Is Peri-Implantitis Curable?

Peri-implant mucositis and peri-implantitis are clinically associated with inflammation of soft tissue around implants; however, peri-implantitis is associated with radiographic bone loss. Recently a new classification scheme—peri-implant health, peri-implant mucositis, peri-implantitis, and peri-implant soft-tissue and hard-tissue deficiencies—was introduced. Although various clinical interventions to treat peri-implant diseases have been suggested, early diagnosis and treatment is the key to successful outcomes. Clinicians can select nonsurgical or surgical techniques according to the clinical parameters present, although surgical intervention seems to be more effective in treating peri-implantitis. The best approach to treat peri-implantitis remains controversial.

Key points

  • Diagnosis of peri-implant mucositis and peri-implantitis is based on the combination of clinical and radiographic findings.

  • Prevention of peri-implant mucositis and peri-implantitis remains the fundamental strategy for a long-term successful outcome of implants.

  • Treatment of peri-implantitis is not standardized and several surgical techniques are available. However, none provides an evidence-based approach nor predictable therapeutic outcome. Peri-implantitis, like periodontitis, is manageable but not curable.

Peri-implantitis: definition and diagnosis

Peri-implant diseases were originally classified into 2 categories; peri-implant mucositis and peri-implantitis. Both diagnoses involve mucosal tissue inflammation around implants with clinical signs that include redness, swelling, and bleeding on probing. Peri-implant mucositis is characterized by the marginal inflammation of mucosal tissues around the implant with no loss of supporting bone following initial bone remodeling, whereas peri-implantitis is characterized by inflammation of mucosal tissues around the implant including progressive loss of supporting bone beyond initial biological remodeling.

The 2017 World Workshop on the classification of periodontitis and peri-implant diseases introduced a new classification scheme to further expand the definitions of peri-implant health, peri-implant mucositis, peri-implantitis, and peri-implant soft-tissue and hard-tissue deficiencies. This expansion includes more stringent criteria for disease assessment to include patients with and without previous evaluation by the clinician. Based on these factors, a diagnostic tree can be used ( Fig. 1 ):

Fig. 1
Peri-implant evaluation flowchart.

Peri-implant health is characterized by absence of peri-implant signs of soft-tissue inflammation (redness, swelling, and profuse bleeding on probing) and absence of further additional bone loss following initial healing/bone remodeling ( Fig. 2 ).

Fig. 2
Peri-implant health is demonstrated in site #9. ( A ) No evidence of radiographic bone loss around the implant. ( B ) Healthy mucosal tissue around the implant at 3-year follow-up.

Peri-implant mucositis is characterized by the presence of peri-implant signs of inflammation (redness, swelling, line or drop of bleeding, and/or suppuration within 30 seconds following probing), combined with no additional bone loss following initial healing ( Fig. 3 ).

Fig. 3
Peri-implant mucositis around implant #9 at 2-year follow-up. ( A ) The radiographic bone level around implants #7 and #9 do not show additional bone loss following initial healing. ( B ) Marginal inflammation of mucosal tissue exists around implant #9.

Peri-implantitis is based on following criteria:

  • 1.

    Presence of peri-implant signs of inflammation

  • 2.

    Radiographic evidence of progressive bone loss (≥2 mm) 1 year following delivery of implant prosthesis

  • 3.

    Increasing probing depth compared with probing depth values collected after placement of the prosthetic reconstruction

In the absence of previous radiographs, a radiographic bone level of ≥3 mm along with bleeding on probing (BoP) and probing depths ≥6 mm along with bleeding indicates peri-implantitis as shown in Fig. 4 .

Fig. 4
Peri-implantitis of implant #13. ( A ) Radiographic bone level is normal at the time of implant loading ( B ) Radiographic crestal bone loss is present around the implant after 3 years of function. ( C ) Healthy mucosal tissue around implant at the time of implant loading. ( D ) After 3 years of function, circumferential bone loss around the implant as seen after the reflection of mucoperiosteal flap.

Peri-implant soft-tissue and hard-tissue deficiencies may result from a multitude of factors including systemic and local diseases, medications, tissue healing, turnover, response to interventions, trauma, iatrogenic factors, malpositioned implants, biochemical factors, and tissue morphology and phenotype ( Fig. 5 ). Furthermore, peri-implantitis can be further classified as mild, moderate, and severe according to probing depth, bone loss, and presence of bleeding and suppuration ( Fig. 6 ).

