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Peri-implant tissues inflammation: do we have the means to prevent it?

Andrea Pilloni

Key words: peri-implantitis • peri-implant mucositis • risk factors

IntroductionThe introductory sentence of almost every scientifi c article on the subjects of implants, and peri-implant tissues, emphasises how dental implants have revolutionised the replacement of missing teeth, enhancing the comfort of the patient. Indeed, dental implants are a predictably successful treatment with a survival rate of 95.7% still in function after 10-14 years.1 But, can implants last forever? And why should this not be possible when the clinician creates the conditions required to encourage the best healthy maintainable state by the dental professional and, above all, by the patient? On the other hand, once the implant is inserted and prosthetically restored, following a comprehensive plan in relation to the adjacent teeth, are anatomical structures and occlusion still at risk? The answer has, for a long period of time, reported to be “yes!”

Plaque accumulation can cause mucositis, just as it can cause gingivitis in the experimentally induced infl ammation.2-4 (Figures 1-3). It is interesting to note the data observing the higher quantity4 and frequency of bacteria in plaque accumulated around natural teeth, compared to dental implants.5

Peri-implant mucositis, as the infl ammation is limited to the soft tissues, can be reversible4 but if not treated it may progress to peri-implantitis, i.e. peri-implant bone loss. The treatment of this infl ammation has been thoroughly discussed and it has been found that peri-implantitis has no predictably successful treatment: whereas peri-implant mucositis can be treated. But not one adjunctive treatment is superior to others, or to the mechanical treatment itself. Presently, even though treatable, there is no other protocol for peri-implant tissue maintenance, other than the CIST protocol of Lang et al 6 that recognizes the two conditions arising from the lack of peri-implant bone loss, based on the probing depth above or below 4 mm, as two different treatment protocol conditions.

As clinicians, we are all responsible for its prevention, until further studies on peri-implant infl ammation treatments are published. Prevention prior to the implant being placed means creating conditions enabling the patient and the dental hygienist to remove the plaque. The aim of this article is to

give three different perspectives: from the patient level, site level and the implant surrounding soft tissues level.

PatientWhen deciding on the suitability of a patient for implants, consideration of the following factors which infl uence the long term health of peri-implant tissues are essential.

AgeThe risk for peri-implantitis development increases with age.7,8

Systemic conditionsCurrently it appears that an association with peri-implantitis can be found only with cardiovascular diseases but not with other well known diseases such as diabetes mellitus, osteoporosis, lung disease, rheumatoid arthritis, depression and smoking.7

Periodontal health Periodontally healthy patients present a lower risk from peri-implantitis - the incidence is currently 1.8% peri-implantitis in periodontally healthy patients9 compared to 37% peri-implantitis in periodontally compromised patients.8 A recent study reports the risk of developing peri-implantitis is fourteen times higher in patients treated for aggressive periodontal disease, compared to periodontally healthy patients.10 Similarly, Roccuzzo et al 201011 report higher levels of peri-implantitis in severe and moderate cases of chronic periodontitis with both groups being at a higher risk, compared to periodontally healthy patients. Even though periodontal diseases are treatable, the history of such disease represents a risk factor for peri-implantitis.7,12,13 In addition, patients with a history of periodontitis, and following supportive periodontal therapy continue to develop periodontal pockets, are at higher risk than patients in that same group who show stability in the maintenance programme.14

Oral hygiene levelPoor oral hygiene is a risk factor for peri-implantitis.15

Adherence to SPT Supportive periodontal therapy is of crucial importance for the

AbstractPeri-implant infl ammation is becoming an increasingly important challenge for clinicians, as the management of these infl ammatory complications remains unclear. This article aims to highlight the most recent data on some issues that are thought to be important in the prevention of peri-implant infl ammation and the long-term maintenance of healthy tissues.

