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At least 1,225 records · Page 68Linked to original sources
PubMed2004

Alendronate may protect against increased periodontitis-related bone loss in estrogen-deficient rats.

BACKGROUND: The aim of this study was to evaluate the impact of alendronate (ALD) and estrogen (EST) therapies and their withdrawal on bone loss in experimental periodontitis in ovariectomized rats. METHODS: Eighty-seven Wistar rats were divided into six groups: group 1 (N = 15): sham surgery; group 2 (N = 15): ovariectomy (OVX); group 3 (N = 15): OVX plus alendronate administration for 80 days (AT); group 4 (N = 14): OVX plus alendronate administration for 40 days (AW); group 5 (N = 14): OVX plus 17beta estradiol administration for 80 days (ET); and group 6 (N = 14): OVX plus 17beta estradiol administration for 40 days (EW). Twenty-one days after ovariectomy or sham surgery, one mandibular molar was randomly assigned to receive a ligature, while the contralateral tooth was left unligated. Sixty days later, the animals were sacrificed and the specimens processed. RESULTS: OVX presented a direct impact on alveolar bone, regardless of plaque accumulation and significantly increased bone loss resulting from periodontitis (P < 0.05). The effect of OVX on unligated sites was significantly reduced by AT, AW, and ET (P < 0.05), but not by EW (P > 0.05). In addition, alendronate administration (AT/AW) significantly reduced the impact of OVX on periodontitis-related bone loss (P < 0.05), while estradiol did not (P > 0.05). CONCLUSION: Within the limits of this study, alendronate administration, but not estrogen replacement, may protect against the impact of estrogen deficiency on alveolar bone presenting a significant residual effect after its withdrawal.

Alendronate↗
PubMed1997

Pulmonary alveolar proteinosis: diagnosis using routinely processed smears of bronchoalveolar lavage fluid.

AIMS: For the diagnosis of pulmonary alveolar proteinosis from bronchoalveolar lavage specimens it is normally necessary to make an ultrastructural examination. However, this is thought to be impractical for bronchoalveolar lavage specimens that have been routinely fixed in ethanol. In the present study, bronchoalveolar lavage cytology smears on slide glasses were examined directly ultrastructurally to make a diagnosis of pulmonary alveolar proteinosis. METHODS: Bronchoalveolar lavage smears from three pulmonary alveolar proteinosis patients were stained with Papanicolaou and periodic acid-Schiff (PAS) for identification of amorphous globular structures. Subsequently, they were refixed with glutaraldehyde and osmium tetroxide, and embedded in epoxy resin. Ultrathin sections were cut and examined ultrastructurally. RESULTS: Papanicolaou stained specimens from pulmonary alveolar proteinosis patients contained scattered amorphous or granular globules, 20-50 microns in diameter, which were PAS positive. Ultrastructural examination of the globules revealed multilamellated structures, characteristic of pulmonary alveolar proteinosis, in all cases. CONCLUSIONS: In general, it is thought that the morphological diagnosis of pulmonary alveolar proteinosis from bronchoalveolar lavage specimens requires both cytological and ultrastructural examination. However, the amorphous globules evident on cytology smears proved to contain multilamellated structures so that they can themselves be used as diagnostic evidence.

Adult↗
PubMed1989

The distribution of phenotypically distinct macrophage subsets in the lungs of patients with cryptogenic fibrosing alveolitis.

Monoclonal antibodies that identify phenotypically distinct macrophage subsets were used to analyse the macrophages in lung biopsy specimens and bronchoalveolar lavage fluid from patients with cryptogenic fibrosing alveolitis. Among the antibodies were RFD1, an interdigitating cell marker, RFD7, a marker for mature tissue macrophages, and RFD9, which identifies epithelioid cells as well as germinal centre macrophages. The lavage fluid was found to contain abnormally high numbers of cells staining with each of the antibodies, a finding that could be explained, at least in part, by an increased frequency of cells expressing more than one marker. In lung tissue macrophage phenotypes within the interstitium were found to differ significantly from those in the alveolar space. Most strikingly, cells bearing the antigen recognized by RFD9 were entirely absent from the interstitial macrophage population, whereas the vast majority in the alveolar lumen were RFD9-positive. The discrete compartmentalization of phenotypically different macrophages within the lung suggests that macrophages may contribute differently to lung pathology in each microenvironment. The functional capacity of the unusual RFD9-positive alveolar macrophages remains to be determined, but their close association with the process of alveolar occlusion indicates a role in the fibrotic process.

Aged↗
PubMed1986

Alveolar macrophage and its participation in the inflammatory processes of allergic asthma.

Purified alveolar macrophages (AM) obtained by bronchoalveolar lavage of allergic asthmatic patients are stimulated by incubation with anti IgE or the exposure to the related allergen. Confirming the demonstration of a receptor for the Fc fragment of IgE on the surface of macrophages, IgE was characterised on AMs by a rosette-assay, showing an increased percentage of cells forming rosettes with red blood cells coated with anti-IgE or the specific allergen. The IgE-dependent secretion of arachidonic acid metabolites, PAF-acether and chemotactic factors for neutrophils and eosinophils demonstrated in vitro, together with the in vivo demonstration of the activation of AMs by a local provocation test, suggest that besides mast cell, AM do participate in the inflammatory processes of allergic asthma.

