Radiographic evaluation of immediately loaded implants supporting 2-3 units fixed bridges in the posterior maxilla: a 3-year follow-up prospective randomized controlled multicenter clinical study.

OBJECTIVE: To compare the survival rate and alveolar bone levels at implants installed in healed sites and functionally loaded within 1 h from installation or after 3 months. MATERIAL AND METHODS: A total of 30 patients (17 male and 13 female) were recruited and 71 implants with a SLA(®) surface, 4.1 mm in diameter and 8-12 mm long, were installed in a fully healed alveolar ridge, 36 as test and 35 as control implants. The test implants were immediately loaded with a temporary reconstruction in proper occlusion, while the randomly selected control sites received the final reconstruction after 3 months. Radiographic bone levels were determined after implant installation, prosthesis delivery, and at annual intervals thereafter. RESULTS: One patient of the control and one patient of the test were excluded from evaluation. No further losses of implants or patients were seen up to the 3-year follow-up. Hence, data from 28 patients were accounted for. A total of 37 and 36 metal-ceramic crowns were provided at the test and control sites, respectively. No biological and technical complications were observed during the 3-year follow-up. Bone levels at the time of implant installation were at 1.6 ± 0.8 and 1.7 ± 0.9 mm from the implant shoulder at the test and control sites, respectively. At prosthesis delivery, the bone levels were located at 2.4 ± 0.7 mm at the control sites 3 months after implant placement. After 1 year of function, similar bone levels were observed at both sites, displaying 2.4 ± 1.0 and 2.5 ± 0.8 mm at the test and control sites, respectively. No differences were found in the subsequent observation periods. CONCLUSION: Survival rates and radiographic bone levels after 1, 2, and 3 years of observation did not differ between conventionally installed implants loaded immediately or delayed (after 3 months). Moreover, insertion torque values did not affect osseointegration.

Implants in fresh extraction sockets: a prospective 5-year follow-up clinical study.

OBJECTIVE: The aim of this prospective study was to evaluate the 5-year clinical outcome of the 'immediate implants.' MATERIAL AND METHODS: One week after the cementation of the prosthesis, a clinical baseline examination was carried out. Clinical measurements were performed of the following: plaque, mucositis, probing pocket depth, and soft tissue position. The height of the keratinized mucosa was measured at the buccal/lingual aspects. Standardized intra-oral radiographs were taken. The marginal level of bone to implant contact [radiographic (Rx) bone level] was measured, and Rx bone level change over time was evaluated. The clinical/radiographic measurements were repeated on a yearly basis. The subjects were enrolled in a carefully supervised oral hygiene program. RESULTS AND CONCLUSION: It was demonstrated that 'immediate implants' that were loaded after 5-7 months had a high success rate. During the 5-year interval, no implant was lost, and the mean Rx bone level at the implants was maintained or even improved. The plaque and mucositis scores were low (<20%) at baseline and at all re-examinations. Implant sites located adjacent to the teeth showed bone gain during the initial period while sites that were facing edentulous zones lost some bone.

Damage of the medial preoptic area impairs peripheral pilocarpine-induced salivary secretion.

The existence of neural connections between the medial preoptic area (MPOA) and the salivary glands and the increase in salivation by thermal or electrical stimulation of the MPOA have suggested an important role of MPOA in the control of salivary gland function. Although direct cholinergic activation of the salivary glands induces salivation, recent studies have suggested that salivation produced by i.p. pilocarpine may also depend on the activation of central mechanisms. Therefore, in the present study, we investigated the effects of bilateral electrolytic lesions of the MPOA on the salivation induced by i.p. pilocarpine. Adult male Holtzman rats (n = 11-12/group) with bilateral sham or electrolytic lesions of the MPOA were used. One, five, and fifteen days after the brain surgery, under ketamine anesthesia, the salivation was induced by i.p. pilocarpine (1 mg/kg of body weight), and saliva was collected using pre-weighed small cotton balls inserted into the animal's mouth. Pilocarpine-induced salivation was reduced 1 and 5 days after MPOA lesion (341 +/- 41 and 310 +/- 35 mg/7 min, respectively, vs. sham lesions: 428 +/- 32 and 495 +/- 36 mg/7 min, respectively), but it was fully recovered at the 15th day post-lesion (561 +/- 49 vs. sham lesion: 618 +/- 27 mg/7 min). Lesions of the MPOA did not affect baseline non-stimulated salivary secretion. The results confirm the importance of MPOA in the control of salivation and suggest that its integrity is necessary for the full sialogogue effect of pilocarpine. However, alternative mechanisms probably involving other central nuclei can replace MPOA function in chronically lesioned rats allowing the complete recovery of the effects of pilocarpine.

