Implant Esthetics:
Form Meeting Function

Treatment of Peri-implantitis – A Literature Review
Vavalekas, Michail; Hanawa, Yasufumi; Dunca, Flaviu; Tetri, Baruch; Froum, Scott; Bral Michael, Cho, Sang-choon; Froum, Stuart; Elian, Nicolas; Tarnow, Dennis. Dennis. Ashman Department of Periodontology and Implant Dentistry, New York University

New York University
INTRODUCTION
eri-implantitis is an inflammatory process affecting the soft and hard tissues surrounding an implant. This disease is associated with loss of supporting bone
bleeding on probing and occasionally suppuration. The etiopathogenesis ofperi-implantitis is complex and related to a variety of factors that affect the peri-implant
environment. Peri-implantitis can influenced by:(1) Patient related factors including
systemic diseases (e.g diabetes, osteoporosis) and prior dental history (periodontitis),2) social factors such as (inadequate oral hygiene, smoking, drug abuse) and 3) parafunctional habits (bruxism & malocclusion). In addition to the above, iatrogenic factors such as faulty restorations, cement left following restoration delivery and loose
components can also play a significant role in the development of peri-implantitis.

P

Although restorations of endosseous implants have demonstrated a very high survivalrate(1), one study suggested that over a 5 year period, 0 to 14.4% of dental implants
demonstrated peri-implant inflammatory reactions associated with crestal bone loss
(2).

Moreover, only one study showed 5-year post treatment results with a 58 percent success rate.
Pontoriero (21) demonstrated the importance of bacterial plaque accumulation in thedevelopment of inflammation around implants (peri-implantitis) and Mombelli (15)showed that, if this condition is left untreated and the surface is not decontaminated,
it will lead to peri- implant pocketing, alveolar bone loss, and eventually to implantloss. Because there are biologic differences between teeth and implants, the progression of infection around implants is also different than natural teeth. The inflammatory cell infiltrate around implants was reported to be larger and extend more apicalwhen compared to a corresponding lesion in the gingival tissue around natural teeth(29). In addition, the tissues around implants are more susceptible to plaque associated infections which spread into the alveolar bone (29).
Implant surface bacterial decontamination is essential in treating peri-implantitis infections. Systemic administration of antibiotics has been used in the treatment of periimplantitis resulting in a reduction of inflammation. However, in a systematic reviewof treatment Lindhe et al. questioned the use of antibiotics as a sole therapy for treatment (29). Moreover,in one study a 3-month recurrence of peri-implantitis was

bleeding on probing was statistically significantly greater and an improvement in mean
peri-implant PD (from 3.9mm to 3.6 mm) was seen. These results suggest that the topical application of chlorhexidine provides limited or no adjunctive clinical improvement when treating shallow peri-implant lesions as compared with using mechanicaldebridement alone. (33)
Karring et al. (2005) studied the efficacy of sub-mucosal debridement without antibiotics for the therapy of peri-implantitis utilizing an ultrasonic device or carbon fiber
curettes. Karring concluded that there was no statistically significant difference reported for the implants treated either by the ultrasonic device or manually scalers frombaseline, three, and six months regarding reduction in bleeding on probing and radiographical bone loss. (34)
Schwarz et al. (2005, 2006a) compared the efficacy of the Er:YAG laser with that of
the combination of mechanical debridement (using plastic curettes) and antiseptic(0.2% chlorhexidine digluconate) administration for the treatment of peri-implantitis.
In both studies the results obtained at 6 months after therapy suggested that the treatment modalities were equally efficacious in significantly improving peri-implant probing pocket depth (PPD) and clinical attachment level (CAL). However, at 12 months,

bination of bovine bone mineral and the collagen membrane seemed to yield greater
improvements in clinical parameters showing 0.9 +/- 0.2mm more in PD reduction
and 1.0 +/- 0.3 more clinical attachment gain (32).

In this review several modalities have been evaluated as for treatment for peri-implantitis. To date, none of the techniques have been shown to be predictable (Table 1.). At
best, a 5-year follow-up study showed a 58% success rate. Moreover, no histologicalstudy has reported has reported significant re-osseointegration of a peri-implantitis
affected surface. Wetzel 1999 (39).

