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Table of Contents
REVIEW ARTICLE
Year : 2013  |  Volume : 3  |  Issue : 1  |  Page : 58-61

Bacteria and dental implants: A review


15640 Redmond Way, Redmond, USA

Date of Web Publication10-May-2013

Correspondence Address:
Aravind Buddula
15640 Redmond Way, Redmond
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-6781.111698

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   Abstract 

Dental implants have been shown to be an excellent method for replacing natural teeth. Dental implants like natural teeth can be affected by microorganisms. Various terms have been proposed to describe inflammation around dental implant. The ones that are commonly used include peri-implantitis and peri-implant mucositis. Studies were conducted that described the bacteriology of dental implants. Most studies reported that the microbiota associated with stable implants is similar to the one seen in periodontal health. Similarly, bacteria associated with failing implants have also been studied. These studies predominantly showed that the bacteria associated with failing implant are similar to the ones seen in periodontal disease. One should be very cautious in placing dental implants in subjects with significant periodontal disease as there is a risk for failure. Implants are not immune for infections. The present review briefly describes the bacteriology associated with stable and failing implants.

Keywords: Bacteria, implants, peri-implantitis


How to cite this article:
Buddula A. Bacteria and dental implants: A review. J Dent Implant 2013;3:58-61

How to cite this URL:
Buddula A. Bacteria and dental implants: A review. J Dent Implant [serial online] 2013 [cited 2022 Jan 25];3:58-61. Available from: https://www.jdionline.org/text.asp?2013/3/1/58/111698


   Introduction Top


Dental implants like natural teeth are colonized by microorganisms. There are various terminologies associated with ailing and failing implants. Terms such as peri-implant disease, peri-implant mucositis, and peri-implantitis have been proposed that describe pathologic conditions around dental implants. Dental implants are being used more frequently to restore partially edentulous or completely edentulous patients. Clinicians now are facing problems that they encountered with natural teeth. Like natural teeth dental implants are susceptible to inflammation of the supporting tissues by colonization of pathogenic bacteria.

Implant failure has been defined as the inadequacy of the host tissue to establish or maintain osseointegration. [1] Implant failures can be classified based on the time of failure as early or late and based on the etiopathogenesis as infectious or noninfectious. [2],[3] Early failures are due to failure to establish osseointegration and late failure is due to failure to maintain osseointegration. [4] Osseointegration is defined as a "direct structural and functional connection between ordered living bone and surface of a load-carrying implant". [5],[6] Early failures can occur as a result of surgical trauma, premature loading of the implant, and bacterial infection. Late failures can occur following prosthetic rehabilitation. [2] Late failures can again be divided as "soon" late failures which occur during the first year of loading and as "delayed" late failures occurring in subsequent years. "Soon' late failures can be attributed to overloading of the implant placed in bone that is poor both qualitatively and quantitatively. " Delayed late failures can occur when there are changes in the loading conditions in relation to bone quality and volume and also as a result of peri-implantitis". [2],[7]

The present review will focus on the microbiota associated with dental implants in healthy and diseased states.


   Definition and Prevalence of Peri-Implant Disease Top


European workshop on periodontology proposed the following definitions for inflammatory lesions that develop around implants. [8]

  • Peri-implant disease: The inflammatory lesions that develop in the tissues around the implants
  • Peri-implant mucositis: Reversible inflammatory reaction in the soft tissues surrounding a functioning implant
  • Peri-implantitis: Inflammatory reactions associated with loss of supporting bone around an implant in function.
However, Zitzmann, et al.[9] provided new definitions for these inflammatory lesions.

  • Peri-implant Disease: Inflammatory reactions in the tissues surrounding an implant
  • Peri-implant Mucositis: Presence of inflammation in the mucosa at an implant with no signs of loss of supporting bone
  • Peri-implantitis: Presence of inflammation and loss of supporting bone.
Authors in their latest definition eliminated the words reversible and irreversible proposed by the European workshop on periodontology as it might imply that the process cannot be treated. Authors were of the opinion that peri-implantitis is treatable hence it cannot be considered irreversible. Peri-implant mucositis is comparable to gingivitis around natural teeth as there is no loss of supporting structure and peri-implantitis is comparable to periodontitis around natural teeth as there is bone loss associated with it.


