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Periimplantitis and Management

 

 

ABSTRACT
Replacement of teeth through the use of implants offers very high success rates. In this article, some of the complications involved with this technique, such as periimplant disease and, within this category, periimplantitis, an inflammatory reaction in which there is a loss of the bony support of the implant accompanied by inflammation. Peri–implantitis is probably one of the main causes of implant loss. The frequency of periimplantitis has been reported to be in the range of 1-19%3. This article attempts to review periimplantitis, its clinical features and management.

 

Introduction
Installation of oral implants is a routine procedure in the reconstruction of fully or partially edentulous individuals. High short- and long-term success rates are achieved. However the progressive loss of alveolar bone surrounding the implant is perhaps a very common complication limiting the success rates. The name periimplant disease refers to the pathological inflammatory changes that take place in the tissue surrounding a loadbearing implant.
Peri-implantitis is defined as an inflammatory reaction, with the loss of supporting bone in the tissues surrounding a functioning implant. Mombelli et al. defined it as “a site-specific infection yielding many features in common with chronic adult periodontitis.” Tonetti defined it as “an inflammatory, bacterial-driven destruction of the implant-supporting apparatus.”

Periimplant disease refers to 2 entities as follows -
- Mucositis: a clinical manifestation characterized by the appearance of inflammatory changes restricted to the periimplant mucosa. If treated properly, it is a reversible process.
- Periimplantitis: a clinical manifestation where clinically and radiologically evident loss of the bony support for the implant occurs, together with an inflammatory reaction of the periimplant mucosa.

 

Periimplant tissue
Healthy periimplant tissue plays an important role as a biological barrier to some of the agents that cause periimplant disease. If we compare the tooth and the implant, we see that the tooth is endowed with certain specific protective mechanisms such as: the junctional epithelium, connective tissue and cells belonging to the immune system.
The epithelium and the interface between the supraalveolar connective tissue and the titanium surface of an implant differ from the interface of the dental-gingival unit. The outer surface of the peri-implant mucosa is lined by a stratified keratinized oral epithelium that is continous with a junctional epithelium attached to the titanium surface by a basal lamina and by hemidesmosomes. The 2 mm. long nonkeratinized junctional epithelium is only a few cells thick in the apical portion and separated from the alveolar bone by 1 to 2 mm. of collagen rich connective tissue. This 3 to 4 mm. “biological barrier” protects the zone of osseointegration from factors released from plaque and the oral cavity.

 

Implant structure

The implants superficial roughness favors bacterial plaque adhesion when the surface is exposed to the oral environment. Poor alignment of the components that comprise an implant prosthesis system may foster the retention of bacterial plaque, as well as enabling microorganisms to pass inside the transepithelial abutment.

 

Microbial infection
Another cause of periimplantitis, as previously mentioned, is the bacterial colonization of the periimplant pocket. The microorganisms most commonly related to the failure of an implant to integrate through this mechanism are: rods and mobile forms of Gram-negative anaerobes. In partially edentulous patients with active periodontal disease, colonization of the periimplant sulcus by these microorganisms is observed one month following connection of the implant to its prosthetic abutment.
Risk factors for periimplant disease include poorly controlled diabetes, long term treatment with corticoids, radiation and chemo-therapy, smoking and excessive mechanical stresses on the implant.

 

MICROBIOLOGY OF THE PERI-IMPLANT AREA

The transmucosal attachment of osseointegrated dental implants serves as a surface for bacterial colonization of microbial biofilms. In partially edentulous subjects, the developing microbiota around implants closely resembles the microflora of naturally remaining teeth. Quirynen and Listgarten found that the subgingival microflora around implants and deep peri-implant pockets showed significantly higher proportions of spirochetes and motile rods. In addition, other bacterial species are associated with peri-implant infections. (eg. Bacteroides forsythus, Fusobacterium nucleatum, Campylobacter, Peptostreptococcus micros and Prevotella intermedia.) Organisms that are less frequently associated with periodontitis, such as Staphylococcus spp., enterics and Candida spp, have also been found in peri-implant infections.

