Implantology occupies an increasingly important place in the modern management of patients affected by one or more tooth losses.

Studies on implant survival rates have multiplied, highlighting a high survival rate, ranging from 82 to 95% over a period of 5 to 16 years [1-4]. However, the term "survival" is not synonymous with success. Indeed, survival involves the persistence of implants in the oral cavity, regardless of any biological and/or mechanical complications, whereas success is defined as the survival of these implants in the absence of any complication [5,6].

Alongside the increasing use of implants, complications, particularly biological ones, tend to rise. They can be classified into two categories: so-called primary complications, which concern the absence of osseointegration, and so-called secondary complications, which concern implants for which osseointegration has been achieved. In this article, we will focus on peri-implantitis, biological complications of infectious origin that occur on osteointegrated implants.

The diagnosis and management of peri-implantitis remain complex [7] due to the diversity of manifestations and implant anatomy to date, there is no consensus regarding the management of peri-implantitis, but lasers are increasingly being proposed as adjuncts in the treatment of peri-implant lesions. The aim of this presentation is to highlight the qualities of Erbium Yag and diode lasers in the reduction of peri-implantitis.

First, a review of the epidemiological and biological characteristics of the peri-implant periodontium highlights the reasons for the difficulty in treating peri-implantitis. Then, a reproducible laser-assisted management protocol is described, with the precise methods for peri-implant decontamination while respecting the therapeutic gradient, namely first a non-surgical approach and then, when necessary, a more surgical approach. This protocol is inspired by the existing literature on the management of peri-implantitis and precised by clinical experience.

Peri-Implantitis: Definition and Epidemiological Datas

Peri-implantitis is defined as an inflammatory pathology associated with a biofilm, characterized by bleeding on probing, an increase in pocket depths, and progressive bone loss (Fig 1). Its prevalence is estimated to be between 6.6% and 18% of implants, depending on diagnostic criteria and the populations studied (with or without peri-implant maintenance, exposure to a risk factor or not…) [8-10]. It tends to increase over time [3,4,11].

Peri-implantitis was introduced in the new classification of periodontal and peri-implant diseases following the 2017 Workshop [12,13]. Another classification, more focused on bone defects and the number of implants involved, was proposed in 2019 by Para, the APARA classification [14].

Peri-Implantitis: Biological Datas

The peri-implant mucosa, although it presents numerous similarities with the gingiva surrounding the teeth [15], has its own particularities that explain its fragility [7]: its collagen fibers are inserted parallel to the axis of the implant [16], its vascularization comes from periosteal tissues, and the absence of the periodontal ligament would explain why it is less developed than around a tooth. There is also a zone of avascular connective tissue adjacent to the implant [15].

Figure 1: Peri-Implantitis Caracterized by Bone-Loss and Suppuration in a Context of Lack of Keratinized Gum.

The lack of organization of the peri-implant mucosa therefore makes it more vulnerable to the presence of bacteria. Very quickly after the implant is placed, within the first 30 minutes, the peri-implant mucosa is colonized by bacteria (Porphyromonas gingivalis, Tanarella forsythia, Treponema denticola, Staphylococcus aureus …) [17].

The tissue response to bacterial aggression is similar at the level of the gingiva and the peri-implant mucosa [15], but the defense potential would be lower around implants [18] due to the tissue fragility mentioned above, and the inflammatory response around the implant is more intense [19] with a different distribution of pro-inflammatory molecules [20]. Bone destruction around the implant is therefore more severe than around teeth.

Treatment of Peri-Implantitis

As with periodontitis, there is a significant therapeutic range for the management of peri-implantitis. The treatment of peri-implantitis is based on a multimodal strategy, which varies according to the severity of the lesion with the aim of controlling infection and stabilizing peri-implant tissues. Although there is still no consensus or protocol to date regarding the management of these treatments, many therapeutic proposals have been made with several common points. Two main approaches are distinguished: either non-surgical treatments based on mechanical debridement alone or with the addition of antiseptics and/or antibiotics, on the one hand, or surgical treatments on the other hand with mechanical debridement associated or not with a bone grafting technique.