Fig. 5
Peri-implant soft-tissue and hard-tissue deficiencies in implant #8. ( A ) Bone deficiency around the implant is due to implant malposition (implant is more apically and facially positioned). ( B ) Mucosal deficiency is present on midfacial of the implant.

Fig. 6
Classification of peri-implant severity.
( Data from Froum SJ, Rosen, PS. A proposed classification for peri-implantitis. Int J Periodontics Restorative Dent 2012;32(5):533–40.)

Prevalence and risk factors

Joos-Jansaker et. al. reported that peri-implant mucositis is present in 48% of implants followed from 9 to 14 years. However, this prevalence could be underreported because peri-implant mucositis is reversible. The prevalence of peri-implantitis is more difficult to assess because study methodologies, specifically in terms of peri-implantitis criteria, vary greatly. Peri-implantitis has been reported to range from 1.1% to 85% of implants and in 3% of nonsmokers to 53% of smokers with periodontitis history. Prevalence of peri-implantitis also increases in patients without regular maintenance care (18% vs 9% in patients with regular maintenance). Incidence of peri-implantitis also seems to increase with time: from 0.4% within 3 years after implant placement to 43.9% within 5 years after implant placement. According to a recent meta-analysis, the risk factors for peri-implant diseases include: smoking (odds ratio [OR] 1.7, 95% confidence interval [CI] 1.25–2.3), diabetes mellitus (OR 2.5, 95% CI 1.4–4.5), lack of prophylaxis, and a current or previous history of periodontal disease that has been shown to increase the incidence of peri-implant diseases. Thus, these risk factors need to be taken into consideration when managing peri-implantitis.

Prevention and maintenance

Peri-implantitis is known to be preceded by peri-mucositis; thus, preventive therapy aiming at the preservation and maintenance of mucosal health around an implant is essential. The “epithelial sealing” around implants is like that of teeth, and there is no evidence that structural differences affects the host response to bacterial challenge. Therefore, the process of mucositis is very similar to that of gingivitis. Additionally there is evidence to suggest that, like gingivitis, peri-implant mucositis is reversible when it is effectively treated. Initial studies showing implant surface damage from the use of probe or common mechanical instruments, such as Cavitron tips and regular scalers, deter practitioners from using basic prevention techniques, especially in the disruption of subgingival biofilm around implants. Subgingival biofilm disruption on a regular basis is essential to avoid initial inflammation (peri-mucositis). Instruments, such as titanium scalers, regular sonic and ultrasonic scalers with plastic tips, or piezoelectric scalers with carbon or plastic tips, can be used around implant abutments and seem to be safe with regard to subgingival biofilm disruption.

There is a notable paucity of clinical trials addressing the efficacy of preventive measures, and most of these studies evaluated professional plaque control versus patient self-plaque control. There is a lack of a standard preventive measure with demonstrated efficacy to preserve peri-implant health. It has been reported that the use of a triclosan/copolymer toothpaste significantly reduced plaque and gingivitis and BoP as well as microbiological variables compared with a routine fluoride dentifrice after 6 months of application.

Managing periodontitis before implant placement

Periodontitis should be treated before the placement of a dental implant. A systematic review revealed that significantly more patients developed peri-implantitis when a prior history of periodontitis-associated tooth loss was present (risk ratio, 9; 95% CI 3.94–20.57). Moreover, significantly increased peri-implant marginal bone loss was observed in patients with periodontitis-associated tooth loss after 5 years, mean difference 0.5 mm (95% CI 0.06–0.94). Regular maintenance care must be emphasized in patients with a history of periodontitis to avoid the initiation of peri-implant disease.

Management of peri-implant diseases

Once the diagnosis of peri-implant mucositis or peri-implantitis has been made, several nonsurgical and surgical treatment modalities are available.

Nonsurgical Approaches

Peri-implant mucositis

Treatment of peri-implant mucositis is essential for the prevention of peri-implantitis. Mechanical therapy (with or without adjunctive use of antiseptic rinses) is usually the initial treatment of choice for this condition. Graziani and colleagues published a recent systematic review on the treatment of peri-implant mucositis. This publication concluded that only 6 parallel-arm randomized controlled trials (RCTs) evaluated the adjunctive effect of antimicrobial compounds (chlorhexidine [CHX], triclosan, essential oils, and tetracycline fibers) in the treatment of peri-implant mucositis. The results of these were as follows.