 

 

Inflammation leading to tissue destruction

Inflammation is a complex reaction of the body in response to an infectious agent, antigen challenge, or injury. Within 10 to 20 days of plaque accumulation on teeth, clinical signs of inflammation can be seen. The cells in the inflammatory lesion cause considerable tissue damage in their effort to combat the invading microorganisms. Degradation of connective tissue is followed by epithelial migration and bone resorption. Berglundh et al, reported that there were numerous polymorphonuclear cells in the connective tissue areas adjacent to the pocket epithelium and in the perivascular compartments in more central areas of the inflammatory cell infiltrate among which plasma cells dominated.

 

 

DIAGNOSIS OF PERIIMPLANTITIS
Periimplantitis can be diagnosed early or once clear clinical evidence has developed.

 

Bleeding on probing
‘‘Bleeding on probing’’ (BOP) represents a clinical parameter which is defined as the presence of bleeding noticed after the penetration of a periodontal probe into the periimplant sulcus or pocket using gentle force. Obviously, the size (point diameter) of the probe applied as well as the application force should be standardized. In the healthy and normal periodontium, the probing force used is 0.25 N. Standardized probes which produce standardized probing forces may be recommended. Absence of BOP around implants would indicate healthy periimplant tissues.

 

Modified Gingival Index (mod GI)
The Loe & Silness Gingival Index System has been modified and adapted by Mombelli et al. for application around oral implants. While the mod GI may very well be used with success to assess the status of health or inflammation in periimplant mucosal tissues, and hence, to indicate
mucositis in clinical research, it may be preferable to use BOP for routine clinical documentation.

 

Probing depth and ‘‘loss of attachment’’
Periodontal probing to determine probing depth and the level of periodontal attachment in relation to the cemento-enamel junction (CEJ) is the most widely used clinical parameter in periodontal practice. Instead of relating probing depth to the CEJ, examiners may use the implant shoulder, which provides a landmark easy to localize in clinical practice.

 

 

Mobility
Since periimplant infections represent lesions originating from the marginal periimplant sulcus, the bone loss encountered in association with the development of such infections is also observed to be marginal and results in the formation of intrabony defects. 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. Therefore, increase in clinical mobility is not at all a sensitive parameter for monitoring clinical stability. Assessment of implant mobility in routine evaluations and clinical monitoring of implants is, therefore, not essential, but when used must always be performed in conjunction with the evaluation of other parameters.

 

 

Radiographic interpretation
Conventional radiography
In evaluating the bony structures adjacent to the implants over long periods of time, conventional radiography is a widely applied technique in clinical practice. 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. Nevertheless, DIB (the Distance from the Implant shoulder to the alveolar Bone crest) represents a reliable radiographic parameter for long term monitoring in clinical practice provided that optimal exposure geometry has been achieved. Usually, the apical termination of the cylindrical part of implant fixtures is used as a reference point in two stage systems, despite the fact that subcrestal placement utilizing a countersink procedure is recommended for most submerged implant systems.

 

Digital Subtraction Radiography (DSR)
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. For clinical research, DSR is highly recommended and has been successfully applied in longitudinal studies.
Hence the most common signs and symptoms of periimplantitis are:
- Colour changes in keratinized gum tissue or in the oral mucosa.
- Bleeding on probing.
- Increased probing depth of periimplant pockets.
- Suppuration.
- Periimplant radiolucency.
- Progressive loss of bone height around the implant.


The absence of bleeding on probing is indicative of good health.
Use of probes calibrated to a force of 0.25 n (25 g) to avoid test errors is advocated1. Higher gingival and plaque indices, pain on chewing and the presence of granulation tissue surrounding the implant are all detected.
Analysis of the fluid in the periimplant sulcus reveals certain early changes that demonstrate the existence of bone resorption, for instance, increased levels of chondroitin sulfate, elastase, β-glucuronidase, aminotransferase and prostaglandin E2 levels. Recording of gingival temperature and peri-implant fluid volume are other testing procedures that are elevated in the presence of periimplantitis.

