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BERGLUNDH et al .
PERI‐IMPLANTITIS
diabetes as potential risk indicators for peri‐implantitis are inconclusive. Implants that have been placed under less than ideal circum ‐ stances are often encountered in day‐to‐day practice. As a re ‐ sult, there may be an increased prevalence of peri‐implantitis associated with these situations. There is some limited evidence linking peri‐implantitis to factors such as post‐restorative presence of submucosal cement and positioning of implants that does not facilitate oral hygiene and maintenance. The role of peri‐implant keratinized mucosa, oc ‐ clusal overload, titanium particles, bone compression necrosis, overheating, micromotion and biocorrosion as risk indicators for peri‐implantitis remains to be determined. There is a high priority to conduct studies that are designed to develop diagnostic, preventive, and intervention strategies for the management of these peri‐implant issues. 9. Does progressive crestal bone loss around implants occur in the ab‐ sence of soft tissue inflammation? Observational studies have indicated that crestal bone level changes at implants are typically associated with clinical signs of inflammation. However, there are situations in which peri‐im ‐ plant bone loss may occur due to iatrogenic factors, including malpositioning of the implant or surgical trauma.
1. What is peri‐implantitis? Peri‐implantitis is a plaque‐associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri‐implant mucosa and subsequent pro ‐ gressive loss of supporting bone. 2. What is the evidence for plaque/biofilm as a principal etiological fac‐ tor for peri‐implantitis? There is evidence from observational studies that patients exhib ‐ iting poor plaque control and not attending regular maintenance therapy are at higher risk of developing peri‐implantitis. Studies on treatment of peri‐implantitis reveal that anti‐infective treat ‐ ment strategies are successful in decreasing soft tissue inflam‐ mation and in suppressing disease progression. 3. What are the clinical characteristics of peri‐implantitis? Peri‐implantitis sites exhibit clinical signs of inflammation, bleed ‐ ing on probing and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radio‐ graphic bone loss compared to previous examinations. At sites presenting with peri‐implantitis, probing depth is correlated with bone loss and is, hence, an indicator for the severity of disease. It is important to recognize that rate of progression of bone loss may vary between patients. 4. What are the histological characteristics of peri‐implantitis? Peri‐implantitis lesions extend apical of the junctional/pocket epithelium and contain large numbers and densities of plasma cells, macrophages and neutrophils. In addition, peri‐implantitis lesions are larger than those at peri‐implant mucositis sites. 5. Are there any specific microbiological and immunological characteris‐ tics of peri‐implantitis? No specific or unique bacteria or proinflammatory cytokines have been identified. 6. What is the evidence for peri‐implant mucositis being the precursor of peri‐implantitis? Peri‐implant mucositis is assumed to precede peri‐implantitis. Data indicate that patients diagnosed with peri‐implant mucosi‐ tis may develop peri‐implantitis, especially in the absence of regular maintenance care. However, the features or conditions characterizing the progression from peri‐implant mucositis to peri‐implantitis in susceptible patients have not been identified. 7. What is known about the onset and progression pattern of peri‐implantitis? The onset of peri‐implantitis may occur early during follow‐up as indicated by radiographic data. Peri‐implantitis, in the absence of treatment, seems to progress in a non‐linear and accelerating pattern. Data suggest that the progression of peri‐implantitis ap ‐ pears to be faster than that observed in periodontitis. 8. What are the major risk indicators for peri‐implantitis? There is strong evidence that there is an increased risk of devel ‐ oping peri‐implantitis in patients who have a history of severe periodontitis, poor plaque control, and no regular maintenance care after implant therapy. Data identifying smoking and
HARD‐ AND SOFT‐TISSUE DEFICIENCIES
1. What are the main factors associated with hard‐ and soft‐tissue deficiencies at potential implant sites? The healing process following tooth loss leads to diminished dimensions of the alveolar process/ridge representing hard‐ and soft‐tissue deficiencies. Larger deficiencies may occur at sites exposed to the following factors: loss of periodontal support, endodontic infections, longitudinal root fractures, thin buccal bone plates, buccal/lingual tooth position in relation to the arch, extraction with additional trauma to the tissues, injury, pneumatization of the maxillary sinus, medications, and systemic diseases reducing the amount of naturally formed bone, agenesis of teeth, pressure from soft‐tissue supported removable prosthesis, and combinations. 2. What factors are associated with recession of the peri‐implant mucosa? The principal factors for recession of the peri‐implant mucosa are malpositioning of implants, lack of buccal bone, thin soft tis ‐ sue, lack of keratinized tissue, status of attachment of the adja ‐ cent teeth and surgical trauma. 3. Does the presence/absence of keratinized mucosa play a role in the long‐term maintenance of peri‐implant health? The evidence is equivocal regarding the effect of keratinized mu ‐ cosa on the long‐term health of the peri‐implant tissue. It ap ‐ pears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal.
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