29Volume 53 No 1 of 6 January 2014

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maintenance of peri-implant tissue health to a point that it overcomes the importance of a history of peridontitis when it comes to the risk of peri-implantitis.16 Poor compliance or adherence to supportive periodontal therapy is a risk factor for the development of peri-implantitis.13,15,17 On the other hand, it has been reported that the insertion of the dental implant enhances the adherence of the patient to SPT and that it is possible to obtain an excellent degree of compliance to this programme.18

Site Periodontal disease develops in a periodontal pocket and there are no reasons to consider it differently to the counterpart situation at the implant level. From CIST protocol, the treatment applied in a peri-implant pocket of 4-5 mm in depth (Fig. 4) requires an adjunctive antiseptic treatment besides the mechanical removal of plaque,6 but no adjunctive therapy is superior to others or mechanical treatment alone.19 This rationale leads to the prevention of a peri-implant “sulcus” deeper than 3 mm. Deeper pockets, more than 4 mm, even at an healthy stage, provide an appropriate environment for the growth of anaerobic bacteria. This then poses the question as to how this physiological bone loss around implants can be prevented?

Theories related to the physiology of peri-implant bone loss in the first year of function are related to the establishment of biological width (2mm of junctional epithelial and 1-1.5 mm of connective tissue, as reported by Berglundh & Lindhe 20 and to the inflammatory response of the tissues to the presence of bacteria at the abutment-implant junction.21

Recently it is speculated that this initial peri-implant bone reaction can be a response to a foreign body.22 This assumption can be supported by the in vitro results of Quabius et al., 2012 observing an enhanced expression of IL-8 when the human blood is in contact with dental implants.23 Similarly, but in vivo results, Salvi et al report levels of MMP-8 activity at the implant level higher at all the time-points, even in healthy conditions, compared to the tooth level during the development of 21 days experimental mucositis and gingivitis. Both biomarkers are involved in periodontal tissue destruction during inflammation. In addition, Salvi et al., 2012 4 concluded that the peri-implant tissue response is stronger to plaque accumulation than periodontal tissues. Once again we need to ask whether it could be that we are indeed dealing with a permanent inflammatory or forein body reaction to the dental implant and that could this really be the reason why, even when there is less quantity of plaque and percentages of periopathogens, the peri-implant tissues respond more strongly? We currently do not have the answer to these questions but, meanwhile, platform- switching and the insertion of the implants at the level of, or 1 mm above, the alveolar crest can reduce the dimensions of biological width mainly for the epithelial component.24 Furthermore, the most recent data on bone loss at the first year in function report figures of 0.02 mm25 compared to previously accepted physiological bone loss of 1.5 mm.26

Cases of regrowth of bone around dental implants following the first year in function, contradict all this theory and indicate the need for further examination and epidemiological evaluation of similar patients.

Soft tissue Keratinized mucosa as a surrounding dental and peri-implant soft tissue presents two components: the width (distance from the free gingival margin to the mucogingival junction) and the thickness (evaluated as thick biotype when it is thicker or equal to 2 mm) and thin biotype when is thinner than 1.5 mm.27 Both components have been the centre of controversial discussions on the importance that the presence of a thick biotype of a minimum width of 2 mm might have on the oral hygiene and prevention of the inflammation of tissues with subsequent prevention of bone loss.28(Fig. 5)

Biotype: The most recent data comes from a study on the importance of biotype and SPT on the peri-implant bone loss during the first year in function.25 The statistically significant lower bone loss in the group of thick biotype that followed SPT compared to thin biotype not following SPT (0.09mm vs 0.78mm), permitted the authors to conclude that the

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References1. Roos-Jansåker AM. Long time follow up of implant therapy and treatment of peri- implantitis. Swed Dent J Suppl. 2007; (188): 7-66.

2. Pontoriero R, Tonelli MP, Carnevale G et al. Experimentally induced peri-implant mucositis. A clinical study in humans. Clin Oral Implants Res. 1994; 5(4): 254-9.

3. Zitzmann NU, Berglundh T, Marinello CP et al. Experimental peri-implant mucositis in man. J Clin Periodontol. 2001; 28(6): 517-23.

4. Salvi GE, Aglietta M, Eick S et al. Reversibility of experimental peri-implant mucositis compared with experimental gingivitis in humans. Clin Oral Implants Res. 2012; 23(2):182-90.

