Immunohistochemical analysis of soft tissues in implants with healthy and peri‐implantitis condition, and aggressive periodontitis
Identifieur interne : 007A08 ( Main/Curation ); précédent : 007A07; suivant : 007A09Immunohistochemical analysis of soft tissues in implants with healthy and peri‐implantitis condition, and aggressive periodontitis
Auteurs : P. Bullon [Espagne] ; M. Fioroni [Italie] ; G. Goteri [Italie] ; C. Rubini [Italie] ; M. Battino [Italie]Source :
- Clinical Oral Implants Research [ 0905-7161 ] ; 2004-10.
Descripteurs français
- Wicri :
- topic : Analyse quantitative.
English descriptors
- KwdEn :
- Aggressive periodontitis, Agressive periodontitis gingiva, Antibody marker, Apoptosis, Basal, Basal epithelial cells, Basal layer, Biopsy specimens, Bone loss, Branemark implants, Bullon, Cd1a, Cd1a cell number, Cd1a cells, Cd1a mib1, Cinco casos, Clin, Clinical periodontology, Connective tissue, Dental implants, Dental school, Endothelial cells, Epithelial, Epithelial cells, Epithelium, European workshop, Factor viii, Fviii vegf bcl2, General status, Gingival, Gingival tissues, Growth factor, Healthy group, Healthy mucosa, Immature dendritic cells, Immunohistochemical, Immunohistochemical analysis, Immunohistochemical results, Impl, Implant, Implant data, Implants research, International journal, Junctional epithelium, Lamina propria, Lang, Langerhans, Langerhans cells, Late failures, Lesion, Load factors, Longitudinal studies, Lymphocyte, Mandibular edentulism, Marginal bone loss, Mib1, Mib1 index, Occlusal overload, Oral impl, Oral maxillofacial implants, Oral microbiology, Osseointegration, Osseointegration loss process, Parabasal, Parabasal layer, Parabasal layers, Periimplant, Periimplant mucosa, Periimplantitis, Periodontal, Periodontal disease, Periodontitis, Periodontitis agresiva, Periodontitis groups, Periodontitis patients, Periodontology, Plaque, Plaque accumulation, Plaque index, Positive cells, Quantitative analysis, Quantitative evaluation, Reliable treatment modality, Soft tissues, Squamous epithelium, Tres grupos, Universita politecnica delle marche, Vascular, Vascular proliferation, Vegf, Vessel density, Viii.
- Teeft :
- Aggressive periodontitis, Agressive periodontitis gingiva, Antibody marker, Apoptosis, Basal, Basal epithelial cells, Basal layer, Biopsy specimens, Bone loss, Branemark implants, Bullon, Cd1a, Cd1a cell number, Cd1a cells, Cd1a mib1, Cinco casos, Clin, Clinical periodontology, Connective tissue, Dental implants, Dental school, Endothelial cells, Epithelial, Epithelial cells, Epithelium, European workshop, Factor viii, Fviii vegf bcl2, General status, Gingival, Gingival tissues, Growth factor, Healthy group, Healthy mucosa, Immature dendritic cells, Immunohistochemical, Immunohistochemical analysis, Immunohistochemical results, Impl, Implant, Implant data, Implants research, International journal, Junctional epithelium, Lamina propria, Lang, Langerhans, Langerhans cells, Late failures, Lesion, Load factors, Longitudinal studies, Lymphocyte, Mandibular edentulism, Marginal bone loss, Mib1, Mib1 index, Occlusal overload, Oral impl, Oral maxillofacial implants, Oral microbiology, Osseointegration, Osseointegration loss process, Parabasal, Parabasal layer, Parabasal layers, Periimplant, Periimplant mucosa, Periimplantitis, Periodontal, Periodontal disease, Periodontitis, Periodontitis agresiva, Periodontitis groups, Periodontitis patients, Periodontology, Plaque, Plaque accumulation, Plaque index, Positive cells, Quantitative analysis, Quantitative evaluation, Reliable treatment modality, Soft tissues, Squamous epithelium, Tres grupos, Universita politecnica delle marche, Vascular, Vascular proliferation, Vegf, Vessel density, Viii.
