Management of peri‐implant mucositis and peri‐implantitis

Peri‐implant diseases are defined as inflammatory lesions of the surrounding peri‐implant tissues and include peri‐implant mucositis (an inflammatory lesion limited to the surrounding mucosa of an implant) and peri‐implantitis (an inflammatory lesion of the mucosa that affects the supporting bone with resulting loss of osseointegration). This review aims to describe the different approaches to manage both entities and to provide a critical evaluation of the evidence available on their efficacy. Therapy of peri‐implant mucositis and nonsurgical therapy of peri‐implantitis usually involve mechanical debridement of the implant surface using curettes, ultrasonic devices, air‐abrasive devices or lasers, with or without the adjunctive use of local antibiotics or antiseptics. The efficacy of these therapies has been demonstrated for mucositis: controlled clinical trials show an improvement in clinical parameters, especially in bleeding on probing. For peri‐implantitis, the results are limited, especially in terms of probing pocket‐depth reduction. Surgical therapy of peri‐implantitis is indicated when nonsurgical therapy fails to control the inflammatory changes. Selection of the surgical technique should be based on the characteristics of the peri‐implant lesion. In the presence of deep circumferential and intrabony defects, surgical interventions should aim to provide thorough debridement, implant‐surface decontamination and defect reconstruction. In the presence of defects without clear bony walls or with a predominant suprabony component, the aim of the surgical intervention should be the thorough debridement and the repositioning of the marginal mucosa to enable the patient to perform effective oral‐hygiene practices, although this aim may compromise the esthetic result of the implant‐supported restoration.     

Animal models for peri‐implant mucositis and peri‐implantitis

The treatment of infectious diseases affecting osseointegrated implants in function has become a demanding issue in implant dentistry. Since the early 1990s, preclinical data from animal studies have provided important insights into the etiology, pathogenesis and therapy of peri‐implant diseases. Established lesions in animals have shown many features in common with those found in human biopsy material. The current review focuses on animal studies, employing different models to induce peri‐implant mucositis and peri‐implantitis.     

Clinical approaches to treat peri‐implant mucositis and peri‐implantitis

Therapies proposed for the treatment of peri‐implant diseases are primarily based on the evidence available from treating periodontitis. The primary objective is elimination of the biofilm from the implant surface, and nonsurgical therapy is a commonly used treatment. A number of adjunctive therapies have been introduced to overcome accessibility problems or difficulties with decontamination of implant surfaces as a result of specific surface characteristics. It is now accepted that following successful decontamination, clinicians can attempt to regenerate the bone that was lost as a result of infection. The ultimate goal is re‐osseointegration, and a number of regenerative techniques have been introduced. By reviewing the existing evidence, it seems that peri‐implant mucositis is reversible when appropriately treated. Additionally, a combined therapy (mechanical therapy with local antimicrobials as adjuncts) can serve as an alternative to surgical intervention when treating peri‐implantits in cases not suitable for surgery. Surgical therapy is an effective method for treating peri‐implantitis, and various degrees of success of the use of regenerative procedures have been reported, regardless of whether or not radiographic evidence of defect fill has been achieved. Finally, no matter which therapy is employed, a prerequisite for the long‐term stability of treatment results obtained is the ability of the patient to maintain good oral hygiene.     

Risk factors of peri‐implant pathology

This study aimed to identify risk factors for the incidence of peri‐implant pathology. One‐thousand, two‐hundred and seventy‐fifty patients (255 cases and 1020 controls), rehabilitated with dental implants, were included. Peri‐implant pathology was defined as the presence of peri‐implant pockets ≥ 5 mm, bleeding on probing, vertical bone loss, and loss of attachment ≥2 mm. Cases and controls were matched for age, gender, and duration of follow‐up. A logistic regression model was used, with estimation of the OR for each variable and interaction, with a level of significance of 5%. The risk factors for peri‐implant pathology were: history of periodontitis (OR = 19), bacterial plaque (OR = 3.6), bleeding (OR = 2.9), bone level on the medium third of the implant (OR = 13.9), lack of prosthetic fit or non‐optimal screw joint (OR = 5.9), metal–ceramic restorations (OR = 3.9), and the interaction between bacterial plaque and the proximity of other teeth or implants (PROXI) (OR = 4.3). PROXI (OR = 0.44) exerted a protective effect when independent. Based on the results, peri‐implant pathology represents a group of multifactorial situations with interaction of biological and biomechanical components in its pathogenesis. It was possible to model the condition and to assess, with high precision, the risk profile of each patient.     

