Case Report

Regenerative Reconstructive Treatment of A Peri- Implantitis Case: New Perspectives for Implant Surface Decontamination

by Giovanni Barbagallo1,3*, Federica di Gregorio1,3, Gianluca Monaca1,3, Gloria Alì1,3, Vanina Porto2,3, Giovanni Assenza1,3

1DDS, DMD, Italy

2BDH, MSAT, Italy

3Centro Odontoiatrico Mediterraneo in Agreement with NHS, Private Dental Practice, Catania, Sicily, Italy

*Corresponding author: Giovanni Barbagallo, Centro Odontoiatrico Mediterraneo in Agreement with NHS, Private Dental Practice, Catania, Sicily, Italy

Received Date: 18 January, 2024

Accepted Date: 22 January, 2024

Published Date: 24 January, 2024

Citation: Barbagallo G, di Gregorio F, Monaca G, Alì G, Porto V, et al. (2024) Regenerative Reconstructive Treatment of A PeriImplantitis Case: New Perspectives for Implant Surface Decontamination. J Surg 9: 1984.


Introduction: Implantology is a therapeutic approach that has allowed the fixed prosthetic treatment of an increasing number of patients who would otherwise be destined for removable prosthetics. Peri-implant diseases are inflammatory conditions caused by biofilm that affect the tissues around dental implants; they are distinguished into peri-implant mucositis and peri-implantitis. Studies have shown a prevalence of 43-46.8% for mucositis and 19.83-22% for peri-implantitis. The primary goal of peri-implantitis treatment is to halt progressive bone loss by controlling bacterial infection.

Case Presentation: In 2013, a 68-year-old patient underwent rehabilitation with a fixed prosthesis on 5 implants in the lower arch. Despite regular check-ups, the implant in position 4.5 developed peri-implantitis. The patient is a non-smoker and maintains good plaque control. Reconstructive surgery was performed on the implant, with the treatment goal being not only conditioning and decontamination of the implant surface but also bone defect regeneration/reconstruction. Decontamination of implant threads, was carried out using ultrasonic instruments and 24% EDTA. At the 6-month postoperative follow-up, the implant showed no signs of inflammation (bleeding on probing and/or suppuration). Radiographic examination revealed clinically significant bone remineralization around the implant.

Conclusion: For the surgical treatment of peri-implantitis, reconstructive treatment involving mechanical debridement with ultrasonics and chemical decontamination, in addition to resolving peri-implant inflammation, allows for bone reconstruction around the implant. The use of multiple aids, both chemical and mechanical, for decontaminating the implant threads is key to achieving greater predictability in the procedure.


The absence of proper oral health in the adult population is a condition that can have significant socio-economic implications. In fact, poor oral hygiene negatively impacts an individual’s quality of life, both in terms of interpersonal relationships and common daily activities such as eating or smiling. Furthermore, clinical studies have linked poor oral hygiene, particularly periodontal disease, to numerous acute and chronic systemic conditions, including pneumonia, cerebrovascular diseases, heart attack, and diabetes [1-2]. The lack of one or more teeth is still a relatively common situation in the global population [3]. We are still far from achieving the goals set by the World Health Organization (WHO), which aimed for less than 5% edentulism at ages 64-74 and 75% of individuals with at least 20 functional teeth by 2001 [4-5].

Osseointegrated implantology has offered new perspectives in the field of prosthetic rehabilitation, showing significant development in the last thirty years. Today, it is considered the preferred choice for replacing a single missing tooth due to decay, periodontal disease, trauma, or agenesis, as well as for restoring entire dental arches. The biological complications affecting osseointegrated implants are of great interest in contemporary dentistry.Two clinical varieties can be distinguished: periimplant mucositis and peri-implantitis. While the presence of an inflammatory lesion is a common characteristic of both conditions, only the latter involves a loss of supporting bone [6]. Implantology has modified the traditional therapeutic approach, making fixed prosthesis treatments possible for an increasing number of patients who would otherwise be destined for removable prosthetics. However, after the significant expansion of the last forty years, driven by the belief that osseointegrated implants could be considered a “definitive” treatment, clinical observations of technical and biological complications have multiplied [6]. Following implant placement, a trans-mucosal passage forms around the implant abutment. Peri-implant mucosa and the gum surrounding adjacent teeth share common characteristics but also have differences [7].It has been demonstrated that healed periimplant mucosa contains a core of connective tissue, primarily composed of collagen fibers and matrix elements (85%), few fibroblasts (3%), and vascular units (5%). The surface facing the implant consists of two distinct parts: a “coronal” part covered by sulcular epithelium and a thin epithelium similar in appearance to the junctional epithelium of the gum, and a more “apical” part where connective tissue seems to be in direct contact with the implant surface (connective tissue attachment zone). Around the implants, the main bundles of collagen fibers are anchored in the crestal bone and extend parallel to the implant surface [8].Renewal of exposed surfaces through the exfoliation process counteracts bacterial accumulation. Teeth are non-exfoliating surfaces and, as such, provide an excellent substrate for the deposition and proliferation of bacterial aggregates. Depending on the type of bacteria and the location of the accumulation, carious lesions, gingivitis, and periodontitis may develop. The ability to adhere to surfaces is characteristic of almost all bacteria and depends on the type of surface, the more or less fluid environment, and the type of bacteria. Plaque is defined as a deposit of numerous species, yet to be fully identified, of bacteria organized in a complex matrix of extracellular bacterial polymers and salivary exudate products [9].