Abstract
Abstract: Today, implant‐supported prostheses are widely accepted as a reliable treatment modality, but failures in longitudinal studies have been shown. In some cases, peri‐implantitis with a progressive periodontal bone loss takes place, and mechanical or load factors and biological or plaque‐induced lesions have been claimed as main etiologic factors. We compared five cases of peri‐implantitis, with five cases of healthy peri‐implant tissues and five cases of aggressive periodontitis in order to give new findings on the osseointegration loss process. Biopsy specimens from the peri‐implant tissues including oral (O), sulcular, and junctional epithelium and the underlying and supracrestal connective tissue, were taken in all cases for histological and immunohistochemical analysis. T lymphocytes were the most prominent cell in the peri‐implantitis (PG) and aggressive periodontitis (AG) groups, but not in the peri‐implant healthy group (HG). CD1a‐positive cells (Langerhans and immature dendritic cells) were observed more frequently in the O than in the sulcular–junctional (S–J) epithelium: they were located in the basal and parabasal layers, without any differences between the three groups. Vascular proliferation analysed by immunoreactivity for CD34, Factor VIII, and vascular endothelial growth factor was more prominent in the PG comparing with HG and AG in the S–J area. Apoptosis, analysed by bcl2 and p53 immunoreactivity, was similar in the three groups. In conclusion, we suggest that the osseointegration loss process is due to an inflammatory process similar to that observed in aggressive periodontitis according to the number of T lymphocytes, but not to the vascular proliferation.
Url:
DOI: 10.1111/j.1600-0501.2004.01072.x
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aggressive periodontitis</term>
<term>Agressive periodontitis gingiva</term>
<term>Antibody marker</term>
<term>Apoptosis</term>
<term>Basal</term>
<term>Basal epithelial cells</term>
<term>Basal layer</term>
<term>Biopsy specimens</term>
<term>Bone loss</term>
<term>Branemark implants</term>
<term>Bullon</term>
<term>Cd1a</term>
<term>Cd1a cell number</term>
<term>Cd1a cells</term>
<term>Cd1a mib1</term>
<term>Cinco casos</term>
<term>Clin</term>
<term>Clinical periodontology</term>
<term>Connective tissue</term>
<term>Dental implants</term>
<term>Dental school</term>
<term>Endothelial cells</term>
<term>Epithelial</term>
<term>Epithelial cells</term>
<term>Epithelium</term>
<term>European workshop</term>
<term>Factor viii</term>
<term>Fviii vegf bcl2</term>
<term>General status</term>
<term>Gingival</term>
<term>Gingival tissues</term>
<term>Growth factor</term>
<term>Healthy group</term>
<term>Healthy mucosa</term>
<term>Immature dendritic cells</term>
<term>Immunohistochemical</term>
<term>Immunohistochemical analysis</term>
<term>Immunohistochemical results</term>
<term>Impl</term>
<term>Implant</term>
<term>Implant data</term>
<term>Implants research</term>
<term>International journal</term>
<term>Junctional epithelium</term>
<term>Lamina propria</term>
<term>Lang</term>
<term>Langerhans</term>
<term>Langerhans cells</term>
<term>Late failures</term>
<term>Lesion</term>
<term>Load factors</term>
<term>Longitudinal studies</term>
<term>Lymphocyte</term>
<term>Mandibular edentulism</term>
<term>Marginal bone loss</term>
<term>Mib1</term>
<term>Mib1 index</term>
<term>Occlusal overload</term>
<term>Oral impl</term>
<term>Oral maxillofacial implants</term>
<term>Oral microbiology</term>
<term>Osseointegration</term>
<term>Osseointegration loss process</term>
<term>Parabasal</term>
<term>Parabasal layer</term>
<term>Parabasal layers</term>
<term>Periimplant</term>
<term>Periimplant mucosa</term>
<term>Periimplantitis</term>
<term>Periodontal</term>
<term>Periodontal disease</term>
<term>Periodontitis</term>
<term>Periodontitis agresiva</term>
<term>Periodontitis groups</term>
<term>Periodontitis patients</term>
<term>Periodontology</term>
<term>Plaque</term>
<term>Plaque accumulation</term>
<term>Plaque index</term>
<term>Positive cells</term>
<term>Quantitative analysis</term>
<term>Quantitative evaluation</term>
<term>Reliable treatment modality</term>
<term>Soft tissues</term>
<term>Squamous epithelium</term>
<term>Tres grupos</term>
<term>Universita politecnica delle marche</term>
<term>Vascular</term>
<term>Vascular proliferation</term>
<term>Vegf</term>
<term>Vessel density</term>
<term>Viii</term>
</keywords>