5. Cortelli SC, Cortelli JR, Romeiro RL et al. Frequency of periodontal pathogens in equivalent peri-implant and periodontal clinical statuses. Arch Oral Biol. 2013; 58(1): 67- 74. doi: 10.1016/j.archoralbio.2012.09.004. Epub 2012 Nov 3

6. Lang NP, Berglundh T, Heitz- Mayfi eld LJ et al. Consensus statements and recommended clinical procedures regarding implant serviva and complications. Int J Oral Maxillofac Implants. 2004; 19 Suppl: 150-4.

7. Renvert S, Aghazadeh A, Hallström H et al. Factors related to peri-implantitis - a

About the author: Professor Pilloni is the Chairman and Director of Postgraduate Programme, Section of Periodontics, School of Dentistry and Dental Hygiene, Sapienza, University of Rome. He is also a clinical instructor and lecturer in the department. Prof Pilloni is a member of the Editorial Board of Dental Health.

Address for correspondence: Prof. Andrea Pilloni, Dipartimento di Scienze OdontostomatologicheSapienza, Università di Roma, Via Caserta 6, Rome Italy 00161Email: andrea.pilloni@uniroma1.it

presence of a thin biotype could be considered a risk factor for additional peri-implant bone loss.

Width: the latest meta-analysis and review on the correlation between presence of wider or equal KT to 2 mm and infl ammation parameters at implant level, concluded that indeed the presence of a minimum of 1-2mm of KT decreases plaque accumulation and the risk for marginal recession and attachment loss. Interestingly, this amount of keratinized mucosa was seen to be associated with greater probing depth but a tendency to less bleeding on probing, even though this differences did not reach statistical signifi cance.28

ConclusionIt can be concluded that even though recent studies focussed on important factors in peri-implant infl ammation prevention, they all raise the alarm that further research is needed.

retrospective study. Clin Oral Implants Res. 2013 Jun 17. doi: 10.1111/clr.12208. [Epub ahead of print]

8. Marrone A, Lasserre J, Bercy P, et al. Prevalence and risk factors for peri-implant disease in Belgian adults. Clin Oral Implants Res. 2013; 24(8): 934-40. doi: 10.1111/j.1600-0501.2012.02476.x. Epub 2012 May 3.

9. Buser D, Janner SF, Wittneben JG et al. 10-year survival and success rates of 511 titanium implants with a sandblasted and acid-etched surface: a retrospective study in 303 partially edentulous patients. Clin Implant Dent Relat Res. 2012; 14(6): 839-51.

10. Swierkot K, Lottholz P, Flores-de-Jacoby L et al. Mucositis, peri-implantitis, implant success, and survival of implants in patients with treated generalized aggressive periodontitis: 3- to 16-year results of a prospective long-term cohort study. J Periodontol. 2012; 83(10): 1213-25. Epub 2012 Jan 20.

11. Roccuzzo M, Bonino F, Aglietta M et al. Ten-year results of a three arms prospective cohort study on implants in periodontally compromised patients. Part 2: clinical results. Clin Oral Implants Res. 2012; 23(4): 389-95. doi: 10.1111/j.1600-0501.2011.02309.x. Epub 2011 Sep 28.

12. De Boever AL, Quirynen M, Coucke W et al. Clinical and radiographic study of implant treatment outcome in periodontally susceptible and non-susceptible patients: a prospective long-term study. Clin Oral Implants Res. 2009; 20(12):1341-50. doi: 10.1111/j.1600- 0501.2009.01750.x. Epub 2009 Sep 30.

13. Koldsland OC, Scheie AA, Aass AM. Prevalence of peri-implantitis related to severity of the disease with different degrees of bone loss. J Periodontol. 2010; 81(2): 231-8. doi: 10.1902/jop.2009.090269.

14. Pjetursson BE, Helbling C, Weber HP et al. Peri-implantitis susceptibility as it relates to periodontal therapy and supportive care. Clin Oral Implants Res. 2012; 23(7): 888-94. doi: 10.1111/j.1600-0501.2012.02474.x. Epub 2012 Apr 24.

