Peri-implant mucositis and peri-implantitis: key features and differences.

Peri-implant diseases are frequent complications that occur around osseointegrated endosseous implants and are the result of an imbalance between the bacterial challenge and host response. Peri-implant diseases may affect the peri-implant mucosa only (peri-implant mucositis) or also involve the supporting bone (peri-implantitis). Early detection of peri-implant diseases and timely treatment is important for the success of dental implant treatment. Peri-implant probing is essential to assess the peri-implant health status and should be done at each recall visit. Dental practitioners should be familiar with the clinical and radiological features of both conditions in order to make an accurate diagnosis and determine the appropriate treatment required. This article aims to provide clinicians with an understanding of the key differences between peri-implant health, peri-implant mucositis and peri-implantitis.

Occurrence, associated factors and soft tissue reconstructive therapy for buccal soft tissue dehiscence at dental implants: Consensus report of group 3 of the DGI/SEPA/Osteology Workshop.

OBJECTIVES: To systematically assess the literature and report on (1) the frequency of occurrence of buccal soft tissue dehiscence (BSTD) at implants, (2) factors associated with the occurrence of BSTD and (3) treatment outcomes of reconstructive therapy for the coverage of BSTD. MATERIALS AND METHODS: Two systematic reviews addressing focused questions related to implant BSTD occurrence, associated factors and the treatment outcomes of BSTD coverage served as the basis for group discussions and the consensus statements. The main findings of the systematic reviews, consensus statements and implications for clinical practice and for future research were formulated within group 3 and were further discussed and reached final approval within the plenary session. RESULTS: Buccally positioned implants were the factor most strongly associated with the risk of occurrence of BSTD, followed by thin tissue phenotype. At immediate implants, it was identified that the use of a connective tissue graft (CTG) may act as a protective factor for BSTD. Coverage of BSTD may be achieved with a combination of a coronally advanced flap (CAF) and a connective tissue graft, with or without prosthesis modification/removal, although feasibility of the procedure depends upon multiple local and patient-related factors. Soft tissue substitutes showed limited BSTD coverage. CONCLUSION: Correct three-dimensional (3D) positioning of the implant is of utmost relevance to prevent the occurrence of BSTD. If present, BSTD may be covered by CAF +CTG, however the evidence comes from a low number of observational studies. Therefore, future research is needed for the development of further evidence-based clinical recommendations.

Implant Disease Risk Assessment IDRA-a tool for preventing peri-implant disease.

OBJECTIVE: This treatment concept paper introduces a risk assessment tool, the Implant Disease Risk Assessment, (IDRA) which estimates the risk for a patient to develop peri-implantitis. MATERIALS AND METHODS: The functional risk assessment diagram was constructed incorporating eight parameters, each with documented evidence for an association with peri-implantitis. RESULTS: The eight vectors of the diagram include (1) assessment of a history of periodontitis (2) percentage of sites with bleeding on probing (BOP) (3) number of teeth/implants with probing depths (PD) ≥5 mm (4) the ratio of periodontal bone loss (evaluated from a radiograph) divided by the patient's age (5) periodontitis susceptibility as described by the staging and grading categories from the 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases (Journal of Periodontology, 89 Suppl 1, S159-S172, 2018) (6) the frequency/compliance with supportive periodontal therapy (7) the distance in mm from the restorative margin of the implant-supported prosthesis to the marginal bone crest and (8) prosthesis-related factors including cleanability and fit of the implant-supported prosthesis. CONCLUSION: The combination of these factors in a risk assessment tool, IDRA, may be useful in identifying individuals at risk for development of peri-implantitis.

Peri-implant mucositis.

