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Surgical anti-infective mechanical therapy for peri-implantitis: A clinical report with a 12-month follow-up Posted on Monday, April 27, 2009 |
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According to previous studies, bacterial infection plays the most important role in the late failures of dental implants. Peri-implantitis has been described as a site-specific infection that causes soft tissue inflammation and bone loss around osseointegrated implants that have performed masticatory functions. To reduce the number of pathogenic species and improve the clinical parameters (that is, probing depth, bleeding on probing, and suppuration) around dental implants, several anti-infective therapies have been developed for peri-implantitis. However, recent reviews have not identified sufficient evidence to support an ideal anti-infective protocol for this disease. This article presents a case of advanced peri-implantitis that was treated with a single surgical anti-infective mechanical therapy. A follow-up visit 12 months post-treatment showed improved clinical features. Received: July 18, 2008 Accepted: October 1, 2008 Osseointegrated titanium implants are used routinely to rehabilitate totally and partially edentulous patients. Successful long-term results have been reported in the literature; however, as demand for dental implants increases, early and late complications have increased as well.1,2 Early failures have been attributed to surgical trauma, inadequate bone quality and quantity, lack of primary stability, and premature loading during the healing period.3-6 Late failures, which may not be detectable for many years, have been attributed to biomechanical overload, peri-implantitis, or a combination of both.3-6 Peri-implantitis is a site-specific infectious disease that causes an inflammatory process in soft tissues and bone loss around an osseointegrated implant in function.7 Previous studies have demonstrated that the microbiota related to peri-implantitis resemble those associated with periodontitis, with high levels of pathogenic species, including Prevotella intermedia, Porphyromonas gingivalis, Tanerella forsythia, and Treponema denticola.8-11 Anti-infective therapies for peri-implantitis have been developed to reduce both the probing depth (PD) measurement and the number of pathogens and to improve the clinical signs of inflammation, such as bleeding on probing and suppuration.12-15 Surgical and nonsurgical mechanical anti-infective procedures (frequently in combination with topical and/or systemic antimicrobials and/or regenerative techniques) have been described in the literature.12-15 However, data regarding treating peri-implantitis by using surgical anti-infective mechanical procedures alone are limited.11 This case report investigated the effect of using surgical anti-infective mechanical therapy alone for the treatment of advanced peri-implantitis. Case report The patient was a 54-year-old man; he was systemically healthy, did not smoke, and was not taking any medications (such as anti-inflammatory and antibiotics) or using local antimicrobial agents. The patient was totally edentulous in both jaws and his dental history revealed tooth loss due to periodontitis. The The first clinical peri-implant examination revealed severe signs of inflammation. The peri-implant soft tissues were characterized by redness, friability, and pain. The patient’s oral hygiene was poor, with marked plaque and calculus accumulating around the implants and the prosthesis (Fig. 1). Although the patient claimed to brush the implants daily, he was not removing plaque effectively due to pain and the prosthesis design, which presented no room for toothbrush access.
The prosthesis was removed (Fig. 2) and a periodontal probe was used to evaluate visible plaque index (PI) (the presence of plaque along the mucosal/gingival margin), marginal bleeding (the presence of bleeding recorded by running a probe along the soft tissue margin); bleeding on probing (BOP) (that is, bleeding up to 15 seconds after gentle probing); suppuration (SUP), either spontaneous or as the result of probing; PD (the distance between the mucosal margin and the bottom of the sulcus/pocket); and marginal recession (the distance between the abutments and the mucosal margin (in mm)) at six sites on each implant.16
For each implant, the number of sites with visible plaque, marginal bleeding, BOP, and SUP was computed, together with the mean values of PD and marginal recession. Periapical radiographs showed generalized horizontal peri-implant bone resorption. Radiographic bone loss was more pronounced in the central implant. All implants had probing depths of 5 mm or more, in addition to BOP and SUP associated with radiographic bone loss involving five or more threads of the implant. Based on these factors, peri-implantitis was diagnosed for all implants. Treatment Initially, the patient was instructed to perform a brushing technique that utilized dental floss and conventional and interdental toothbrushes. Supramucosal removal of plaque and calculus was performed. Intra-sulcular incisions made under local anesthesia (2% lidocaine with 1:100,000 epinephrine) completed a flap that extended horizontally beyond the most posterior implants. Buccal and lingual full-thickness flaps were dissected. Granulation tissue was removed as necessary to expose the implant threads and bone defect; at that point, it was confirmed that all implants had one-wall or horizontal bone defects (Fig. 3). The implant surface was scaled using plastic curettes (Implacare, Hu-Friedy Co, Chicago, IL; 800.483.7433) and decontaminated with an abrasive sodium carbonate air-powder system (Jet Sonic, Gnatus, Ribeirao Preto, SP, Brazil; 55.16.2102.5000) (Fig. 4). The flap was placed in its original position and stabilized with interrupted sutures (Fig. 5). ![]() ![]() Chlorhexidine gluconate (0.12%) mouthwash was prescribed twice a day for one week and analgesics were recommended to control postoperative discomfort. The sutures were removed after 10 days. A maintenance care program was performed once every four months for one year; at that time, supra-gingival intervention (supragingival plaque removal and peri-implant hygiene re-instruction) was performed. The 12-month clinical outcomes are presented in Tables 1 and 2. Improved clinical features were observed at the 12-month post-treatment evaluation (Fig. 6). This treatment protocol had previously been approved by the Institutional Committee of Ethics in Dental Research,