Many authors agree that at a later stage of mucositis, non-surgical treatment would be ineffective and that surgical treatment would be necessary in the management of peri-implantitis [7,14]. However, the use of lasers also allows for very satisfactory results in certain situations without the need for surgical intervention. When this access becomes insufficient, flap elevation then becomes necessary.

The following protocol concerns the management of localized peri-implantitis, in the context of a healthy or generally stabilized periodontium [21]. If necessary, the first step is to restore generalized periodontal health, and the initial management of the implant is included in the periodontal etiological therapy.

Non-Surgical Treatment of Peri-Implantitis Assisted By Laser Diode

As for periodontitis, mechanical debridement is the basis of treatment. It can be carried out using ultrasound, plastic or titanium curettes, titanium brushes, or air-flow. It may be combined or not with antiseptic agents (povidone-iodine, 0.12% chlorhexidine, 3% or 10-volume hydrogen peroxide) or local antibiotics. However, conventional instruments have limitations when faced with the complexity of implant surfaces [22].

Figure 2: Decontamination with Diode Laser (OHLLT Protocol).

Decontamination constitutes a key step, made difficult by the microtopography of the implants. Diode lasers, notably used in photochemical or photodynamic protocols (PDT, OHLLT), have shown significant antibacterial effects and represent an excellent alternative for combating bacterial resistance with better results than with ultrasounds alone [23,24]. Highlighted a significant reduction in bacterial load with the use of a diode laser in addition to conventional treatment.

The diode laser decontamination protocol proposed here follows the principle developed by Rey G [25] under the name of dye-free dynamic phototherapy and now called the OHLLT photochemical protocol (Oxygen High Level Laser Therapy).

The implant is initially debrided conventionally using ultrasound and air-flow. The peri-implant pocket is then irrigated with 3% or 10-volume hydrogen peroxide for about 1 to 3 minutes for decontamination by diode laser.

The diode laser is a photonic device that produces light radiation that is spatially and temporally coherent, based on the principle of stimulated emission. Coherent light is light whose parameters are all predictable and correlated at every point in time or space. The aim of OHLLT is to lead the beam of light to interact with the molecular oxygen present locally. When the target tissues are oxygenated (hydrogen peroxide at 3% or 10 volumes), a photo-oxidative reaction allows the formation of singlet oxygen and triplet oxygen which will have a decontaminating action by destroying the bacterial membrane of the microorganisms contained and sensitive to tissue oxygenation [26,27].

The diode laser used in this protocol has a wavelength of 980 nm (also possible at 808 nm). The radiation is applied using a 400 µm diameter fiber. The fiber is introduced tangentially to the implant (Fig 2) and is kept in constant back-and-forth motion for about 20 to 30 seconds per side at a power of 2 to 3 Watts. The fiber must not remain static or stuck at the bottom of the pocket, as this could cause carbonization of its tip, altering its properties. The diode laser is a so-called penetrating laser, meaning that it acts deeply on the tissues concerned. Its effect is not immediately visible.

This protocol results in satisfactory and reproducible bone healing in the case of pockets up to 6 mm deep (Fig 3, Fig 4).

Figure 3: Peri-Implantitis Grade PA1d (APARA) On Implant in Position 35 Treated By Laser Assistance through OHLLT Protocol. A. Initial Situation. B. One Year after Treatment. C. Two Years after Treatment.

Figure 4: Peri-Implant Treatment in 35-36 Laser-Assisted By OHLLT. Coverage of One Thread for Each Implant and Bone Densification at 3 Months Post-Operation. A, B. Initial Situation, Peri-Implantitis Grade PA2c (APARA). C. Result at 3 Months.

There is another laser diode decontamination protocol, photodynamic therapy, which uses a dye as a sensitizing agent to laser radiation. This protocol is used at a wavelength around 660 nm and will not be detailed in this article.

Non-Surgical Treatment of Peri-Implantitis Assisted By Laser Erbium-Yag (Er-Yag) Combined to Laser Diode

Beyond a pocket depth of 6 mm, conventional mechanical debridement, even when combined with diode laser decontamination, is no longer sufficient for a lasting result. Current data suggest that no single approach allows for optimal management. Protocols combining mechanical debridement (Er-YAG) AND antibacterial decontamination (diode laser), and even surgical procedures if needed (implantoplasty, regeneration), seem to offer the best clinical results.

