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

被引:73
作者
Bullon, P
Fioroni, M
Goteri, G
Rubini, C
Battino, M
机构
[1] Univ Sevilla, Fac Odontol, Sch Dent, E-41009 Seville, Spain
[2] Univ Politecn Marche, Inst Anat & Pathol Histol, Ancona, Italy
[3] Univ Politecn Marche, Inst Biochem, Ancona, Italy
[4] Univ Politecn Marche, Sch Dent, Ancona, Italy
关键词
aggressive periodontitis; angiogenesis; apoptosis; dendritic cell; implant failure; lymphocyte; peri-implantitis;
D O I
10.1111/j.1600-0501.2004.01072.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
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.
引用
收藏
页码:553 / 559
页数:7
相关论文
共 36 条
  • [1] ALBREKTSSON T, 1994, PROCEEDINGS OF THE 1ST EUROPEAN WORKSHOP ON PERIODONTOLOGY, P365
  • [2] Histological characteristics of peri-implant mucosa around Branemark and single-crystal sapphire implants
    Arvidson, K
    Fartash, B
    Hilliges, M
    Kondell, PA
    [J]. CLINICAL ORAL IMPLANTS RESEARCH, 1996, 7 (01) : 1 - 10
  • [3] Dendritic cells and the control of immunity
    Banchereau, J
    Steinman, RM
    [J]. NATURE, 1998, 392 (6673) : 245 - 252
  • [4] Local and systemic TCR V gene expression in advanced periodontal disease
    Berglundh, T
    Liljenberg, B
    Tarkowski, A
    Lindhe, J
    [J]. JOURNAL OF CLINICAL PERIODONTOLOGY, 1998, 25 (02) : 125 - 133
  • [5] Booth V, 1998, J PERIODONTAL RES, V33, P491
  • [6] Long-term evaluation of non-submerged ITI implants .1. 8-year life table analysis of a prospective multi-center study with 2359 implants
    Buser, D
    MericskeStern, R
    Bernard, JP
    Behneke, A
    Behneke, N
    Hirt, HP
    Belser, UC
    Lang, NP
    [J]. CLINICAL ORAL IMPLANTS RESEARCH, 1997, 8 (03) : 161 - 172
  • [7] Cornelini R, 2001, INT J ORAL MAX IMPL, V16, P389
  • [8] Crawford J M, 1989, Reg Immunol, V2, P91
  • [9] De Smet E, 2001, INT J PERIODONT REST, V21, P381
  • [10] Immunohistochemistry of soft tissues surrounding late failures of Branemark implants
    Esposito, M
    Thomsen, P
    Molne, J
    Gretzer, C
    Ericson, LE
    Lekholm, U
    [J]. CLINICAL ORAL IMPLANTS RESEARCH, 1997, 8 (05) : 352 - 366