From the many courses I attended at EuroPerio8, one thing is clear: There is no consensus on how to treat peri-implant mucositis and implantitis. Some speakers say that, lacking clear guidelines, we should maintain implants the same as natural teeth, and treat peri-implant mucositis and implantitis like we treat gingivitis and periodontitis. Others vehemently disagree with this approach. I will try to dissect the literature and report the findings.
According to a Journal of Clinical Periodontology article, peri-implant mucositis (PM) is “the presence of a plaque-related inflammatory soft tissue infiltrate without the concurrent loss of peri-implant bone tissue” and peri-implantitis “presents with inflammation in combination with bone loss.” (1) There are similarities and differences between periodontal and peri-implant diseases in regard to the host response and bacterial features. As the outcome of therapy of peri-implantitis is unpredictable, it is important to emphasize prevention. PM can progress into “peri-implantitis if left untreated, but may be reversible if adequately treated.” (1) Treating disease early is key.
One group examined the existing evidence in identifying risk indicators in the etiology of PM. (2) They found limited studies that provided data on risk indicators for the development of PM, with plaque biofilm accumulation at the site of the implant one of them. Smoking is considered an independent risk factor. Genetics, sex, maintenance visits, residual cement, and systemic diseases have limited or weak data to support their role as risk factors. (2)
Mechanical and chemical plaque control
Another group evaluated the efficacy of patient-administered protocols of mechanical plaque control and/or chemical plaque control in the management of PM. (3) Out of the 11 randomized and controlled clinical trials, not one reported incidence of peri-implantitis. One study reported resolution of PM in 38% of patients. The researchers concluded that “professionally and patient-administered mechanical plaque control alone should be considered the standard of care in the management of PM” for the prevention of peri-implantitis. (3) No specific recommendations or guidelines were rendered, as the reported control interventions in the studies were very varied. The efficacy of powered toothbrushes, triclosan-containing toothpaste, and adjunctive antiseptics, irrigation, and gels have not been established. The evidence on the efficacy of patient-administered inter-proximal cleaning is limited, and the adjunctive delivery of systemic antibiotics does not have supporting data. (3)
Another group focused on a different question: “In patients with [PM], what is the efficacy of professionally administered plaque removal (PARP) with adjunctive measures on changing signs of inflammation compared with PARP alone?” (4) They looked at bleeding on probing as the primary outcome, gingival index, and probing pocket depth reductions. The results were not better with adjunctive antiseptic, local or systemic antibiotic therapy, or with air abrasive devices over PARP alone. (4)
Controlling inflammation
Another paper considered the etiology of the peri-implant disease in the treatment options. They suggested controlling the inflammation and infection through mechanical debridement, localized and/or systemic antimicrobial therapy, and improved patient compliance with self-care. (5) If these measures do not work, it is suggested to look for signs of retained cement. Detoxification of the implant surface can be attempted by mechanical devices (e.g., air powder abrasives, lasers). Application of chemotherapeutic c agents such as tetracycline may also be employed. They conclude that many methods for detoxification have been used, but there is no standard protocol to date. Surgery is the last option suggested, with antibiotics. (5)
Risk factors
As there is so much debate and experts are still unsure about risk factors and proper prevention and treatment, one group of researchers suggest a model with risk factors for the incidence of peri-implant pathology based on multivariable analysis. (6) The variables shown to be risk factors by multivariable logistic regression analysis were: history of periodontitis, presence of bacterial plaque, presence of bleeding, bone level localized on the medium third of the implant, lack of prosthetic fit or non-optimal screw joint, metal-ceramic restorations, and the interaction between the presence of bacterial plaque and proximity of that implant to other teeth or implants. (6) Smoking did not directly influence the incidence of peri-implant pathology after being adjusted for the presence of other variables of interest.
The direction of ginigival fibers is key
According to one study, the health of peri-implant soft tissues is one of the most important critical aspects of osseointegration necessary for the long-term survival of dental implants. The peri-implant interface was revealed to be less effective than natural teeth in resisting bacterial assault because gingival fiber alignment and reduced vascular supply make it more susceptible to peri-implant disease and future bone loss. (7) One of the key findings was the direction of gingival fibers around implants as compared to natural teeth. In natural teeth the collagen fibers are in a perpendicular direction, from the cementum to the alveolar bone. In implants, the fibers run parallel, making them less of a barrier and easier to penetrate. This difference in fibers explains why bacteria can more easily penetrate the epithelial and connective tissue layer, increasing the susceptibility of the soft tissue to inflammation and infection.
