Simvastatin therapy in cyclosporine A-induced alveolar bone loss in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Intermittent Therapy with 1,25 Vitamin D and Calcitonin Prevents Cyclosporin-Induced Alveolar Bone Loss in Rats

Bone loss associated with cyclosporin A (CsA) therapy can result in serious morbidity to patients. Intermittent administration of 1,25 Vitamin D and calcitonin reduces osteopenia in a murine model of postmenopausal osteoporosis. The purpose of this study was to evaluate the effects of this therapeutic approach on CsA-induced alveolar bone loss in rats. Forty male Wistar rats were allocated to four experimental groups according to the treatment received during 8 weeks: (1) CsA (10 mg/kg/day, s.c.); (2) 1,25 Vitamin D (2 mu g/kg, p.o.; in weeks 1, 3, 5, and 7) plus calcitonin (2 mu g/kg, i.p.; in weeks 2, 4, 6, and 8); (3) CsA concurrently with intermittent 1,25 Vitamin D and calcitonin administration; and (4) the control treatment group (vehicle). At the end of the 8-week treatment period, serum concentrations of bone-specific alkaline phosphatase, tartrate-resistant acid phosphatase (TRAP-5b), osteocalcin, interleukin (IL)-1 beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) were measured and an analysis of bone volume, bone surface, number of osteoblasts, and osteoclasts was performed. CsA administration resulted in significant alveolar bone resorption, as assessed by a lower bone volume and an increased number of osteoclasts, and increased serum bone-specific alkaline phosphatase, TRAP-5b, IL-1 beta, IL-6, and TNF-alpha concentrations. The intermittent administration of calcitriol and calcitonin prevented the CsA-induced osteopenic changes and the increased serum concentrations of TRAP-5b and inflammatory cytokines. Intermittent calcitriol/calcitonin therapy prevents CsA-induced alveolar bone loss in rats and normalizes the production of associated inflammatory mediators.

iNOS-Derived Nitric Oxide Stimulates Osteoclast Activity and Alveolar Bone Loss in Ligature-Induced Periodontitis in Rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Decrease in the number and apoptosis of alveolar bone osteoclasts in estrogen-treated rats

Bone is a mineralized tissue that is under the influence of several systemic, local and environmental factors. Among systemic factors, estrogen is a hormone well known for its inhibitory function on bone resorption. As alveolar bone of young rats undergoes continuous and intense remodeling to accommodate the growing and erupting tooth, it is a suitable in vivo model for using to study the possible action of estrogen on bone. Thus, in an attempt to investigate the possibility that estrogen may induce the death of osteoclasts, we examined the alveolar bone of estrogen-treated rats.Fifteen, 22-d-old female rats were divided into estrogen, sham and control groups. The estrogen group received estrogen and the sham group received corn oil used as the dilution vehicle. After 8 d, fragments containing alveolar bone were removed and processed for light microscopy and transmission electron microscopy. Sections were stained with hematoxylin and eosin and tartrate-resistant acid phosphatase (TRAP)-an osteoclast marker. Quantitative analysis of the number of TRAP-positive osteoclasts per mm of bone surface was carried out. For detecting apoptosis, sections were analyzed by the Terminal deoxynucleotidyl transferase-mediated dUTP Nick-End Labeling (TUNEL) method; TUNEL/TRAP combined methods were also used.The number of TRAP-positive osteoclasts per mm of bone surface was significantly reduced in the estrogen group compared with the sham and control groups. TRAP-positive osteoclasts exhibiting TUNEL-positive nuclei were observed only in the estrogen group. In addition, in the estrogen group the ultrastructural images revealed shrunken osteoclasts exhibiting nuclei with conspicuous and tortuous masses of condensed chromatin, typical of apoptosis.Our results reinforce the idea that estrogen inhibits bone resorption by promoting a reduction in the number of osteoclasts, thus indicating that this reduction may be, at least in part, a consequence of osteoclast apoptosis.

Immunohistochemical detection of estrogen receptor beta in alveolar bone cells of estradiol-treated female rats: possible direct action of estrogen on osteoclast life span

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Structural and functional changes in the alveolar bone osteoclasts of estrogen-treated rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Atypical dento-alveolar fracture fixed with screws: a technical note

Dento-alveolar process fracture is an important and common event in the dental office practice usually managed under the well-established protocols, but sometimes this kind of lesion is evaluated in the hospital emergency rooms without attention to the dental injuries. In this type of trauma, the time between the injury and the definitive resolution is essential for the treatment success, usually 1 h in cases of dento-alveolar fractures (tooth and alveolar bone). This paper describes the management of a patient with unusual dento-alveolar fracture caused by gunshot and treated using screw fixation.

Influence of chronic alcoholism and oestrogen deficiency on the variation of stoichiometry of hydroxyapatite within alveolar bone crest of rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influence of different durations of estrogen deficiency on alveolar bone loss in rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Response of human alveolar bone-derived cells to a novel poly(vinylidene fluoride-trifluoroethylene)/barium titanate membrane

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Response activity of alveolar macrophages in pulmonary dysfunction caused by Leptospira infection

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of nitrous oxide on minimum alveolar concentration of desflurane in dogs

Estudaram-se os efeitos do óxido nitroso (N2O) sobre a concentração alveolar mínima (CAM) do desfluorano. Trinta cães foram distribuídos em dois grupos: desfluorano (GD) e N2O e desfluorano (GDN). Os do GD receberam propofol (8,9±1,65mg/kg) para intubação orotraqueal e após, 11,5V% de desfluorano em 100% de O2. Após 30 minutos, os animais receberam estímulo elétrico e não havendo reação do animal, reduziu-se a concentração em 1,5V%. Repetiu-se o protocolo a cada 15 minutos, cessando-se os estímulos quando observada reação voluntária. Os GDN foram submetidos ao mesmo protocolo, substituindo-se o fluxo diluente por 30% O2 e 70% N2O. Mensuraram-se freqüências cardíaca (FC) e respiratória (FR), pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM), concentração de dióxido de carbono ao final da expiração (ETCO2), saturação de oxihemoglobina (SpO2), temperatura corpórea (TC) e a CAM do desfluorano. Observou-se aumento da FC, ETCO2 e SpO2, e redução da FR e da TC concomitantemente à administração da maior dose de desfluorano, além de redução da CAM do desfluorano. As pressões arteriais diminuíram em M30 aumentando posteriormente. Concluiu-se que o N2O associado ao desfluorano reduz em 16% a CAM do anestésico volátil. Além disso, essa associação promoveu aumento da FC e depressão respiratória.