New strategies and developments for peri-implant disease

Abstract

The aim of this illustrated review is to present the new strategies and developments to treatment and diagnosis of periimplant diseases. Periimplant disease is a subject of great concern for modern dentistry. The numbers of implant exhibiting biological complications grows as implant dentistry expands thought-out the world. Diagnosis and treatment of those diseases are still controversial and difficult. We present novel treatment for infection control and biological rationale of additional use of guided bone regeneration, with an illustrative explanation of the treatments presented with two cases.

Peri-Iimplantitis; Bone Regeneration; Infection Control

Introduction

Periimplantitis is an inflammatory disease that affects the bone and mucosa around osseointegrated implants. It is suggested to be an evolution of a previous periimplant disease, mucositis, and differs from it due to the presence of progressive bone loss.¹

Mucositis has been shown to be a plaque-induced inflammation of periimplant mucosa. Its reversibility is obtained with proper treatment by means of professional and patient mechanical plaque control.² On the other hand, when having periimplantitis onset, it cannot be reversed with plaque control only and more complex treatment are needed.

Periimplantitis has been an issue of great concern for implant dentistry in the past 20 years. Its prevalence has shown to increase with the number of patients receiving dental implants around the world. It has been difficult to obtain reliable numbers of incidence and prevalence of the disease due to remarked discrepancies on diagnostic criteria.³ However, a prevalence of around 20% in subjects non compliant to a supportive care regime,⁴ and around 14.5% in compliant patients⁵ is, to date, accepted.

The aetiology appears to be bacterial and its composition has shown to be more complex then in periodontitis.⁶ .Most of the proposed treatments rely on strategies of disinfection used on periodontitis such as debridement with curettes and use of local/systemic broad-spectrum antibiotics associated or not with anti-infective solutions, such as used for chemical plaque control. The rationale of using adjunctive broad-spectrum antibiotics to treat a site-specific lesion is questionable due to the risk of development of bacterial resistance and the well known side effects for the rest of the body.

The primary treatment goal is to disinfect and to reduce the inflammation (bleeding on probing). As a secondary goal, restoration of the periimplant tissue lost due to the disease progression, usually with regenerative approaches using biologics and/or growth factors.

The aim of this review is to present the developments and new strategies to the treatment and diagnosis of periimplant disease, and help to draw lines for future research.

Diagnosis

Currently, the tools for diagnosing periimplant conditions are still the periodontal probe and the dental x-ray,¹ both not accurate as it would be desirable for a diagnostic tool. Bleeding on probing has been a measure of periodontal inflammation for decades⁷ and is still the main diagnostic tool for this condition, despite the possibilities of false negative. To overcome those limitations, recently, authors had proposed a system based on optical spectroscopy for quantification of mucosal inflammation around implants.⁸ This system would be failure proof for inconsistencies found on probing, especially in implants, such as excessive force/pressure on probing, and difficulties in the positioning of the probe due to prosthetic reasons.

The spectroscopy system is composed by a light irradiation emitter surrounded by a fluorescence receptor, the diagnosis is based on an algorithm analysis trough a computer that will measure the amount of oxygenated haemoglobin and concentration of oxygenated/non oxygenated haemoglobin in the tissue.⁹ In the future this method might be a user-friendly, chairside, site-specific, diagnostic and prognostic test for periodontitis and periimplantitis.

Other studies are focusing on analysis of gingival crevicular fluid in order to obtain a non-invasive chairside diagnosis.¹⁰ To date, it is still an expensive and non user-friendly method. Molecular diagnostic may be valuable in the future, but seems to be far from daily basis clinical application.

Treatment

Disinfection and antiinfective therapies

As we stated before, peri-implant diseases have microbial aetiology and the treatment primary goal should be cleansing the implant surface for restoring the bone implant contact. Studies demonstrate that mechanical debriding is not sufficient to provide condition for re-osseointegration¹¹ or even to solve inflammation,¹² this can be easily explained by the complexity of the implant surface and difficulty to access areas of the implant, even with surgical approach.¹³

Some authors had proposed the use of titanium brushes mounted on handpiece with irrigation to mechanically treat the contaminated implant surface¹⁴ . The efficiency of this treatment is still unclear. At the authors experience, those brushes seem to polish the implant surface without reducing it ( Figure 1 ). A more radical treatment of the implant surface includes the total removal of implant threads and outer surface by means of a tungsten bur and metal polishing rubber.¹⁵ , ¹⁶ Clinical data suggests a good defect resolution in small case series,¹⁷ but reducing the outer surface of the a narrow implant can cause future biomechanical problems leading to factures, especially on internal connection implants.¹⁸

Figure 1
A) implant surface before the use of titanium brush; B) polished surface as result of titanium brush instrumentation.