Antibodies↗
PubMed1980

Histologic study of the effects of occlusal hypofunction following antagonist tooth extraction in the rat.

A histologic study was done to observe the influence of occlusal hypofunction on periodontal tissues and the physiologic drift process, and to elucidate the origin of periodontal ligament narrowing. Twenty-four Wistar rats were used. Hypofunction was induced by extracting the right maxillary molars. Histologic observations were reported on the right lower jaws which were fixed, decalcified, sectioned and stained according to classical histologic methods. Two groups of five animals each were used for a complementary study study using sequential fluorescent labeling in order to evaluate the bone formation rate. After 15 days of hypofunction, the periodontal ligament was obviously narrowed and its structure was disorganized. Woven-bone formation was noted at the top of the interradicular septa, at the bottom of the sockets and along their modeling sides. At 30 days and at intervals up to 3 months, the periodontal ligament remained disorganized and narrowed. The newly-formed bone was engaged in a maturation process. Nevertheless, osteoporosis was also observed at the inferior part of the interradicular septa. Fluorescent labeling confirmed the histologic findings and showed that the induced bone formation is related to periodontal ligament narrowing and the supra-eruption process.

Alveolar Process↗
PubMed1993

Development of the murine periodontium. II. Role of the epithelial root sheath in formation of the periodontal attachment.

Experimental manipulation of the developing murine tooth germ has provided evidence that basement membrane components on the forming root surface are involved in early periodontal attachment formation. The purpose of this investigation was to determine the role of epithelial root sheath (ERS) cells in murine cementogenesis and periodontal ligament formation using tissue separation and recombination techniques. Root dentin specimens, with and without root-associated basement membrane components (D + RBM or D - RBM), were recombined with dental sac in the presence or absence of ERS. Recombinations were cultured for 2 weeks, harvested, and examined by light, electron, and immunofluorescence microscopy. Mineralized tissue formed in all tissue recombinations. However, when ERS was included in recombinations between D + RBM and dental sac, 25% of recombinations formed a periodontal ligament with fibrous attachment of the root specimen to adjacent bone. These results support the hypothesis that root and periodontal ligament formation is influenced by epithelio-mesenchymal interactions and further support a key role for ERS in these processes.

Alveolar Process↗
PubMed1978

Dental implant fixation by electrically mediated process. I. Interfacial strength.

In order to determine the effect of electrical stimulation on canine alveolar bone, porous PMMA dental implants with a solid core (on which a Pt-13% Rh electrode was wound) were implanted in the mesial socket of the canine mandibular fourth premolars bilaterally. The positive electrode was implanted into the distal socket. The power pack was placed over the masseteric fossa. The implants, wires and power packs were all implanted subcutaneously. Each animal had an experimental and control implant. Mechanical push-out samples were prepared by sectioning a 2mm thick section of the mandible with the implant in the middle. The samples were tested immediately and the load-deflection curves were obtained.

Alveolar Process↗
PubMed1992

Reactivity of alveolar epithelial cells in primary culture with type I cell monoclonal antibodies.

An understanding of the process of alveolar epithelial cell growth and differentiation requires the ability to trace and analyze the phenotypic transitions that the cells undergo. This analysis demands specific phenotypic probes to type II and, especially, type I pneumocytes. To this end, monoclonal antibodies have been generated to type I alveolar epithelial cells using an approach designed to enhance production of lung-specific clones from a crude lung membrane preparation. The monoclonal antibodies were screened by a combination of enzyme-linked immunosorbent assay and immunohistochemical techniques, with the determination of type I cell specificity resting primarily on immunoelectron microscopic localization. Two of these new markers of the type I pneumocyte phenotype (II F1 and VIII B2) were used to analyze primary cultures of type II cells growing on standard tissue culture plastic and on a variety of substrata reported to affect the morphology of these cells in culture. On tissue culture plastic, the antibodies fail to react with early (days 1 to 3) type II cell cultures. The cells become progressively more reactive with time in culture to a plateau of approximately 6 times background by day 8, with a maximum rate of increase between days 3 and 5. This finding is consistent with the hypothesis that type II cells in primary culture undergo at least partial differentiation into type I cells. Type II cells grown on laminin, which reportedly delays the loss of type II cell appearance, and on fibronectin, which has been reported to facilitate cell spreading and loss of type II cell features, develop the type I cell markers during cultivation in vitro with kinetics similar to those on uncoated tissue culture plastic. Cells on type I collagen and on tissue culture-treated Nuclepore filters, which have been reported to support monolayers with type I cell-like morphology, also increase their expression of the II F1 and VIII B2 epitopes around days 3 to 5. Taken together with available morphologic information, these data suggest that expression of different alveolar epithelial cell phenotypic markers by type II cells in primary culture may be independently regulated. The monoclonal antibody probes described in this report should prove useful in the continued investigation of the mechanisms and regulation of alveolar epithelial cell differentiation.

Animals↗