OBJECTIVES: This narrative review was prepared for the 2017 World Workshop of the American Academy of Periodontology and European Federation of Periodontology to address key questions related to the clinical condition of peri-implant mucositis, including: 1) the definition of peri-implant mucositis, 2) conversion of peri-implant health to the biofilm-induced peri-implant mucositis lesion, 3) reversibility of peri-implant mucositis, 4) the long-standing peri-implant mucositis lesion, 5) similarities and differences between peri-implant mucositis at implants and gingivitis at teeth, and 6) risk indicators/factors for peri-implant mucositis. METHODS: A literature search of MEDLINE (PubMed) and The Cochrane Library up to and including July 31, 2016, was carried out using the search strategy (peri-implant[All Fields] AND ("mucositis"[MeSH Terms] OR "mucositis"[All Fields])) OR (periimplant[All Fields] AND mucosits[All Fields]). Prospective, retrospective, and cross-sectional studies and review papers that focused on risk factors/indicators for peri-implant mucositis as well as experimental peri-implant mucositis studies in animals and humans were included. FINDINGS: Peri-implant mucositis is an inflammatory lesion of the soft tissues surrounding an endosseous implant in the absence of loss of supporting bone or continuing marginal bone loss. A cause-and-effect relationship between experimental accumulation of bacterial biofilms around titanium dental implants and the development of an inflammatory response has been demonstrated. The experimental peri-implant mucositis lesion is characterized by an inflammatory cell infiltrate present within the connective tissue lateral to the barrier epithelium. In long-standing peri-implant mucositis, the inflammatory cell infiltrate is larger in size than in the early (3-week) experimental peri-implant mucositis lesion. Biofilm-induced peri-implant mucositis is reversible at the host biomarker level once biofilm control is reinstituted. Reversal of the clinical signs of inflammation may take longer than 3 weeks. Factors identified as risk indicators for peri-implant mucositis include biofilm accumulation, smoking, and radiation. Further evidence is required for potential risk factors, including diabetes, lack of keratinized mucosa, and presence of excess luting cement. CONCLUSIONS: Peri-implant mucositis is caused by biofilm accumulation which disrupts the host-microbe homeostasis at the implant-mucosa interface, resulting in an inflammatory lesion. Peri-implant mucositis is a reversible condition at the host biomarker level. Therefore, the clinical implication is that optimal biofilm removal is a prerequisite for the prevention and management of peri-implant mucositis. An understanding of peri-implant mucositis is important because it is considered a precursor for peri-implantitis.

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.

A classification for peri-implant diseases and conditions was presented. Focused questions on the characteristics of peri-implant health, peri-implant mucositis, peri-implantitis, and soft- and hard-tissue deficiencies were addressed. Peri-implant health is characterized by the absence of erythema, bleeding on probing, swelling, and suppuration. It is not possible to define a range of probing depths compatible with health; Peri-implant health can exist around implants with reduced bone support. The main clinical characteristic of peri-implant mucositis is bleeding on gentle probing. Erythema, swelling, and/or suppuration may also be present. An increase in probing depth is often observed in the presence of peri-implant mucositis due to swelling or decrease in probing resistance. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis. Peri-implantitis is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone. Peri-implantitis sites exhibit clinical signs of inflammation, bleeding on probing, and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radiographic bone loss. The evidence is equivocal regarding the effect of keratinized mucosa on the long-term health of the peri-implant tissue. It appears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal. Case definitions in day-to-day clinical practice and in epidemiological or disease-surveillance studies for peri-implant health, peri-implant mucositis, and peri-implantitis were introduced. The proposed case definitions should be viewed within the context that there is no generic implant and that there are numerous implant designs with different surface characteristics, surgical and loading protocols. It is recommended that the clinician obtain baseline radiographic and probing measurements following the completion of the implant-supported prosthesis.

Peri-implant mucositis.

