PERI-IMPLANTITIS ETIOPATHOGENESIS – THERAPIES

INTRODUCTION

1. Particularities of peri-implant soft tissues
2. Definitions of peri-implantitis
3. Etiopathogenesis
4. Risk factors for peri-implantitis:
   1. History of periodontitis
   2. License plate check
   3. Diabetes
   4. Tobacco consumption
   5. Presence of keratinized tissue
   6. Excess cement in implant-supported cemented prostheses
   7. Nature of the implant surface
   8. Occlusal factor

5. Morphological classifications of peri-implant lesions
6. Diagnosis
7. Therapeutics for peri-implant lesions:
   1. Non-surgical therapies:
      1. Mechanical treatment
      2. Complementary treatments
   2. Surgical therapies:
      1. Access flap / osteoplasty
      2. Filling/Regeneration Techniques
      3. Explantation
8. Peri-implant maintenance CONCLUSION

INTRODUCTION :

Nowadays, implants are an integral part of the therapeutic arsenal for treating partial or total edentulism in our patients. Physiological bone remodeling at the implant collar is systematic and necessary to establish a biological space around the implants. However, pathological bone loss may occur due to bacterial colonization of the peri-implant tissues, causing peri-implantitis.

1. Particularities of peri-implant soft tissues :

• The peri-implant soft tissues are called “peri-implant mucosa” with a pale pink color that differentiates it from the alveolar mucosa with the presence of surface pitting due to the insertion of collagen fiber bundles under the lining epithelium.
• The height of the peri-implant junctional epithelium is significantly close to its counterpart at the gingivo-dental junction (1 mm).
• The collagen fibers of the peri-implant connective tissue are oriented parallel to the implant surface into which no insertion of these fibers is possible.
• The peri-implant connective tissue is particularly rich in collagen fibers but not in fibroblasts, which ensures slow tissue renewal.
• The peri-implant vascular network is less extensive due to the absence of vascularization from the periodontal ligament which can irrigate the peri-implant connective tissue.

2. Definitions :

• European Workshop of Periodontology, 1980 : “A destructive inflammatory process affecting the hard and soft tissues around osseointegrated implants leading to the formation of a peri-implant pocket with bone loss.”
• Alberktsson, 1986 : “Peri-implantitis is defined as a progressive loss of peri-implant bone exceeding accepted norms and simultaneous with inflammation of the soft tissues.”
• Smith and Zarb, 1989 : “Peri-implantitis is defined as an inflammatory process that involves the peri-implant mucosa and bone and may result in progressive loss of implant-supporting tissues.”
• A definition has been adopted: “peri-implant diseases are infections. Peri-implant mucositis describes an inflammatory lesion within the mucosa, while peri-implantitis also affects the bone support” (Lindhe and Meyle, 2008) .

3. Etiopathogenesis :

Dental implants replace missing tooth roots. The bacterial flora found around implants and in the peri-implant grooves is derived from the natural flora of the oral cavity. The composition of this peri-implant flora is similar to that of the gingival grooves.

In partially edentulous people, colonization of the peri-implant grooves will occur very quickly from the germs of the gingivo-dental grooves. In totally edentulous people, the absence of teeth reduces the number of

microbial reservoirs. However, the tonsillar crypts and the tongue harbor mainly anaerobic germs that will recolonize the new implant sites within 12 to 18 months.

• Formation of primary biofilm :

The peri-implant plaque is organized into a biofilm. The film allows bacteria to be absorbed thanks to the constituents of their wall. This first organic layer is deposited immediately after the implant is exposed in the oral cavity. Within the first few minutes, isolated bacteria adhere to it. These then begin their division process and, within a few hours, form large bacterial aggregates.

• Similarities with periodontitis :

Primary colonizations are mainly Gram-positive, rather aerobic cocci. The appearance of inflammatory phenomena corresponds to an anaerobic drift of the flora in which Gram-negative bacteria become more numerous. Most periodontal pathogenic bacteria are also involved in the genesis of peri-implantitis. The only particularity concerns the presence of Stylococcus aureus which has the capacity to colonize foreign bodies and in particular those made of titanium.

