Peri-implant diseases, which include mucositis and peri-implantitis, are common conditions affecting the tissues surrounding the implant. It is a complication that can occur following implant placement. Untreated, it can lead to gradual bone resorption and loss of the implant.
The prevalence varies from one study to another. However, the values range from 6% to 25% for implants and 15% to 47% for patients.
In this article, we will discuss the difference between peri-implant and periodontal tissues, risk factors, diagnosis, pathogenesis, and treatment of peri-implantitis.
What is peri-implantitis?
Peri-implant disease is an inflammatory condition of bacterial origin. There are two clinical varieties: mucositis and peri-implantitis.
Mucositis is an inflammatory infection of the soft tissue surrounding the implant without bone loss. Untreated, it can evolve into peri-implantitis.
Peri-implantitis is an inflammatory process affecting both the soft tissue and the bone surrounding the implant. Unlike mucositis, it is irreversible and can lead to implant loss.
Diagnosis of peri-implantitis
The diagnosis of peri-implantitis is often based on three criteria: probing depth, bleeding, and bone loss.
- Probing depth:
Probing depth is performed with a fine instrument called a periodontal probe. It is determined by gently inserting the periodontal probe in the sulcus (the space under the gum line) until resistance is encountered. Then the distance between the top of the gingival margin and the base of the sulcus is evaluated. The value should not be greater than 5mm.
An increase in this distance indicates a loss of attachment, an evident sign of peri-implantitis.
- Bleeding on probing:
Bleeding on probing assessment is also done with the periodontal probe. The instrument is inserted into the sulcus to evaluate the condition of the soft tissue surrounding the implant. Bleeding indicates the presence of active inflammation.
- Bone loss:
Bone loss is confirmed by comparing radiographic images before and after implant placement. Bone resorption greater than 3 mm from the top of the alveolar crest is an indicator of peri-implantitis.
Implant mobility is one of the less commonly used signs because sometimes bone loss occurs without any signs of loosening. When it happens, it indicates the final stage of peri-implantitis, which may result in implant loss.
The difference between periodontal and peri-implant tissues
Although peri-implant and periodontal tissues share common microscopic characteristics, they differ in many ways, which explains the evolution and progression of peri-implant disease. Among the main differences:
- Periodontal ligament space: Often abbreviated as the PDL, it refers to the space surrounding the root, which contains ligaments that attach the tooth to the bone. Implants do not have a PDL as they are directly connected to the bone.
- Probing depth: The peri-implant mucosa is more fragile, which makes it less resistant to probing. The periodontal probe penetrates deeper into the sulcus, resulting in overestimated values even under healthy conditions.
- The connective tissue: The peri-implant connective tissue is similar to scar tissue with a predominance of collagen fibres and a lack of fibroblasts.
- Vascularisation: The vascularisation of the periodontium comes from three sources: gingiva, bone, and PDL. Peri-implant tissues are only vascularised by bone and gingiva since the PDL is absent.
- The orientation of the collagen fibres: The collagen fibres are perpendicular to the root of the teeth but parallel to the implants. The perpendicular fibres allow a proper tooth attachment and limit the extension of the lesions toward the bone.
Peri-implant tissues have some unique characteristics, including:
- Connective tissue is similar to scar tissue.
- Peri-implant tissue vascularisation is weaker.
- Absence of periodontal ligament.
- Collagen fibres are parallel to the implant.
All these factors contribute to the low defence potential of the tissues around the implant, increasing the rapidity and severity of lesions.
The bacteria involved in periodontitis and peri-implantitis are almost similar. They include Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg).
Furthermore, the mechanisms of plaque formation are identical for implant materials and dental surfaces.
Therefore, peri-implantitis and periodontitis involve the interaction between bacterial factors and the immune response. Some other factors increase the risk of peri-implantitis occurrence. Among them:
- Poor oral hygiene: Poor oral hygiene leads to plaque accumulation on implant sites. This may trigger an inflammatory response resulting in mucositis, which may progress to peri-implantitis.
- History of periodontal disease: Bacteria from pre-existing periodontitis could contaminate implant sites and trigger peri-implantitis.
- Smoking: Smoking is a major risk factor for peri-implant disease. Nicotine and its by-products compromise the host response to infection by reducing immune cell function and narrowing blood vessels in peri-implant tissues (vasoconstriction). This decreases the defense potential and worsens the progression of peri-implantitis.
- Lack of keratinised tissue: The keratinised tissues include the free and attached gingiva. Their role is to protect and increase the resistance of the periodontium in addition to facilitating oral hygiene. Their lack or absence is associated with a greater risk of peri-implantitis.
- Occlusal overload: Excessive occlusal forces can stress peri-implant tissues and worsen bone resorption.
- Certain chronic diseases: Chronic diseases such as diabetes and cardiovascular disease may increase the risk of peri-implantitis by compromising the immune system response.
The evolution of peri-implant disease follows the same process as periodontal disease. The inflammation first affects the soft tissue (mucositis) and then spreads to the bone (peri-implantitis).
