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Soft Tissue Retraction With Osseointegrated Implants

Gingival retraction techniques for fixed prosthodontics have traditionally been advocated to increase the clarity and accuracy of impressions for die fabrication. When mechanical irritation or inflammation prevents a bloodless field, the use of cords with hemostatic agents may assist the operator to control hemorrhage.1,2 The concept of margin placement in accordance with biological width has resulted in well-established axioms for the prevention of gingival irritation and subsequent marginal recession of the dentogingival complex.3,4 The peri-implant soft tissues have been previously investigated and described in detail.5 Berglundh et al have subsequently demonstrated that the dentogingival fiber network extends from the alveolar crest parallel to the abutment interface, indicating that a bond exists between these two structures. These investigators determined that the connective tissue architecture surrounding the natural dentition is oriented in a different manner compared to that of the implant connective tissues.6  

Coronal to this connective tissue cuff, the epithelial attachment is hemidesmosomal. In comparison to that of the natural dentition, however, smaller cellular populations of desmosomes have been demonstrated in peri-implant tissues.7 The attachments of these soft tissues to a variety of materials should be of particular interest to clinicians. Hemidesmosomal attachments to alumina and titanium abutment materials are significantly greater than such attachments to dental porcelain and alloys.8 Consequently, the clinical management of peri-implant tissues associated with restorative procedures should be approached differently than similar procedures with the natural dentition. The recession of soft tissues around osseointegrated implants has been previously described as a model of inflammation with destruction of the connective tissues, and the subsequent invasion of the epithelium into this denuded area.9 Impression procedures for cement-retained implant-supported restorations may involve a transfer of the implant position following a series of healing and restorative abutment removal and placement sequences. The repeated movement of abutments may cause some degree of concern, as remodeling of the connective tissues may be affected by the inflammation produced by the impression procedure.10

Conventional crown and bridge procedures that use custom abutments, which are often fabricated of alloy materials, require gingival retraction by mechanical means. Although innocuous by themselves, hemostatic agents may sufficiently constrict microscopic blood vessels to precipitate inflammation. When retraction is necessary around the implants, a plain cord may provide a safe treatment alternative, since minimal soft tissue attachment and mechanical/chemical trauma may result in inflammation that causes recession.

The use of plain retraction cord may be suggested for retrieving cementation material to prevent excessive soft tissue manipulation and to facilitate ease of clean up. The extrapolation of elementary peri-implant manipulation principles to the clinical situation may be controversial. There is inherent concern, however, in treating these tissues in a similar manner when manipulating them in preparation for impression procedures. A careful, systematic approach is therefore recommended to avoid the potential detrimental effects of injudicious retraction methods for peri-implant soft tissues.

 

References:

  1. Harrison JD. Effect of retraction materials on the gingival sulcus epithelium. J Prosthet Dent 1961;11:514.
  2. Weir DJ, Williams BH. Clinical effectiveness of mechanical-chemical tissue displacement methods. J Prosthet Dent 1984;51(3):326-329.
  3. Ingber JS, Rose LF, Coslet JG. The "biologic width" - a concept in periodontics and restorative dentistry. Alpha Omegan 1977;70(3):62-65.
  4. Wilson RD, Maynard G. Intracrevicular restorative dentistry. Int J Periodont Rest Dent 1981;1(4):35-49.
  5. Waerhaug J. Anatomy, physiology, and pathology of the gingival pocket. Revue Belge de Medecine Dentaire1966;21(1):9-15.
  6. Berglundh T, Lindhe J, Ericsson I, et al. The soft tissue barrier at implants and teeth. Clin Oral Impl Res 1991;2(2):81-90.
  7. Carmichael RP, McCulloch CA, Zarb GA. Quantitative immunohistochemical analysis of keratins and desmoplakins in human gingiva and peri-implant mucosa. J Dent Res 1991;70(5):899-905.
  8. Abrahamsson et al. J Clin Periodontol 1998;25:721-727.
  9. Baker DL, Seymour GJ. The possible pathogenesis of gingival recession. A histological study of induced recession in the rat. J Clin Periodontol 1976;3(4):208-219.
  10. Abrahamsson I, Berglundh T, Lindhe J. The mucosal barrier following abutment dis/reconnection. An experimental study in dogs. J Clin Periodontol 1997;24(8)568-572.
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