<keywords scheme="Teeft" xml:lang="en"><term>Aggressive periodontitis</term>
<term>Agressive periodontitis gingiva</term>
<term>Antibody marker</term>
<term>Apoptosis</term>
<term>Basal</term>
<term>Basal epithelial cells</term>
<term>Basal layer</term>
<term>Biopsy specimens</term>
<term>Bone loss</term>
<term>Branemark implants</term>
<term>Bullon</term>
<term>Cd1a</term>
<term>Cd1a cell number</term>
<term>Cd1a cells</term>
<term>Cd1a mib1</term>
<term>Cinco casos</term>
<term>Clin</term>
<term>Clinical periodontology</term>
<term>Connective tissue</term>
<term>Dental implants</term>
<term>Dental school</term>
<term>Endothelial cells</term>
<term>Epithelial</term>
<term>Epithelial cells</term>
<term>Epithelium</term>
<term>European workshop</term>
<term>Factor viii</term>
<term>Fviii vegf bcl2</term>
<term>General status</term>
<term>Gingival</term>
<term>Gingival tissues</term>
<term>Growth factor</term>
<term>Healthy group</term>
<term>Healthy mucosa</term>
<term>Immature dendritic cells</term>
<term>Immunohistochemical</term>
<term>Immunohistochemical analysis</term>
<term>Immunohistochemical results</term>
<term>Impl</term>
<term>Implant</term>
<term>Implant data</term>
<term>Implants research</term>
<term>International journal</term>
<term>Junctional epithelium</term>
<term>Lamina propria</term>
<term>Lang</term>
<term>Langerhans</term>
<term>Langerhans cells</term>
<term>Late failures</term>
<term>Lesion</term>
<term>Load factors</term>
<term>Longitudinal studies</term>
<term>Lymphocyte</term>
<term>Mandibular edentulism</term>
<term>Marginal bone loss</term>
<term>Mib1</term>
<term>Mib1 index</term>
<term>Occlusal overload</term>
<term>Oral impl</term>
<term>Oral maxillofacial implants</term>
<term>Oral microbiology</term>
<term>Osseointegration</term>
<term>Osseointegration loss process</term>
<term>Parabasal</term>
<term>Parabasal layer</term>
<term>Parabasal layers</term>
<term>Periimplant</term>
<term>Periimplant mucosa</term>
<term>Periimplantitis</term>
<term>Periodontal</term>
<term>Periodontal disease</term>
<term>Periodontitis</term>
<term>Periodontitis agresiva</term>
<term>Periodontitis groups</term>
<term>Periodontitis patients</term>
<term>Periodontology</term>
<term>Plaque</term>
<term>Plaque accumulation</term>
<term>Plaque index</term>
<term>Positive cells</term>
<term>Quantitative analysis</term>
<term>Quantitative evaluation</term>
<term>Reliable treatment modality</term>
<term>Soft tissues</term>
<term>Squamous epithelium</term>
<term>Tres grupos</term>
<term>Universita politecnica delle marche</term>
<term>Vascular</term>
<term>Vascular proliferation</term>
<term>Vegf</term>
<term>Vessel density</term>
<term>Viii</term>
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<front><div type="abstract">Abstract: Today, implant‐supported prostheses are widely accepted as a reliable treatment modality, but failures in longitudinal studies have been shown. In some cases, peri‐implantitis with a progressive periodontal bone loss takes place, and mechanical or load factors and biological or plaque‐induced lesions have been claimed as main etiologic factors. We compared five cases of peri‐implantitis, with five cases of healthy peri‐implant tissues and five cases of aggressive periodontitis in order to give new findings on the osseointegration loss process. Biopsy specimens from the peri‐implant tissues including oral (O), sulcular, and junctional epithelium and the underlying and supracrestal connective tissue, were taken in all cases for histological and immunohistochemical analysis. T lymphocytes were the most prominent cell in the peri‐implantitis (PG) and aggressive periodontitis (AG) groups, but not in the peri‐implant healthy group (HG). CD1a‐positive cells (Langerhans and immature dendritic cells) were observed more frequently in the O than in the sulcular–junctional (S–J) epithelium: they were located in the basal and parabasal layers, without any differences between the three groups. Vascular proliferation analysed by immunoreactivity for CD34, Factor VIII, and vascular endothelial growth factor was more prominent in the PG comparing with HG and AG in the S–J area. Apoptosis, analysed by bcl2 and p53 immunoreactivity, was similar in the three groups. In conclusion, we suggest that the osseointegration loss process is due to an inflammatory process similar to that observed in aggressive periodontitis according to the number of T lymphocytes, but not to the vascular proliferation.</div>
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