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Peri-implant Inflammation Defined by the Implant-Abutment Interface

N. Broggini1,5, L.M. McManus1,2, J.S. Hermann1,3, R. Medina4, R.K. Schenk5, D. Buser5, and D.L. Cochran1,*

1 Departments of Periodontics and
2 Pathology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA;
3 Division of Periodontics and Implant Dentistry, Stuttgart Continuing Education Center, German Dental Association, Stuttgart, Germany;
4 Department of Dental Research, Universidad Autonoma de Coahuila Facultad de Odontologia, Torreon, Mexico; and
5 Department of Oral Surgery and Stomatology, School of Dental Medicine, University of Bern, Switzerland


Figure 1
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Figure 1. Implant design and placement, histomorphometric study area, and histology. (A) At the time of initial surgery, implants were positioned so that the implant-abutment interface was either supracrestal, crestal, or subcrestal to the alveolar bone, i.e., 1 mm coronal to, at, or 1 mm apical to the alveolar bone crest, respectively. Three months later, abutments (outlined in a dashed line) were connected to implants. After 3 additional mos, specimens were derived for histomorphometric analyses. (B) Sequential histological (test) fields of apico-coronal peri-implant soft tissue were digitally captured; morphometric assessment of peri-implant tissue was confined to connective tissue immediately adjacent to the implant surface from gingival epithelium to alveolar bone. All non-vascular interstitial cells were assessed and designated as either neutrophils or mononuclear cells. For the latter, lymphocytes, plasma cells, monocytes, and macrophages were collectively considered as a single population of cells. (C) Photomicrographs of representative soft tissues immediately adjacent to the implant-abutment interface. Although neutrophils are abundant in the specimen with crestal or subcrestal placement, these cells were infrequent in the supracrestal specimen. Toluidine blue, basic fuchsin stain. A = abutment; AB = alveolar bone; BC = bone crest; CT = connective tissue; GE = gingival epithelium; IAI = implant-abutment interface; R = rough portion of implant (SLA surface); S = smooth-machined collar of implant.

 

Figure 2
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Figure 2. Effect of the implant-abutment interface position on the distribution of peri-implant inflammatory cells. Histomorphometric quantitation of neutrophils and mononuclear cells at specific locations relative to the original alveolar bone were averaged for a given implant type in each animal. These results were then used to calculate the group mean (± SEM; n = 5). (A) Total inflammatory cells. (B) Neutrophils. (C) Mononuclear cells. * = significant differences between crestal and subcrestal implants, # = significant differences between crestal and supracrestal implants, and o = significant differences between subcrestal and supracrestal implants (p < 0.05).

 

Figure 3
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Figure 3. Relationship between inflammatory cells below the original bone crest and bone loss. For a given animal, results from duplicate samples were averaged.

 





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