Effects of AV3V lesion on pilocarpine-induced pressor response and salivary gland vasodilation.

The cholinergic agonist pilocarpine injected intraperitoneally (ip) increases mean arterial pressure (MAP) and superior mesenteric (SM) vascular resistance and reduces submandibular/sublingual gland (SSG) vascular resistance. In the present study, we investigated the effects of electrolytic lesions of the anteroventral third ventricle (AV3V) region on the changes in MAP, SM, and SSG vascular resistances induced by ip pilocarpine. Male Holtzman rats anesthetized with urethane (1.0 g/kg) and chloralose (60 mg/kg) were submitted to sham or electrolytic AV3V lesions and had pulsed Doppler flow probes implanted around the arteries. Contrary to sham rats, in 1-h and 2-day AV3V-lesioned rats, pilocarpine (4 micromol/kg) ip decreased MAP (-41 +/- 4 and -26 +/- 4 mm Hg, respectively, vs. sham: 19 +/- 4 mm Hg) and SM (-48 +/- 11 and -45 +/- 10%, respectively, vs. sham: 41 +/- 10%) and hindlimb vascular resistances (-65 +/- 32 and -113 +/- 29%, respectively, vs. sham: 19 +/- 29%). In 7-day AV3V-lesioned rats, pilocarpine produced no changes on MAP and SM and hindlimb vascular resistances. Similar to sham rats, pilocarpine reduced SSG vascular resistance 1 h after AV3V lesions (-46 +/- 6%, vs. sham: -40 +/- 6%), but it produced no effect 2 days after AV3V lesions and increased SSG vascular resistance (37 +/- 6%) in 7-day AV3V-lesioned rats. The responses to ip pilocarpine were similar in 15-day sham and AV3V-lesioned rats. The cholinergic antagonist atropine methyl bromide (10 nmol) iv slightly increased the pressor response to ip pilocarpine in sham rats and abolished for 40 min the fall in MAP induced by ip pilocarpine in 1-h AV3V-lesioned rats. The results suggest that central mechanisms dependent on the AV3V region are involved in the pressor responses to ip pilocarpine. Although it was impaired 2 and 7 days after AV3V lesions, pilocarpine-induced salivary gland vasodilation was not altered 1 h after AV3V lesions which suggests that this vasodilation is not directly dependent on the AV3V region.

Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine.

Peripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the alpha2-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with intraperitoneal (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 micromol/kg of body weight) i.p. reduced SSG vascular resistance (-50+/-13% vs. vehicle: 5+/-3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15+/-5% vs. vehicle: 2+/-3%) and MAP (16+/-3 mmHg, vs. vehicle: 2+/-3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88+/-12% vs. vehicle: 7+/-4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine.

Central alpha(2) adrenergic receptors and cholinergic-induced salivation in rats.