OBJECTIVES: This narrative review was prepared for the 2017 World Workshop of the American Academy of Periodontology and European Federation of Periodontology to address key questions related to the clinical condition of peri-implant mucositis, including: 1) the definition of peri-implant mucositis, 2) conversion of peri-implant health to the biofilm-induced peri-implant mucositis lesion, 3) reversibility of peri-implant mucositis, 4) the long-standing peri-implant mucositis lesion, 5) similarities and differences between peri-implant mucositis at implants and gingivitis at teeth, and 6) risk indicators/factors for peri-implant mucositis. METHODS: A literature search of MEDLINE (PubMed) and The Cochrane Library up to and including July 31, 2016, was carried out using the search strategy (peri-implant[All Fields] AND ("mucositis"[MeSH Terms] OR "mucositis"[All Fields])) OR (periimplant[All Fields] AND mucosits[All Fields]). Prospective, retrospective, and cross-sectional studies and review papers that focused on risk factors/indicators for peri-implant mucositis as well as experimental peri-implant mucositis studies in animals and humans were included. FINDINGS: Peri-implant mucositis is an inflammatory lesion of the soft tissues surrounding an endosseous implant in the absence of loss of supporting bone or continuing marginal bone loss. A cause-and-effect relationship between experimental accumulation of bacterial biofilms around titanium dental implants and the development of an inflammatory response has been demonstrated. The experimental peri-implant mucositis lesion is characterized by an inflammatory cell infiltrate present within the connective tissue lateral to the barrier epithelium. In long-standing peri-implant mucositis, the inflammatory cell infiltrate is larger in size than in the early (3-week) experimental peri-implant mucositis lesion. Biofilm-induced peri-implant mucositis is reversible at the host biomarker level once biofilm control is reinstituted. Reversal of the clinical signs of inflammation may take longer than 3 weeks. Factors identified as risk indicators for peri-implant mucositis include biofilm accumulation, smoking, and radiation. Further evidence is required for potential risk factors, including diabetes, lack of keratinized mucosa, and presence of excess luting cement. CONCLUSIONS: Peri-implant mucositis is caused by biofilm accumulation which disrupts the host-microbe homeostasis at the implant-mucosa interface, resulting in an inflammatory lesion. Peri-implant mucositis is a reversible condition at the host biomarker level. Therefore, the clinical implication is that optimal biofilm removal is a prerequisite for the prevention and management of peri-implant mucositis. An understanding of peri-implant mucositis is important because it is considered a precursor for peri-implantitis.

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.

A classification for peri-implant diseases and conditions was presented. Focused questions on the characteristics of peri-implant health, peri-implant mucositis, peri-implantitis, and soft- and hard-tissue deficiencies were addressed. Peri-implant health is characterized by the absence of erythema, bleeding on probing, swelling, and suppuration. It is not possible to define a range of probing depths compatible with health; Peri-implant health can exist around implants with reduced bone support. The main clinical characteristic of peri-implant mucositis is bleeding on gentle probing. Erythema, swelling, and/or suppuration may also be present. An increase in probing depth is often observed in the presence of peri-implant mucositis due to swelling or decrease in probing resistance. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis. Peri-implantitis is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone. Peri-implantitis sites exhibit clinical signs of inflammation, bleeding on probing, and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radiographic bone loss. The evidence is equivocal regarding the effect of keratinized mucosa on the long-term health of the peri-implant tissue. It appears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal. Case definitions in day-to-day clinical practice and in epidemiological or disease-surveillance studies for peri-implant health, peri-implant mucositis, and peri-implantitis were introduced. The proposed case definitions should be viewed within the context that there is no generic implant and that there are numerous implant designs with different surface characteristics, surgical and loading protocols. It is recommended that the clinician obtain baseline radiographic and probing measurements following the completion of the implant-supported prosthesis.

Supportive peri-implant therapy following anti-infective surgical peri-implantitis treatment: 5-year survival and success.

OBJECTIVES: To evaluate clinical outcomes of supportive peri-implant therapy (SPIT) following surgical treatment of peri-implantitis. MATERIALS AND METHODS: Twenty-four partially dentate patients with 36 dental implants diagnosed with peri-implantitis were treated by an anti-infective surgical protocol followed by regular supportive therapy. SPIT included removal of supra- and submucosal biofilm at the treated implants using titanium or carbon fibre curettes, or ultrasonic devices. In addition, professional prophylaxis (calculus/biofilm removal) at other implants/teeth and oral hygiene reinforcement was provided. Clinical measurements and radiographs were obtained at 1, 3 and 5 years. A successful treatment outcome was defined as implant survival with the absence of peri-implant probing depths (PD) ≥ 5 mm with concomitant bleeding/suppuration and absence of progression of peri-implant bone loss. RESULTS: Twelve months after treatment, there was 100% survival of the treated implants and 79% of patients (19 of 24) had a successful treatment outcome according to the defined success criteria. At 3 years, 75% of the patients (18 of 24) had a successful treatment outcome, two patients (8%) were lost to follow-up (LTF), while 8% lost an implant, and two patients had recurrence of peri-implantitis. Between 3 and 5 years, an additional two patients were LTF, and an additional two patients each lost one implant. Thus, at 5 years 63% of patients (15 of 24) had a successful treatment outcome. Complete resolution of peri-implantitis, defined as absence of bleeding at all sites, was achieved in 42% of implants (N = 15) at 5 years. CONCLUSION: Five years following regular supportive therapy, the peri-implant conditions established following peri-implantitis surgery were maintained in the majority of patients and implants. Some patients had recurrence of peri-implantitis and some lost implants over the 5-year period.