15. Rinke S, Ohl S, Ziebolz D et al. Prevalence of periimplant disease in partially edentulous patients: a practice-based cross-sectional study. Clin Oral Implants Res. 2011; 22(8): 826-33. doi: 10.1111/j.1600-0501.2010.02061.x. Epub 2010 Dec 28.

16. Cho-Yan Lee J, Mattheos N, Nixon KC et al. Residual periodontal pockets are a risk indicator for peri-implantitis in patients treated for periodontitis. Clin Oral Implants Res. 2012; 23(3): 325-33. doi: 10.1111/j.1600-0501.2011.02264.x. Epub 2011 Aug 5.

17. Costa FO, Takenaka-Martinez S, Cota LO et al. Peri-implant disease in subjects with and without preventive maintenance: a 5-year follow-up. J Clin Periodontol. 2012; 39(2):173-81. doi: 10.1111/j.1600-051X.2011.01819.x. Epub 2011 Nov 23.

18. Cardaropoli D, Gaveglio L. Supportive periodontal therapy and dental implants: an analysis of patients’ compliance. Clin Oral Implants Res. 2012; 23(12):1385-8. doi: 10.1111/j.1600-0501.2011.02316.x. Epub 2011 Oct 21.

19. Esposito M, Maghaireh H, Grusovin MG et al. Interventions for replacing missing teeth: management of soft tissues for dental implants. Cochrane Database Syst Rev. 2012 Feb 15;2:CD006697. doi: 10.1002/14651858.CD006697.pub2. Review.

20. Berglundh T, Lindhe J. Dimension of the periimplant mucosa. Biological width revisited. J Clin Periodontol. 1996; 23(10):971-3.

21. Schwarz F, Alcoforado G, Nelson K et al. Impact of implant-abutment connection, positioning of the machined collar/microgap, and platform switching on crestal bone level changes. Camlog Foundation Consensus Report. Clin Oral Implants Res. 2013 Oct 21. doi: 10.1111/clr.12269. [Epub ahead of print]

22. Albrektsson T, Dahlin C, Jemt T et al. Is marginal bone loss around oral implants the result of a provoked foreign body reaction? Int J Oral Maxillofac Implants. 2013; 28(2):494-502. doi: 10.11607/jomi.3081. Clin Implant Dent Relat Res. 2013 Sep 4. doi: 10.1111/cid.12142. [Epub ahead of print]

23. Quabius ES, Ossenkop L, Harder S et al. Dental implants stimulate expression of Interleukin-8 and its receptor in human blood--an in vitro approach. J Biomed Mater Res B Appl Biomater. 2012; 100(5):1283-8.

24. Cochran DL, Mau LP, Higginbottom FL et al. Soft and hard tissue histologic dimensions around dental implants in the canine restored with smaller-diameter abutments: a paradigm shift in peri-implant biology. J Periodontol. 2013 Mar 1. [Epub ahead of print]

25. Aguirre-Zorzano LA, Vallejo-Aisa FJ, Estefanía-Fresco R. Supportive periodontal therapy and periodontal biotype as prognostic factors in implants placed in patients with a history of periodontitis. Med Oral Patol Oral Cir Bucal. 2013; 18(5):e786-92.

26. Albrektsson T, Zarb GA. Current interpretations of the osseointegrated response: clinical signifi cance. Int J Prosthodont. 1993; 6(2): 95-105.

27. Claffey N, Shanley D. Relationship of gingival thickness and bleeding to loss of probing attachment in shallow sites following nonsurgical periodontal therapy. J Clin Periodontol. 1986; 13(7): 654-7.

28. Lin GH, Chan HL, Wang HL. The signifi cance of keratinized mucosa on implant health: A systematic review. J Periodontol. 2013; 84(12):1755-67. doi: 10.1902/jop.2013.120688. Epub 2013 Mar 1.2013

Acknowledgements:The authors declare lack of direct or indirect interests in the products or information listed in the paper. This study was not fi nancially supported.

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