As a more conservative approach and in an attempt to preserve the implant surface, adjuvant therapies have been proposed to overcome the the mechanical debridement access difficulty and enhance decontamination. They are usually based on therapeutic strategies for treatment the of periodontitis such as systemic¹⁹ and local antibiotics and disinfectant solution ( i.e. , Chlorexidine),²⁰ with questionable additional effects.

Last decades, as a consequence of the growing worry with the development of microbial resistance, efforts are being made to find novel antibacterial therapies at all fields of medicine, leading to alternative treatments.

One of the options that have been emerged is the antimicrobial photodynamic therapy²¹ (aPDT) that will be the main focus of this review. aPDT consist on the use of a dye, or photosensitizer in association with a light source, usually a laser , to induce photokilling of certain cells, in this case, bacterial pathogens. Despite it involves a series of complex reaction that goes through photophysics and photochemistry, it is important to understand the mechanisms and the factors that may enhance/jeopardize its efficacy and thus, adapt and redesign protocols to maximize efficiency.

There are basically two pathways to photokilling promoted by aPDT, the first one involves reactions with surrounding oxygen molecules, generating superoxide radicals, toxic to bacterial cells. The other pathway involve quenching H⁺ or OH^-from aminoacids/proteic molecules, and RNA and DNA, leading to a bacterial death, similar to apoptosis of mammalians cells.²¹ This mechanisms are very different from the ones of common antimicrobials and transform aPDT on an important agent to avoid microbial resistance.²²

In dentistry, aPDT uses photosensitizers from the family of phenothiazine (ie. Toluidine blue and methylene blue), and the protocols may vary according to the laser device used, power density, and photosensitizer concentration. When dealing with protocols reproducibility, clinicians should lay special attention to the power density used in the studies to obtain similar results.

aPDT has been extensively used on the treatment of infections such as periodontal diseases, with good results, especially when applied in deep pockets.²³ , ²⁴ Due to its powerful disinfection potential and ability to target regions not reached by curettes and others mechanical cleansing methods, aPDT has been proposed as an alternative for the treatment of periimplantitis.

As an example of the treatment, this illustrated review will show 2 cases that were treated with an aPDT protocol in order to discuss biological and clinical results obtained.

Case 1

A diabetic patient with one internal conical connection implant presented mucosal inflammation with bleeding on probing and great loss of attachment ( Figure 2 ). The first treatment approach was to perform a surgical access in the area without vertical incisions ( Figure 3 ). Then, a mechanical debridement was performed with titanium curettes in order to remove any calculus or visible plaque at the implant surface, followed by the application of a phenothiazine chloride ( Figure 4 ), a pre-irradiation time of 5 minutes, rinsing with saline and red laser irradiation ( Figure 5 ) in a total power density of 44J/cm² equally distributed on the 6 aspects of the implant (mesial lingual, lingual, disto-lingual, mesial-buccal, buccal, disto-buccal). The flap, then was closed with two simple sutures ( Figure 6 ). Six weeks after, the treatment showed a considerable mucosal recession, but an inflammation resolution ( Figure 7 ). Thus, a new surgical access was performed in an attempt to gain the hard tissue loss due to the disease progression trough guided bone regeneration. Two vertical releasing incisions were made ( Figure 8 ) and a flap was raised to visualize a circumferential defect ( Figure 9 ). The internal connection of the implant was protected and the defect was filled with a bovine bone mineral ( Figure 10 ). A collagen membrane was placed, with a hole in its center to allow the connection of an abutment at the implant ( Figure 11 ). Flap closure was performed with simple sutures ( Figure 12 ) and a new crown was installed. After 6 months, there were no sign of inflammation and the defect was completely filled with biomaterial/bone ( Figure 13 ).

Figure 2
Initial probing depth associated with bleeding.

Figure 3
Coronal aspect after opening the flap.

Figure 4
Rinsing with phenotiazinium chloride.

Figure 5
Aspect of the flap after 5 minutes of pre-irradiation time followed by rinsing with saline. The optical fiber in position.

Figure 6
Immediate post-op.

Figure 7
Surgical result of the disinfection showing resolution of inflammation and probing depth, exhibiting mucosal recession.

Figure 8
Flap design with two vertical releasing incisions.

Figure 9
A) coronal aspect of the surgical site; B) Buccal aspect of the surgical site.

Figure 10
Defect filled with bovine hydroxyapatite, the internal connection was protected with a sulcus measuring pin. A) Coronal Aspect; B) Buccal aspect.

Figure 11
The collagen membrane was positioned with the aid of a sulcus measuring pin (A- buccal aspect; B- coronal aspect) and a hole was made in the center, followed by the connection of the abutment (C).

Figure 12
Immediate post-op.

