RGUHS Nat. J. Pub. Heal. Sci Vol No: 16 Issue No: 3 pISSN:
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Akshata Kutre, Sandeep Katti*
Department of Periodontology, Maratha Mandal’s Nathajirao G Halgekar Institute of Dental Sciences & Research Centre, Belagavi.
*Corresponding author:
Dr. Sandeep Katti, Professor, Department of Periodontology, Maratha Mandal’s Nathajirao G Halgekar Institute of Dental Sciences & Research Centre, Belagavi. Email address: zorb@rediffmail.com
Received date: October 29, 2021; Accepted date: March 2, 2022; Published date: June 30, 2022
Abstract
Retrograde peri-implantitis is a clinically symptomatic lesion diagnosed as radiolucency in the periapical region of an osseointegrated implant. Retrograde peri-implantitis is one of the causes of implant failure, which is usually diagnosed symptomatically with pain, tenderness, swelling, and the presence of the fistulous tract. There are very limited studies that describe the etiology and the treatment protocols for retrograde periimplantitis. Therefore, this review attempts to compile and discuss the etiology, classification, diagnosis, and treatment plan for retrograde peri-implantitis available in the literature
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Introduction
Periodontal disease is defined as a chronic infection in which the pathogenic microorganisms initiate the host immune response leading to the destruction of toothsupporting tissue and eventually tooth loss. Dental implant placement is a standard and most accepted treatment modality for replacing single or multiple missing teeth.1 Although dental implants have a high success rate, there is a risk of developing complications that can lead to implant failure.2 Implant failure is defined as the total failure of an implant to fulfill its purpose (functional, esthetic, or phonetic) because of mechanical or biological reasons.3 Biological complications comprise peri-implant diseases such as peri-implant mucositis, peri-implantitis, and retrograde/apical periimplantitis. Hence, this review discusses retrograde peri-implantitis; its prevalence, classification, etiology, and treatment plan.
Retrograde peri-implantitis (periapical implant lesion; implant periapical pathology, apical peri-implantitis) was first described by McAllister et al. in 1992.4 It is defined as a “clinically symptomatic periapical lesion (diagnosed as radiolucency) that develops shortly after the implant insertion while the coronal portion of the implant achieves a normal bone to implant interface.”5 In 1993, Sussman and Moss defined it as “localized osteomyelitis secondary, due to endodontic pathology”. In 1995 Reiser and Nevins described retrograde periimplantitis as “active implant periapical lesion”.6
Retrograde peri-implantitis is not a common sequel of dental implant failure, but it has a prevalence of 1.6% in upper teeth and 2.7% in lower teeth, before abutment connection.5 The incidence of retrograde peri-implantitis is reported to increase to 7.8% when the teeth adjacent to the implant site have a history of root canal therapy.7 A 2mm space between the implant and the adjacent teeth and a minimum of 4 weeks between completion of endodontic treatment and actual implant placement decreases the incidence of retrograde peri-implantitis.8
Etiology: 13
According to the source of the infection:
a) Contamination of the surgical bed: implant surface contamination and overheating of bone during drilling
b) Pre-existing pathology: immediate implant placement, periapical pathology associated with the extracted tooth or adjacent teeth, pre-existing bone pathology/ poor bone quality, and the presence of residual root fragments or foreign bodies.
Diagnosis
Retrograde peri-implantitis is diagnosed by clinical features such as pain, tenderness, swelling, and occasionally with the presence of the fistulous tract. Radiographically, the presence of periapical radiolucency around the apical area of the implant is noted.1 The periapical lesion around the dental implant can be divided into an active and an inactive lesion. Active lesions are symptomatic while in the inactive lesions, radiographic features are not comparable with the clinical findings and/or the patient’s symptoms. Clinically asymptomatic, periapical radiolucency caused by placing implants shorter than the drilled cavity or by heat-induced aseptic bone necrosis is considered to be inactive.5, 6
A decision-making tree for the management of retrograde peri-implantitis was developed (Figure 2). It was used for proper diagnosis and management of the pathology aiming to save the implant.2 Conventional bitewings and periapical radiographs are used to evaluate the bone around the implant.2
For diagnosis of marginal peri-implantitis, a radiographic marginal bone loss >2mm beyond the crown/abutmentimplant junction is seen with bleeding on probing and/or suppuration and pocket depth of ≥ 4mm. 3
If radiographic bone loss is observed at the apex of an implant, the diagnosis is retrograde peri-implantitis.4 Retrograde peri-implantitis is classified according to the etiology as— infective (adjacent tooth with endodontic pathology or root fracture of an adjacent tooth or persisting pathology in the bone or chronic periodontitis of adjacent tooth) and traumatic (bone overheating or bone over-compression during fixture treatment or impaired osseointegration). It can also occur due to other etiological risk factors.2
If there is implant mobility with or without clinical symptoms, the implant must be removed. If there is swelling, fistula, pain, or no clinical symptoms, then endodontic treatment or retreatment has to be done. In case of a radiographic periapical lesion with an adjacent tooth having a periapical lesion or incomplete endodontic treatment or root fracture, endodontic treatment or retreatment has to be done. In case of a root fracture in the neighboring tooth, the tooth has to be removed. The patient should be followed up every 2 weeks, 1 month, 2 months, 3 months, and 6 months for the next 2 years to ensure that the healing takes place and the symptoms resolve. If the symptoms do not resolve, surgical treatment should be indicated.2
Surgical treatment includes debridement of granulation tissue, decontamination of the implant surface, apicectomy, and guided bone regeneration.
Quirynen et al. (2005) suggested that complete removal of granulation tissue prevents further progression of the disease, as it eliminates the bacteria colonized over the implant surface.5 Decontamination of implant surface is considered one of the modalities for successful treatment outcomes. The aim is to eliminate bacterial contamination and allow the implant surface to be conducive for bone regeneration and re-osseointegration. Ntrouka et al. (2011) demonstrated that 0.2% chlorhexidine digluconate successfully eliminated the bacterial biofilm.14 Kutlu et al. (2016) recommended that there will be a recurrence of retrograde peri-implantitis if the implant apicectomy is not performed15
Bone replacement grafts (BRGs) with or without barrier membrane used in guided bone regeneration (GBR) act as a scaffold for the growth of new bone cells, maintenance of space, clot stabilization, and prevention of soft tissue overgrowth in the bony defects. They are used in the treatment of retrograde peri-implantitis. In his recent retrospective cohort study covering over 20-year period, Bianca Di Murro et al. (2021) concluded that retrograde peri-implantitis can be successfully treated with surgical curettage and bone replacement grafts; all implants are still in place after a mean follow-up of 8.83±5.34 years.16
Wassdrop and Reynolds (2010) suggested that the use of antibiotics resolved the radiographic lesions within 9 months of follow-up with any other adjunctive treatment.17 Systemic antibiotics like amoxicillin, metronidazole, or a combination of these, used as an adjunct to surgical treatment, were successful in the treatment of retrograde peri-implantitis.18
Conclusion
Retrograde peri-implantitis is caused due to periapical pathology of an adjacent tooth or the contamination of the surgical bed which is often diagnosed as radiolucency at the implant apex. The treatment for retrograde periimplantitis is usually empirical. The most successful treatment regimen is surgical debridement and the use of bone replacement grafts with or without barrier membrane. However, there is no clear consensus in the literature about the etiology, clinical symptoms, and treatment plan, therefore, additional research is required with a large sample size to conclude this review.
Conflicts of Interest
None.
Supporting File
References
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