Chlorhexidine

  • No adjunctive effect was noted with the use of CHX on these studies (with the exception of one study that had low quality of evaluation methods )

  • Irrigation of sulcus with CHX did not enhance clinical outcomes in terms of reducing periodontal parameters and periodontopathogens

  • BoP sites did not decrease with the application of CHX gel

Essential oils

  • Superior plaque control of mouth rinse essential oils (Listerine) occurred when compared with the control in the absence of mechanical therapy

Triclosan

  • Less BoP was noted after daily usage of triclosan/copolymer-containing toothpaste when compared with a sodium fluoride toothpaste

Tetracycline fibers

  • In a controlled case series study, little effect was observed from the submucosal placement of tetracycline fibers

Peri-implantitis

Until recently, there was neither any standardized classification of peri-implantitis nor treatment approaches. In addition, the methods of decontamination of implant surfaces are still controversial. Most RCTs in the literature on this topic evaluate small sample sizes and are mostly of short duration.

Renvert and Polyzois examined all recent case series and controlled trials that used mechanical debridement and an adjunctive therapy (local antimicrobial, laser, ultrasonic, or air-abrasive devices). No additional benefits were found with the use of different debridement approaches such as air abrasion, ultrasonic scaling, or Erbium:YAG lasers in peri-implantitis lesions at 6 to 12 months after treatment. Table 1 shows controlled studies evaluating different nonsurgical approaches in the treatment of peri-implantitis and their outcomes in terms of reduction of clinical parameters obtained from the different treatment modalities applied.

Table 1
Nonsurgical treatment studies, treatment approaches, and clinical parameter reductions
Data from Renvert S, Polyzois IN. Clinical approaches to treat peri-implant mucositis and peri-implantitis. Periodontol 2000 2015;68(1):369–404.
Studies Treatment Approach Time (mo) PD/CAL Reduction Other Parameters/Notes
Nonsurgical approach: mechanical
Karring et al, 2005
  • a.

    OHI + carbon-fiber tip and aerosol spray with HA

  • b.

    OHI + carbon-fiber curette

6 Not significant from baseline Reduction on PI and BoP (a only)
Renvert et al, 2009
  • a.

    Titanium curette

  • b.

    Ultrasonic system with specially designed tip

6 Not significant from baseline Plaque index: mean difference from baseline to 6 mo (both groups) ( P <.01)
BoP: mean difference from baseline to 6 mo (both groups) ( P = .026)
Sahm et al, 2011
  • a.

    Air-abrasive device vs

  • b.

    Mechanical debridement (carbon-fiber curettes)

6
  • a.

    • PD: 0.6 mm

    • CAL: 0.4 mm

  • b.

    • PD: 0.5 mm

    • CAL: 0.5 mm

  • a.

    • PI: 0.1

    • BoP: 43.5%

    • R: 0.2 mm

  • b.

    • PI: 0.2

    • BoP: 11%

    • R: 0.0 mm

Nonsurgical approach: local antimicrobials
Buchter et al, 2004
  • Removal of prosthetic restoration + abutment sterilized + CHX irrigation (0.2%) + scaling (plastic instruments) +

    • a.

      8.5% doxycycline hyclate

    • b.

      No additional treatment

4
  • PD:

    • a.

      0.4 mm a

    • b.

      0.3 mm a

  • CAL:

    • a.

      1.1 mm a

    • b.

      0.3 mm a , b

  • BI:

Renvert et al, 2004
  • OHI + supra- and submucosal scaling + rubber cup polishing + submucosal administration of:

    • a.

      1 mg of Arestin

    • b.

      1 mL of 1% CHX gel

3
  • a.

    PD: 0.4 mm a

  • b.

    PD: no change

a. PI: 24% a ; BoP: 43% a , b
b. PI: 23%; BoP: 15%
Renvert et al, 2006
  • OHI + supra- and submucosal scaling + rubber cup polishing + submucosal administration of

    • a.

      1 mg of Arestin

    • b.

      1 mL of 1% chlorhexidine gel

12
  • a.

    PD: 0.3 mm a , b

  • b.

    PD: no change

  • a.

    PI: 23% a ; BoP: 17% a , b

  • b.

    PI: 24%; BoP: 8%

  • Microbiological improvements in both groups

Renvert et al, 2008
  • a.

    Minocycline HCl microspheres (Arestin)

  • b.