The evaluation of peri‐implant sulcus fluid osteocalcin,osteopontin, and osteonectin levels in peri‐implant diseases

1 Background

Peri‐implant mucositis is an inflammation of the soft tissues surrounding an implant. Peri‐implantitis refers to a process characterized by peri‐implant bone loss along with an inflammation of the soft tissues. Osteocalcin, osteopontin, and osteonectin proteins are related to bone remodeling. The aim of the present study was to investigate peri‐implant sulcus fluid (PISF) osteocalcin, osteopontin, and osteonectin levels in peri‐implant mucositis and peri‐implantitis.

2 Methods

Fifty‐two implants with peri‐implantitis, 46 implants with peri‐implant mucositis, and 47 control implants were included in the study. Clinical parameters including probing depth, modified sulcus bleeding index and modified plaque index were recorded. PISF osteocalcin, osteopontin, and osteonectin levels were analyzed by ELISA kits.

3 Results

There were no significant differences in PISF osteocalcin, osteopontin, and osteonectin total amounts between healthy controls, peri‐implant mucositis and peri‐implantitis groups (P > 0.05). Probing depths were not correlated with PISF osteocalcin, osteopontin, and osteonectin levels in the study groups (P > 0.05).

4 Conclusions

Soft tissue inflammation around dental implants does not cause a change in osteocalcin, osteopontin, and osteonectin levels in PISF. Also, peri‐implantitis does not seem to give rise to an increase in PISF levels of osteocalcin, osteopontin, and osteonectin.     

Soft‐tissue dehiscence coverage at peri‐implant sites

Soft‐tissue dehiscence at the facial aspect of an osteointegrated implant is a common complication which impacts on the final esthetic result. The etiology and ways of diagnosing this condition are still controversial. Many factors seem to influence the position of the peri‐implant soft‐tissue margin, and some of these have been studied more carefully than others. Various surgical and combination surgical‐prosthetic approaches have been described to treat soft‐tissue dehiscence, with the latter appearing to be more predictable. This paper focuses on the factors affecting peri‐implant soft‐tissue margins and describes the different treatment approaches, reported in the literature, to treat buccal soft‐tissue dehiscence, with more focus on the prosthetic–surgical–prosthetic approach.     

Implant‐abutment connection as contributing factor to peri‐implant diseases

Dental implant–supported prostheses are an established treatment modality for the functional and esthetic rehabilitation of partial and/or complete edentulous patients. One of the most essential factors for successful treatment outcomes stems from preservation of the peri‐implant bone. Early peri‐implant crestal bone loss has been a common observation, coincides with the time period where most treatment manipulations occur and has been considered as a complex multifactorial event. Microbial leakage at the implant‐abutment interface has been associated with inflammatory reactions that may jeopardize peri‐implant crestal bone stability. Prevention of microbial leakage at the implant‐abutment interface is a major challenge in the construction of two‐piece implant systems. Changes in the implant‐abutment complex design achieved reduction in the magnitude of microbial leakage and/or separation of the implant‐abutment interface from the osseous surface. However, it is still unclear if microbial leakage at the implant‐abutment interface plays a role beyond the initial crestal bone remodeling, namely on the development of peri‐implantitis. Therefore, the aim of this review is to analyze the knowledge available on the integrity of different types of implant‐abutment connections and their potential role on the development of peri‐implant crestal bone loss and peri‐implant diseases.