Journal of Dental Implants

PRACTITIONER SECTION
Year
: 2014  |  Volume : 4  |  Issue : 1  |  Page : 82--85

Nip it in the bud- therapeutic strategies in the management of peri-implant infections: Literature review


K Harikumar, Sameera G Nath, Raghunath Arun 
 Department of Periodontics, Government Dental College, Calicut, Kerala, India

Correspondence Address:
K Harikumar
Associate Professor, Department of Periodontics, Government Dental College, Calicut - 673 008, Kerala
India

Abstract

Oral implants represent hard, non-shedding surfaces in a fluid system, as do teeth. As such, they are subjected to biofilm formation and if left unattended may lead to peri-implant infections and ultimately failure of implants. Proper utilization of diagnostic tools may help in predicting the prognosis of implants during the maintenance visits. Depending on continuing diagnosis during maintenance, developing peri-implant lesions should be treated according to the cumulative interceptive supportive therapy protocols.



How to cite this article:
Harikumar K, Nath SG, Arun R. Nip it in the bud- therapeutic strategies in the management of peri-implant infections: Literature review.J Dent Implant 2014;4:82-85


How to cite this URL:
Harikumar K, Nath SG, Arun R. Nip it in the bud- therapeutic strategies in the management of peri-implant infections: Literature review. J Dent Implant [serial online] 2014 [cited 2022 Oct 6 ];4:82-85
Available from: https://www.jdionline.org/text.asp?2014/4/1/82/131013


Full Text

 Introduction



Oral implants represent hard, non-shedding surfaces in a fluid system, as do teeth. [1] As such, they are subjected to biofilm formation. A layer of glycoproteins will coat the implant surfaces that are exposed to the oral environment. After a few minutes to hours after implant installation, single bacterial colonies usually predominated by a Gram-positive coccoidal and rod microbiota will adhere to the pellicle coat. As time passes, the biofilm development will result in a more complex microbiota.

Basically, the microbiota associated with healthy peri-implant tissues closely resembles the microbiota associated with gingival health. In contrast, the microbiotas identified in peri-implant infections in many cases were identical to that encountered in pockets with advanced periodontitis. [2] This means that during the development of the biofilm the colonization pattern may substantially be influenced by bacterial colonization from various niches within the oral environment. [3] Thus, untreated periodontitis may represent a risk for the establishment of a pathogenic microbiota in the peri-implant sulcus.

The First European Workshop on Periodontology in 1993 identified two disease patterns associated with oral implants. Peri-implant mucositis, a term used to describe reversible inflammatory reactions in the mucosa adjacent to an implant; and Peri-implantitis, an inflammatory process that affects the tissues around an osseointegrated implant in function and results in loss of supporting bone. The pattern of spread of inflammation is different in periodontal and peri-implant tissues. The lesions in plaque-associated periodontitis are limited to the connective tissue, whereas in the peri-implant tissues the lesions also involve the alveolar bone. In contrast to the periodontal tissues, peri-implant tissues appear to be poorly encapsulated to resolve progressive, plaque-associated lesions and extend into the marginal bone tissue and may, if they are allowed to progress, lead to the loss of the implant.

Diagnostic tools for assessing implant failure

Mobility

Since peri-implant infections represent lesions originating from the marginal peri-implant sulcus, the bone loss associated with such infection is also observed to be marginal and results in the formation of an intrabony saucer-shaped defects around the implant. This, in turn, means that the implant still remains fully osseointegrated in the apical portion and hence, an increase in implant mobility cannot be expected. In contrast, loss of clinical stability as a result of complete loss of three osseointegration would be reflected in a sudden increase in implant mobility. Therefore, an increase in clinical mobility represents a highly specific, but not at all sensitive, parameter for monitoring clinical stability. Assessment of implant mobility must always be performed in conjunction with the evaluation of other parameters.

Bleeding on probing (BOP)

In the healthy periodontium and in periodontally reduced dentition, the probing force used is 0.25 N. [4],[5] The application of the same probing force for the determination of BOP around oral implants has been established. [6] The absence of BOP is a very reliable indicator for periodontal stability. [7] Hence, from a clinical point of view, absence of BOP around implants would indicate healthy peri-implant tissues.

Probing depth and loss of attachment

Instead of relating probing depth to the cementoenamel junction in natural tooth, clinicians may use the implant shoulder, as a landmark for probing depth. In a study done by Christensen et al. [8] found that clinical probing depth determined by three automatic probing devices yielded slightly higher values around oral implants (approximately 0.5 mm higher) than around healthy contralateral control teeth. Furthermore, the buccal and lingual aspects of oral implants generally scored 0.5-1.0 mm less than the interproximal aspects. Probing depth around oral implants may be system specific and dependent on access of the probe to the peri-implant sulcular region. Hence, different probing depth values may be considered as "normal" in different implant systems. A soft-tissue seal inhibits the probe tip penetration in healthy and slightly inflamed peri-implant soft-tissues, but not so in peri-implantitis. Probing around oral implants must be considered a sensitive and reliable clinical parameter for long-term clinical monitoring of peri-implant mucosal tissues. Repeated subsequent comparisons of probing depth and loss of implant support (loss of attachment) in comparison with baseline measurements are highly recommended.