Salivation induced by intraperitoneal (i.p.) injections of pilocarpine (cholinergic agonist) is reduced by intracerebroventricular (i.c.v.) injections of moxonidine (alpha(2) adrenergic and imidazoline receptor agonist). In the present study, we investigated the involvement of central alpha(2) adrenergic receptors in the inhibitory effect of i.c.v. moxonidine on i.p. pilocarpine-induced salivation. Male Holtzman rats with stainless steel cannula implanted into the lateral ventricle (LV) were used. Saliva was collected using pre-weighted small cotton balls inserted into the animal's mouth under ketamine (100 mg x kg(-1)) anesthesia. Salivation was induced by i.p. injection of pilocarpine (4 micromol x kg(-1)). Pilocarpine-induced salivation was reduced by i.c.v. injection of moxonidine (10 nmol) and enhanced by i.c.v. injections of either RX 821002 (160 nmol) or yohimbine (320 nmol). The inhibitory effect of i.c.v. moxonidine on pilocarpine-induced salivation was abolished by prior i.c.v. injections of the alpha(2) adrenergic receptor antagonists, RX 821002 (160 nmol) or yohimbine (160 and 320 nmol). The alpha(1) adrenergic receptor antagonist prazosin (320 nmol) injected i.c.v. did not change the effect of moxonidine on pilocarpine-induced salivation. The results suggest that moxonidine acts on central alpha(2) adrenergic receptors to inhibit pilocarpine-induced salivation, and that this salivation is tonically inhibited by central alpha(2) adrenergic receptors.

Inhibition of pilocarpine-induced salivation in rats by central noradrenaline.

Peripheral treatment with cholinergic or adrenergic agonists results in salivation and the possibility of synergy between cholinergic and adrenergic efferent mechanisms in the control of salivation has been proposed. Central injections of the cholinergic agonist pilocarpine also induce salivation, while the effects of central injections of noradrenaline (norepinephrine) are not known. Here (a) the effects of intracerebroventricular (i.c.v.) injection of noradrenaline on the salivation induced by i.c.v. or intraperitoneal (i.p.) injection of pilocarpine and (b) the receptors involved in the effects of central noradrenaline on pilocarpine-induced salivation were investigated. Male Holtzman rats with a stainless-steel guide cannula implanted into the lateral ventricle were used. Rats were anaesthetized with tribromoethanol (200mg/kg body weight) and saliva was collected on small, preweighed cotton balls inserted into the animal's mouth. Noradrenaline (40, 80 and 160 nmol/1 microl) injected i.c.v. reduced the salivary secretion induced by pilocarpine (0.5 micro mol/1 microl) injected i.c.v.. Noradrenaline (80 and 160 nmol/1 microl) injected i.c.v. also reduced the salivation induced by pilocarpine (4 micromol/kg) injected i.p. Previous treatment with the alpha(2)-adrenergic receptor antagonists RX 821002 (40, 80 and 160 nmol/1 microl) or yohimbine (160 and 320 nmol/1 microl) abolished the inhibitory effect produced by i.c.v. injection of noradrenaline on pilocarpine-induced salivation in rats. Prazosin (alpha(1)-adrenergic receptor antagonist) injected icv did not change the effect of noradrenaline on pilocarpine-induced salivation. Prior icv injection of only RX 821002 (80 or 160 nmol/1 microl) or yohimbine (320 nmol/1 microl) increased pilocarpine-induced salivation. The results show that (1) contrary to its peripheral effects, noradrenaline acting centrally inhibits cholinergic-induced salivation in rats; (2) central mechanisms involving alpha(2)-adrenergic receptors inhibit pilocarpine-induced salivation.

Morphological alterations of the rat submandibular gland caused by lesion of the ventromedial nucleus of the hypothalamus

As características morfológicas da glândula submandibular de ratos foram estudadas em diferentes períodos de tempo (5, 10, 20, 40 e 90 dias) após a lesäo do núcleo ventromedial do hipotálamo. O arranjo estrutural da glândula submandibular foi o mesmo em ratos com lesäo do núcleo ventromedial e nos ratos controle ou com lesäo fictícia. No primeiro grupo, entretanto, o septo estava estreito, dificultando a definiçäo dos compartimentos lobulares. Alteraçöes do parênquima foram bastante evidentes nos ratos lesados, com hipotrofia acinar e aumento no número de ductos granulosos. Os componentes submandibulares restantes, entretanto, näo apresentaram alteraçöes quando comparados com aqueles dos animais controles. Em resumo, a lesäo do núcleo ventromedial do hipotálamo produz as seguintes mudanças na glândula submandibular do rato: 1) diminuiçäo da massa glandular; 2) hipotrofia acinar; e 3) aumento no número de ductos granulosos