CONCLUSIONS
he ideal management of peri-implant infections should focus both on infection
control of the lesion, detoxification of the implant surface, and regeneration oflost support. Treatment options can be surgical or non-surgical. In this review
was concluded that non-surgical treatment of peri-implantitis was unpredictable, whileT“…implant surface bacterial decontamination is the essential in treating
peri-implantitis infections. In the studies described, establishing an adequate healthy tissue environment
proved to be difficult since inflammation was still present in a significant
number of patients…”

Implant failure has been attributed to a variety of causes including: 1) bacterial infection 2) poor surgical technique 3) premature fixture overload (7), 4) faulty or incorrect
prosthetic design and/or 5) improper surgical placement (17). In cases where is evidence of progressive infection caused by bacterial plaque and resulting in progressivebone loss of bone around the implant, the etiology is considered to be peri-implantitis.
Many methods of treating peri-implantitis treatment have been documented in the literature. This paper will focus on treatments that address bacterial contamination as the
etiologic agent. Therefore methods of implant surface decontamination will be
described along with procedures designed to treat the bone loss caused by periimplantitis (6, 10). These treatments include 1) administration of systemic antibiotics
alone, 2) Mechanical debridement with or without systemic antibiotic treatment (38),3) Mechanical debridement with or without chlorhexidine oral rinses (38), 4)
Mechanical debridement combined with LASER decontamination (30,38), 5) Surgical
Debridement (32) and more recently, 6) Surgical debridement with guided boneregeneration (GBR) for reparation of bony and soft tissue defects (6, 7, 8). To date,
GBR using a bone graft and membrane has had the best success as in demonstratingbone fill of the defects associated with peri-implantitis as described in the literature (6,9).

Fig 1a. Peri-implantitis around on internal hex implant

Fig 1b. Implant removal site

Fig 2a. Peri-implantitis around a RTs implantFig 2b. Peri-implantitis lesions surrounding implants

Fig 3a. Peri-implantitis around on external hex

Fig 3b. Removed implants showing extend bone loss
Author

The purpose of this literature review was to discuss different treatment modalities for
peri-implantitis and the compare of the treatment outcomes.

Patients and implants

Follow-up

Survival rate

Open flap debridement,
Leonhardt, A et Antibiotic: Systemic administraal. (2003)
tion of Amoxicillin and metronidazole

9 patients, 26 implants

6 months, 1 and5 years

58%

Karring et al.
(2005)

Ultrasound debridement, No
Antibiotic used

11 patients, 22 implants

6 months

100%

Schwartz et al.
(2005) (2006a)

No flap, Er:YAG laser, mechanical debridement, chlorohexidine

20 patients, 32 implants(2005), 20 patients, 40
implants (2006a)

6 months(2005), 12
months(2006a)

100%

Schwartz et al.
(2006b) (2008)

Open flap, nanocrystalinehydroxyapatite, or bovine bone
combined with a collagen membrane

22 patients, 22 implants

6 months(2006b), 2
years (2008)

100%, 100%

Renvert et al.
(2006)

Sub-mucosal mechanicaldebridement, Topical minocycline
microspheres or 1% chlorhexidine gel application

30 patients, 87 implants

12 months

100%

MATERIALS AND METHODS
linical data in this study was obtained from the Implant Database (ID). This data
was extracted as de-identified information from the routine treatment ofpatients at the Ashman Department of Periodontology and Implant Dentistry at
the New York University College of Dentistry (NYUCD) Kriser Dental Center. The ID
was certified by the Office of Quality Assurance at NYUCD. This study is in compliance with the Health Insurance Portability and Accountability Act (HIPAA) requirements and approved by the University Committee on Activities involving Human
Subjects.
This literature review includes a total of 358 articles referring to “periimplantitis”,”Peri-implant diseases” (311 articles), ” treatment of peri-implantitis” (250articles), “surgical treatment of peri-implantitis” (218 articles), “re-osseointegration of
implants” (188 articles), “microbiology in peri-implantitis” (94 articles), “laser treatment of peri-implantitis” (32 articles), “implant surfaces and peri-implantitis” (50 articles), “peri-implantitis infection” (67 articles).The inclusion criteria for article consideration included:
1.
Treatment of peri-implantitis in human clinical studies.
2.
Treatment of peri-implantitis in animal clinical studies
3.
Re osseointegration of implants
4.
Peri-implant diseases
5.
Laser treatment of peri-implantitis

C

RESULTS AND DISCUSSION
Based on this literature review, 39 of the 358 articles were included in this evaluation.
he results of the literature review revealed that although there are a number ofstudies using different modalities to treat peri-implantitis most of the studies only
to have 6 to 12 month follow-up, with one study showing a 24-month follow up.