Pus formation

Pus formation is always a sign of infection with active tissue destructive processes taking place. Peri-implantitis lesions usually yield some pus formation upon provocation by pressing on the mucosal tissues, whereas mucositis lesions may not. Hence, pus formation represents a specific diagnostic sign for the presence of peri-implantitis.

Radiographic interpretation

Conventional radiography is widely used in clinical practice to evaluate the bony structures adjacent to the implants over long periods. However, it should be noted that minor changes in bone morphology in the crestal area may not be revealed until they reach a significant size and shape. [9] In digitizing radiographs of identical exposure geometry, minute changes in the level and density of the alveolar bone may be revealed by subtracting subsequent images from a baseline radiograph. By doing this, the sensitivity of radiographs may be increased significantly. [10]

Proper utilization of these diagnostic tools may help in predicting the prognosis of implants during the maintenance visits. Based on these tools, therapeutic strategies could be planned and "tailor made" for specific individual needs.

Therapeutic strategies

Cumulative interceptive supportive therapy (CIST)

Depending on the clinical and the radiographic diagnosis, a protocol of therapeutic measures, called CIST, has been designed to head off the development of peri-implant lesions. [11] This protocol is cumulative in nature and includes four steps (A-D) which should not be used as single procedures, but rather as a sequence of therapeutic procedures with increasing antibacterial potential, depending on the severity and extent of the lesion. Diagnosis, therefore, represents a key characteristic of this maintenance care program. The major clinical parameters to be used have been discussed above and include assessment of the following presence or absence of dental plaque, presence or absence of gentle BOP, presence or absence of suppuration, peri-implant probing depth and radiographic evidence of bone loss. [12]

Oral implants without evident plaque or calculus adjacent to healthy peri-implant tissues as revealed by absence of BOP, absence of suppuration and probing depth usually not exceeding 3-4 mm, can be considered clinically stable and not currently at risk for peri-implant disease. These implants should be re-evaluated at least on an annual basis. The frequency of and interval between supportive therapy visits should be determined by the patient's oral health status.

Mechanical debridement (supportive therapy protocol A)

Oral implants with evident plaque or calculus deposits adjacent to only slightly inflamed peri-implant tissues (BOP positive), but lacking suppuration and having a probing depth not exceeding 3-4 mm, are to be subjected to mechanical debridement. Although calculus may be chipped off using carbon-fiber curettes or plastic instruments, plaque is removed by means of polishing using the rubber cups and polishing paste. Conventional steel curettes or ultrasonic instruments with metal tips leave marked damage on the implant surface and render it conducive to future plaque accumulation and hence should not be used. [13]

Antiseptic treatment (supportive therapy protocol B)

In addition to performing protocol A, antiseptic treatment is performed in situations where, in addition to the presence of plaque and BOP, probing depth is increased to 4-6 mm and suppuration may or may not be present. The antiseptic treatment is performed in conjunction with the mechanical treatment (protocol A) and comprises of the application of the most potent antiseptic available, i.e., chlorhexidine digluconate, either in the form of a daily rinse of 0.1%, 0.12%, or 0.2%, or as a gel applied to the site of desired action. [14] In general, 3-4 weeks of regular administration is necessary to achieve positive treatment results.

Antibiotic treatment (supportive therapy protocol C)

When probing depth values of the peri-implant sulcus or pocket increase to 6 mm or more, plaque deposits and BOP are usually encountered, suppuration may or may not be present and peri-implant lesion evident radiographically, then protocol C should be considered. The pocket with increased depth represents an ecologic niche, which is conducive to colonization with Gram-negative anaerobic, periodontopathic microorganisms. [15] The antibacterial treatment approach must then include antibiotics to eliminate or at least significantly reduce the pathogens in this submucosal ecosystem. This, in turn, will allow soft-tissue healing. [16] Before administering antibiotics, the mechanical (A) and the antiseptic (B) treatment protocols have to be applied. During the last 10 days of the antiseptic treatment, an antibiotic directed at the elimination of Gram-negative anaerobic bacteria is administered. Subsequently, prophylactic procedures are instituted to prevent reinfection.

As an alternative to administration of systemic antibiotics, the application of local antibiotics through the use of controlled delivery devices has emerged as a suitable treatment concept. However, only release devices with adequate release kinetics may be used to ensure successful clinical outcomes. The antibiotic must remain at the site of action for at least 7-10 days in a concentration high enough to penetrate the submucosal biofilm. As of today, only a limited number of products have been shown to demonstrate the appropriate characteristics. [17] Tetracycline periodontal fibers, microspheres of minocycline hyclate have successfully been applied in some case studies. The therapeutic effect appears to be identical to the effect documented for the systemic administration of antibiotics, [18] provided that treatment protocols A and B are used as well. Hence, it appears that peri-implant infections may be controlled successfully by cumulatively providing mechanical, antiseptic and antibiotic supportive therapy.