![]() ![]() Discussion The relationship between biofilm accumulation and inflammatory processes surrounding oral implants has been documented, with the literature recognizing specific pathogenic species as the etiological factor of peri-implantitis.8-11 Various mechanical and chemical techniques have been suggested for removing peri-implant biofilm, reducing the number of pathogens, and improving the clinical profile around diseased implants.12-15,17-20 An increasing number of studies have proposed local and/or systemic antimicrobials as an adjunct to nonsurgical mechanical debridement of the implant surface.18-20 Surgical strategies also have been associated frequently with antimicrobial therapies and/or regenerative procedures.8,21,22 The present case demonstrated a positive outcome 12 months after peri-implantitis was treated by using only a surgical anti-infective mechanical therapy. A 2005 article by Karring et al reported no clinical benefits six months after treating peri-implantitis with single mechanical non-surgical therapy.23 Because bacterial adherence increases in the micro-irregularities and the threads of dental implants, open debridement was chosen in the present case to improve access to the infected implant surfaces. Initially, the major deposits of calculus and biofilm were removed with plastic curettes. The tips of the curettes that currently are available for implant debridement are too large to reach the deepest parts of the threads; as a result, abrasive sodium carbonate air-powder was applied to remove the most adhered biofilm. In vitro studies have supported the importance of the use of specific instruments (such as plastic curettes and abrasive air-powder) to debride implants and minimize surface roughness.24,25 It has been demonstrated that both plastic curettes and abrasive air-powder are effective for implant decontamination without causing severe implant topographical changes or damaging fibroblast attachments.24-27 Inappropriate use of abrasive air-powder (for example, using high pressure air-spray or incorrect angulation of the tip) may result in subcutaneous emphysema due to air in the interstices of connective tissue.28,29 Although subcutaneous emphysema was not observed in the present case—and there are few reports in the literature concerning the possibility of serious lesions appearing after air-powder abrasive application—it is important to be careful when applying an air-powder abrasive system to the surgical site. As described above, regenerative therapies (where the ultimate goal is the regeneration of lost bone tissue) can be applied in conjunction with anti-infective procedures to treat peri-implantitis.12-15,22 However, the type of bone defect will indicate whether a regenerative procedure is appropriate. Regeneration techniques are recommended primarily for three- or four-wall intrabony defects, to increase bone support and sometimes prevent further thread exposure. The horizontal or one-wall bone defects observed in the present case would jeopardize the success of regenerative therapy. Surgical anti-infective mechanical therapy remained the best option for this case. At the 12-month follow-up, levels of bleeding, SUP, and PD were reduced for all implants (see Tables 1 and 2); however, marginal recession had been induced (Fig. 6). Marginal soft tissue recession can expose the implant surface. The exposed metal from the implant can compromise the esthetics of the implant-supported prostheses, especially in the A 2007 study by Romeo et al observed that implantoplasty (modifying surface roughness with polishing) had a positive influence on both clinical parameters (that is, PD, BOP, and SUP) and survival rates of rough-surfaced implants affected by peri-implantitis.21,30 Implantoplasty could have been used in the present case to improve the hygiene of the exposed threads. Maximo et al utilized a single surgical anti-infective mechanical therapy for treating peri-implantitis and reported clinical and microbiological benefits after a short-term evaluation of three months.11 However, to date, no clinical trials have been published offering long-term assessments of access flap surgery alone for treating peri-implantitis. It also is important to note that there is a risk of re-infection due to deficient implant toothbrushing and the fact that the oral sites (tongue, teeth, mucosa) may act as reservoir for the pathogenic species. The long-term success of any peri-implant treatment strategy requires a program of periodic maintenance, including supragingival plaque removal and reinstruction in proper hygiene. Summary Several methods for the treatment of peri-implantitis have been proposed; however, there is still insufficient evidence to support an ideal universal therapy for peri-implant diseases. The present case report indicated that surgical anti-infective mechanical therapy was effective for treating peri-implantitis, with clinical features improved at 12 months post-treatment. Further evaluations will be essential to determine whether, and to what extent, these initial improvements of surgical mechanical anti-infective therapy can be sustained. Author information Dr. Santos is a master's student, Department of Periodontics, Dental Research Division, References 1. Astrand P, Engquist B, Anzen B, Bergendal T, Hallman M, Karlsson U, Kvint S, Lysell L, Rundcranz T. A three-year follow-up report of a comparative study of ITI dental implants and Branemark system implants in the treatment of the partially edentulous 2. Roos-Jansaker AM, Lindahl C, Renvert H, Renvert S. Nine- to fourteen-year follow-up of implant treatment. Part 1: Implant loss and associations to various factors. J Clin Periodontol 2006;33(4):283-289. 3. Esposito M, Hirch J-M, Lekholm U, Thomsen P. Biological factors contributing to failures of osseointegrated oral implants. (II). Etiopathogenesis. Eur J Oral Sci 1998;106(3):721-764. 4. Tonetti MS. Risk factors for osseodisintegration. Periodontol 2000 1998;17:55-62. 5. Berglundh T, Persson L, Klinge B. 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