Journal of ISSN: 2373-4345JDHODT

Dental Health, Oral Disorders & Therapy
Opinion
Volume 4 Issue 5 - 2016
The Microbiological Diagnosis Of The Peri-Implant Disease: Can It Really Have A Practical Significance?
Nicola Alberto Valente*
Department of Periodontics and Endodontics, State University of New York at Buffalo, USA
Received: March 12, 2015 | Published: July 05, 2016
*Corresponding author: Nicola Alberto Valente, Department of Periodontics and Endodontics, State University of New York at Buffalo, SUNY at Buffalo, 3435 Main St., Buffalo NY 14214, USA, Tel: 393385932069; Email:
Citation: Valente NA (2016) The Microbiological Diagnosis Of The Peri-Implant Disease: Can It Really Have A Practical Significance?. J Dent Health Oral Disord Ther 4(5): 00127. 10.15406/jdhodt.2016.04.00127

Opinion

The peri-implant disease, like periodontal disease, is supported by a bacterial load that is at the base of both its onset and, above all, of its progression. For a long time, we have been wondering about the similarity of the peri-implant mucositis with gingivitis and peri-implantitis with periodontitis. If clear and obvious are the anatomical and histological differences, rather less obvious it is the similarity on a microbiological level [1,2].

The most credited theory until recent times, and in many ways even today, is that the microflora that supports the peri-implant disease is exactly the same as that responsible for periodontal disease. To give strength to this theory, several studies conducted between the years 90 and 2000 have revealed the presence, in the peri-implant sulci of human subjects with peri-implatitis and animal models with induced peri-implantitis, of species normally present in the diseased periodontal sulcus: Porphyromonas gingivalis, Fusobacterium nucleatum, Tannerella forsythia, Treponema denticola and various species of prevotellaceae [3-13]. In addition to these findings, many studies analyzing the microflora of peri-implant crevice in fully edentulous subjects noted the almost total, or total, absence of those bacteria commonly found in the periodontal crevice, thus reinforcing the theory of the close similarity of the two environments and the bacterial reservoir role of natural teeth [14-16].

From a conceptual point of view this theory is useful to explain the importance of a correct periodontal diagnosis before starting any implant rehabilitation plan, is well known, in fact, that the presence or a history of periodontitis are indicators of risk for the onset of peri-implantitis. However, the same theory is at odds with the evidence that the peri-implant and periodontal crevices are two completely different environments and, as such, should favor or impede the development of different bacterial species or at least they should have more differentiated bacterial compositions. In fact, it is known that the promoters of bacterial adhesion, namely the formation of biofilms, are, in the first instance, the so-called van der Waals forces, repulsive or attractive forces between molecules, weaker than the bonds that form in more advanced biofilms but fundamental in the adhesion of pioneers or early colonizers. These adhesion forces are strictly dependent on the surface free energy (SFE) of the substrate on which are formed. Microorganisms with high free energy will adhere to surfaces with high SFE and vice versa. Enamel and titanium, in this case, have different SFE, 0.088 ± 0.009 J m-2 and 0.051 ± 0.001 J m-2, respectively, so they should elicit the adhesion of different bacterial populations [17,18].

In this regard, a study by Leonhardt et al. [5], analyzing the bacterial composition of periodontal and peri-implant sulci in disease and in health, had found that, if in healthy conditions the two different environments had an overlapping microflora, in sulci around implants affected by peri-implantitis was found a presence of staphylococci, enterics and yeasts with almost the same frequency of periodontopathogens, indicating a substantial difference in the compositions of the two bacterial crevices [5]. What is the difference between Leonhardt et al. study and the majority of modern studies that indicate, instead, a complete similarity between the microbial composition around teeth and implants? The study by Leonhardt et al. [5] uses an old-fashioned technique, bacterial culture, which, however, has the advantage of being “open-ended”. However, the biggest drawbacks of culturing methods are the long time required and the uncultivability of numerous species.