Anti-infective treatment of peri-implant mucositis: a randomised controlled clinical trial.

AIM: To compare the effectiveness of two anti-infective protocols for the treatment of peri-implant mucositis. MATERIALS AND METHODS: Twenty-nine patients with one implant diagnosed with peri-implant mucositis (bleeding on probing [BOP] with no loss of supporting bone) were randomly assigned to a control or test group. Following an assessment of baseline parameters (probing depth, BOP, suppuration, presence of plaque), all patients received non-surgical mechanical debridement at the implant sites and were instructed to brush around the implant twice daily using a gel provided for a period of 4 weeks. The test group (15 patients) received a chlorhexidine gel (0.5%), and the control group (14 patients) received a placebo gel. The study was performed double blind. After 4 weeks, patients were instructed to discontinue using the gel and to continue with routine oral hygiene at the implant sites. Baseline parameters were repeated at 1 and 3 months. RESULTS: At 1 month, there was a statistically significant reduction in the mean number of sites with BOP and mean probing depth measurements at implants in both groups. There were also some statistically significant changes in these parameters from 1 to 3 months. However, there were no statistically significant differences between test and control groups. One month following treatment, 76% of implants had a reduction in BOP. Complete resolution of BOP at 3 months was achieved in 38% of the treated implants. The presence of a submucosal restoration margin resulted in significantly lower reductions in probing depth following treatment. CONCLUSIONS: Non-surgical debridement and oral hygiene were effective in reducing peri-implant mucositis, but did not always result in complete resolution of inflammation. Adjunctive chlorhexidine gel application did not enhance the results compared with mechanical cleansing alone. Implants with supramucosal restoration margins showed greater therapeutic improvement compared with those with submucosal restoration margins.

Comparative biology of chronic and aggressive periodontitis vs. peri-implantitis.

This review was undertaken to address the similarities and dissimilarities between the two disease entities of periodontitis and peri-implantitis. The overall analysis of the literature on the etiology and pathogenesis of periodontitis and peri-implantitis provided an impression that these two diseases have more similarities than differences. First, the initiation of the two diseases is dependent on the presence of a biofilm containing pathogens. While the microbiota associated with periodontitis is rich in gram-negative bacteria, a similar composition has been identified in peri-implant diseases. However, increasing evidence suggests that S. aureus may be an important pathogen in the initiation of some cases of peri-implantitis. Further research into the role of this gram-positive facultative coccus, and other putative pathogens, in the development of peri-implantitis is indicated. While the initial host response to the bacterial challenge in peri-implant mucositis appears to be identical to that encountered in gingivitis, persistent biofilm accumulation may elicit a more pronounced inflammatory response in peri-implant mucosal tissues than in the dentogingival unit. This may be a result of structural differences (such as vascularity and fibroblast-to-collagen ratios). When periodontitis and peri-implantitis were produced experimentally by applying plaque-retaining ligatures, the progression of mucositis to peri-implantitis followed a very similar sequence of events as the development of gingivitis to periodontitis. However, some of the peri-implantitis lesions appeared to have periods of rapid progression, in which the infective lesion reached the alveolar bone marrow. It is therefore reasonable to assume that peri-implantitis in humans may also display periods of accelerated destruction that are more pronounced than that observed in cases of chronic periodontitis. From a clinical point of view the identified and confirmed risk factors for periodontitis may be considered as identical to those for peri-implantitis. In addition, patients susceptible to periodontitis appear to be more susceptible to peri-implantitis than patients without a history of periodontitis. As both periodontitis and peri-implantitis are opportunistic infections, their therapy must be antiinfective in nature. The same clinical principles apply to debridement of the lesions and the maintenance of an infection-free oral cavity. However, in daily practice, such principles may occasionally be difficult to apply in peri-implantitis treatment. Owing to implant surface characteristics and limited access to the microbial habitats, surgical access may be required more frequently, and at an earlier stage, in periimplantitis treatment than in periodontal therapy. In conclusion, it is evident that periodontitis and peri-implantitis are not fundamentally different from the perspectives of etiology, pathogenesis, risk assessment, diagnosis and therapy. Nevertheless, some difference in the host response to these two infections may explain the occasional rapid progression of peri-implantitis lesions. Consequently, a diagnosed peri-implantitis should be treated without delay.