Effect of adrenergic stimulation of the amygdalois complex on water intake

O efeito da noradrenalina, isoproterenol, fentolamina e propanolol, injetados no núcleo basolateral da amigdala, sobre a ingestäo de água, foi investigado em ratos Holtzman. A injeçäo de noradrenalina (40nmol) no complexo amigdalóide (CA) de ratos saciados näo produziu nenhuma mudança na ingestäo de água em ratos saciados (1,93 ñ 0,23 ml/lh). A noradrenalina injetada no CA produziu uma diminuiçäo na ingestäo de água de ratos privados (0,40 ñ 0,19 ml/lh). A injeçäo de isoproterenol no CA de ratos privados näo produziu nenhuma mudança na ingestäo de água em comparaçäo aos controles (11,65 ñ 1,02 e 10,92 ñ 0,88 ml/lh, respectivamente). Quando comparado com valores controles, a fentolamina injetada prévia à noradrenalina bloqueou o efeito inibitório da noradrenalina sobre a ingestäo de água em ratos privados 10,40 ñ 1,31 ml/lh). O propanolol bloqueou o efeito do isorpoterenol em ratos saciados (0,85 ñ 0,49 ml/lh) e também bloqueou a ingestäo água induzida por privaçäo (0,53 ñ 0,38 ml/lh). Tanto em animais saciados quanto em privados, a injeçäo de fentolamina, antes da administraçäo de hexametônio, bloqueou o efeito inibitório do hexametônio na ingestäo de água. Em animais saciados, quando o hexametônio foi injetado sozinho, a ingestäo de água foi de 0,39 ñ 0,25 ml/lh; quando acompanhado de fentolamina, a ingestäo de água foi de 1,04 ñ 0,3 ml/lh. Em ratos privados, o hexametônio sozinho bloqueou a ingestäo de água (0,40 ñ 0,17 ml/lh) e quando injetado com fentolamina produziu uma ingestäo de 9,7 ñ 1,8 ml/lh. Este resultados demonstram claramente a participaçäo de receptores catecolaminérgicos do CA na regulaçäo da ingestäo de água.

Effect of nicotinic stimulation of the amygdaloid complex on water and sodium chloride intake

No presente trabalho foi estudado o efeito da estimulaçäo e nicotínica do complexo amigdalóide (CA) sobre a ingestäo de sódio e água em ratos saciados e privados de água. A nicotina näo produziu nenhuma alteraçäo no apetite ao sódio e água em ratos saciados. Em ratos privados, a nicotina injetada no núcleo basolateral somente bloqueou a ingestäo de cloreto de sódio. Nós demonstramos previamente que o carbacol, injetado no CA, inibiu a ingestäo de água e cloreto de sódio em ratos saciados e privados de água. A injeçäo de hexametônio no CA bloqueou totalmente a ingestäo de água em ratos saciados e privados de água. A administraçäo de hexametônio no CA, antes da injeçäo de nicotina,näo produziu alteraçäo na ingestäo de sódio. Assim, estes resultados sugerem que a populaçäo de neurônios colinoceptivos específicos do CA medeiam a ingestäo de água e cloreto de sódio

Morphometric study of the alterations in the submandibular glands of young mice treated with cocaine

Injetaram-se, intraperitonealmente, soluçäo fisiológica ou 50 µg/kg/dia de cloridrato de cocaína em camundongos albinos com 23 dias de idade. O volume nuclear das células acinares e ductulares foi determinado morfometricamente. Foi observada uma reduçäo estatisticamente significativa na média dos volumes nucleares das células dos ductos granulosos e nas acinares de glândulas submandibulares provenientes de animais tratados com cocaína quando comparados com o controle. Estas alteraçöes induzidas pela cocaína podem ser devidas ao bloqueio da captaçäo neuronal induzido pela droga ou a interferência da droga com a atividade das gonadas ou outras glândulas endócrinas

