Nonsurgical Treatment of Peri-implant Mucositis

By determining the etiology of the lesion and initiating appropriate treatment, oral health professionals can reverse the disease process and prevent bone loss

Implant gingivitis, known to clinicians as peri-implant mucositis, is a reversible inflammatory process in the soft tissue surrounding an osseointegrated dental implant without the loss of marginal bone beyond normal resorption.1 Like gingivitis around natural teeth, the etiology of this disease is related to biofilm accumulation in the soft tissues surrounding the implant, combined with a susceptible host response.2

Animal and human studies have confirmed that peri-implant mucositis is comparable to gingivitis around teeth, both from histological and clinical perspectives.3 Pontoriero et al studied 20 partially edentulous patients who received implant therapy. After six months of supervised oral hygiene, the patients were asked to stop all oral hygiene practices for three weeks — after which plaque control was resumed. When the implants were compared with natural teeth, no differences in plaque index, gingival index or pocket depths were noted.4 Another study looked at the differences in the inflammatory response between teeth and implants after three weeks of suspended oral hygiene, followed by a return to optimal plaque control. Biopsies of the connective tissue taken around each group revealed similar increases in B and T lymphocyte volumes.5

Although these earlier studies demonstrated that the magnitude and severity of tissue inflammation around an implant experiencing peri-implant mucositis are similar to the dento-gingival complex, more recent studies suggest the inflammatory process around implants may be more severe and harder to reverse with treatment than is seen with natural dentition.

Using protocols similar to the studies previously discussed, Salvi et al looked at experimentally induced mucositis around implants that was treated through nonsurgical mechanical debridement. Unlike earlier studies, this research demonstrated that, compared to gingiva around teeth, the bacterial challenge presented by the cessation of oral hygiene elicited a greater inflammatory response in the peri-implant mucosa. Although treatment helped reduce inflammation, reversibility did not extend to pre-experimental levels, as denoted by inflammatory biomarkers (IL-1B and MMP-8) in the crevicular fluid.6

A study by Schierano et al showed that reversibility of tissue inflammation to pre-experimental levels was possible after oral hygiene care was suspended and reinstituted, but it took three times as long as with natural teeth (69 days versus 21 days).7 In summary, more recent studies examining peri-implant mucositis have shown that, compared to treating gingivitis in natural teeth, the degree and severity of inflammation are greater, and true reversibility takes longer and is harder to establish when treating implants.

PREVALENCE

Peri-implant mucositis is common among patients not enrolled in regular periodontal maintenance programs. Among implant patients observed over a period of 9 to 14 years, 48% experienced peri-implant mucositis.8 A similar study showed that prevalence could be cut to 20% when patients were actively involved in a supportive periodontal therapy program.9 That said, because peri-implant mucositis is widely prevalent, progresses quickly, and is harder to resolve than gingivitis around teeth, an aggressive nonsurgical approach is warranted following diagnosis. In addition, the patient should be placed on a strict maintenance protocol.

ANTI-INFECTIVE THERAPY

When treating patients with peri-implant mucositis lesions, anti-infective therapy in the form of mechanical debridement — with or without local/systemic antibiotics — has been shown to be effective in animal and human studies. Trejo et al showed that mechanical debridement, with or without adjunctive chlorhexidine, resolved mucosal inflammation in monkeys affected by peri-implant mucositis on both clinical and histological levels.10 In human studies in which successful treatment was defined as implant survival with no mean pocket depths greater than 5 mm and no further bone loss, Mombelli et al reported that 84% of the 25 patients treated with nonsurgical mechanical debridement and an adjunctive tetracycline fiber had successful treatment outcomes 12 months post-therapy.11 A systematic review of the literature by Renvert and colleagues showed that nonsurgical treatment of peri-implant mucositis lesions was effective, and the adjunct use of antimicrobial rinses in conjunction with debridement procedures yielded even better results.12 Another study by Salvi et al reported that 76% of patients with implants affected by mucositis lesions had successful resolution at 12 months following nonsurgical mechanical debridement in conjunction with 1 mg minocycline spheres.13 Although the Mombelli study and Salvi study each showed a significant reduction in bleeding upon probing and pocket depths, complete resolution of the lesion was not achieved, with 41%11 and 44%13 of the sites (respectively) still showing bleeding upon probing.