The most modern techniques of PCR and DNA-DNA hybridization have the considerable advantage of requiring very short time, however, they are "targeted" techniques, that is, the bacteria that will be analyzed are pre-selected by choosing a certain number of DNA probes. This is the reason why all of the studies using these techniques have a strong bias due to the fact that knowledge of the crevices in terms of bacterial composition derives from the periodontal literature, therefore the analysis of peri-implant sulcus is, a priori, directed towards the search of bacteria commonly found around the teeth.

In very recent years new bacterial analysis techniques have been developed, known as metagenomics, which uses 16S rRNA sequencing, and that overcome the limits of both the cultivation and molecular methods. The metagenomic analysis is in fact both fast and "open ended". With this advancement in the microbiological field we arrived at the concept of "microbiome” intended as all the species that inhabit a certain environment in their genetic diversity and, as a result of this discovery, the human oral microbiome database (HOMD) project has been developed, with the discovery of 619 taxa arranged in 13 phyla, 54% of which has been officially named, 14% are unnamed but cultivated, the remaining 32% are categorized only as uncultivated phylotypes [19].

The, so far few, studies using these modern metagenomics methods seem to now direct towards the affirmation of a theory of bacterial diversity of the peri-implant sulcus from the periodontal one [20-23]. However, can these informations be useful in practical terms in the everyday clinical practice? Can the awareness that the bacteria around implants are different from those around natural teeth change something in our therapeutic strategies?

Surely the time is not yet ripe to answer these question with certainty, more and more detailed and complex studies may someday lead us to find a microbiological trend that is most frequently associated with the onset of peri-implant disease, thus guaranteeing an early diagnosis and more effective preventive measures. For now, we remain of the view that, although convinced that the microflora of implants and natural teeth are distinct, the host response, as in periodontal disease, certainly plays a very important role in peri-implantitis.23 Patients with a history of aggressive periodontitis, can develop forms of severe peri-implantitis, not much for the bacterial population that characterizes their oral microbiome, as for the genetic characteristics that characterize these patients (phagocyte abnormalities, hyperresponsive macrophage phenotype, elevated levels of PGE2 and IL-1, tissue destruction inconsistent with microbial deposit, etc.) [24,25]. Finally, whatever the bacterial flora, the prevention of peri-implant disease cannot be separated from the treatment of the pre-existing periodontal disease, and from a correct maintenance program after the implant rehabilitation [26,27].

