5.1Treatment of Peri-implant Mucositis

Therapy of peri-implant mucositis should be considered as a preventive measure for the onset of peri-implantitis (Salvi and Zitzmann 2014). Treatment of peri-implant mucositis includes a thorough removal of the supra- and submucosal peri-implant biofilm in combination with reinforcement of self-performed oral hygiene. Non-surgical mechanical removal of calculus and biofilm can be performed using a range of instruments, including hand curettes and ultrasonic devices with plastic, carbon-fiber, or titanium tips. Peri-implant biofilms can also be removed using air-abrasive devices, Erbium-YAG lasers, photodynamic therapy, or rubber polishing cups. The clinician should choose a method that minimizes damage to the surface of the transmucosal parts of the prosthesis or implant. Antiseptics such as chlorhexidine solution or gel can also be recommended as an adjunct to mechanical cleaning.

Importantly, if contributing factors such as an ill-fitting or overcontoured prosthesis, a loose abutment or screw, or the presence of a foreign body are identified, these must be corrected in order to achieve a satisfactory treatment outcome.

Peri-implant mucositis is considered to be a reversible condition, as was demonstrated in an experimental human study where clinical signs of peri-implant inflammation (bleeding on probing) resolved when oral hygiene was reinstated after a period of three weeks of undisturbed plaque accumulation (Salvi and coworkers 2012).

Studies evaluating various treatment protocols using a variety of antiseptic agents and toothpastes have shown significant clinical improvements with a reduction in bleeding on probing, and probing depths following treatment (Figs 1a-c and 2a-b).

However, in these studies complete resolution of the peri-implant mucositis in all cases is infrequently reported. The location of the implant-supported restoration margin may influence the treatment response. This was shown in a clinical study where implants diagnosed with peri-implant mucositis with submucosal restoration margins had less favorable treatment outcomes compared to those with equi- or supramucosal margins (Heitz-Mayfield and coworkers 2011).

The use of systemic antibiotics for the treatment of peri-implant mucositis is not justified (Hallström and coworkers 2012).

Fig 1a Peri-implant mucositis at implant site 11. Bleeding on probing caused by inadequate oral hygiene resulting in plaque accumulation and inflammation.

Fig 1b Periapical radiograph. No marginal bone loss at sites 11 and 12, confirming the diagnosis of peri-implant mucositis.

Fig 1c Resolution of the of peri-implant mucositis at site 11 (no bleeding on probing) four weeks following non-surgical debridement and oral hygiene instructions (flossing and brushing).

Fig 2a Implant at site 35 diagnosed with peri-implant mucositis caused by an impacted food particle. Swelling and redness of the peri-implant mucosa. There was also bleeding on probing.

Fig 2b Resolution of the peri-implant mucositis following debridement, oral hygiene instructions and application of chlorhexidine solution twice daily for one week.

5.2Treatment of Peri-implantitis

Once a patient is diagnosed with peri-implantitis, it is important to implement an anti-infective treatment protocol. If left untreated, it is likely that there will be progression of bone loss and possible eventual loss of the implant.

The primary goal of peri-implantitis treatment should be to establish healthy peri-implant tissues. A cause-related treatment approach is required, aimed at resolution of the infection and the prevention of disease progression. Secondary goals may include peri-implant bone regeneration and fill of the intrabony defect.

There are many different peri-implantitis treatment approaches reported in the literature; however, it is not yet known which is the most effective (Esposito and coworkers 2012).

A recent systematic review prepared for the 5th ITI Consensus Conference identified a number of study protocols where successful treatment outcomes were achieved in the majority of patients at twelve months (Heitz-Mayfield and Mombelli 2014). This systematic review also found that, while favorable short-term outcomes were documented in many studies, a lack of disease resolution as well as progression and recurrence of the disease and implant loss despite treatment were also reported (Heitz-Mayfield and Mombelli 2014).

The following sequence of treatment is recommended, based on similarities in the treatment approaches between studies included in this systematic review (Heitz-Mayfield and coworkers 2014):

5.2.1Pre-treatment Phase

•Assessment of the peri-implant soft tissues, bone levels and the prosthesis in order to make a diagnosis and to establish the cause of the infection.
A correctly aligned radiograph showing the marginal bone levels should be made and clinical probing measurements recorded. This will give an indication of the severity of the bone loss, and allow identification of any hardware or technical complication that may manifest itself as a biological complication, for example an inadequate fit of prosthetic components. In addition, obtaining previous radiographic records from the time of the prosthesis insertion will allow a comparison with the current marginal bone levels.

•Reduction of risk factors for peri-implant infection—in particular poor oral hygiene, inadequate prosthesis design, tobacco use, presence of periodontal diseases and systemic diseases that may predispose to peri-implant infection.

•If the prosthesis is screw-retained, it may have to be removed to assess the prosthetic components or modify the prosthesis’ contours. Removal may also improve access to the implant surface for subsequent debridement.

5.2.2Non-surgical Debridement

Non-surgical debridement should be aimed at the removal of calculus and biofilm supramucosally, and on the contaminated implant surface if accessible (Figs 3 and 6a-b). This can be achieved using a range of instruments including curettes or ultrasonic instruments with carbon-fiber or plastic tips (Fig 3), air-abrasive devices using sodium bicarbonate or glycine powder (Fig 4), Er:YAG lasers, or photodynamic therapy.

Due to the topography of the implant and the limited access to the implant surface, care should be taken using instruments submucosally in deep pockets to avoid breakage of the instrument, or damage to the surrounding tissues.

Antiseptics (e.g. chlorhexidine), local antimicrobials (e.g. minocycline-HCL microspheres) (Figs 5a–b), or systemic antimicrobials may be used in conjunction with the non-surgical debridement. The severity of the peri-implantitis lesion appears to play a role in the success of non-surgical therapy, with a more favorable treatment outcome at implants without advanced bone loss and without deep peri-implant probing depths.

Fig 3 Removing calculus and biofilm using a titanium curette from an implant with peri-implantitis.

Fig 4 Non-surgical debridement using an air-abrasive device (glycine powder). The flexible tip of the air-abrasive device is placed approximately 3 mm submucosally.

Figs 5a-b Applying a local antimicrobial agent (minocycline microspheres) following non-surgical debridement using a titanium curette for the treatment of peri-implantitis at site 15.