   Prevalence of Peri-Implant Diseases Top


There is the scant literature available about the prevalence of peri-implant diseases. Cross-sectional studies on prevalence of implant related disease are rare. Hence, there is a scarcity in the available literature about the prevalence of implant related diseases.

Based on the available literature, peri-implant mucositis occurred in approximately 80% of the subjects and in 50% of the implants. [10],[11]

Peri-implantitis was identified in 28% of the subjects and ≥56% of subjects and in 12 and 43% of implant sites, respectively. [10],[11],[12],[13],[14]


   Microbiota Around Healthy and Diseased Teeth in the Absence of Implants Top


Studies have shown that flora associated with healthy implants is similar to the flora in natural teeth and also that the flora associated with ailing/failing implants is similar to the one associated with periodontal disease. [15],[16],[17],[18] Hence, it is important for the clinician to evaluate the periodontal status of the subject before implant placement.

Samples from healthy gingival sulcus consist of predominantly gram-positive anaerobic cocci and rods. Principally found are A. naeslundii, A. gerencseriae, S oralis, and Peptostreptococcus species which account for more than 50% of the bacteria. [19],[20],[21] With the development of periodontitis, there are a higher proportion of gram-negative rods and decreased gram-positive species. Increased proportions of P. gingivalis, B. forsythus and species of Prevotella, Fusobacterium, Campylobacter, and Treponema have been detected. [18],[19]


   Bacteriology of Stable Implants Top


There are only two longitudinal studies to date that report microbial colonization of stable dental implants. The first study was done by Nakou, et al.[22] in 1987. They found that supragingival plaque in stable implants predominantly consists of gram-positive cocci and subgingival plaque is dominated by Haemophilus spp and Veillonella parula. Second longitudinal study was done by Mombelli, et al.[23] in 1988. They studied microbial colonization of ITI implants in edentulous patients. Samples were taken from peri-implant crevice. They found that the flora was established shortly after installation of the dental implant. Over 85% of the organisms were identified as coccoid cells and over 80% were gram-positive facultative cocci. No, noteworthy, changes were found in the flora in the first 6 months. Spirochetes were never detected and Fusobacteria and black-pigmenting gram-negative rods were found occasionally. Authors' concluded from the study that bacteria around the implants in edentulous patients were similar to that found in the sulci of subjects with healthy periodontium. Mombelli, et al.[24] conducted a follow-up study in which they assess the microbial flora associated with stable osseointegrated dental implants. Majority of the patients were followed to the fifth year of implantation. No significant change was noted in the microbial flora during follow-up examinations.

However, cross-sectional studies are available in the literature that talks about bacteriology of stable implants. Lekholm, et al.[25] studied 20 patients with Brånemark implants. Mean observation time was 7.6 years. Coccoid and nonmotile rods dominated in up to 94% in the samples taken. Similarly, Apse, et al.[26] compared bacteriology of tooth and implant crevices. Microbiology included dark field microscopy and anaerobic culturing. The results were interpreted by the authors as an indication that crevices around teeth may be reservoirs of bacteria for implant colonization. The authors were trying to explain higher percentages of black pigmenting anaerobes on implants in partially edentulous patients as opposed to completely edentulous patients. Rams, et al.[27] compared microbiota associated with osseointegrated hydroxyapatite coated titanium implants to pure titanium implants. No significant differences in the microbiota between the implant types. Strep. sanguis and Strep. mitis were the predominant organisms. Conclusions based on various studies about bacteriology of stable implants are as follows:

  • Peri-implant microbiota is established soon after implant placement
  • Significant shifts in the flora do not occur over time
  • Microflora is stable in healthy patients comprising a microbiota in which periodontal pathogens present only at low or below detectable levels.
  • Composition of the subgingival microflora around implants in partially edentulous patients is a resultant of the composition of the flora around the teeth.
Microbiota around failing implants

