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Immunohistochemical analysis of soft tissues in implants with healthy and peri‐implantitis condition, and aggressive periodontitis
Author(s) -
Bullon P.,
Fioroni M.,
Goteri G.,
Rubini C.,
Battino M.
Publication year - 2004
Publication title -
clinical oral implants research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.407
H-Index - 161
eISSN - 1600-0501
pISSN - 0905-7161
DOI - 10.1111/j.1600-0501.2004.01072.x
Subject(s) - periodontitis , peri implantitis , connective tissue , junctional epithelium , immunohistochemistry , medicine , cd34 , implant , soft tissue , aggressive periodontitis , pathology , osseointegration , dentistry , biology , surgery , stem cell , genetics
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.