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Träfflista för sökning "WFRF:(Zitzmann Nicola 1967 ) ;pers:(Lindhe Jan 1935)"

Sökning: WFRF:(Zitzmann Nicola 1967 ) > Lindhe Jan 1935

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  • Berglundh, Tord, 1954, et al. (författare)
  • Spontaneous progression of ligature induced peri-implantitis at implants with different surface roughness: an experimental study in dogs.
  • 2007
  • Ingår i: Clinical oral implants research. - : Wiley. - 0905-7161 .- 1600-0501. ; 18:5, s. 655-61
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Peri-implantitis is associated with the presence of submarginal plaque, soft-tissue inflammation and advanced breakdown of the supporting bone. The progression of peri-implantitis following varying periods of continuing plaque accumulation has been studied in animal models. OBJECTIVE: The aim of the current experiment was to study the progression of peri-implantitis around implants with different surface roughness. MATERIAL AND METHODS: In five beagle dogs, three implants with either a sandblasted acid-etched surface (SLA) or a polished surface (P) were installed bilaterally in the edentulous premolar regions. After 3 months on a plaque control regimen, experimental peri-implantitis was induced by ligature placement and plaque accumulation was allowed to progress until about 40% of the height of the supporting bone had been lost. After this 4-month period, ligatures were removed and plaque accumulation was continued for an additional 5 months. Radiographs of all implant sites were obtained before and after 'active' experimental peri-implantitis as well as at the end of the experiment. Biopsies were harvested and the tissue samples were prepared for light microscopy. The sections were used for histometric and morphometric examinations. RESULTS: The radiographic examinations indicated that similar amounts of bone loss occurred at SLA and P sites during the active breakdown period, while the progression of bone loss was larger at SLA than at polished sites following ligature removal. The histological examination revealed that both bone loss and the size of the inflammatory lesion in the connective tissue were larger in SLA than in polished implant sites. The area of plaque was also larger at implants with an SLA surface than at implants with a polished surface. CONCLUSION: It is suggested that the progression of peri-implantitis, if left untreated, is more pronounced at implants with a moderately rough surface than at implants with a polished surface.
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  • Zitzmann, Nicola, 1967, et al. (författare)
  • Host response to microbial challenge following resective/non-resective periodontal therapy.
  • 2005
  • Ingår i: Journal of clinical periodontology. - 0303-6979. ; 32:11, s. 1175-80
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The host response to microbial challenge depends on the recruitment of homing leucocytes and may be related to the experience to infectious insults over years. PURPOSE: The aim of this study was to investigate the soft tissue reactions to de novo plaque formation at sites treated with either open flap debridement or with the use of resective means during periodontal therapy. MATERIAL AND METHODS: Fifteen patients, who had been treated for periodontal disease (severe generalized chronic periodontitis), participated in the study. Surgical therapy was performed using either gingivectomy (GV) or open flap debridement (OFD) procedures in a split mouth design. After 6 months of healing (day 0), two gingival biopsies were obtained, one from the GV- and one from the OFD-treated sites. The experimental gingivitis model was applied and plaque accumulation was allowed for 3 weeks. New biopsies were obtained from the remaining quadrants on day 21 of plaque formation. The biopsies were snap frozen and prepared for immunohistochemical analysis. RESULTS: Following 3 weeks of plaque accumulation, the size of the lesion in OFD sites was more than twice as large than that in GV sites (0.42 versus 0.19 mm2). In the GV units, the lesion was characterized by almost similar proportions of T cells (CD3+, 6.0%) and B cells (CD19+, 6.6%), while the ICT in OFD sites was dominated by B cells (13.8%). During the 3-week period of plaque formation the increase in cell densities of T and B cells was three times larger in OFD than in GV sites. The proportion of ELAM-1 (CD62+ cells) decreased in GV (-0.4%) and increased in OFD (0.9%) sites. CONCLUSIONS: The host response that occurred in the gingival sites treated with OFD was more pronounced than the reaction that under similar experimental conditions took place in the regenerated gingiva at sites treated by resective means.