 

 

Treatment
Depending on continuing diagnosis during maintenance, developing periimplant lesions should be treated according to the Cumulative Interceptive Supportive Therapy (CIST) protocols.
CIST includes as a first sequence mechanical, antiseptic and antibiotic treatment to control ongoing infection. Following this, periimplant bony lesions may be corrected by regenerative or resective surgical techniques. It is evident that preventive measures have to be reinstituted following such therapy.


Table 1. Cumulative Interceptive Supportive Therapy (CIST) (Mombelli & Lang 1998)

 


PII

BOP

Suppuration

PD mm.

RX defect

Maintenance Classification

CIST

 

 

 

 

 

 

 

+, -

-

-

<4

-

0

(A)

+

+

-

<4

-

I

A

+

+

+, -

4-5

+

II

A+B

+

+

+, -

>5

++

III

A+B+C

+

+

+, -

>5

+++

IV

A+B+C+D

+

+

+, -

>5

++++

V

E

 

 

CIST modalities
Mechanical debridement (Supportive therapy protocol A)
Oral implants with evident plaque or calculus deposits adjacent to only slightly inflamed periimplant tissues (BOP positive), but lacking suppuration and having a probing depth not exceeding 3 mm, are to be subjected to mechanical debridement. While calculus may be chipped off using carbon fiber curettes, plaque is removed by means of polishing using rubber cups and polishing paste. Carbon fiber curettes do not sever the implant surface, but are sharp and strong enough to remove light to moderate calcified deposits on implants. Conventional steel curettes or ultrasonic instruments with metal tips leave severe damage on the implant surface and render it conducive to future plaque accumulation, hence should not be used.

 

Antiseptic treatment (Supportive therapy protocol B)

In addition to performing supportive therapy protocol A (i.e. mechanical debridement), antiseptic treatment is performed in situations where – in addition to the presence of plaque and BOP – probing depth is increased to 4–5 mm. Suppuration may or may not be present. The antiseptic treatment (protocol B) is performed in conjunction with the mechanical treatment (protocol A). Antiseptic treatment comprises 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. Generally, 3–4 weeks of regular administration are necessary to achieve positive treatment results.

 

Antibiotic treatment (Supportive therapy protocol C)
When probing depth values of the periimplant sulcus or pocket increase to 6 mm or more, plaque deposits and BOP are usually encountered. Suppuration may or may not be present. Such a periimplant lesion is usually radiographically evident. The antibacterial treatment approach must then include antibiotics to eliminate or at least significantly reduce the pathogens in this submucosal ecosystem. Prior to administering antibiotics, the mechanical (A) and the antiseptic (B) treatment protocols have to be applied. During the last ten days of the antiseptic treatment, an antibiotic directed at the elimination of gram negative anaerobic bacteria – e.g. metronidazole or ornidazole is administered. Periimplant infections were treated successfully and remained stable for a documented period of one year. Subsequently, prophylactic procedures were instituted to prevent reinfection.
Instead of administration of systemic antibiotics, the application of local antibiotics through the use of controlled delivery devices has emerged recently as a suitable treatment concept. The antibiotic must remain at the site of action for at least 7–10 days in a concentration high enough to be effective. Tetracycline periodontal fibers (Actisite) have successfully been applied. The therapeutic effect appears to be identical to the effect documented for the systemic administration of antibiotics. Mombelli et al.  treated 30 lesions with mechanical debridement and placement of tetracycline fibers. Mean improvements in clinical parameters resulted, which were sustained over a 12-month observation period.
Hence, it appears that periimplant infections may be controlled successfully by cumulatively providing mechanical, antiseptic and antibiotic supportive therapy.
Dennison et al carried out an in vitro study of the relationship between implant surface and decontamination technique, in which the decontaminating efficacy of air-power abrasives, citric acid solution, hydrogen peroxide and chlorhexidine on different implant surfaces (hydroxyapatite, titanium plasma and machined titanium) was assessed. They coincided with Zablotsky et al. in their conclusions that air abrasion, using bicarbonate particles with saline solution is the best way to eliminate endotoxins and remains from all surfaces, and that 40% citric acid with a pH of 1 for 30-60 seconds is an effective means of decontamination for hydroxyapatite coated implants; chlorhexidine is not effective in these cases. They also determined that machined titanium surfaces are the easiest to decontaminate and that topical tetracyclines (the content of one 250-mg capsule mixed with saline serum until a creamy consistency is obtained) are the antibiotic of choice in these cases. Furthermore, it appears that tetracycline stimulates fibroblast growth in the affected area.
Surgical laser when used as a method of decontamination on different implant surfaces depending on power intensities, bacteria kill rates of up to 99.4% have been attained. The CO2 and Er:YAG lasers are recommended, since it appears that they do not exert a negative impact on the implant surface. The Er:YAG laser generates the least amount of heat in the bone tissue surrounding the implant16. Another type of laser with a low thermal effect on the bone and implant surface is the Er, Cr, YSGG (Waterlase), which represents an improvement over the technical properties of the Er:YAG and which surely has a bright future in this field.