The Er-YAG laser appears to be an interesting alternative due to its high absorption in water and its low thermal effect. The study by Schwarz et al [28].  Showed a significant clinical improvement after treatment with the Er-YAG laser, notably a reduction in pocket depths and bleeding on probing. Its mechanism is based on a photo-mechanical effect that allows the disorganization of the biofilm and the removal of contaminated tissues.

The mechanical debridement protocol with Erbium-Yag laser is similar to that proposed for the treatment of periodontal pockets. It has the advantage, in the case of implants, of not altering the implant surface and of improving access to the threads that are devoid of bone and not yet exposed at the gingival level [29].  A tip of approximately 600 µm is introduced into the peri-implant pocket tangentially and then directed toward the gingival tissue as a first step in order to vaporize the granulation tissue at a power of P = 2 to 3 Watts with a frequency of F = 15 Hz. Then, the tip is directed toward the implant at a power of P = 1.5 Watts and a frequency of F = 30 Hz. The site is then irrigated with hydrogen peroxide, and decontamination according to the OHLLT protocol completes the process (Fig 5).

Figure 5: Combined protocol with Erbium-Yag laser debridement and diode laser decontamination. a and f. Initial situation class PA1d (APARA). b. Debridement with Erbium-Yag laser. c. Decontamination with diode laser according to OHLLT protocol. d. Healing at day 15. e and g. Healing at 18 months.

Surgical Treatment of Peri-Implantitis Assisted by Laser Erbium-Yag (Er-Yag) Combined to Laser Diode without Bone Grafting

When non-surgical therapy does not yield satisfactory results, access surgery with or without implantoplasty is performed with the aim of eliminating peri-implant granulation tissue under visual control and possibly smoothing the implant threads along the entire length of the alveolysis. Making the implant smooth allows certain access to the bacteria and subsequently prevents recontamination of the threads. The surgery can be resective to reshape the bone and soft tissues when regeneration is not possible [30].

The lifting of a flap facilitates access for better debridement assisted by Erbium-Yag laser and decontamination with a diode laser according to the photochemical protocol or PDT, or with the diode laser-only protocol [26]. Thanks to the photostimulatory effect of the diode laser, host bone repair can be achieved more quickly (Fig 6, Fig 7).

Figure 6: Surgical Treatment of Peri-Implantitis at 15 (PA1d APARA Class) Using A Combined Laser Protocol without Bone Grafting and Without Modification of the Implant Surface. A And B. Initial Situation. C. Bone Healing At 1 Year.

This combined protocol with Erbium-Yag laser debridement and diode laser decontamination allows reproducible bone repair, without altering the implant anatomy. Bone repair is achieved quickly despite the absence of bone filling.

Figure 7: Surgical Treatment of Peri-Implantitis at 46 and 47 (Class PA2c APARA) Using A Combined Laser Protocol without Bone Grafting and Without Modification of the Implant Surface. A. Initial Situation. B. Healing At 5 Months.

Surgical Treatment of Peri-Implantitis Assisted by Laser Erbium-Yag (Er-Yag) Combined to Laser Diode without Bone Grafting

Peri-implant debridement and decontamination can be combined with bone grafting as part of regenerative surgery, with the aim of reconstructing the peri-implant bone environment. According to some authors, the results would be better than in the case of debridement alone [31-33]. The management protocol is the same as in non-surgical treatment once the flap is raised. The Er-Yag laser allows for optimal debridement and better access to the underlying bone and implant structure. Through its micro-perforations in the bone, it promotes vascularization of the site and, thereby, bone healing. Next comes the decontamination of the site and the implant surface using the diode laser according to the OHLLT protocol. Depending on the size of the bone defect, bone grafting then allows for improvement of the bone environment and architecture (Fig 8, Fig 9). However, the results obtained by bone graft doesn’t appear to be superior to that without biomaterial.

Figure 8: Surgical treatment of peri-implantitis at 15 (class PA1c (APARA)) using a combined laser protocol with bone grafting and without modification of the implant surface. a. Initial situation. b. Healing at 5 years.

Figure 9: Surgical Treatment of Peri-Implantitis at 16 (PA1d (APARA)) Using a Combined Laser Protocol with Bone Grafting and Modification of the Implant Surface.