Influência dos adrenoceptores alfa1 e alfa2 do hipotálamo médio sobre a pressao arterial sistêmica em ratos / Role of the alfa1 and alfa2 adrenoceptores in the medial hypothalamus on the arterial pressure in rats

Foram estudados os efeitos sobre a pressäo arterial sistêmica após a administraçäo de noradrenalina e de dois antagonistas de alfa-adrenoceptores no hipotálamo médio de ratos normotensos. Tanto o prazosin quanto a ioimbina antagonizaram a açäo do agonista misto de alfa1/alfa2-adrenoceptores, a noradrenalina ; entretanto a administraçäo prévia de prazosin mostrou uma maior interaçäo da noradrenalina pelos adrenoceptores alfa1. Estes resultados sugerem que os adrenoceptores alfa1 do hipotálamo médio exerceriam uma maior influência que os adrenoceptores alfa2 no controle de pressäo arterial sistêmica

Sistema renina-angiotensina cerebral e sua interaçäo com o sistema renina-angiotensina renal / Interaction between central and peripheric renin-angiotensin system

O objetivo deste trabalho foi o de investigar a existência de angiotensina II (AII) no líquido cefalorraquideano (LCR) independente daquela originada nos rins. A concentraçäo de AII foi medida no LCR de ratos normais e nefrectomizados, tratados com AII central ou perifericamente, isoproterenol e polietilenoglicol. Nos animais nefrectomizados, houve um aumento de quatro vezes da AII no LCR em relaçäo aos animais normais. Quando se fez a infusäo intravenosa de AII, nenhuma mudança nos níveis de AII no LCR foi detectada. A aplicaçao do isoproterenol e do polietilenoglicol provocaram uma diminuiçao nos níveis de AII no LCR de ratos normais, mas näo nos nefrectomizados. Esses resultados mostraram que existe AII no LCR tendo interaçäo com a AII vinda do sangue, sugerindo a existência de um sistema renina-angiotensina cerebal. Os efeitos observados durante hipotensäo e hipovolemia sugerem um mecanismo autorregulatório entre AII sistêmica (renal) e renina cerebal

Effects of lesions in some areas of the central nervous system on serum concentrations of glucose, triglycerides, cholesterol, HDL-cholesterol and total lipids

Neste experimento estudamos, através de lesöes eletrolíticas em ratos, a participaçäo do complexo amigdalóide, área preóptica lateral, hipotálamo posterior, área septal e núcleo ventromediano, nos níveis circulantes de glicose, triglicerídeos, colesterol, lipídeos totais e HDL-colesterol. A lesäo no complexo amigdalóide näo determinou nenhuma alteraçäo significativa em nenhum dos componentes estudados, embora apresentasse tendência a aumento ou diminuiçäo de um ou outro componente. A lesäo da área preóptica lateral provocou queda significante nos níveis de triglicerídeos e aumento do HDL-colesterol. A lesäo do hipotálamo posterior provocou queda significante nos níveis de triglicerídeos, colesterol e lipídeos totais. A lesäo da área septal determinou aumento significante nos níveis de lipídeos totais. A lesäo do núcleo ventromediano determinou aumento significativo do HDL-colesterol. Estes resultados sugerem a participaçäo destas áreas do sistema nervoso central na regulaçäo do metabolismo lipídico

Effects of intracerebroventricular infusion of angiotensin II and related peptides on water and sodium ingestion and excretion

The objetive of the present study was to investigate the effects of an angiotensin II (AII) analogue, Des-Asp1-AII and of two competitive blockers, [Leu8]-AII and [octanoyl-Leu8]-AII, infused intracerebroventriculary on the ingestion of water and of a 3% NaCl solution, as well as on diuresis and natriuresis in normal rats and in adrenalectomized and deoxycorticosterone (DOCA)-treated rats. Both AII and Des-Asp1-AII increased water and 3% NaCl intake and increased urine and Na+ excretion, the effect of AII being more intense. Except for 3% NaCl, the responses of all other parameters were totally or partially reduced by previous treatment with [Leu8]-AII or [octanoyl-Leu8]-AII. Subcytaneous DOCA injection caused water ingestion. Previous treatment with DOCA increased the response to AII for the ingestion of 3% NaCl and inhibited sodium excretion. The results obtained for adrenalectomized rats treated with DOCA, AII and analogous agonists did not differ from those observed in normal rats. These data suggest a possible synergism between the cerebral and renal renin-angiotensin systems in the regulation of the physiological parameters studied