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  • Zitzmann, Nicola, 1967, et al. (författare)
  • Inflammatory lesions in the gingiva following resective/non-resective periodontal therapy.
  • 2005
  • Ingår i: Journal of clinical periodontology. - 0303-6979. ; 32:2, s. 139-46
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Findings from previous experiments have revealed that inflammatory cell infiltrates may remain in the gingiva following clinically successful non-surgical periodontal therapy. PURPOSE: To investigate the presence of inflammatory lesions in the gingiva following a periodontal treatment procedure that included either soft-tissue resection [gingivectomy (GV)] or non-resective open-flap debridement (OFD). MATERIAL AND METHODS: Fifteen patients with advanced generalized chronic periodontitis were recruited. Following oral hygiene instruction and supragingival debridement, one tooth site in each quadrant (non-molar, probing pocket depth>5 mm, bleeding on probing(+) and >50% bone loss) was selected and a soft-tissue biopsy was obtained and prepared for immunohistochemical analysis. Using a split-mouth design, two quadrants were randomly selected for periodontal therapy including GV, while the two remaining quadrants were exposed to non-resective OFD procedure. Six months after completion of surgical treatment, a new set of biopsies was obtained from GV and OFD sites. RESULTS: The inflammatory lesions residing in the gingival biopsies obtained prior to surgical therapy were 1.33-1.41 mm(2) large and contained similar proportions of CD19(+)- (B-cells, 15%), CD3(+)- (T-cells, 7%) and elastase(+)- (polymorphonuclear cells, 2%) cells in the two treatment groups. The corresponding lesions identified in the soft-tissue specimens obtained after 6 months of healing were twice as large at OFD as at GV sites (0.19 versus 0.08 mm(2), p=0.002). The densities of CD19(+)- and elastase(+)-cells in these lesions were significantly greater at OFD than at GV sites. CONCLUSION: The findings of the present study indicate that surgical therapy including soft-tissue resection results in regenerated gingival units that contain smaller lesions with lower densities of immunocompetent cells when compared with the lesions remaining in sites treated by non-resective means.
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  • Zitzmann, Nicola, 1967, et al. (författare)
  • Spontaneous progression of experimentally induced periimplantitis.
  • 2004
  • Ingår i: Journal of clinical periodontology. - 0303-6979. ; 31:10, s. 845-9
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Periimplantitis represents an inflammatory condition that is associated with the presence of a submarginal biofilm and with advanced breakdown of soft and mineralized tissues surrounding endosseous implants. Animal models have been used to describe mechanisms involved in the pathogenesis and treatment of the soft and hard tissue lesions of periimplantitis. OBJECTIVE: The aim of the present experiment was to study the presence and progression of inflammatory lesions in tissues surrounding implants exposed to "experimental periimplantitis". MATERIAL AND METHODS: Five Labrador dogs were used. In each dog, 2 or 3 implants were placed in both the left and right edentulous premolar regions of the mandible. Abutment connection was performed 4 months later and a plaque control regimen was initiated and maintained for 5 months. "Experimental periimplantitis" was subsequently induced by ligature placement and plaque accumulation was allowed to progress until about 40% of the height of the supporting bone had been lost. The ligatures were removed, but plaque formation was allowed to continue for an additional 12 months. Radiographs of all implant sites were obtained before and after active "experimental periimplantitis" as well as at the end of the experiment. Biopsies were harvested from the implant sites in 3 of the dogs. The tissue samples were prepared for light microscopy and the sections were used for histometric and morphometric examinations. RESULTS: One implant was lost during the first 2 months of "experimental periimplantitis" and two implants were lost during the 12 months that followed ligature removal. The radiographic examination indicated that varying amounts of additional bone loss occurred in the majority of the implant sites also following ligature removal. The mucosa of all implant sites harbored inflammatory lesions that extended apically of the pocket epithelium. The lesions were separated from the marginal bone by a zone of apparently normal connective tissue. CONCLUSION: A remission of the destructive inflammatory lesion in the periimplant tissues was seen in some sites following ligature removal, but in the majority of sites additional loss of supporting bone occurred.
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