T

Fig 1c. Implant removal with torque wrench

Fig 1d. Healed after implant removal

observed after completion of antibiotic therapy due to bacterial recolonization of theimplant surface (14).
Because non-surgical treatment approaches failed to promote the re-osseointegrationof the exposed implant sites (37), additional surgical interventions have been used inorder to minimize the risk for a re-infection of the peri-implant pocket. Some of thetreatment modalities suggested for peri-implantitis are: 1) Sub-mucosal mechanicaldebridement and antimicrobial minocycline spheres (Arestin), 2) Mechanical ultrasound debridement without antibiotics, 3) Er:YAG laser with mechanical debridement, chlorohexidine, with and without open flap surgery, 4) Antimicrobial therapy
with open flap debridement, 5) Access flap surgery and nanocrystaline hydroxyapatite.
Renvert et al. (2006) compared the combination of oral hygiene instructions, mechanical debridement and topical application of minocycline microspheres (Arestin) in periimplant lesions (with bone loss corresponding to no more than three implant threads)
to the combination of oral hygiene instructions, mechanical debridement and 1%
chlorhexidine gel application. The results obtained after a follow-up period of 12months showed that with the Chlorohexidine group, only a limited reduction in bleeding on probing was achieved and the mean peri-implant probing depth (PD) remained
unchanged (3.9mm). On the other hand, in the minocycline group, the reduction ofFig 2c. Removed implants showing extend of infection

the mean values for both groups of peri-implant PPD and CAL were not statisticallysignificantly different from the corresponding values at baseline. Therefore the resultsof the Er:YAG laser seems to be limited to a 6-month period, particularly for advanced
peri-implantitis lesions. (30)
Leonhardt et al. (2003) evaluated the 5-year outcome of a combined surgical (openflap) and antimicrobial treatment of peri-implantitis in humans. Leonhardt studied theeffect of systemic antimicrobial therapy (amoxicillin and metronidazole) together with
an open flap procedure and in conjunction with mechanical debridement of theimplant surface for decontamination. The treatment was successful in 58% of theimplants treated during follow-up for 5 years (26). Smoking was found to be a negative risk factor for treatment success.
Schwarz et al. (2006b) evaluated and compared the efficacy of two bone regenerative
procedures for the treatment of moderate intra-bony peri-implantitis lesions that
included at a greater than 6mm probing depth and an intrabony component of 3mm
as detected on radiographs. The defects were randomly treated either with a surgicaldebridement and filled with nanocrystalline hydroxyapatite, or surgical debridement
and filled with bovine-derived xenograft (Bio-Osss, Geistlich, Wolhusen, Switzerland)
combined with a bioresorbable porcine-derived collagen membrane (Bio-Gides,
Geistlich, Wolhusen, Switzerland) (31). After two years the study showed that the com-

Fig 2d. Site of implant failure due to peri-implantitis

Fig 4a. Peri-implantitis around on press-fit im

the use of chemical agents such as chlorhexidine had only limited effects on clinicaland microbiological parameters. Adjunctive local or systemic antibiotics were shown
to reduce bleeding on probing and probing depths in combination with mechanicaldebridement. Beneficial effects of laser therapy on peri-implantitis have been shown,
but this approach needs to be further evaluated. Implant surface bacterial decontamination is the essential in treating peri-implantitis infections. In the studies described,
establishing an adequate healthy tissue environment proved to be difficult since
inflammation was still present in a significant number of patients. New treatment
modalities need to be evaluated using long term randomized-controlled studies to
identify predictable and successful treatment of peri-implantitis.

Procedures

Table 1. Comparison of different treatment modalities

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This Presentation was Sponsored by New York University Department of Implant Dentistry
Alumni Association (NYUDIDAA) and the Office for International Program