Salivary glycoproteins are rich in amino acids that establish electrostatic bonds with the enamel surface. This film is bacteriafree and is considered a physiological coating of the dental surface. An intricate microbial aggregation develops on the acquired film, characterized by the secretion of an adhesive and protective matrix known as biofilm. Initially, the biofilm consists of bacterial microcolonies, followed by their multiplication and maturation into a complex structure where bacteria organize a system of canaliculi for the flow of water and substances, further maturing the biofilm. The mechanisms of bacterial biofilm formation on implantprosthetic surfaces are similar to those described for natural dentition. As soon as the implant surface is exposed to the oral cavity, it is covered by a salivary film containing various molecules (high molecular weight mucins, IgA, α-amylase, etc.) that provide an anchoring medium for microorganism attachment. Although the key role played by bacterial biofilm in the etiology of peri-implant diseases is clear, the role of individual bacterial species and/or their specific interaction in the onset and development of the disease is still not well understood. The complexity and high number of bacterial species present in peri-implant sites on one hand, and the difficulty in establishing a correct temporal relationship between the colonization of sites by certain pathogenic microorganisms and the formation of lesions on the other, have so far hindered a clearer understanding of the pathogenic role of individual species or their interaction within the biofilm. In any case, bacterial colonization of the peri-implant sulcus plays a key role and consequently represents the primary target of peri-implantitis therapy (Lindhe and Meyle 2008) [10]. Mucositis is characterized by inflammation of the peri-implant support tissues resulting from the accumulation of bacterial biofilm on implant and/or prosthetic surfaces [6].

In predisposed individuals, prolonged plaque accumulation and consequent inflammation of peri-implant mucosal tissues may eventually be followed by involvement in the lesion of supporting peri-implant bone tissue, leading to its coronal-apical resorption, defining the picture of peri-implantitis [6]. In this case as well, some similarities with periodontitis are evident, particularly the formation of a pocket at the peri-implant sulcus level, the presence of inflammation clinically manifested as bleeding on probing, and the loss of peri-implant bone tissue that develops coronally-apically [6]. The presence of non-physiological probing is related to the extent of the pathology: in advanced stages of peri-implantitis, probing may exceed 7-8 millimeters. The radiographic appearance is pathognomonic: peri-implant disease is evident in the form of a “bowl” lesion, an osseous crater surrounding the implant, possibly involving adjacent teeth. However, there are some important differences between the two pathologies, probably due to profound anatomical (absence of a ligamentous tissue between the implant surface and the bone) and histological differences (peri-implant mucosal tissues have less blood supply and exhibit characteristics more similar to scar tissue) [6].

Human histological studies have shown that the inflammatory infiltrate is more extensive in peri-implantitis, especially apically to the junctional epithelium, and that there is often a portion of connective tissue not covered by epithelial cells directly in contact with the bacterial biofilm. Furthermore, despite dominant cellular populations characterized by the presence of lymphocytes and plasma cells in both periodontal and peri-implant lesions, the latter also show a high number of macrophages and polymorphonuclear cells (Berglundh et al., 2011) [11]. Another very important difference is the rate of lesion progression. These differences have a relevant clinical impact and require a different therapeutic approach than periodontitis treatment [6]. Numerous epidemiological studies have presented data on the incidence of peri-implant biological complications. However, published data show high variability, a consequence of the fact that, despite a certain consensus on clinical definitions, diagnostic parameters vary significantly across studies [12,13]. This limitation can now be successfully addressed with the introduction of the new classification and agreement on diagnostic parameters. Various factors have been correlated with an increased incidence of peri-implant mucositis and periimplantitis, many of which are common to periodontal disease [14]. General risk factors that could influence host susceptibility to biofilm-induced peri-implant mucositis have been investigated. Cigarette smoking has been identified, in three studies, as a risk indicator for peri-implant mucositis. There is also evidence that radiation therapy is a possible risk indicator for mucositis. There is some evidence for diabetes mellitus; poorly controlled diabetes (HbA1c levels > 10.1) has been associated with increased bleeding on probing of implants. Although a history of cardiovascular disease has been associated with an increased risk of periimplantitis, there is no evidence of an association with mucositis [15]. Ferreira et al. have also reported an association between periimplant mucositis and systemic diseases. However, the described systemic diseases included “diabetes mellitus, hormonal changes, menopause, chemotherapy, thyroid alterations, heart problems, and alcohol consumption,” making the interpretation of the study results challenging [15]. Finally, among the main local risk factors are: oral hygiene; adherence/lack of adherence to implant-support therapy (IST); implant material and surface characteristics; design of implant-supported prostheses; size of peri-implant keratinized mucosa and excess cement [15].

Case Presentation

The case presented in this study focuses on a patient with peri-implantitis affecting an implant placed a decade earlier. The patient, B.E., 68 years old and a non-smoker, has a medical history of bilateral otosclerosis surgery and subsequent thyroidectomy, currently taking Eutirox. In 2013, the patient’s edentulous mandible was rehabilitated with a fixed prosthesis (Toronto Bridge) supported by 5 implants (Figure 1).


Figure 1

Despite regular check-ups over the years, peri-implantitis developed in the most distal implant in the right hemi-arch, despite the patient’s good oral hygiene. In January 2023, it was decided to intervene. The initial state of the affected implant pre-surgical treatment is visible in the intraoral image (Figure 2).


Figure 2

The surgical intervention proceeded as follows: Local anesthesia with articaine was administered around the implant affected by peri-implantitis.

Removal of the prosthetic structure began by eliminating cement covering the prostethic abutment (Figures 3-5), followed by unscrewing the abutment (Figure 6) to facilitate the removal of the prosthesis.


Figure 3


Figure 4