Most studies reported that microbiota around failing dental implants harbored periodontopathic bacteria. Mombelli, et al.[17] reported data from seven cases with hollow cylinder titanium implants. Implant sites with pocket depth greater than 6 mm with bleeding on probing and suppuration were compared to successfully osseointegrated implants. Failing implants harbored a flora similar to adult periodontitis. Increased proportions of P. intermedia, Fusobacterium spp, and spirochetes were found around failing implants. Quirynen, et al.[28] conducted a retrospective study with four Brånemark implants and four patients. Implants failing due to overload demonstrated flora similar to periodontal health and failing implants due to infection harbored periodontopathic flora. Rosenberg, et al.[29] studied 32 implants in subjects. This was a prospective study. Subjects were followed for 2-18 months. Implants failing due to infection had periodontopathic bacteria and implants failing due to traumatic influences had flora similar to periodontal health. One study reported higher levels of P. gingivalis in failed implants. [30] Based on the observations from the above-mentioned studies, it can be concluded that implants that fail due to infection have microbiota similar to those associated with periodontal disease. This could possibly be one of the reasons why implants fail more in subjects with periodontal disease compared to implants placed in otherwise healthy mouth.


   Conclusion Top


A review of the literature so far leads to the conclusion that dental implants are not immune to infections. Like natural teeth, dental implants are colonized by bacteria. However there is a difference in the nature of microorganisms colonizing stable and failing implants. Most studies reported that stable implants have microbiota similar to that found in healthy periodontium. Gram-positive anaerobic cocci and rods are the predominant species colonizing stable implants. In contrast, failing implants have bacteria similar to the ones seen in periodontal disease. This is based on the majority of the studies. Like any topic in periodontics, there are studies that refute these findings. No matter what the studies show, it is wise to be cautious in placing dental implants in subjects with significant periodontal disease. It is important to treat the disease first and then treatment plan for dental implants.

 
   References Top

1.Heydenrijk K, Meijer HJ, Van der Reijden WA, Raghoebar GM, Vissink A, Stegenga B. Microbiota around root-form endosseous implants: A review of the literature. Int J Oral Maxillofac Implants 2002;17:829-38.  Back to cited text no. 1
    
2.Esposito M, Hirsch JM, Lekholm U, Thomsen P. Biological factors contributing to failures of osseointegrated oral implants. Etiopathogenesis. Euro J Oral Sci 1998;106:721-64.  Back to cited text no. 2
    
3.Buddula A, Assad DA, Salinas TJ, Garces YI, Volz JE, Weaver AL. Survival of dental implants in irradiated head and neck cancer patients: A retrospective analysis. Clin Imp Dent Relat Res 2012;14:716-22.  Back to cited text no. 3
    
4.Tabanella G, Nowzari H, Slots J. Clinica and microbiological determinants of ailing dental implants. Clin Implant Dent Relat Research 2009;11:24-26.  Back to cited text no. 4
    
5.Brånemerk PI. Introduction to osseointegration. In: Brånemark PI, editor. Tissue-integrated prosthesis: Osseointegration in clinical dentistry. Chicago, IL: Quintessence; 1985. p. 11-76.  Back to cited text no. 5
    
6.Adell R, Lekholm U, Rockler B, Brånemark PI. A 15-year study of osseointegrated implants in the treatment of the edentulous jaw. Int J Ora Surg 1981;10:387-416.  Back to cited text no. 6
    
7.Tonetti MS, Schmid J. Pathogenesis of implant failures. Periodontol 2000 1994;4:127-38.  Back to cited text no. 7
    
8.Albrektsson T, Isidor F. Consensus report. In: Lang NP, Karring T, editors. Proceedings of the 1 st European workshop on periodontology; 1994. p. 365-9.  Back to cited text no. 8
    
9.Zitzmann NU, Berglundh T. Definition and prevalences of peri-implant diseases. J Clin Periodontol 2008;35:286-91.  Back to cited text no. 9
    
10.Fransson C, Lekholm U, Jemt T, Berglundh T. Prevalence of subjects with progressive bone loss at implants. Clin Oral Implant Res 2005;16:440-6.  Back to cited text no. 10
    
11.Fransson C, Wennstrom J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implant Res 2008;19:142-7.  Back to cited text no. 11
    
12.Karoussis IK, Salvi GE, Heitz-Mayfield L, Bragger J, Hammerle CH, Lang NP. Long-term implant prognosis in patients with and without a history of chronic periodontitis: A 10 year prospective cohort study of the ITI dental implant system. Clin Oral Implant Res 2003;14:329-39.  Back to cited text no. 12
    