References

  1. Carcuac O, Berglundh T (2014) Composition of human peri-implantitis and periodontitis lesions. J Dent Res 93(11): 1083-1088.
  2. Emecen Huja P, Eubank TD, Shapiro V, Yildiz V, Tatakis DN, et al. (2013) Peri-implant versus periodontal wound healing. J Clin Periodontol 40(8): 816-824.
  3. Mombelli A, van Oosten MA, Schurch E, Land NP (1987) The microbiota associated with successful or failing osseointegrated titanium implants. Oral Microbiol Immunol 2(4): 145-151.
  4. Augthun M, Conrads G (1997) Microbial Findings of Deep Peri-implant Bone Defects. Int J Oral Maxillofac Implants 12(1): 106-112.
  5. Leonhardt A , Renvert S, Dahlén G (1999) Microbial findings at failing implants. Clin Oral Implants Res 10(5): 339-345.
  6. Albertini M, Lopez Cerero L, O'Sullivan MG, Chereguini CF, Ballesta S, et al. (2014) Assessment of periodontal and opportunistic flora in patients with peri-implantitis. Clin Oral Implants Res 26(8): 937-941.
  7. Botero JE, Gonzalez AM, Mercado RA, Olave G, Contreras A (2005) Subgingival microbiota in peri-implant mucosa lesions and adjacent teeth in partially edentulous patients. J Periodontol 76(9): 1490-1495.
  8. Salvi GE, Furst MM, Lang NP, Persson GR (2008) One-year bacterial colonization patterns of Staphylococcus aureus and other bacteria at implants and adjacent teeth. Clin Oral Implants Res 19(3): 242-248.
  9. Furst MM, Salvi GE, Lang NP, Persson GR (2007) Bacterial colonization immediately after installation on oral titanium implants. Clin Oral Implants Res 18(4): 501-508.
  10. Hickey JS, O'Neal RB, Scheidt MJ, Strong SL, Turgeon D et al. (1991) Microbiologic characterization of ligature-induced peri-implantitis in the microswine model. J Periodontol 62(9): 548-543.
  11. Hanisch O, Cortella CA, Boskovic MM, James RA, Slots J, et al. (1997) Experimental peri-implant tissue breakdown around hydroxyapatite- coated implants. J Periodontol 68(1): 59-66.
  12. Charalampakis G, Abrahamsson I, Carcuac O, Dahlen G, Berglundh T (2014) Microbiota in experimental periodontitis and peri-implantitis in dogs. Clin Oral Implants Res 25(9): 1094-1098.
  13. Zhuang LF, Watt RM, Mattheos N, Si MS, Lai HC, et al. (2016) Periodontal and peri-implant microbiota in patients with healthy and inflamed periodontal and peri-implant tissues. Clin Oral Implants Res 27(1): 13-21.
  14. Danser MM, van Winkelhoff, van der Velden U (1997) Periodontal bacteria colonizing oral mucous membranes in edentulous patients wearing dental implants. J Periodontol 68(3): 209-216.
  15. Mombelli A, Lang NP (1994) Microbial aspects of implant dentistry. Periodontol 2000: 74-80.
  16. Mombelli A, Buser D, Lang NP (1988) Coloniza- tion of osseointegrated titanium implants in edentulous patients. Early results. Oral Microbiol Immunol 3(3): 113-120.
  17. Busscher HJ, de Jong H, van Pelt AW, Arends J (1984) The surface free energy of human dental enamel. Biomater Med Devices Artif Organs 12(1-2): 37-49.
  18. Ponsonnet L, Reybier K, Jaffrezic N (2003) Relationship between surface properties (roughness, wettability) of titanium and titanium alloys and cell behaviour. Materials Science and Engineering: C 23: 551-560.
  19. Dewhirst FE, Chen T, Izard J, Paster BJ, Tanner AC, et al. (2010) The human oral microbiome. J Bacteriol 192(19): 5002-5017.
  20. Kumar PS, Mason MR, Brooker MR, O’Brien K (2012) Pyrosequencing reveals unique microbial signa- tures associated with healthy and failing dental implants. J Clin Periodontol 39(5): 425-433.
  21. Dabdoub SM, Tsigarida AA, Kumar (2013) Patient-specific analysis of periodontal and peri-implant microbiomes. J Dent Res 92(12 Suppl): 168S-175S.
  22. Koyanagi T, Sakamoto M, Takeuchi Y, Maruyama, N, Ohkuma M, et al. (2013) Comprehensive microbiological findings in peri-implantitis and periodonti- tis. J Clin Periodontol 40(3): 218-226.
  23. Kornman KS, Page RC, Tonetti MS (1997) The host response to the microbial challenge in periodontitis: assembling the players. Periodontol 2000 14: 33-53.
  24. Armitage GC (1999) Development of a classification system for periodontal diseases and conditions. Ann Periodontol 4(1): 1-6.
  25. Malmstrom HS, Fritz ME, Timmis DP, Van Dyke TE (1990) Osseo-integrated implant treatment of a patient with rapidly progressive periodontitis. A case report. J Periodontol 61(5): 300-304.
  26. Rokn A, Akbari S, Roosta Ha, Najafi H, Zayeri F, et al. (2016) Prevalence of peri-implantitis in patients not participating in well-designed supportive periodontal treatments: a cross- sectional study. Clin Oral Impl Res.
  27. Roccuzzo M, Bonino L, Dalmasso P, Aglietta M (2014) Long-term results of a three arms prospective cohort study on implants in periodontally compromised patients: 10-year data around sandblasted and acid-etched (SLA) surface. Clin Oral Impl Res 25(10): 1105-1112.
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