, Reem Atout1, Nader Hamdan2 and Ioannis Tsourounakis3
1.1 Definitions
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Peri-implant mucositis: A disease in which the presence of inflammation is confined to the mucosa surrounding a dental implant with no signs of loss of supporting bone.
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Peri-implantitis: An inflammatory process around a dental implant which includes both soft tissue inflammation and loss of supporting bone.
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Biotype: The thickness or dimension of the soft and hard tissue surrounding natural teeth or dental implants.
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Osseointegration: A direct contact, on the light microscopic level, between living bone tissue and a dental implant.
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Fibro-osseous integration: The interposition of healthy dense collagenous tissue between a dental implant and bone. Also known as fibro-osteal integration.
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Implant, oral: Endosseous root-form implant – an implant placed into the alveolar process and/or basal bone that derives its support from a vertical length of bone and supports a prosthesis or other devices. Most commonly made of titanium, it can be cylindrical, tapered, etc.
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Implant fixture: A synonym for a dental implant, especially an endosseous implant.
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Implant abutment: That part of an implant system that connects the dental implant with a prosthesis or other devices.
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Overdenture: Complete or partial removable denture supported by soft tissue and retained roots or implants to provide support, retention, and stability and reduce ridge resorption.
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Recession: The migration of the marginal soft tissue to a point apical to the cementoenamel junction of a tooth or the platform of a dental implant.
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Biologic width: The dimension of soft tissue composed of a connective tissue and epithelial attachment extending from the crest of bone to the most apical extent of the pocket or sulcus.
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Occlusal trauma: Injury resulting in tissue changes within the attachment apparatus due to physiologic or parafunctional forces which may exceed its adaptive capacity.
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Piezoelectric surgery: A surgery performed using an instrument which generates micro-vibrating motion via the application of electromagnetic forces on a polycrystal; the micro-vibration of the metallic tip results in ostectomy and osteoplasty of the bone in contact with the tip.
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Peri-implant mucositis is a disease confined to the mucosa and is reversible.
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Peri-implantitis includes both soft tissue inflammation and loss of supporting bone and is irreversible.
1.2 Epidemiology
The prevalence of peri-implant diseases has been reported to range from 5 to 63.4% according to different reports [2]. This variability is due to various studies reporting different findings depending on the study design, the definitions (threshold of bone loss) adopted for peri-implant diseases, population size, and other factors.
A better understanding of peri-implant diseases and a consensus on the diagnostic criteria will eventually help in reducing some of this variability in the prevalence of peri-implant mucositis and peri-implantitis.
1.3 Classification of Peri-Implant Diseases
A classification system for peri-implant diseases is highly desirable. This will assist healthcare professionals in determining accurate prevalence estimates, providing clear diagnoses, and assigning prognoses. It will also improve the communication between health professionals and researchers, as well as the evaluation of treatment outcomes. However, to date, there is no consensus on a certain classification system as far as the authors know. This is consistent with the lack of clarity on established diagnostic criteria, as well as management protocols of peri-implant diseases.
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The first was proposed by Froum and Rosen in [3]. This classification for peri-implantitis is based on the severity of the disease. A combination of bleeding on probing and/or suppuration, probing depth, and extent of radiographic bone loss around the dental implant is used to classify the severity of peri-implantitis into early, moderate, and advanced categories (Table 1.1, Figs. 1.1, 1.2 and 1.3).
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The second classification system was proposed by Ata-Ali et al. in [4]. In their article Ata-Ali et al. proposed a classification for peri-implant mucositis and peri-implantitis based on the severity of the disease, using a combination of peri-implant clinical and radiological parameters to classify severity into several stages (stage 0A and 0B = peri-implant mucositis and stage 1 to 4 = peri-implantitis) (Tables 1.2 and 1.3).