Peri-implant mucositis is common among patients not enrolled in regular periodontal maintenance programs

Many studies have questioned the need for adjunctive therapy beyond mechanical debridement when treating peri-implant mucositis lesions nonsurgically. Recently, case reports have shown that decontamination of the mucositis lesion can occur without mechanical debridement. Pini-Prato and colleagues used a concentrated aqueous mixture of hydroxybenzenesulfonic and hydroxymethoxybenzenesulfonic acids and sulfuric acid, and injected this solution into the sulcus of the affected implants. After 30 seconds, the solution was removed and the area was irrigated. Preliminary results showed resolution of the lesions and significant areas of recession.14


key takeaways

  • Compared to gingivitis in tissues proximate to natural dentition, studies of peri-implant mucositis show that the degree and severity of inflammation are greater and disease reversal more difficult when found near implants.
  • The incidence of peri-implant disease can be significantly reduced when patients are involved in a supportive periodontal therapy program.9
  • Because peri-implant mucositis can progress quickly, and become more difficult to resolve than gingivitis, an aggressive nonsurgical approach is warranted.
  • Among the most important determinants of successful outcomes when using nonsurgical mechanical debridement to treat peri-implant lesions are the initial depth of the lesions, amount of bone loss associated with the lesions, and the ability to fully debride implant surfaces.15

KEY DETERMINANTS

FIGURE 1A and FIGURE 1B. Periodontal lesions are limited to the soft tissue without bone loss. In this case, complete implant surface decontamination is possible.

FIGURE 1A and FIGURE 1B. Periodontal lesions are limited to the soft tissue without bone loss. In this case, complete implant surface decontamination is possible.

It has been well demonstrated in the literature that among the most important determinants of a successful outcome when using nonsurgical mechanical debridement to treat a peri-implant lesion are the initial depth of the lesion, amount of bone-loss associated with the lesion, and the ability to fully debride the implant surface.15 Nonsurgical therapy is most effective when the lesion is confined solely to the soft tissue, without bone loss present. A consensus has not been reached in regard to nonsurgical therapy when bone loss has occurred. Some authors suggest that nonsurgical interventions can be effective when bone loss is present, but only when it is less than 25% of the implant length.16

FIGURE 2A and FIGURE 2B. After four weeks (A) and 12 months (B) of treatment, the patient from Figure 1 still exhibits gingival recession.

FIGURE 2A and FIGURE 2B. After four weeks (A) and 12 months (B) of treatment, the patient from Figure 1 still exhibits gingival recession.

When a patient presents with peri-implant mucositis, the current treatment by this author is to determine the etiology. If plaque biofilm is determined to be the cause, a diagnosis is made according to the peri-implantitis lesion classification system proposed by Froum and Rosen.17 If the lesion is confined to the soft tissue without bone loss (Figures 1A and 1B), and complete implant surface decontamination is possible, the area is anesthetized and mechanical debridement is performed with implant-appropriate curets. Multiple doses of 1 mg minocycline spheres are placed on the mesial and distal of the implant lesion. The patient is instructed to use a compounded mouthrinse consisting of nystatin/metronidazole and amoxicillin (if not allergic) in the amount of 3 ml, three times a day for 30 seconds. For large inflammatory lesions, the patient is prescribed a course of systemic antibiotics consisting of 500 mg metronidazole and 500 mg amoxicillin twice a day for 10 days (substitute ciprofloxacin 500 mg for penicillin allergies). Follow-up is performed at two-week and four-week intervals.

FIGURE 3A and FIGURE 3B. These images show the periodontal status of a patient with peri-implant mucositis after undergoing nonsurgical therapy for four weeks. Note the debris (cement) on the mesial of the implant. If cement is still present and/or inflammation has not resolved with nonsurgical treatment, surgical intervention may be necessary.

FIGURE 3A and FIGURE 3B. These images show the periodontal status of a patient with peri-implant mucositis after undergoing nonsurgical therapy for four weeks. Note the debris (cement) on the mesial of the implant. If cement is still present and/or inflammation has not resolved with nonsurgical treatment, surgical intervention may be necessary.

This protocol has proven successful in resolving inflammation, although there are exceptions. As seen in Figures 2A and 2B, gingival recession is present at both the four-week and 12-month intervals. Prior to receiving treatment, patients should be advised about this possible sequelae. After four weeks of nonsurgical therapy, if cement is still detected (Figures 3A and 3B) and/or the inflammation has not resolved, surgical intervention may be necessary in the form of flap surgery with or without regenerative therapy. If the dentist is not familiar with this treatment, a referral to a specialist is recommended.

