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11. |
Antimicrobial Susceptibility of Periodontopathic Bacteria Associated With Failing Implants |
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The Journal of Periodontology,
Volume 66,
Issue 1,
1995,
Page 69-74
Ludovico Sbordone,
Antonio Barone,
Luca Ramaglia,
Renato N. Ciaglia,
Vincent J. Iacono,
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摘要:
The aim of this studywas to examine the subgingival microflora associated with failing implants, and to determine their susceptibility to commonly used antibiotics in periodontal therapy and dental practice. Thirteen partially edentulous patients with 19 failing implants were selected. Clinical examination included probing depth, attachment level, gingival index, plaque index, and radiographic analyses. Two subgingival plaque samples were taken from each failing implant and analyzed for microbial composition.Fusobacterium nucleatum, Porphyromonas gingivalis, andPrevotella intermediawere the prevalent cultivable microflora. Antimicrobial susceptibility of isolates was determined by the agar dilution technique. Antibacterial activity of penicillin G, amoxicillin, amoxicillin‐clavulanate, and the combination amoxicillin‐metronidazole was significantly higher than with other antibiotics tested. These data indicated that the commonly‐used antibiotics were highly effective against bacteria isolated around failing implants, which would suggest the use of these antibiotics to control peri‐implant infections.J Periodontol 1995; 66:69–74.
ISSN:1049-8885
DOI:10.1902/jop.1995.66.1.69
出版商:Wiley
年代:1995
数据来源: WILEY
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12. |
Hereditary Gingival Fibromatosis Associated With Hearing Loss and Supernumerary Teeth — A New Syndrome |
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The Journal of Periodontology,
Volume 66,
Issue 1,
1995,
Page 75-79
Susan E. Wynne,
Michael J. Aldred,
P. Mark Bartold,
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摘要:
Hereditary gingival fibromatosiscan occur as an isolated trait or as part of a syndrome. We report on three generations of one family featuring an autosomal dominant syndrome with variable expression of gingival fibromatosis with associated hearing deficiencies, hypertelorism, and supernumerary teeth. We propose that this represents a new syndrome within the spectrum of those including gingival enlargement.J Periodontol 1995; 66:75–79.
ISSN:1049-8885
DOI:10.1902/jop.1995.66.1.75
出版商:Wiley
年代:1995
数据来源: WILEY
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13. |
Fibroblasts, Mononuclear Phagocytes, and Endothelial Cells Express Monocyte Chemoattractant Protein‐1 (MCP‐1) in Inflamed Human Gingiva† |
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The Journal of Periodontology,
Volume 66,
Issue 1,
1995,
Page 80-88
Xiaohui Yu,
Dana T. Graves,
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摘要:
Gingival inflammation is initiatedby bacterial colonization of the tooth surface. It is characterized by infiltration of mononuclear cells, a feature of many forms of chronic inflammation. Monocyte chemoattractant protein‐1 (MCP‐1) is the predominant monocyte chemoattractant secreted by a variety of cells in vitro. We examined MCP‐1 expression in chronic gingival inflammation by double antibody immunohistochemistry that utilized rabbit anti‐MCP‐1 antibody simultaneously with mouse monoclonal antibodies to specific cellular markers. MCP‐1 mRNA expression by fibroblasts in inflamed gingival tissues was examined byin situhybridization. We report here that in human chronic gingival inflammation the principal cell type expressing MCP‐1 in dense inflammatory infiltrates is the mononuclear phagocyte. The cells expressing MCP‐1 in moderately inflamed areas and in adjacent areas to inflammatory infiltrates are mononuclear phagocytes and fibroblasts, while in areas of fibroblastic hyperplasia, MCP‐1 positive cells are predominantly fibroblasts. We also demonstrate that in moderately and highly inflamed areas, the extent of MCP‐1 expression is greater than that in adjacent normal/mildly inflamed areas. As the degree of inflammation increased, there is also a concomitant increase in the number of mononuclear phagocytes. Furthermore, it is apparent that most of the infiltrating monocytes/macrophages are positive for MCP‐1 in vivo. Our finding that MCP‐1 expression is unambiguously identified in fibroblasts suggests that they can play a role in host defense by initiating the recruitment of monocytes. In addition, the expression of chemokines such as MCP‐1 may represent a mechanism for amplification of inflammatory signals in gingival inflammation.J Periodontol 1995; 66:80–88.
ISSN:1049-8885
DOI:10.1902/jop.1995.66.1.80
出版商:Wiley
年代:1995
数据来源: WILEY
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