Regenerative or resective therapy (supportive therapy protocol D)

Only if infection is controlled successfully, as evidenced by an absence of suppuration and reduced edema, is it reasonable to consider treatment approaches either to restore the bony support of the implant by means of regenerative techniques or to reshape the peri-implant soft-tissues and/or bony architecture by means of resective surgical techniques depending on the size and morphologic characteristics of the lesion. Regarding attempts for surface decontamination of the implant surface during surgical exposure, no conclusive evidence identifies one particular approach as being most effective. Hence, it appears that irrigating the lesions under a flap surgery using chlorhexidine digluconate followed by sterile saline, is the most simple and effective protocol for surface decontamination. [19]

 Conclusions and Clinical Implications



Oral implants are anchored in the jawbone and yet penetrate the mucosa, reaching the highly contaminated environment of the oral cavity. There, biofilms will form on titanium implants and will trigger a host response, resulting in the development of mucositis. If plaque is allowed to accumulate over prolonged periods, peri-implant mucositis may develop into lesions extending farther apically, with associated loss of alveolar bone in angular fashion extending around the entire circumference of the implant termed peri-implantitis. Owing to the infectious nature of peri-implant mucositis and peri-implantitis, preventive procedures have to be rendered in a well-organized recall program to assure adequate supportive therapy for a lifetime. Depending on continuing diagnosis during maintenance, developing peri-implant lesions should be treated according to the CIST protocols.

References

1Gristina AG. Biomaterial-centered infection: Microbial adhesion versus tissue integration. Science 1987;237:1588-95.
2van Winkelhoff AJ, Goené RJ, Benschop C, Folmer T. Early colonization of dental implants by putative periodontal pathogens in partially edentulous patients. Clin Oral Implants Res 2000;11:511-20.
3Leonhardt A, Renvert S, Dahlén G. Microbial findings at failing implants. Clin Oral Implants Res 1999;10:339-45.
4Lang NP, Nyman S, Senn C, Joss A. Bleeding on probing as it relates to probing pressure and gingival health. J Clin Periodontol 1991;18:257-61.
5Karayiannis A, Lang NP, Joss A, Nyman S. Bleeding on probing as it relates to probing pressure and gingival health in patients with a reduced but healthy periodontium. A clinical study. J Clin Periodontol 1992;19:471-5.
6Gerber JA, Tan WC, Balmer TE, Salvi GE, Lang NP. Bleeding on probing and pocket probing depth in relation to probing pressure and mucosal health around oral implants. Clin Oral Implants Res 2009;20:75-8.
7Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding on probing. An indicator of periodontal stability. J Clin Periodontol 1990;17:714-21.
8Christensen MM, Joss A, Lang NP. Reproducibility of automated periodontal probing around teeth and osseointegrated oral implants. Clin Oral Implants Res 1997;8:455-64.
9Lang NP, Hill RW. Radiographs in periodontics. J Clin Periodontol 1977;4:16-28.
10Brägger U, Pasquali L, Rylander H, Carnes D, Kornman KS. Computer-assisted densitometric image analysis in periodontal radiography. A methodological study. J Clin Periodontol 1988;15:27-37.
11Lang NP, Berglundh T, Heitz-Mayfield LJ, Pjetursson BE, Salvi GE, Sanz M. Consensus statements and recommended clinical procedures regarding implant survival and complications. Int J Oral Maxillofac Implants 2004;19 Suppl:150-4.
12Mombelli A, Lang NP. Clinical parameters for the evaluation of dental implants. Periodontol 2000 1994;4:81-6.
13Matarasso S, Quaremba G, Coraggio F, Vaia E, Cafiero C, Lang NP. Maintenance of implants: An in vitro study of titanium implant surface modifications subsequent to the application of different prophylaxis procedures. Clin Oral Implants Res 1996;7:64-72.
14Lang NP, Brecx M. Chlorhexidine digluconate: an agent for chemical plaque control and prevention of gingival inflammation. J Periodontal Res 1986;21 Suppl 18:74-89.
15Mombelli A, van Oosten MA, Schurch E Jr, Land NP. The microbiota associated with successful or failing osseointegrated titanium implants. Oral Microbiol Immunol 1987;2:145-51.
16Mombelli A, Lang NP. Antimicrobial treatment of peri-implant infections. Clin Oral Implants Res 1992;3:162-8.
17Tonetti MS. Local delivery of tetracycline: From concept to clinical application. J Clin Periodontol 1998;25:969-77.
18Mombelli A, Lang NP. The diagnosis and treatment of peri-implantitis. Periodontol 2000 1998;17:63-76.
19Schou S, Berglundh T, Lang NP. Surgical treatment of peri-implantitis. Int J Oral Maxillofac Implants 2004;19 Suppl:140-9.