| 1. |
|
|
| 2. |
|
|
| 3. |
- Berglundh, Tord, 1954, et al.
(författare)
-
Are peri-implantitis lesions different from periodontitis lesions?
- 2011
-
Ingår i: Journal of clinical periodontology. - 1600-051X. ; 38 Suppl 11, s. 188-202
-
Forskningsöversikt (refereegranskat)abstract
- Aim:To compare histopathological characteristics of peri-implantitis and periodontitis lesions. METHODS: A search was conducted on publications up to July 2010. Studies carried out on human biopsy material and animal experiments were considered. RESULTS: While comprehensive information exists regarding histopathological characteristics of human periodontitis lesions, few studies evaluated peri-implantitis lesions in human biopsy material. Experimental peri-implantitis lesions were evaluated in 10 studies and three of the studies included comparisons to experimental periodontitis. Human biopsy material: the apical extension of the inflammatory cell infiltrate (ICT) was more pronounced in peri-implantitis than in periodontitis and was in most cases located apical of the pocket epithelium. Plasma cells and lymphocytes dominated among cells in both types of lesions, whereas neutrophil granulocytes and macrophages occurred in larger proportions in peri-implantitis. Experimental studies: placement of ligatures together with plaque formation resulted in loss of supporting tissues and large ICTs around implants and teeth. Following ligature removal, a "self-limiting" process occurred in the tissues around teeth with a connective tissue capsule that separated the ICT from bone, while in peri-implant tissues the ICT extended to the bone crest. CONCLUSION: Despite similarities regarding clinical features and aetiology of peri-implantitis and periodontitis, critical histopathological differences exist between the two lesions
|
|
| 4. |
|
|
| 5. |
- 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.
|
|
| 6. |
- Donati, Mauro, 1966, et al.
(författare)
-
B-1a cells and plasma cells in periodontitis lesions.
- 2009
-
Ingår i: Journal of periodontal research. - : Wiley. - 1600-0765 .- 0022-3484. ; 44:5, s. 683-8
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND OBJECTIVE: Host response mechanisms in periodontal tissues are complex and involve numerous systems of interactions between cells. The B-cell lineage seems to predominate in chronic periodontitis lesions. The aim of the present investigation was to study the correlation between inflammatory cells and some functional markers in gingival lesions obtained from subjects with severe chronic periodontitis. MATERIAL AND METHODS: Thirty-eight Caucasian subjects volunteered to take part in the study. A gingival biopsy from one randomly selected diseased proximal site (probing pocket depth > 6 mm and bleeding on probing positive) was obtained from each patient. Immunohistochemical preparation was used to identify inflammatory cells and functional markers. Correlations between the different percentages of cell markers were analyzed by pairwise correlation. RESULTS: B cells (B-1a and B-2 cells) occurred in larger proportions than T cells and plasma cells. A statistically significant correlation was found between the percentage of B-1a cells and plasma cells and between all B lymphocytes and plasma cells. About 60% of B lymphocytes exhibited autoreactive features. CONCLUSION: It is suggested that B-1a cells constitute a significant part of the host response in periodontitis lesions and that plasma cells may develop from both B-2 and B-1a cells.
|
|
| 7. |
- Donati, Mauro, 1966, et al.
(författare)
-
B-1a cells in experimental gingivitis in humans.
- 2009
-
Ingår i: Journal of periodontology. - : Wiley. - 0022-3492 .- 1943-3670. ; 80:7, s. 1141-5
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Although previous studies revealed the presence of autoreactive B cells (B-1a cells) in periodontitis lesions, no evidence was provided for an active role of such cells in the host response to microbial challenge. The aim of the present investigation was to study the reaction of B-1a cells to de novo plaque formation in subjects who were treated for severe chronic periodontitis. METHODS: Fifteen white subjects with generalized, severe chronic periodontitis volunteered. Surgical periodontal therapy was performed in all quadrants of each subject after a period of infection control. After 6 months of healing (baseline), two gingival biopsies were harvested from each patient (probing depth <4 mm and no bleeding on probing; healed sites). The experimental gingivitis model was applied, and plaque accumulation was allowed for 3 weeks. Two additional biopsies were collected and prepared for immunohistochemical analysis on day 21. RESULTS: The biopsies retrieved after 3 weeks of plaque accumulation contained larger proportions of CD19+ and CD5+ cells (B-1a cells) than biopsies representing baseline (healed sites) (7.38% +/- 2.80% versus 5.96% +/- 2.48%). The tissue fraction of cells carrying the markers for CD3 (T cells), CD19 (B cells), and Bcl2 (apoptosis-associated marker) were significantly larger in tissue samples collected after 3 weeks of plaque accumulation than in specimens from baseline (healed sites). CONCLUSION: Autoreactive B cells (B-1a cells) are involved in the host response to microbial challenge in subjects with chronic periodontitis.
|
|
| 8. |
- Jepsen, Sören, et al.
(författare)
-
Primary prevention of peri-implantitis: Managing peri-implant mucositis.
- 2015
-
Ingår i: Journal of clinical periodontology. - : Wiley. - 1600-051X .- 0303-6979. ; 42 Suppl 16, s. S152-7
-
Forskningsöversikt (refereegranskat)abstract
- Over the past decades, the placement of dental implants has become a routine procedure in the oral rehabilitation of fully and partially edentulous patients. However, the number of patients/implants affected by peri-implant diseases is increasing. As there are - in contrast to periodontitis - at present no established and predictable concepts for the treatment of peri-implantitis, primary prevention is of key importance. The management of peri-implant mucositis is considered as a preventive measure for the onset of peri-implantitis. Therefore, the remit of this working group was to assess the prevalence of peri-implant diseases, as well as risks for peri-implant mucositis and to evaluate measures for the management of peri-implant mucositis.
|
|
| 9. |
- Zitzmann, Nicola, 1967, et al.
(författare)
-
Definition and prevalence of peri-implant diseases.
- 2008
-
Ingår i: Journal of clinical periodontology. - 1600-051X. ; 35:8 Suppl, s. 286-91
-
Forskningsöversikt (refereegranskat)abstract
- OBJECTIVES: The aim of the current review was to describe the prevalence of peri-implant diseases including peri-implant mucositis and peri-implantitis. MATERIAL AND METHODS: A MEDLINE search (PubMed) until December 2007 was conducted and different keywords related to the prevalence of peri-implant diseases were used. Cross-sectional and longitudinal studies including > or =50 implant-treated subjects exhibiting a function time of > or =5 years were considered. RESULTS AND CONCLUSION: The current review revealed that only a few studies provided data on the prevalence of peri-implant diseases. Cross-sectional studies on implant-treated subjects are rare and data from only two study samples were available. Peri-implant mucositis occurred in approximately 80% of the subjects and in 50% of the implants. Peri-implantitis was found in 28% and > or =56% of subjects and in 12% and 43% of implant sites.
|
|
| 10. |
- 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.
|
|
