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Peri-implantitis is a destructive inflammatory process affecting the soft and hard tissues surrounding dental implants.[1] The soft tissues become inflamed whereas the alveolar bone (hard tissue), which surrounds the implant for the purposes of retention, is lost over time. The bone loss involved in peri-implantitis differentiates this condition from peri-mucositis, a reversible inflammatory reaction involving only the soft tissues around the implant.[2][3][4]

A radiograph 2 years after implant placement, then 7 years later in a heavy smoker, demonstrating progression of bone loss due to peri-implantitis.

Signs and Symptoms[edit]

Peri-implantitis does not present in the same way for all patients.[4] Patients are recommended to regularly attend dental appointments and to seek advice from their dentist if they have any concerns for their oral health.[5]

Before the signs and symptoms are explained, it is worth noting that healthy peri-implant tissue should not be swollen, bleeding, producing pus, or have a reddened appearance.[2]

From a patient’s perspective, he/she may notice loosening or wobbling of the implant.[5] This symptom does not usually present at the early stages of peri-implantitis as the implant will still be fused to bone at its deeper aspects.[4][6] It is more likely that the patient will notice bleeding whilst brushing their teeth. A patient may also notice swelling around the implant, bad breath and/or foul taste.[5]

Clinically, peri-implantitis involves both inflammation of soft tissues and destruction of bone, therefore, there is usually evidence of both bone loss (assessed by a radiograph) and bleeding when nearby tissues are probed, a common finding for soft tissue inflammation. There have been reports of bone loss without any accompanying sign of soft tissue inflammation. Without evidence of bone loss, the diagnosis is restricted to peri-mucositis (see comparison between peri-implantitis and peri-implant mucositis below for more information).[2][3][4][5][7]

Other reported features include pain and gingival hyperplasia.[3][6] Pain is thought to be a rare symptom and is usually linked to an acute infection.[3]

Bone loss[edit]

In health, there should be no sign of bone loss other than potential bone remodelling at the alveolar crest following implant placement.[2]

The shape of the alveolar bone in regions of bone loss varies depending on the buccal-lingual length (or cheek-to-tongue length) of the bone. Where this length is greater than the extent of the peri-implantitis, the region of bone loss can take the shape of a crater, with walls of bone surrounding the pathology;[4] this is the most common presentation of bone loss.[3] Where the buccal-lingual length is smaller, there may be no walls of bone surrounding the pathology.[4]


Bleeding on probing is considered normal whilst tissues are healing shortly after implant placement, however, if bleeding is present months or years after placement, inflammation should be suspected.[5] Other features which may be present whilst probing include pus, the presence of a pocket around the implant and/or recession of the gums. The dental professional may also notice swelling and redness of the gums, the latter of which is termed erythema.[2][3][4][6][7]

During probing, it is important to note that the pocket depth around an implant is typically greater than around natural teeth.[8] Also, the value for the pocket depth around an implant is variable in health, therefore, diagnosis of a pocket is reliant on a change in pocket depth when comparing measurements from different appointments.[2] For this reason, a Basic Periodontal Examination (BPE) is not appropriate, and a 4 or 6 point pocket chart is instead recommended.[8]

Below is a summary table of signs and symptoms associated with peri-implantitis.[2][3][4][5][6][7]

Signs and symptoms of peri-implantitis
Signs (identified by health professional) Symptoms (patient presents with these issues)
Bleeding (and possible discharge of pus) on probing Bleeding when brushing teeth
Swelling Swelling around implant
Pocket formation and/or gum recession Foul taste
Redness (erythema) Bad breath
Hyperplasia Loose implant
Radiographic evidence of bone loss around implant Pain (rare)

Causes & Pathology[edit]

Studies in both human and animal specimens found that the presence of plaque and its conglomeration around tissues invariably concluded in inflammation around the peri-implant soft tissue.

To find the pathology of peri-implantitis, experiments were compared to peri-mucositis, and found that in peri-implantitis, there were more neutrophil granulocytes and a bigger proportion of (CD19+) B-cells. Similarly in periodontitis, peri-implantitis lesions contained many plasma cells and lymphocytes, however there were a larger ratio of macrophage cells and leukocytic cells.[9][10]

Risk Factors[edit]

The risk factors have been sub-divided to distinguish those with strong supporting evidence (below the sub-heading ‘risk factor’) from those with conflicting evidence (below the sub-heading ‘potential risk factors’).

Risk factors[edit]

Poor plaque control - this highlights the importance of cleaning the tissues around an implant between dental appointments. It is understood that patients sometimes feel discomfort whilst brushing around implants and are advised to speak to their dentist about this. Also, patients may sometimes be unable to access some sites for cleaning.

