects on FSH-stimulated progesterone production. Genistein at 10(-5) M was inhibitory, while apigenin significantly potentiated the response at 19(-7) M. In contrast, DDT had no effect on the FSH-induced response, though 10(-7) M octyl-phenol nearly doubled the response. While all these chemicals are known to interact with the estrogen receptor to a greater or lesser extent, these studies suggest that like genistein, these different endocrine-disrupting chemicals may have other actions apart from those on the estrogen receptor.

Comparison of two stylus methods for measuring surface texture.

OBJECTIVES: The purpose of this study was to evaluate and compare two "stylus" methods for measuring surface texture of dental tissues and materials. METHODS: The two styli chosen were a contact diamond stylus and a non-contact focussed laser stylus attached to the same measuring apparatus. RESULTS: These indicate that there are significant differences between those obtained from surface texture measurements using a non-contact laser stylus and a diamond contact stylus method despite being mounted in the same profilometer. This is valid for both the test specimens of known surface texture, provided by the manufacturers, and for a "real world" simulation using contoured and finished Dicor ceramic blocks. The only significant agreement between the two styli was found for the Ra parameter. This should not be used alone to describe the roughness of a surface because the parameter is not sensitive to profile shape. Owing to the properties of the stylus used it is essential that the limitations of surface profilometry be recognised. SIGNIFICANCE: Caution should be exercised when comparing the results of surface texture studies of dental hard tissues and restorative materials using varying types of stylus attached to a surface profilometer.

Surface texture changes of a composite brushed with "tooth whitening" dentifrices.

OBJECTIVES: The aim of this investigation was to evaluate the significance of selected surface texture parameters used to describe and quantify the effect of tooth brushing with various "tooth whitening" dentifrices on a resin composite surface in vitro. METHODS: Specimens of a microfil resin composite were brushed with selected dentifrices. Surface texture profiles were acquired and analyzed both pre- and post-brushing using a contact diamond stylus. The selected parameters chosen to describe the surface texture were Ra, Rz, Rpm and the Rpm:Rz ratio. Differences between toothpastes were assessed using an ANOVA and a multiple comparisons test, the Student Newman-Keuls procedure. P and t values were calculated to determine if any of the surface roughness parameters were significantly changed by brushing. RESULTS: The results indicate that there were significant changes in the surface texture of the resin composite following tooth brushing with the selected dentifrices. For example, the use of Clinomyn significantly increased the surface roughness of the resin composite, as measured by the Rz parameter, from 2.19 +/- 1.67 microns to 10.02 +/- 2.57 microns (p < 0.05). In addition, the surface texture parameters chosen to describe the properties of the surface should reflect a knowledge of profile shape such as Rpm:Rz ratio, and care should be taken if measurements of surface texture of dental restorative materials are to be used as predictors of clinical performance. SIGNIFICANCE: All the toothpastes chosen for this investigation left a surface on the resin composite which may be prone to crack propagation during "vertical barrelling" movements generated during mastication. However, this may be more of a function of the rigidity of the restorative material rather than the surface left after tooth brushing.