4. Risk factors :
   1. History of periodontitis :

Before any implant treatment, periodontal disease must be treated and then stabilized, because placing implants in an inadequate periodontal environment could compromise implant success. Treating this periodontal pathology, which affects the remaining teeth, reduces the risk of peri-implant disease but does not eliminate it. Therefore, very regular monitoring of implant patients is essential.

2. License plate check :

Very poor oral hygiene (plaque index ≥2) is strongly associated with the presence of peri-implantitis (Ferreira et al. 2006).

The prevalence of bleeding on probing increases as the plaque index increases.

Plaque control around implants is no different from that around teeth. It is important to brush the implant healing abutments during the osseointegration period with a soft brush. However, accessibility sometimes requires the use of single-tufted brushes or special floss such as Superfloss.

3. Diabetes :

Diabetes is a systemic disease that affects healing capacity at multiple levels, increasing patients’ susceptibility to infections and implant failure rates ( Fiorellini and Nevins 2000 ). Diabetes is associated with an increased risk of peri-implantitis, particularly in subjects with poor diabetes control.

4. Tobacco consumption :

Studies on risk indicators of peri-implant diseases report a significant association of smoking with peri-implant mucositis, marginal bone loss and peri-implantitis (Roos-Jansaker et al. 2006, Fransson et al 2008 ).

5. Presence of keratinized tissue :

A lack of keratinized tissue around implants is linked to plaque accumulation, tissue inflammation, gingival recession, and attachment loss. ( Lin et al, 2013 ).

6. Excess cement for sealing implant-supported prostheses :

Studies have shown that excess cement sealant is associated with signs of peri-implant disease in the majority of cases and that after removal of this excess, no clinical signs of peri-implant disease were observed.

7. Nature of the implant surface :

The characteristics of an implant surface depend on its relief (surface irregularity), roughness, and chemical composition. Studies have shown no statistically significant differences between implant types (machined or rough surfaces), except for the higher incidence of peri-implantitis in implants with a rough surface.

8. Occlusal factor :

It has been observed that peri-implant tissue destruction begins to occur with 250µm of excessive occlusal height. When this occlusal load is transmitted to the peri-implant tissues, it causes more bone destruction than that induced by bacterial plaque. According to Renvert, occlusal overload cannot be the cause of peri-implantitis. According to him, since occlusal trauma systematically leads to implant fibrointegration, the etiology of peri-implantitis remains exclusively infectious.

5. Morphological classifications of peri-implant lesions :

• Classification of Spickermann et al, 1995:

Class 1 : bone destruction only horizontal and not very marked.

Class 2 : moderate bone destruction with possibly isolated vertical damage.

Class 3 : more advanced horizontal and circular bone destruction.

Class 4 : Severe bone destruction with extensive circular lesions and, possibly, complete loss of a bone wall.

Classes 3 and 4 require implant removal.

• Classification of Behnecke et al, 1997 : based on radiographic diagnosis of bone lesions:
  • Horizontal lesions.
  • Columnar or crevasse lesions.
  • Funnel-shaped lesions.
  • Bowl-shaped lesions.
  • Lesions combining the previous forms.
• Classification by Schwartz et al, 2007 :

Class 1 : The implant tray remains at the crestal level

Class 2 : the implant tray is located above the crestal level

6. Diagnosis :

The diagnosis of peri-implantitis is based on different criteria: probing, suppuration, radiographic analysis and mobility (Heitz-Mayfield 2008).

• The survey :

• Essential for the diagnosis of peri-implant diseases.
• Probe with light force (0.25N) and avoid damaging the peri-implant tissues.
• Bleeding on probing indicates the presence of inflammation of the peri-implant mucosa and can be used as an indicator of loss of supporting tissues.
• An increase in probing depth over time is associated with attachment loss.

• Suppuration : is the sign of an infectious lesion and an advanced state of peri-implant inflammation, generally at the level of a deep pocket.
• X-rays : are required to assess and compare bone level around implants, particularly at the proximal level. Panoramic X-rays provide a comprehensive view but are not precise enough; long cone X-rays are preferred, allowing us to visualize bone loss mesially and distally.
• Mobility : the implant indicates a complete loss of osseointegration, its removal is then indicated.

7. Therapeutics for peri-implant lesions :

The key element in the management of peri-implantitis is the need to intervene as early as possible. All authors agree on the following points:

• Implementation of effective oral hygiene.
• Balancing occlusal forces.
• Supra- and subgingival mechanical debridement of the peri-implant lesion associated with local antibacterial treatment.
• Systemic antibiotic therapy.
• Mechanical polishing and chemical disinfection of the implant surface.