Pathogenic bacteria first infiltrate the peri-implant soft tissue, triggering inflammation. The immune response is intended to protect us. However, when it lasts too long or faces virulent bacteria, it releases destructive substances in excess called inflammatory mediators. Those most correlated with peri-implant diseases are interleukin-1 (IL1) and tumour necrosis factor alpha (TNF-).
But, the way peri-implantitis progresses is different. Inflammation around implants spreads rapidly and more deeply into the bone compared to periodontitis. This is mainly due to the low resistance of peri-implant tissues, the absence of the periodontal ligament, and the orientation of the collagen fibres, which does not prevent the lesion from progressing deep into the bone.
The treatment goal of peri-implantitis is to eliminate inflammation, stop the disease progression, and maintain the implant site.
There are two categories of treatment: surgical and non-surgical.
Also called initial therapy, it is the first phase of peri-implantitis treatment. It consists of several therapies that can be combined as needed:
- Oral hygiene instruction:
Oral hygiene by the patient is important to prevent peri-implant disease and maintain long-term treatment results. It helps to reduce the amount of plaque and pathogenic bacteria in the mouth, which are the primary factors of peri-implantitis.
Without oral hygiene, treatment success will be minimal and only temporary.
- Management of risk factors:
Risk factors should be carefully assessed and properly managed to reduce their interaction with peri-implant disease. This can include:
-Stopping or reducing tobacco use
-Managing chronic diseases such as diabetes and cardiovascular disease
-Treating existing periodontitis
-Restoring favourable conditions for oral hygiene
-Improving the occlusion
-Increasing the keratinised mucosa if it is absent or insufficient
- Mechanical debridement:
It consists in cleaning the implant surface with manual or ultrasonic instruments. It removes plaque and calculus and sanitises the surface of the implant to ensure optimal healing.
Drug treatment is never performed alone but in conjunction with mechanical debridement. It includes antiseptics and antibiotics.
Antiseptic treatment consists of applying a strong agent (Betadine or Chlorhexidine) in the form of a mouthwash or gel directly to the affected site.
Antibiotics are applied either topically in case of localised peri-implantitis or systemically in diffuse forms.
2. Surgical treatment:
The first phase is often insufficient to treat severe peri-implantitis. Deep pockets and bleeding on probing may persist after the initial treatment, requiring surgical therapy.
Surgical treatment consists of incising and elevating the soft tissue overlying the implant. It allows access to the lesion and the implant surface to perform a debridement under direct vision.
Depending on the objective and the type of bone lesion, the method can be resective or regenerative.
- The resective method:
Resecting surgery consists of surgically removing the persisting pockets. It is indicated in cases of moderate to severe horizontal bone lysis. The disadvantage of this technique is that it does not allow the regeneration of the bone surrounding the implant.
- The regenerative method:
The regenerative technique is indicated when the bone lysis is vertical, deep, and narrow. It induces a repair of the destroyed bone. This can be achieved with simple mechanical debridement or regenerative techniques such as bone grafts or guided tissue regeneration.
- Peri-implant diseases are inflammatory conditions affecting the tissues surrounding the implant. There are two clinical varieties: mucositis and peri-implantitis.
- Diagnosis is based mainly on three criteria: probing depth, bleeding, and bone loss.
- It is the result of the interaction between bacterial factors and immune response. However, other factors increase the risk, including poor oral hygiene, smoking, pre-existing periodontal disease, diabetes, and cardiovascular disease.
- Peri-implant tissues have some unique characteristics, making peri-implantitis progress faster toward the bone.
- The peri-implantitis treatment goal is to stop its progression. It includes two phases: non-surgical and surgical. Non-surgical treatment is the first phase and consists of eliminating the disease factors. It can be effective on its own, but sometimes the response to treatment is insufficient, requiring another surgical step.
Useful Links & Recommended Reading
- The Good Practitioner’s Guide to Periodontology
- Periodontology at a Glance
- Single Best Answer Questions for Dentistry
- Renvert S, Polyzois I. Treatment of pathologic peri-implant pockets. Periodontol 2000. 2018;Feb; 76(1):180–90.
- H.F. Wolf, E.M. Rateitschak, K.H. Rateitschak & T.M. Hassell. Color atlas of dental medicine: Periodontology.
- Rokaya D, Srimaneepong V, Wisitrasameewon W, Humagain M, Thunyakitpisal P. Peri-implantitis Update: Risk Indicators, Diagnosis, and Treatment. Eur J Dent. 2020 Oct;14(4):672-682.
- Renvert S, Persson GR, Pirih FQ, Camargo PM. Peri-implant health, peri-implant mucositis, and peri-implantitis: Case definitions and diagnostic considerations: Diagnostic criteria of peri-implant health and diseases. J Clin Periodontol. 2018 Jun;45:S278–85.
- Kumar PS. Systemic Risk Factors for the Development of Periimplant Diseases: Implant Dent. 2019 Apr;28(2):115–9.
- Renvert S, Hirooka H, Polyzois I, Kelekis‐Cholakis A, Wang H, Working Group 3. Diagnosis and non‐surgical treatment of peri‐implant diseases and maintenance care of patients with dental implants – Consensus report of working group 3. Int Dent J. 2019 Sep;69(Suppl 2):12–7.
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