Classification of peri-implantitis as proposed by Froum and Rosen [3]
Staging |
Definition |
---|---|
Early |
PD ≥ 4 mm (bleeding and/or suppuration on probinga) Bone loss <25% of the implant lengthb |
Moderate |
PD ≥ 6 mm (bleeding and/or suppuration on probinga) Bone loss 25% to 50% of the implant lengthb |
Advanced |
PD ≥ 8 mm (bleeding and/or suppuration on probinga) Bone loss >50% of the implant lengthb |
Classification of peri-implant mucositis as proposed by Ata-Ali [4]
Staging |
Definition |
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Stage 0A |
PPD ≤ 4 mm and BoP and/or SUP, with no signs of loss of supporting bone following initial bone remodeling during healing |
Stage 0B |
PPD > 4 mm and BoP and/or SUP, with no signs of loss of supporting bone following initial bone remodeling during healing |
Classification of peri-implantitis as proposed by Ata-Ali [4]
Staging |
Definition |
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Stage I |
BoP and/or SUP and bone loss ≤3 mm beyond biological bone remodeling |
Stage II |
BoP and/or SUP and bone loss >3 mm and <5 mm beyond biological bone remodeling |
Stage III |
BoP and/or SUP and bone loss ≥5 mm beyond biological bone remodeling |
Stage IV |
BoP and/or SUP and bone loss ≥50% of the implant lengtha beyond biological bone remodeling |
Currently, there is no consensus on a classification system for peri-implant diseases.
1.4 Peri-Implant Mucositis vs. Peri-Implantitis
1.4.1 Peri-Implant Mucositis
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It has been proven that the disease process around dental implants is similar to that which occurs around teeth. Peri-implant mucositis around dental implants is seen as the equivalent of gingivitis around natural teeth. Peri-implant mucositis may or may not progress to peri-implantitis as gingivitis may or may not progress to periodontitis [5, 6].
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Plaque accumulation on the titanium surface and the formation of a biofilm seem to be essential for the initiation and progression of peri-implant diseases in a way similar to that found around natural teeth [7–9].
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Peri-implant diseases are linked to similar gram-negative bacteria associated with severe chronic periodontitis [5, 6, 10, 11].
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When effectively treated, peri-implant mucositis can be reversed back to health [5, 6].
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The relatively weak epithelial seal around dental implants is similar in function to that around natural teeth [12].
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The structural difference between teeth and dental implants does not seem to influence the host response to the bacterial insult [13, 14].
The removal of the biofilm from the dental implant surface is the primary objective when treating peri-implant mucositis and will lead to the reversal of disease to a state of health the majority of the time if adequately performed.
1.4.2 Peri-Implantitis
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Peri-implantitis is seen as the equivalent of periodontitis around natural teeth and similarly occurs when the overwhelming bacterial insult leads to a destructive host immune response.
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Studies have shown that peri-implantitis and periodontitis lesions from human biopsies have many features in common [13, 15].
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Bacterial species associated with periodontitis and peri-implantitis are similar. Moreover, Staphylococcus aureus may also be an important pathogen in the initiation of peri-implantitis [13, 16, 17].
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The connective tissue adjacent to the pocket epithelium is infiltrated by inflammatory cells, with B-lymphocytes and plasma cells being the most dominant cell types. Similar markers are upregulated between peri-implantitis and periodontitis, including proinflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8, IL-12, and tumor necrosis factor (TNF)-alpha [18, 19].
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Despite those many similarities between teeth and dental implants, the severity and rate of disease progression may differ significantly in peri-implantitis when compared to periodontitis. Experiments that allowed undisturbed dental plaque formation on dental implants and teeth in humans and in dogs demonstrated a more advanced inflammatory cell infiltrate in the peri-implant mucosa. Features of experimentally created peri-implantitis and periodontitis have also been compared. The results suggested that clinical and radiographic signs of tissue destruction were more pronounced in peri-implantitis cases. Furthermore, the size of the inflammatory cell infiltrate in the connective tissue was larger, approaching the crestal bone around implants [13, 20–23]. This could be attributed to the differences in the orientation and insertion of collagen fibers around teeth compared to those around dental implants [22].
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All implants appear to be susceptible to peri-implantitis [24, 25].
Despite the similarities in both the bacterial etiology and the immune host response components between periodontitis and peri-implantitis, peri-implantitis progresses at a faster rate with more pronounced bone loss. This could be attributed to the differences in orientation and insertion of collagen fibers around teeth compared to those around dental implants.