Oral hygiene must be meticulous to be effective in preventing peri-implantitis disease progression. The authors concluded that there is a difference between peri-implant interface and natural teeth, and we need to be aware that the maintenance and recovery of soft tissues around implants is necessary to prevent peri-implantitis. (7)
A recent paper provides some insight in the proper way to maintain implants. (7) Both manual and powered brushes are effective, and should be used twice daily. Traditional dental floss and interdental brushes are recommended, with the width of the interdental space the deciding factor. Other methods, such as water floss, are options with sparse clinical data.
READ MORE | The debate rages on – triclosan/copolymer: debunking the myths
Regarding chlorhexidine (CHX), a study compared the effect of rinsing with 0.12% CHX mouth rinse to the use of the Pik Pocket Tip with 0.06% CHX. (12) The use of the Pik Pocket Tip reduced plaque scores more significantly, as well as the gingival, calculus and stain indices. No difference was found in bleeding with the rinse or the Pik Pocket Tip. (12)
As can be seen, there is some controversy in the literature. More studies are needed to provide concrete guidelines for clinical practice.
References
1. Derks J, Tomasi C. Peri-implant health and disease. A systematic review of current epidemiology. J Clin Periodontol. 2015;42(suppl 16):S158–S171. doi: 10.1111/jcpe.12334.
2. Renvert S, Polyzois I. Risk indicators for peri-implant mucositis: a systematic literature review. J Clin Periodontol. 2015;42(suppl 16):S172–S186. doi:10.1111/jcpe.12346.
3. Salvi GE, Ramseier CA. Efficacy of patient-administered mechanical and/or chemical plaque control protocols in the management of peri-implant mucositis. A systematic review. J Clin Periodontol. 2015;42 (suppl 16):S187–S201. doi:10.1111/jcpe.12321.
4. Schwarz F, Becker K, Sager M. Efficacy of professionally administered plaque removal with or without adjunctive measures for the treatment of peri-implant mucositis. A systematic review and meta-analysis. J Clin Periodontol. 2015;42(suppl 16):S202–S213. doi: 10.1111/jcpe.12349.
5. Hsu A, Kim JW. How to manage a patient with peri-implantitis. JCan Dent Assoc. 2014;79:e24.
6. de Araújo Nobre M, Mano Azul A , Rocha E, Malo P. Risk factors of peri-implant pathology. Eur J Oral Sci. 2015;123:131-9. doi: 10.1111/eos.12185.
7. Wang Y, Zhang Y, Miron RJ. Health, maintenance, and recovery of soft tissues around implants. [published online ahead of print April 15, 2015]. Clin Implant Dent Relat Res. doi: 10.1111/cid.12343.
8. Sreenivasan PK, Vered Y, Zini A, et al. A 6-month study of the effects of 0.3% triclosan/copolymer dentifrice on dental implants. J Clin Periodontol. 2011;38:33–42. doi: 10.1111/j.1600-051X.2010.01617.x.
9. Di Carlo F, Quaranta A, Di Alberti L, Ronconi LF, Quaranta M, Piattelli A. Influence of amine fluoride/stannous fluoride mouthwashes with and without chlorhexidine on secretion of proinflammatory molecules by peri-implant crevicular fluid cells. Minerva Stomatol. 2008;57:215–221, 221–5.
10. Ciancio SG, Lauciello F, Shibly O, Vitello M, Mather M. The effect of an antiseptic mouthrinse on implant maintenance: plaque and peri-implant gingival tissues. J Periodontol. 1995;66:962-5.
11. Al-Radha AS, Younes C, Diab BS, Jenkinson HF. Essential oils and zirconia dental implant materials. Int J Oral Maxillofac Implants. 2013;28:1497–505.
12. Felo A, Shibly O, Ciancio SG, Lauciello FR, Ho A. Effects of subgingival chlorhexidine irrigation on peri-implant maintenance. Am J Dent. 1997;10:107–10.