1. Non-surgical therapies:
   1. Mechanical treatment:

The objective of mechanical debridement is identical to that of periodontal treatment, namely the elimination of supra- and subgingival microbial biofilms. However, the instrumentation used differs from that used in periodontology in order to avoid altering the surface of the implants. It is recommended to use specific plastic or carbon instruments, possibly coated with a gold alloy.

Mechanical debridement can be performed either with specific curettes with shapes adapted to the implants, or with ultrasonic inserts made of Teflon, carbon or composite material.

Accessible metal surfaces will finally be polished with rubber cups and a very low-abrasive paste.

2. Additional treatments :

Different molecules and several administration modalities have been proposed in addition to mechanical treatment.

• Topically, chlorhexidine remains the antibacterial molecule of choice. It is either applied to the implant surface in gel form or administered via irrigation. Slow-release chlorhexidine carriers have shown greater benefits.
• Topical antibiotic therapy appears to be slightly more effective. This involves either tetracycline fibers, which are no longer available, or 25% metronidazole gel, or doxycycline gel, or minocycline microspheres.
• Systemic antibiotic therapy with the use of metronidazole alone or in combination with amoxicillin has also been proposed according to the same protocols as those recommended in periodontology (1.5g/day in 2 or 3 doses for 7 days).
• Laser treatment has been considered based on its bactericidal and detoxifying action. However, the results are not clinically significant and the cost/benefit ratio cannot recommend laser treatment at this time.

2. Surgical therapies :
   1. Access flap/osteoplasty:

Its objective is to eliminate or, at least, reduce the peri-implant pocket and to restore the peri-implant soft tissues to a morphology compatible with satisfactory access to oral hygiene.

The elevation of a mucoperiosteal flap will allow cleaning and possible treatment of the implant surface, the removal of granulation tissue and osteoplasty if necessary. However, mechanical debridement, even under direct vision, is limited; chemical treatment is then often essential.

2. Filling/regeneration techniques:

In the presence of infra-osseous peri-implant bone defects and craters, the use of filling and/or regeneration techniques derived from periodontal surgery may offer hope for reconstruction, even if only partial, of the tissues destroyed by the peri-implant pathology.

Many materials are available and it is possible to identify the following techniques:

• Protocols for filling the lesion with autogenous bone, bank bone, animal bone or synthetic materials (bone substitutes);
• Guided bone regeneration protocols using resorbable or non-resorbable membranes;
• Combination of the two protocols (placement of a filling product held in place by a covering membrane).

3. Explantation :

When all the therapies mentioned above prove ineffective and do not stop the process of bone destruction, it is necessary to make the decision to remove the implant before the bone loss is such that it no longer allows the placement of a new implant.

The explantation of the implant requires the use of a hollow drill (trephine) whose internal diameter will be slightly greater than the external diameter of the implant or the insertion of a screw in the internal part of the implant connected to a torque wrench and thus an unscrewing movement of the implant in its alveolar housing is carried out.

The placement of a new implant will only be considered after bone reconstruction and removal of risk factors that could have contributed to peri-implantitis.

8. Peri-implant maintenance :

Implant maintenance is an integral part of implant treatment. It must be considered during the design phase of the implant project and implemented at every stage of its implementation. This will fully fulfill its role in preventing peri-implantitis and ensuring long-term implant maintenance. It requires ongoing cooperation from the patient.

The frequency of maintenance sessions varies depending on the patients’ risk assessment criteria; these sessions include:

• an analysis of peri-implant tissues;
• preventive bacterial maintenance;
• early treatment of mucositis;
• an occlusion check.

Conclusion :

While implant technology has revolutionized the management of edentulism, the increasing occurrence of infectious complications such as peri-implantitis poses an enormous challenge.

Therefore, attention must be focused on prevention through the selection of cases justifying implantation, periodontal sanitation prior to the placement of implants, oral hygiene instructions, regular monitoring accompanied at each session by careful professional prophylaxis. Such measures are the only ones likely to limit the appearance of these infectious complications that are peri-implantitis .

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PERI-IMPLANTITIS ETIOPATHOGENESIS – THERAPIES