CONCLUSION

Peri-implant mucositis poses a significant threat to successful implant therapy. While research shows that it is similar to gingivitis in natural teeth, studies suggest the effects of peri-implant mucositis can result in greater inflammation, which, in turn, is harder to treat. By determining the etiology of the lesion and developing an effective nonsurgical treatment plan, oral health professionals can help reverse the disease process and prevent bone loss.

References

  1. Berglundh T, Lindhe J, Marinello C, Ericsson I, Liljenberg B. Soft tissue reaction to de novo plaque formation on implants and teeth. An experimental study in the dog. Clin Oral Implants Res.1992;3:1–8.
  2. Ericsson I, Berglundh T, Marinello C, Liljenberg B, Lindhe J. Long-standing plaque and gingivitis at implants and teeth in the dog. Clin Oral Implants Res.1992;3:99–103.
  3. Salcetti JM, Moriarty JD, Cooper LF, et al. The clinical, microbial, and host response characteristics of the failing implant. Int J Oral Maxillofac Implants.1997;12:32–42.
  4. Pontoriero R, Tonelli MP, Carnevale G, Mombelli A, Nyman SR, Lang NP. Experimentally induced peri-implant mucositis. A clinical study in humans. Clin Oral Implants Res.1994;5:254–259.
  5. Zitzmann NU, Berglundh, Marinello CP, Lindhe J. Experimental peri-implant mucositis in man. J Clin Periodontol. 2001;28:517–523.
  6. Salvi GE, Agiletta M, Sculean A, Lang NP, Ramseier CA. Reversibility of experimental peri-implant mucositis compared with experimental gingivitis in humans. Clin Oral Implants Res. 2012;23:182–190.
  7. Schierano G, Pejrone G, Brusco P, et al. TNF-a, TGF-b2, and IL-1B levels in gingival crevicular fluids before and after de novo plaque accumulation. J Clin Periodontol. 2008;35:532–538.
  8. Roos-Jansåker 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;33:283–289.
  9. Rodrigo D, Martin C, Sanz M. Biologic complications and peri-implant clinical and radiographic changes at immediately placed dental implants. A prospective 5-year cohort study. Clin Oral Implants Res. 2012;23:1224–1231.
  10. Trejo PM, Bonaventura G, Weng D, Caffesse RG, Bragger U, Lang NP. Effect of mechanical and antiseptic therapy on peri-implant mucositis: an experimental study in monkeys. Clin Oral Implants Res. 2006;17:294–304.
  11. Mombelli A, Feloutzis A, Brägger U, Lang NP. Treatment of peri-implantitis by local delivery of tetracycline. Clinical, microbiological and radiological results. Clin Oral Implants Res. 2001;12:287–294.
  12. Renvert S, Roos-Jansåker AM, Claffey N. Non-surgical treatment of peri-implant mucositis and peri-implantitis: a literature review. J Clin Periodontol. 2008;35(8 Suppl):305–315.
  13. Salvi GE, Persson GR, Heitz-Mayfield LJ, Frei M, Lang NP. Adjunctive local antibiotic therapy in the treatment of peri-implantitis II: clinical and radiographic outcomes. Clin Oral Implants Res. 2007;18:281–285.
  14. Pini-Prato G, Magnani C, Rotundo R. Nonsurgical treatment of peri-implantitis using the biofilm decontamination approach: a case report study. Int J Periodontics Restorative Dent. 2016;36(3):383–391.
  15. Froum SJ, Froum SH, Rosen PS. A regenerative approach to the successful treatment of peri-implantitis: A consecutive series of 170 implants in 100 patients with 2- to 10-year follow-up. Int J Periodontics Restorative Dent. 2015;35(6):857–863.
  16. Schwarz F, Bieling K, Bonsmann M, Latz T, Becker J. Nonsurgical treatment of moderate and advanced periimplantitis lesions: a controlled clinical study. Clin Oral Investig. 2006;10:279–288.
  17. Froum SJ, Rosen PS. A proposed classification for peri-implantitis. Int J Periodontics Restorative Dent. 2012;32:533–540.

From Decisions in Dentistry. July 2016;1(09):18,21–22.

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