A. Initial Situation. B. Healing At 3 Years.

Photobiomodulation (PBM) or Low-Level Laser Therapy (LLT)

During the healing phase of each stage of this protocol, PBM sessions may be offered, with the frequency varying depending on the severity of the initial condition. PBM involves the use of low-intensity red or near-infrared light to stimulate cellular functions without causing significant tissue heating. The most commonly used wavelengths are usually between 630 and 980 nm, with fluences of 1 to 10 J/cm². PBM mainly relies on the mitochondrial activation of cytochrome c oxidase, resulting in an increase in ATP production, modulation of inflammation, and stimulation of tissue repair mechanisms. This thus helps promote mucosal healing and limit postoperative edema in surgical situations. It can be achieved using a diode laser (with a defocusing lens), or with a low-intensity laser device (e.g., ATP38, Miltadent…) (Fig 10).

Figure 10: “Intrabuccal Photobiomodulation with Diode Laser A or Extrabuccal with LLT Miltadent Laser B.”

The management of peri-implantitis is based on a reasoned approach, founded on current scientific data, and the use of lasers cannot replace conventional approaches. Lasers are valuable adjunct tools that help facilitate and optimize care through faster and more complete debridement (Er-YAG laser), optimal decontamination (diode laser), a less traumatic approach, and more favorable outcomes with accelerated healing (PBM).

The results obtained allow significant bone repairs by stimulating the patient's biological potential. They thus make it possible to do without regenerative techniques, which are more complex and costly.

Laser-assisted management is increasingly emerging as an essential solution if protocols are more standardized for greater comparability. But the best treatment for peri-implantitis remains its prevention with good pre-implant preparation and effective maintenance.