Lack of regular maintenance therapy. To avoid this, regular dental visits should be arranged to enable early detection and management of peri-implantitis.[11]

Potential risk factors[edit]

Diabetes mellitus (commonly known as type 1 and type 2 diabetes)

Excess cement. The cement is used to retain the implant, although its potentially rough surface may aid with plaque retention. Therefore any residual cement surrounding the implant abutment interface can give rise to peri-implantitis. The alternative to cement is a screw-retained implant, although some studies have reported a higher risk of peri-implantitis with these compared to cement-retained implants.

Further research is required to establish whether the following are indeed risk factors for peri-implantitis:

  • Width of keratinised mucosa around the implant. Several studies identified more plaque and inflammation where the keratinised mucosa is 2mm or less in width, although it is unclear if this translates to a higher risk of peri-implantitis.
  • Genetics
  • Systemic conditions other than diabetes, such as cardiovascular disease and rheumatoid arthritis
  • Iatrogenic factors such as implant positioning and bone grafting
  • Occlusal overloading of the implant
  • Titanium particles from the implant which have infiltrated the peri-implant tissue. These particles have also been found in healthy peri-implant tissue, however, the concentration was reported to be higher in individuals with peri-implantitis [10][12]

Smoking is not regarded as a risk factor for peri-implantitis despite its association with periodontitis.[10]

Peri-implantitis vs Peri-implant mucositis[edit]

Peri-implant disease is an umbrella term for inflammatory diseases of tissues including both peri-implantitis and peri-implant mucositis. Peri-implant mucositis is a disease where inflammation is limited to the surrounding mucosa of an implant whereby peri-implantitis an inflammatory disease affecting mucosa as well as bone.[4]

In health, peri-implant mucosa is described as “oral epithelium extending into a non-keratinised barrier epithelium with basal lamina and hemidesmosomes facing the implant or abutment surface”. Healthy peri-implant mucosa becomes peri-implant mucositis when biofilms housing bacteria colonise implants and elicit an inflammatory response.[13] The characteristics of peri-implant mucositis are very similar to that of gingivitis: redness, swelling and inflammation. In order to diagnose peri-implant mucositis, bleeding in response to probing of the gingiva must be identified. Research has stated that the cause of this disease is similar to that of gingivitis: inadequate plaque removal in areas surrounding the implant.[4] Zitzmann et al (2001) enlisted 12 partially dentate participants with implants who had healthy periodontal tissues. They were asked to refrain from carrying out oral hygiene for a period of 3 weeks. The results of this study demonstrated that the accumulation of plaque had led to the development of inflammation coupled with an increase in the gingival infiltrate containing immune cells[14]

Research has highlighted that the mechanisms of peri-implant mucositis and gingivitis are very similar with bacterial invasion from plaque triggering redness, swelling and inflammation within soft tissues. Peri-implant mucositis has the ability to transform into peri-implantitis if no action is taken to reverse signs of peri-implant mucositis, similar to gingivitis and periodontitis. To reverse peri-implant mucositis, good oral hygiene must be performed regularly to remove plaque which initiated this disease.[15]

Peri-implant mucositis becomes peri-implantitis when bone resorption is identified around the implant on a radiograph as well as all the signs associated with peri-implant mucositis is seen. Often times, pus may also exude from the tissues surrounding the implant. However, mobility of the implant isn’t a sign of peri-implantitis as this disease begins at the margins of the implant. Only in the most severe cases of peri-implantitis, implant mobility may be observed where minimal bone tissue remains.


If peri-implant mucositis is present, it must be treated to deter it from progressing to peri-implantitis, for which currently, there are no treatments to reverse its effects.

Patients must carry out plaque removal regularly to prevent and treat peri-implant mucositis by the act of tooth-brushing. Dentists must deliver oral hygiene instruction to ensure their patients are removing plaque sufficiently as well as removing their calculus which is a known plaque-retentive factor. The prognosis for implants are significantly higher in those who don’t smoke compared to those who do, therefore patients should be encouraged to quit smoking in order to achieve the best results.

Dentists are responsible for ensuring that different elements of the implant should be of the correct size to avoid creating additional surfaces which bacteria can colonise. Margins of the restoration should be placed supra-gingivally in order to remove any extruded cement during placement. After implant placement, dentists must carefully and regularly monitor the health of the peri-implant mucosa at suitable intervals e.g. every 3/6/12 months.[7][13][16]


It is challenging to treat peri-implantitis. Depending on the nature of the disease, treatment can vary significantly – from non-surgical therapy with an aim to control the infection and detoxify the implant surface, to surgical procedures to regenerate the alveolar bone that has been lost.[3]