Early diagnosis and intervention by the elimination of the bacterial biofilm and correction of other possible contributory factors is the most effective way in preventing peri-implant diseases.
1.5 Teeth vs. Dental Implants
Teeth are different from dental implants on both the micro- and the macroscopic levels
Teeth |
Dental Implants |
|
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Periodontal fibers |
Insert into cementum on the root surfaces of natural teeth 13 groups |
Extend parallel to the surface of the implant and/or abutment 2 groups |
Connection |
Periodontal ligaments |
Osseointegration |
Connective tissue |
Lower percentage of collagen fibers Higher percentage of cells More vascular |
Higher percentage of collagen fibers Lower percentage of fibroblasts. Looks very similar to a scar tissue Less vascular |
Blood supply to surrounding gingivae |
Three different sources (the periodontal ligament space, the interdental bone, and the supraperiosteal region) |
Two different sources (the supraperiosteal vessels and a few vessels from the bone) |
Periodontal ligament space |
Present |
Absent |
Resistance to mechanical and microbiological insults |
More resistant |
Less resistant |
Biological width (BW) |
JE: 0.97–1.14 mm CT: 0.77–1.07 mm BW: 2.04–2.91 mm |
JE: 1.88 mm CT: 1.05 mm BW: 3.08 mm |
Sulcus depth |
≤ 3 mm when healthy |
Could be >3 mm depending on multiple factors |
Proprioception |
Periodontal mechanoreceptors |
Osseoperception |
Tactile sensitivity |
High |
Low |
Axial mobility |
25–100 μm |
3–5 μm |
Fulcrum when lateral force applied |
Apical third of the root |
Crestal bone |
Possible relief |
Pressure absorption, distribution |
Pressure concentration on the crestal bone |
Many articles and book chapters have reported on the similarities and differences that exist between tissues around teeth and those around dental implants. The reader is encouraged to consult the published literature on this topic including a recent review entitled “Peri-Implant and Periodontal Tissues: A Review of Differences and Similarities” [26]. Part of this section was adapted from this publication.
1.5.1 Soft Tissues around Implants and Teeth
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The anatomy and histology of soft tissues surrounding dental implants and teeth is structurally similar. Those are made up of keratinized oral epithelium, non-keratinized sulcular epithelium, and the underlying connective tissue.
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In a human histologic study, the length of the peri- implant seal was found to be about 4–4.5 mm [88]. When compared to the “biologic width” around teeth, the same attachment around dental implants was longer nearly by the factor of 1.5 mm [89].
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This protective distance that exists between the alveolar crest of bone and the base of the gingival pocket should always be kept constant and respected in order to avoid bone loss around teeth. If for any reason, e.g., deeply placed restorative margin, this biologic distance is not maintained, then bone around the affected tooth will resorb in what seems like an adaptive mechanism, to mitigate the effects of those noxious stimuli. A similar principle applies to dental implants where changes in the soft tissue to bone relationship may be one of the reasons for the early crestal bone loss seen around dental implants [29].
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Upon dental implant placement, the fast-moving epithelial cells will migrate apically until they reach the dental implant surface where they attach themselves rapidly through the basal lamina and the hemidesmosomes [30]. Another possible attachment modality hypothesized is an indirect epithelium-to-implant contact [31]. This is very similar to what happens around teeth following soft tissue flap reflection and healing.
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Human studies have demonstrated that epithelium surrounding dental implants possess similar patterns of differentiation and function to gingival tissues [32]. However, what stops the epithelium from migrating further apically on the implant surface? The presence of granulation tissue adhering to the surface of the transmucosal components is considered the principal factor that prevents the apical migration of epithelium [33]. Berglundh speculated that this most likely occurs due to the interaction of the titanium surface with the soft tissue [34].
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The following sequence of events occur once an dental implant is inserted into bone:
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Formation and adhesion of the fibrin clot to the dental implant surface
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Adsorption of the fibrin clot to the dental implant surface and adsorption of the extracellular matrix (ECM) proteins and connective tissue cells to the dental implant surface
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Transformation of the clot into granulation tissue and migration of epithelial cells on top of the fibrin clot/granulation tissue [35]
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