1. Berglundh T, Persson L, Klinge B. A systematic review of the incidence of biological and technical complications in implant dentistry reported in prospective longitudinal studies of at least 5 years. J Clin Periodontol. 2002; 29: 197-212.
2. Karoussis IK, Salvi GE, Heitz-Mayfield LJ, Bragger U, 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 Implants Res. 2003; 14: 329-39.
3. 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: 290-295.
4. Simonis P, Dufour T, Tenenbaum H. Long-term implant survival and success: a 10–16-year follow-up of non-submerged dental implants. Clin Oral Implants Res. 2010; 21: 772-777.
5. Albrektsson T, Zarb G, Worthington P. The Long-Term Efficacy of Currently-Used Dental Implants: A Review and Proposed Criterion of Success. Int J Oral Maxillofac Implants. 1986; 1: 11-25.
6. Smith DE, Zarb GA. Criteria for success of osseointegrated endosseous implants. J Prosthet Dent. 1989; 62: 567-72.
7. Saadi-Thiers K, Huck O, Davideau JL, Tenenbaum H. Les peri-implantites, donnees actuelles. Journal de Parodontologie et d’Implantologie Orale. 2011; 30: 177-186.
8. Dreyer H, Grischke J, Tiede C, Eberhard J, Schweitzer A, Toikkanen SE, et al. Epidemiology and risk factors of peri-implantitis: A systematic review. J Periodontal Res. 2018; 53: 657-681.
9. Reis INRD, Huaman-Mendoza AA, Ramadan D, Honorio HM, Naenni N, Romito GA, et al. The prevalence of peri-implant mucositis and peri-implantitis based on the world workshop criteria: A systematic review and meta-analysis. J Dent. 2025; 160: 105914.
10. Diaz P, Gonzalo E, Villagra LJG, Miegimolle B, Suarez MJ. What is the prevalence of peri-implantitis? A systematic review and meta-analysis. BMC Oral Health. 2022; 22: 449.
11. Roos-Jansaker AM, Renvert H, Lindahl C, Renvert S. Nine- to fourteen-year follow-up of implant treatment. Part III: factors associated with peri-implant lesions. J Clin Periodontol. 2006; 33: 296-301.
12. Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018; 89: 173-182.
13. Caton JG, Armitage G, Berglundh T, Chapple ILC, Jepsen S, Kornman KS, et al. A new classification scheme for periodontal and peri-implant diseases and conditions - Introduction and key changes from the 1999 classification. J Clin Periodontol. 2018; 45: 1-8.
14. Para A. Peri-implantites: Approche therapeutique. Parresia.Guide clinique pratique. 2019.
15. Davarpanah M, Szmukler-Moncler S, Khoury PM, Jakubowicz-Kohen B, Martinez H. Manuel d’implantologie clinique. Concepts, protocoles et innovations récentes. Rueil-Malmaison. Editions CDP, 2008.
16. Comut AA, Weber HP, Shortkroff S, Cui FZ, Spector M. Connective tissue orientation around dental implants in a canine model. Clin Oral Implants Res. 2001; 12: 433-40.
17. Fürst MM, Salvi GE, Lang NP, Persson GR. Bacterial colonization immediately after installation on oral titanium implants. Clin Oral Implants Res. 2007; 18: 501-8.
18. El Chaar E. Revue sur la peri-implantite. J Parodontol. Implantol. Orale. 2009; 28: 225-236.
19. Ericsson I, Berglundh T, Marinello C, Liljenberg B, Lindhe J. Long-standing plaque and gingivitis at implants and teeth in the dog. Clin Oral Implants Res. 1992; 3: 99-103.
20. Konttinen YT, Lappalainen R, Laine P, Kitti U, Santavirta S, Teronen O. Immunohistochemical evaluation of inflammatory mediators in failing implants. Int J Periodontics Restorative Dent. 2006; 26: 135-41.
21. Roccuzzo M, De Angelis N, Bonino L, Aglietta M. Ten-year results of a three arms prospective cohort study on implants in periodontally compromised patients. 2012.
22. Meyle J, Fischer-Wasels L. Non-surgical treatment of peri-implantitis. Br Dent J. 2024; 237: 780?5.
23. Schwarz F, Bieling K, Nuesry E, Sculean A, Becker J. Clinical and histological healing pattern of peri-implantitis lesions following non-surgical treatment with an Er:YAG laser. Lasers Surg Med. 2006; 38: 663-71.
24. Ar?san V, Karabuda ZC, Ar?c? SV, Topcuoglu N, Kulekci G. A randomized clinical trial of an adjunct diode laser application for the nonsurgical treatment of peri-implantitis. Photomedicine and Laser Surgery. 2015; 33: 547-554.
25. Rey G. Traitement parodontaux et peri-implantaires laser-assistes. Realite scientifique et medicale. Low Price. 2020.
26. Caccianiga G, Rey G, Baldoni M, Paiusco A. Clinical, Radiographic and Microbiological Evaluation of High Level Laser Therapy, a New Photodynamic Therapy Protocol, in Peri-Implantitis Treatment; a Pilot Experience. Biomed Res Int. 2016; 6321906.
27. Courval A, Harmouche L, Mathieu A, Petit C, Huck O, Severac F, et al. Impact of molar furcations on phototherapy dynamic outcomes: A 6-month split-mouth randomized clinical trial. Int J Environ Res Public Health. 2020; 17.
28. Schwarz F, Sculean A, Rothamel D, Schwenzer K, Georg T, Becker J. Clinical evaluation of an Er:YAG laser for nonsurgical treatment of peri-implantitis: a pilot study. Clinical Oral Implants Research. 2005; 16: 44-52.
29. Renvert S, Lindahl C, Roos-Jansaker AM, Persson GR. Treatment of peri-implantitis using an Er:YAG laser or an air-abrasive device: a randomized clinical trial. J Clin Periodontol. 2011; 8: 65-73.
30. Jing C, Liang C, Xian T, Xiang Q, Ruiying L, Jia M, et al. Efficacy of surgical methods for peri-implantitis: a systematic review and network meta-analysis. BMC Oral Health. 2023; 23: 227.
31. Schwarz F, Jepsen S, Herten M, Sager M, Rothamel D, Becker J. Influence of different treatment approaches on non-submerged and submerged healing of ligature induced peri-implantitis lesions: an experimental study in dogs. J Clin Periodontol. 2006; 33: 584-95.
32. Heitz-Mayfield LJA, Salvi GE. Peri-implant mucositis and peri-implantitis. J Clin Periodontol. 2018; 20: 237-245 ;
33. Rey G, Missika P. Traitements parodontaux et lasers en omnipratique dentaire. La simplicite efficace. Ed Masson. Mai 2010. Clinical Oral Implants Research. 2010; 21: 772-778.