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The effect of an inhibitor of gut serotonin (LP533401) during the induction of periodontal disease.
Lima GM, Corazza BJ, Moraes RM, de Oliveira FE, de Oliveira LD, Franco GC, Perrien DS, Elefteriou F, Anbinder AL
(2016) J Periodontal Res 51: 661-8
MeSH Terms: Alveolar Bone Loss, Animals, Collagen, Disease Models, Animal, Gingiva, Ligation, Male, Mandible, Periodontal Attachment Loss, Periodontal Diseases, Periodontitis, Pyrimidines, Rats, Rats, Wistar, Serotonin, X-Ray Microtomography
Show Abstract · Added April 13, 2017
BACKGROUND AND OBJECTIVE - LP533401 is an inhibitor of tryptophan hydroxylase 1, which regulates serotonin production in the gut. Previous work indicates that LP533401 has an anabolic effect in bone. Thus, we hypothesized that inhibition of gut serotonin production may modulate the host response in periodontal disease. In this study, we aimed to analyze the effects of LP533401 in a rat periodontitis model to evaluate the role of gut serotonin in periodontitis pathophysiology.
MATERIAL AND METHODS - Twenty-four rats were divided into three groups: treated group (T: ligature-induced periodontal disease and LP533401, 25 mg/kg/d) by gavage; ligature group (L: ligature-induced periodontal disease only); and control group (C: without ligature-induced periodontal disease). After 28 d, radiographic alveolar bone support was measured on digital radiographs, and alveolar bone volume fraction, tissue mineral density and trabeculae characteristics were quantified by microcomputed tomography in the right hemi-mandible. Left hemi-mandibles were decalcified and alveolar bone loss, attachment loss and area of collagen in the gingiva were histologically analyzed.
RESULTS - Significant difference between the L and C groups was found, confirming that periodontal disease was induced. We observed no difference between the T and L groups regarding alveolar bone destruction and area of collagen.
CONCLUSION - LP533401 (25 mg/kg/d) for 28 d does not prevent bone loss and does not modulate host response in a rat model of induced periodontal disease.
© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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16 MeSH Terms
Coating of titanium alloy with soluble laminin-5 promotes cell attachment and hemidesmosome assembly in gingival epithelial cells: potential application to dental implants.
Tamura RN, Oda D, Quaranta V, Plopper G, Lambert R, Glaser S, Jones JC
(1997) J Periodontal Res 32: 287-94
MeSH Terms: Amino Acid Sequence, Animals, Antigens, CD, Cell Adhesion, Cell Adhesion Molecules, Cells, Cultured, Dental Alloys, Desmosomes, Epithelial Attachment, Humans, Integrin beta4, Microscopy, Electron, Molecular Sequence Data, Periodontal Diseases, Rats, Surface Properties, Titanium
Show Abstract · Added March 27, 2014
The formation of a biological seal around the transmucosal portion of dental implants may be crucial for the long-term success of these therapies. Data to date suggest that the gingival epithelium attaches to dental implants through the formation of hemidesmosomes. Biochemical and genetic data indicate that the laminin isoform, laminin-5, a component of basement membranes, plays a crucial role in the assembly and maintenance of hemidesmosomes. We report the use of soluble laminin-5 as a biological coating of titanium-alloy to promote cell attachment of the gingival epithelial cell line, IHGK. Monoclonal antibodies reactive with laminin-5 depleted the coating solution of all cell attachment activity and blocked cell attachment to laminin-5-coated disks. Immunodepletion with antibodies to fibronectin had no effect. Finally, we demonstrate that IHGK cells assembled hemidesmosomes within 24 h of attachment to laminin-5-coated titanium alloy but not to the titanium alloy alone. These results suggest that soluble laminin-5 may have clinical applications as a dental implant coating to promote the formation of a biological seal.
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17 MeSH Terms