    0.1% chlorhexidine gel

12
  • PD (deepest site):

    • a.

      0.6 mm a

    • b.

      0.5 mm a (significant differences between the groups were found for probing depths up to 6 mo but not at 12 mo)

  • PI: moderate improvements in both groups

  • BoP (deepest site):

  • No difference in mean total viable counts between groups

Machtei et al, 2012
  • a.

    Mechanical therapy + matrix chips

  • b.

    Mechanical therapy + chlorhexidine chips

6
  • PD:

    • a.

      1.59 mm a

    • b.

      2.19 mm a

  • CAL:

    • a.

      1.56 mm a

    • b.

      2.21 mm a

  • BoP:

    • a.

      41% a

    • b.

      57.5% a

Schar et al, 2013
  • a.

    Mechanical therapy + minocycline microspheres

  • b.

    Mechanical therapy + photodynamic therapy

6
  • PD:

    • a.

      0.49 mm

    • b.

      0.36 mm

  • CAL:

    • a.

      0.19 mm

    • b.

      0.16 mm

  • R:

    • a.

      0.3 mm

    • b.

      0.2 mm

  • PI:

    • a.

      0.18

    • b.

      0.13

  • Equally effective treatments

Bassetti et al, 2014
  • a.

    Mechanical therapy + minocycline microspheres

  • b.

    Mechanical therapy + photodynamic therapy

12
  • PD:

    • a.

      0.56 mm

    • b.

      0.11 mm

  • CAL:

    • a.

      0.31 mm

    • b.

      0.08 mm

  • R:

    • a.

      0.27 mm

    • b.

      0.03 mm

  • PI:

    • a.

      0.21

    • b.

      0.1

  • Equally effective treatments

Nonsurgical approach: lasers and air-abrasive devices
Schwarz et al, 2005
  • Hygiene program 2 wk before treatment

    • a.

      Plastic curette + CHX irrigation (0.2%) + CHX gel

    • b.

      Er:YAG laser

6
  • PD:

    • a.

      0.7 mm a

    • b.

      0.8 mm a

  • CAL:

    • a.

      0.6 mm a

    • b.

      0.7 mm a

  • PI: unchanged

  • BoP:

Schwarz et al, 2006
  • Hygiene program 2 wk before treatment

    • a.

      Plastic curette + CHX

    • irrigation (0.2%) + CHX gel

    • b.

      Er:YAG laser

  • Maintenance: supragingival cleaning and OHI (1,3,6 and 12 mo)

  • Moderate disease: PD >4 mm + BoP + bone loss

  • Advanced disease: PD >7 mm + BoP + bone loss

12
  • PD:

    • a.

      0.2 mm (moderate) a ; 0.4 mm (advanced) a

    • b.

      0.5 mm (moderate); 0.4 mm (advanced) a

  • CAL:

    • a.

      0.1 mm (moderate); 0.3 mm (advanced)

    • b.

      0.3 mm (moderate); 0.2 mm (advanced)

  • PI: unchanged (higher at 12 mo)

  • BI:

    • a.

      0.3 (moderate disease) a ; 0.2 (advanced disease) a

    • b.

      0.4 (moderate) a ; 0.2 (advanced) a

Renvert et al, 2011
  • a.

    Perio-Flow monotherapy (n = 21 patients/45 implants)

  • b.

    Er:YAG laser monotherapy (n = 21 patients/55 implants)

  • OHI in both groups

6
  • PD:

    • a.

      0.9 mm

    • b.

      0.8 mm

  • Bone level changes:

    • a.

      −0.1 mm

    • b.

      −0.3 mm

  • BoP:

  • Clinical treatment results were limited and similar between the 2 approaches

Sahm et al, 2011
  • a.

    Air-abrasive device

  • b.

    Mechanical debridement (carbon-fiber curettes) + CHX

6
  • a.

    PD: 0.6 mm a

    • CAL: 0.4 mm a

  • b.

    PD: 0.5 mm a

    • CAL: 0.5 mm a

  • a.

    PI: 0.1

    • BI: 43.5% b

    • R: −0.2 mm

  • b.

    PI: 0.2

    • BI: 11%

    • R: 0.0

Only gold members can continue reading. Log In or Register to continue

Apr 27, 2020 | Posted by in General Dentistry | Comments Off on Is Peri-Implantitis Curable?
Premium Wordpress Themes by UFO Themes