Papel dos adrenoceptores alfa1 e alfa2 do hipotálamo médio sobre a excreçäo de sódio e potássio / Role of alpha1 e alpha2 adrenoceptors of the medial hypothalamus on sodium and potassium excretion

Injeçäo de noradrenalina dentro do hipotálamo médio de ratos produziu uma estimulaçäo da excreçäo urinária de sódio e potássio. Ioimbina (10**-9 e 4.10**-9 M), um bloqueador dos adrenoceptores alfa 2, potencializou a excreçäo dos dois cátions quando injetado antes do agonista enquanto que o prazosin, um antagonista dos adrenoceptores alfa 1, inibiu estas respostas quando injetado nas mesmas doses. Por outro lado, injeçöes de clonidina, um agonista dos adrenoceptores alfa 2, dentro da mesma área produziu uma inibiçäo dose-dependente da excreçäo de Na+ e K+. O prazosin potencializou os efeitos da clonidina enquanto que a ioimbina inibiu estas repostas. Estes resultados sugerem a presença de dois tipos de adrenoceptores alfa para a modulaçäo das vias centrais que interferem com a regulaçäo dos dois cátions: a estimulaçäo dos adrenoceptores alfa 1 facilita enquanto a estimulaçäo dos adrenoceptores alfa 2 inibem a excreçäo dos ions

Variaçäo dos níveis séricos de glicose, triglicerídeos, colesterol e HDL-colesterol em ratos submetidos a lesöes do hipotálamo lateral / Variations of serum levels of glucose, triglycerides, cholesterol and HDL-cholesterol in rats submitted to lesions of lateral hypothalamus

Vários núcleos hipotalâmicos (núcleo ventromediano, hipotálamo lateral, etc.) atuam regulando a atividade enzimática envolvida no metabolismo de lipídeos e carboidratos. Neste trabalho procurou-se avaliar a participaçäo do hipotálamo lateral (HL) nos níveis séricos de glicose, triglicerídeos, colesterol e HDL-colesterol e verificar as variaçöes do peso corpóreo e ingestäo de alimentos - água e raçäo - em ratos controle e ratos submetidos a lesöes eletrolíticas bilaterais do hipotálamo lateral (HL). Foram utilizados ratos Holtzman de peso variável entre 250-300 gramas para as lesöes, e após períodos de 24, 48 horas, 7, 10 e 25 dias os animais lesados foram anestesiados, coletou-se sangue da aorta descendente abdominal e procedeu-se às dosagens bioquímicas e mediçöes da ingestäo de raçäo e água. Os resultados obtidos para os níveis séricos de glicose demonstraram aumento no grupo 24 horas lesäo do hipotálamo lateral (HL) e diminuiçäo nos grupos lesados de 7, 10 e 25 dias em relaçäo ao grupo controle. Para os níveis séricos de triglicerídeos observou-se uma diminuiçäo nos grupos lesados de 24, 48 e 10 dias, em relaçäo ao grupo controle. Os níveis séricos de colesterol apresentaram aumento nos grupos lesados de 48 horas e 25 dias quando comparados ao grupo controle. Os níveis séricos de HDL-colesterol aumentaram no grupo 48 horas de lesäo em relaçäo ao grupo controle. Em todos os grupos de animais com lesäo do hipotálamo lateral (HL) notaram-se alteraçöes características no peso corporal e ingestäo de alimento (raçäo e água). Os resultados demonstraram que a lesäo bilateral do hipotálamo lateral (HL) promove alteraçöes nos níveis séricos de glicose, triglicerídeos, colesterol e HDL-colesterol