Due to the screw-shaped design and titanium surface modifications of the implants, mechanical debridement on the surface of the implant is ineffective in removing all adhering microorganisms. Therefore, to enhance the non-surgical treatment options of peri-implantitis, mechanical debridement can be used in combination with antiseptic, antibiotic therapy and/or resective or regenerative surgery. The combination of treatments can vary depending on the severity of the peri-implantitis, and cumulative interceptive support therapy provides guidance in this aspect.[17]

Cumulative interceptive supportive therapy, a protocol of therapeutic measures, provides guidance for clinicians to decide which regime should be used to treat peri-implantitis, depending on the mucosal condition (whether there is a presence of dental plaque, bleeding on gentle probing, suppuration), peri-implant probing depth and evidence of radiographic bone loss.[17]

Mechanical debridement[edit]

To prevent roughening and damaging of the implant surface, ultrasonic scalers with a non-metallic tip or resin/carbon fiber curettes are used for calculus removal.[3] Conventional steel curettes or ultrasonic instruments with metal tips should be avoided as implant surface can be damaged, and any residual marks increase implant susceptibility to plaque accumulation in the future. Polishing with rubber cups and polishing paste also aids in plaque removal.[17]

Antiseptic treatment[edit]

This is performed in conjunction with mechanical debridement, with application of chlorhexidine digluconate, a potent antiseptic. To achieve positive treatment results, 3–4 weeks of regular administration of chlorhexidine, either in the form of daily rinse (of 0.1%, 0.12% or 0.2%) or as a gel, is necessary. This is also recommended to maintain satisfactory plaque control.[17] Chlorhexidine is shown to significantly improve the mucosal condition in bleeding on probing, probing pocket depth, and clinical attachment level.[18]

Antibiotic treatment[edit]

This approach is aiming to eliminate or at least significantly reduce the pathogens in the submucosal biofilm. An antibiotic targeting gram-negative anaerobic bacteria – e.g. metronidazole or ornidazole is administered during the last ten days of antiseptic treatment, allowing peri-implant infection to be treated successfully and remain stable. Reinfection is subsequently prevented by instituting prophylactic procedures.[17] Alternatively, tetracycline periodontal fibers can be inserted locally for a period of ten days; this creates an environment of sustained high dose of the antimicrobial agent at the affected site for several days.[19] Another method is to use minocycline microspheres in conjunction with mechanical debridement; this has shown to improve probing depths, but the treatment may have to be repeated in future.[20]

Surgical treatment[edit]

Surgical flap management with either (or both) resective and regenerative approaches is only considered if infection is controlled successfully. This treatment is used to restore the bony support through guided bone regeneration, or to reshape the peri-implant soft tissue.[17] This also helps in comprehensive debridement and local decontamination of the affected implant.[3] It is vital to consider the aesthetic and morphological characteristics of the peri-implant lesion when considering resective surgical techniques.[17]