Figure 13
A) Clinical aspect after healing. B)X-ray after healing.

Case 2

Patient with a maxillary overdenture installed 2 years before, presented mucosal inflammation and bleeding on probing and bone loss non-compatible with implant connection at the second implant in the right side ( Figure 14 ). Fifteen days before the surgical access, the implant was non-surgically debrided with plastic curettes to reduce inflammation before surgery. Surgical treatment was performed two weeks after the non-surgical therapy ( Figures 15 ) with two vertical releasing incisions to access the implant surface ( Figure 16 ), and the same decontamination protocol of case 1 ( Figure 17 ). Guided bone regeneration (GBR) was performed with the aid of a xenograft bone substitute and a collagen membrane ( Figure 18 ) and the flap was closed with simple sutures ( Figure 19 ). 24 months after the surgery the implant presented with no clinical signs of inflammation ( Figure 20 ).

Figure 14
A) clinical aspect showing the difference between healthy and diseased implant; B) Probing depth showing bleeding.

Figure 15
Occlusal (A) and Buccal (B) aspects 1 week after non surgical pre treatment.

Figure 16
Aspect of the implant with conical connection exhibiting bone loss.

Figure 17
Aspect of the surgical site after rinsing with methylene blue 1% solution (A) and after a pre irradiation time of 5 minutes and rinsing with saline (B).

Figure 18
Xenogeneic bone substitute covered by a native collagen membrane.

Figure 19
Immediate post op.

Figure 20
Clinical aspect of health after 2 years.

Discussion

Both cases successfully treated periimplantitis, with radiographical defect filling, and resolution of inflammation. All those features might be considered a successful treatment in its state of art. Thus, we have recently assessed the use of aPDT as an antiinfective treatment, and the effect of the GBR- as used on those two cases- on histological and clinical outcomes of induced periimplantitis in a dog model.²⁵ , ²⁶ Those studies had shown that the protocol used on those cases was effective on dramatically reducing pathogenic microbiota at periimplantitis lesions,²⁵ lowering the proportions of bacteria of red and orange complex.

Within the histological data, we could compare the effect of GBR and submerged healing on bone gain and re-osseointegration. Results showed that adding GBR and collagen membrane to the treatment had little or none additional benefits on both outcomes. By means of a statistical analysis with general estimated equation, we could assess the effects of some variables such as early exposure of the implant on the healing period, use of GBR and site of the implant (mesial, distal, lingual and buccal). There was no difference on bone gain and re-osseointegration with or without GBR, buccal sites responded worse independently of the treatment performed and early exposure during healing was the most important factor that modified the treatment outcome. Early exposed implants showed less re-osseointegration, less bone gain and more inflammatory reactions the non-early exposed implant.²⁶ Bone quality was similar to in GBR and non-GBR sites, with GBR site exhibiting particles of bovine bone mineral (BBM) embebed in bone/connective tissue. In this study, no systemic antibiotics were used for the treatment of periimplantitis.

More recently, a randomized clinical trial compared the use and non-use of bone substitute at clinical and radiological parameters after treating periimplantitis.²⁷ The results on radiographic bone gain and clinical attachment level gains failed to present differences between treatments, but according to the authors criteria of treatment success (defect fill ≥ 1.0 mm, with PPD values at the implant was ≤ 5 mm, with no BOP - 1 out of 4 sites per implant with BOP grade 1 accepted- and with no suppuration at any of 4 assessed sites per implant ) the use of BBM had significant advantages.²⁷ If absence of bleeding on probing (absence of inflammation) was considered as success, no differences could be detected between the groups.

Despite those combined clinical results, the additional benefits of using GBR as adjunctive treatment of periimplantitis lesions is still not a consensus. There is a lack of specific case indications to support predictable results for its use, and the weight of other factors such as primary closure, flap stability and, as reported in preclinical studies,²⁶ flap dehiscence after treatment. It is important to highlight, however, that the GBR is a predictable technique for bone augmentation in a great number of situations, but its additional benefits are questionable when treating periimplantitis considering that the own biological response of the host tissues would be as effective as the aid of a GBR, after proper decontamination. The cost effectiveness of the adding a bone substitute and a collagen membrane to obtain limited or no benefits at all on treatment results should be considered.

Future research should aim maneuvers/novel treatments to reduce the incidence of flap dehiscence after surgery in order to maintain stability, especially at the first weeks of healing. The use of growth factors either synthetic (rh-PDGF; amelogenin), or autologous (L-PRF) might be of interest to achieve better and faster healing after decontamination.

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Publication Dates

• Publication in this collection
  30 Sept 2019
• Date of issue
  2019

History

• Received
  11 June 2019
• Accepted
  13 June 2019
• Reviewed
  18 June 2019