 

Regenerative or resective therapy (Supportive therapy protocol D)
Only if infection is controlled successfully, it is reasonable to discuss treatment approaches to either restore the bony support of the implant by means of regenerative techniques or to reshape the periimplant soft tissues and/or bony architecture by means of resective surgical techniques, depending on esthetic considerations and morphological characteristics of the lesion.
So far, evidence that bone fill of periimplant defects resulting from previous periimplantitis may be achieved following anti-infective therapy and using the biological principle of guided tissue regeneration (GTR) However, the re-osseointegration of a previously contaminated implant surface into regenerated bone has not yet been demonstrated histologically.
Treatment of periimplantitis lesions with Autogenous bone grafts/bone graft substitutes may lead to fill of the defects and improved soft tissue conditions. Failures have been reported3. Treatment with e-PTFE membranes may lead to bone fill of the defects and improved soft tissue conditions. Treatment with the combination of grafts and e-PTFE membranes may lead to bone fill and improved soft tissue conditions. Comparison of the overall outcomes of cases treated with grafts alone, e-PTFE membranes alone, or their combination – does not indicate a superiority to the combination.

 

(Supportive therapy protocol E)
A clinical situation characterized by the presence of suppurative exudate, overt BOP, severely increased periimplant probing depth (usually > 8 mm.), eventually reaching perforations or vents of hollow body implants, and may be associated with pain with a periimplant radiolucency extending far along the outline of the implant, it can be concluded that the periimplant infection has advanced to a degree where it cannot be controlled by the therapeutic protocols proposed above.

 

Summary

    • There is a consensus that proper oral hygiene should be established, and that occlusal forces should be evaluated and corrected by occlusal adjustment when deemed traumatic.
    • Supra- and submucosal mechanical debridement and topical antimicrobial treatment should be part of the initial therapy.
    • Various topical antimicrobial treatments are recommended (e.g. patient administered chlorhexidine application; professional irrigation with chlorhexidine, hydrogen peroxide, stannous fluoride or tetracycline solutions; application of tetracycline fibers).
    • The use of systemic antibiotics as part of the initial therapy is recommended in four of the five treatment strategies.
    • In cases with horizontal bone loss or with wide/shallow intraosseous defects showing inadequate resolution after initial therapy, open debridement combined with osseous recontouring and apical flap positioning is suggested in four of the five treatment strategies.
    • As part of the apically positioned flap surgery, all of the recommendations include mechanical implant surface smoothing and chemical surface detoxification. The recommended detoxification agent varies (e.g. abrasive sodium carbonate air-powder, citric acid or an antimicrobial agent).
    • Regenerative surgery is proposed for intrabony two- and three-wall defects, circumferential moat defects and dehiscence defects, and for intrabony defects.
    • The use of postoperative systemic antibiotics following regenerative procedures is proposed.

