Immunohistochemical analysis of soft tissues in implants with healthy and peri‐implantitis condition, and aggressive periodontitis

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.

Regulation of p53 under hypoxic and inflammatory conditions in periodontium

“…Our results confirmed in part the results of Bullon et al (2004), as we could not show elevated p53 levels in tissue samples of periimplantitis compared to healthy periodontal sections. However, samples of chronic periodontitis revealed stronger immunoreactivity implicating different mechanisms in the pathogenesis of chronic and aggressive periodontitis as it has been suggested by recent investigations [38,39].…”

“…In contrast, Bullon et al have not detected an upregulation of p53 immunoreactivity comparing tissue sections of patients with periimplantitis and aggressive periodontitis with samples of healthy sites [36]. Their findings have been in line with those of Bulut et al who have evaluated different indicators for apoptosis (caspase-3, Bcl-2 and p53) in aggressive periodontitis [37].…”

Marginal bone and soft tissue behavior following platform switching abutment connection/disconnection– a dog model study

“…Morphometric measurements show, that in comparison to healthy condition, inflamed peri-implant sulcus epithelium exhibited areas of ulceration, had rete peg formations and contained numerous polymorphonuclear granulocytes, macrophages and leukocytes ). Animal and human histology studies show that there is an increase of inflammatory cell migration through junctional epithelium, in response to bacterial presence (Bullon et al 2004;Sanz et al 1991). These findings support the idea that junctional epithelium of BW around implants serves as a protective mechanism against bacterial invasion.…”

Long term clinical outcome of dental implants placed in a patient with aggressive periodontitis and Glucose-6-phosphate dehydrogenase (G6pd) deficiency

“…7,8 The similarity in the microbial flora responsible for aggressive periodontitis and periimplantitis supports the view that periodontal pathogens may be associated with periimplant infections and failing implants. 9 Glucose-6-phosphate dehydrogenase (G6pd) is the first and rate-limiting enzyme of the pentose phosphate pathway. It is indispensable to the maintenance of the cytosolic pool of NADPH and thus the cellular redox balance.…”