13.Roos-Jansaker AM, Lindahl C, Renvert H, Renvert S. Nine to Fourteen year follow-up of implant treatment. Part II: Presence of peri-implant lesions. J Clin Periodontol 2006;33:290-5.  Back to cited text no. 13
    
14.Bragger U, Karaoussis I, Persson R, Pjetursson B, Salvi G, Lang N. Technical and biological complications/failures with single crowns and fixed partial dentures on implants. A 10 year prospective cohort study. Clin Oral Implant Res 2005;16:326-34.  Back to cited text no. 14
    
15.Quirynen M, Listgarten MA. Distribution of bacterial morphotypes around natural teeth and titanium implants ad modum Branemark. Clin Oral Implant Res 1990;1:8-12.  Back to cited text no. 15
    
16.Apse P, Ellen RP, Overall CM, Zarb GA. Microbiota and crevicular fluid collagenase activity in the osseointegrated dental implant sulcus: A comparison of sites in edentulous and partially edentulous patients. J Periodont Res 1989;24:96-105.  Back to cited text no. 16
    
17.Mombelli A, Van Oosten MA, Schruch E Jr, Land NP. The microbiota associated with successful or failing osseointegrated titanium implants. Oral Microbiol Immunol 1987;2:145-51.  Back to cited text no. 17
    
18.Meffert RM. Periodontitis and periimplantitis: One and the same? Pract Periodont Aesthetic Dent 1993;5:79-82.  Back to cited text no. 18
    
19.Slots J. Microflora in the healthy gingival sulcus in man. Scand J Dent Res 1977;85:247-54.  Back to cited text no. 19
    
20.Tanner A, Maiden MF, Macuch PJ, Murray LL, Kent RL Jr. Microbiota of health, gingivitis and initial periodontitis. J Clin Periodontol 1998;25:85-98.  Back to cited text no. 20
    
21.Haffajee AD, Cugini MA, Tanner A, Pollack RP, Smith C Kent RL Jr, Socransky SS. Subgingival microbiota in healthy, well-maintained elder and periodontitis subjects. J Clin Periodontol 1998;25:346-53.  Back to cited text no. 21
    
22.Nakou M, Mikx FH, Oosterwaal PJ, Kruijsen JC. Early microbial colonization of permucosal implants in edentulous patients. J Dent Res 1987;11:1654-7.  Back to cited text no. 22
    
23.Mombelli A, Buser D, Lang NP. Colonization of osseointegrated titanium implants in edentulous patients. Early results. Oral Microbiol Immunol 1988;3:113-20.  Back to cited text no. 23
    
24.Mombelli A, Mericske-Stern R. Microbiological features of stable osseointegrated implants used as abutments for overdentures. Clin Oral Impl Res 1990;1:1-7.  Back to cited text no. 24
    
25.Lekholm U, Adell R, Lindhe J, Brånemark P, Eriksson B, Rockler B, et al. Marginal tissue reactions at Osseointegrated titanium fixtures. A cross-sectional retrospective study. Int J Oral Maxillofac Surg 1986;15:53-61.  Back to cited text no. 25
    
26.Apse P, Ellen RP, Overall CM, Zarb GA. Microbiota and crevicular fluid collagenase activity in the osseointegrated dental implant sulcus: A comparison of sites in edentulous and partially edentulous patients. J Periodont Res 1989;24:96-105.  Back to cited text no. 26
    
27.Rams TE, Link CC Jr. Microbiology of failing dental implants in humans: Electron microscopic observations. J Oral Implantol 1983;11:93-100.  Back to cited text no. 27
    
28.Quirynen M, De Soete M, Dierickx K, Van Steenberghe D. The intra-oral translocations of periodontopathogens jeopardize the outcome of periodontal therapy. A review of the literature. J Clin Periodontol 2001;28:499-507.  Back to cited text no. 28
    
29.Rosenberg ES, Torosian JP, Slots J. Microbial differences in 2 clinically distinct types of failures of osseointegrated implants. Clin Oral Implants Res 1991;2:135-44.  Back to cited text no. 29
    
30.Van Winklehoff AJ, Goene RJ, Benshop C, Folmer T. Early colonization of dental implants by putative periodontal pathogens in partially edentulous patients. Clin Oral Implants Res 2000;11:511-20.  Back to cited text no. 30
    



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