     

    Conclusion
    Oral implants are anchored in the jawbone and yet penetrate the mucosa, reaching the highly contaminated environment of the oral cavity. Biofilms forming on all hard, non-shedding surfaces will also form on titanium implants. As on teeth, bacterial plaque will develop and trigger a host response, resulting in the development of mucositis. If plaque is allowed to accumulate over prolonged periods of time, periimplant mucositis may develop into lesions extending further apically, with associated loss of alveolar bone. Angular bony defects usually extending around the entire circumference of the implant may result, and are termed ‘‘periimplantitis’’.
    The periimplant mucositis lesion is characterized by BOP and periimplant sulcus depth of usually 2–4 mm. Periimplantitis, however, yields increasing probing depth, with occasional suppuration and radiographic loss of crestal bone. However, clinical stability is not yet jeopardized, since the implant affected is not mobile as yet. Osseointegration in the apical portion of the implant usually persists. Owing to the infectious nature of periimplant mucositis and periimplantitis, preventive procedures have to be rendered in a well-organized recall program to assure adequate supportive therapy for a lifetime.

     

     

    BIBLIOGRAPHY

    1. Sanchez G, Gay-escoda C. Periimplantitis. Med Oral Patol Oral Cir Bucal 2004;9 Suppl:S63-74.
    2. Lang NP, Wilson TG, Corbet EF. Biological complications with dental implants: their prevention, diagnosis and treatment. Clin Oral Impl Res 2000: 11 (Suppl.): 146-155.
    3. Roos-Jansaker A-M, Renvert S, Egelberg J. Treatment of peri-implant infections: a literature review. J Clin Periodontol 2003; 30: 467–485.
    4. Klinge B, Hultin M, Berglundh T. Peri-implantitis. Dent Clin N Am 2005; 49(3): 661-676.
    5. Mombelli A, Van Oosten MA, Schurch E Jr. Et al. The microbiota associated with successful or failing osseointegrated titanium implants. Oral Microbiol Immunol 1987;2;145-151.
    6. Tonetti M. Peri-implantitis: biologic considerations. J Parodontol Implantol Orale 1996:15:284-296.
    7. Mombelli A, Marxer M, Gaberthuel T, et al. The microbiota of osseointegrated implants in patients with a history of periodontal disease. J  Clin Periodontol 1995:22:124-130.
    8. Quirynen M, Listgarten M. The distribution of bacterial morphotypes around natural teeth and titanium implants ad modum Branemark. Clin Oral Implants Res 1990;1:8-13.
    9. Tanner A, Maiden MF, Lee K, et al. Dental implant infections. Clin Infect Dis 1997:25(suppl 2):S213-217.
    10.  Leonhardt A, Renvert S, Dahlen G. Microbial findings at failing implants. Clin Oral Implants Res 1999;10:339-345.
    11.  Berglundh T, Gislason O, Lekholm U, et al. Histopathological observations of human periimplant lesions. J Clin Periodontol 2004;31:341-347.
    12.  Mombelli A, Lang NP. The diagnosis and treatment of periimplantitis. Periodontology 2000:1998;17:63-76.
    13.  Mombelli A, Feloutzis A, Bragger U & Lang NP. Treatment of periimplantitis by local delivery of tetracycline. Clinical, microbiological and radiological results. Clinical Oral Implants Research 2001; 12:287 – 294.
    14.  Dennison DK, Huerzeler MB, Quinones C, Caffesse RG. Contaminated implant surfaces: an invitro comparison of implant surface coating and treatment modalities for decontamination. J Periodontol 1994;65:942-948.
    15.  Zablotsky NH, Diedrich DL, Meffert RM, Wittrig E. The ability of various chemotherapeutic agents to detoxify the endotoxin infected HA-coated implant surface. Int J Oral Implant 1991;8:45-51.
    16. Walsh LJ. The use of laser in implantology: an overview. J Oral Implantol 1992;18:335-340.
     

     

     

     

     

     

     

     

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    Author : - Dr. Rohit Shah

     

     

     

    Article on “Peri-implantitis, Treatment Protocols” published in Dentistry Today, Vol. V, Issue II, Pgs. 25 – 26.

     

     

     

     

     

     

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