  1. ^ Custom made root analogue zirconia implants Fernando Pessoa University. 2017.
  2. ^ a b c d e f g Berglundh, Tord; Armitage, Gary; Araujo, Mauricio G.; Avila-Ortiz, Gustavo; Blanco, Juan; Camargo, Paulo M.; Chen, Stephen; Cochran, David; Derks, Jan (June 2018). "Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions". Journal of Clinical Periodontology. 45 Suppl 20: S286–S291. doi:10.1111/jcpe.12957. ISSN 1600-051X. PMID 29926491.
  3. ^ a b c d e f g h i j Prathapachandran, Jayachandran; Suresh, Neethu (2012). "Management of peri-implantitis". Dental Research Journal. 9 (5): 516–521. doi:10.4103/1735-3327.104867. ISSN 1735-3327. PMC 3612185. PMID 23559913.
  4. ^ a b c d e f g h i j P., Lang, Niklaus (2015). Clinical Periodontology and Implant Dentistry. Wiley. ISBN 9781118940488. OCLC 956687931.
  5. ^ a b c d e f "European Federation of Periodontology". Retrieved 2018-11-26.
  6. ^ a b c d "Peri-implantitis and Management". DGOI (in German). 2016-05-03. Retrieved 2018-11-26.
  7. ^ a b c d Fransson, Christer; Wennström, Jan; Berglundh, Tord (February 2008). "Clinical characteristics at implants with a history of progressive bone loss". Clinical Oral Implants Research. 19 (2): 142–147. doi:10.1111/j.1600-0501.2007.01448.x. ISSN 0905-7161. PMID 18184340.
  8. ^ a b British Society of Periodontology. "The Good Practitioner's Guide to Periodontology" (PDF). British Society of Periodontology. Retrieved 21 January 2019.
  9. ^ Smeets, Ralf; Henningsen, Anders; Jung, Ole; Heiland, Max; Hammächer, Christian; Stein, Jamal M (2014-09-03). "Definition, etiology, prevention and treatment of peri-implantitis – a review". Head & Face Medicine. 10: 34. doi:10.1186/1746-160X-10-34. ISSN 1746-160X. PMC 4164121. PMID 25185675.
  10. ^ a b c Schwarz, Frank; Derks, Jan; Monje, Alberto; Wang, Hom-Lay (2018). "Peri-implantitis". Journal of Clinical Periodontology. 45: S246–S266. doi:10.1111/jcpe.12954. PMID 29926484.
  11. ^ Costa, Fernando Oliveira; Takenaka‐Martinez, Satoshi; Cota, Luís Otávio Miranda; Ferreira, Sergio Diniz; Silva, Geraldo Lúcio Magalhães; Costa, José Eustáquio (2012). "Peri-implant disease in subjects with and without preventive maintenance: a 5-year follow-up". Journal of Clinical Periodontology. 39 (2): 173–181. doi:10.1111/j.1600-051X.2011.01819.x. ISSN 1600-051X. PMID 22111654.
  12. ^ Stacchi, Claudio; Berton, Federico; Perinetti, Giuseppe; Frassetto, Andrea; Lombardi, Teresa; Khoury, Aiman; Andolsek, Francesca; Di Lenarda, Roberto (2016-09-09). "Risk Factors for Peri-Implantitis: Effect of History of Periodontal Disease and Smoking Habits. A Systematic Review and Meta-Analysis". Journal of Oral & Maxillofacial Research. 7 (3): e3. doi:10.5037/jomr.2016.7303. ISSN 2029-283X. PMC 5100643. PMID 27833728.
  13. ^ a b Heitz-Mayfield, Lisa J.A.; Salvi, Giovanni E. (June 2018). "Peri-implant mucositis". Journal of Clinical Periodontology. 45: S237–S245. doi:10.1111/jcpe.12953. ISSN 0303-6979. PMID 29926488.
  14. ^ Zitzmann, N. U.; Berglundh, T.; Marinello, C. P.; Lindhe, J. (June 2001). "Experimental peri-implant mucositis in man". Journal of Clinical Periodontology. 28 (6): 517–523. doi:10.1034/j.1600-051x.2001.028006517.x. ISSN 0303-6979. PMID 11350518.
  15. ^ Caton, Jack G.; Armitage, Gary; Berglundh, Tord; Chapple, Iain L.C.; Jepsen, Søren; Kornman, Kenneth S.; Mealey, Brian L.; Papapanou, Panos N.; Sanz, Mariano (June 2018). "A new classification scheme for periodontal and peri-implant diseases and conditions - Introduction and key changes from the 1999 classification" (PDF). Journal of Clinical Periodontology. 45: S1–S8. doi:10.1111/jcpe.12935. ISSN 0303-6979. PMID 29926489.
  16. ^ Jepsen, Søren; Berglundh, Tord; Genco, Robert; Aass, Anne Merete; Demirel, Korkud; Derks, Jan; Figuero, Elena; Giovannoli, Jean Louis; Goldstein, Moshe (2015-03-31). "Primary prevention of peri-implantitis: Managing peri-implant mucositis". Journal of Clinical Periodontology. 42: S152–S157. doi:10.1111/jcpe.12369. ISSN 0303-6979. PMID 25626479.
  17. ^ a b c d e f g Froum, Stuart J. (2015-10-05). Dental implant complications : etiology, prevention, and treatment. Froum, Stuart J. (Second ed.). Hoboken, New Jersey. ISBN 9781118976463. OCLC 922529540.
  18. ^ Schwarz, Frank; Sculean, Anton; Bieling, Katrin; Ferrari, Daniel; Rothamel, Daniel; Becker, Jürgen (2007-12-18). "Two-year clinical results following treatment of peri-implantitis lesions using a nanocrystalline hydroxyapatite or a natural bone mineral in combination with a collagen membrane". Journal of Clinical Periodontology. 35 (1): 80–87. doi:10.1111/j.1600-051x.2007.01168.x. ISSN 0303-6979. PMID 18173402.
  19. ^ Lang, Niklaus P.; Wilson, Thomas G.; Corbet, Esmonde F. (September 2000). "Biological complications with dental implants: their prevention, diagnosis and treatment". Clinical Oral Implants Research. 11: 146–155. doi:10.1034/j.1600-0501.2000.011s1146.x. ISSN 0905-7161. PMID 11168263.
  20. ^ Renvert, Stefan; Lessem, Jan; Dahlen, Gunnar; Lindahl, Christel; Svensson, Marie (May 2006). "Topical minocycline microspheres versus topical chlorhexidine gel as an adjunct to mechanical debridement of incipient peri-implant infections: a randomized clinical trial". Journal of Clinical Periodontology. 33 (5): 362–369. doi:10.1111/j.1600-051x.2006.00919.x. ISSN 0303-6979. PMID 16634959.