Nd:YAG (1064 nm) laser for the treatment of chronic periodontitis: a pilot study.

AIM: To evaluate the clinical and microbiological effects of neodymium: yttrium-aluminum-garnet laser therapy as an adjunct to scaling and root planing during the hygienic phase. METHODS: In eight patients, sites with a mean probing pocket depth (PPD) of ≥5 mm were treated by either scaling and root planing (n=28) (control) or by scaling and root planing and adjunctive laser therapy (n=28) (power: 5W). Re-evaluation was at 4-6 weeks. Thereafter, remaining pockets (mean PPD ≥5 mm) were eliminated by either laser surgery (power: 7 W) or gingivectomy (control). RESULTS: At baseline, the mean PPD of sites originally presenting with a mean PPD ≥4 mm were 4.69 and 4.73 mm in the test and control sites, respectively. Six months following surgery, there was a similar average mean PPD reduction in the test (1.18 mm, P<0.01) and control sites (1.35 mm, P<0.01). Also, the reduction in bleeding on probing in both groups was statistically significant (P<0.01, paired t-tests). No statistically-significant differences between the test and control sites were found for any clinical or microbiological parameters at baseline, after initial, and 3 or 6 months' post-surgical therapy. CONCLUSION: During the hygienic phase, neodymium: yttrium-aluminum-garnet (1064 nm) laser treatment yielded no superiority in clinical efficacy compared to conventional debridement. Laser gingivectomy resulted in similar treatment outcomes (mean PPD and bleeding on probing reduction), as did conventional gingivectomy.

History of treated periodontitis and smoking as risks for implant therapy.

PURPOSE: The aim of this review was to evaluate a history of treated periodontitis and smoking, both alone and combined, as risk factors for adverse dental implant outcomes. MATERIALS AND METHODS: A literature search of MEDLINE (Ovid) and EMBASE from January 1, 1966, to June 30, 2008, was performed, and the outcome variables implant survival, implant success, occurrence of peri-implantitis and marginal bone loss were evaluated. RESULTS: Considerable heterogeneity in study design was found, and few studies accounted for confounding variables. For patients with a history of treated periodontitis, the majority of studies reported implant survival rates > 90%. Three cohort studies showed a higher risk of peri-implantitis in patients with a history of treated periodontitis compared with those without a history of periodontitis (reported odds ratios from 3.1 to 4.7). In three of four systematic reviews, smoking was found to be a significant risk for adverse implant outcome. While the majority of studies reported implant survival rates ranging from 80% to 96% in smokers, most studies found statistically significantly lower survival rates than for nonsmokers. CONCLUSIONS: There is an increased risk of peri-implantitis in smokers compared with nonsmokers (reported odds ratios from 3.6 to 4.6). The combination of a history of treated periodontitis and smoking increases the risk of implant failure and peri-implant bone loss.

Peri-implant diseases: diagnosis and risk indicators.

BACKGROUND: Peri-implant diseases include peri-implant mucositis, describing an inflammatory lesion of the peri-implant mucosa, and peri-implantitis, which also includes loss of supporting bone. METHODS: A literature search of the Medline database (Ovid), up to 21 January 2008 was carried out using a systematic approach, in order to review the evidence for diagnosis and the risk indicators for peri-implant diseases. RESULTS: Experimental and clinical studies have identified various diagnostic criteria including probing parameters, radiographic assessment and peri-implant crevicular fluid and saliva analyses. Cross-sectional analyses have investigated potential risk indicators for peri-implant disease including poor oral hygiene, smoking, history of periodontitis, diabetes, genetic traits, alcohol consumption and implant surface. There is evidence that probing using a light force (0.25 N) does not damage the peri-implant tissues and that bleeding on probing (BOP) indicates presence of inflammation in the peri-implant mucosa. The probing depth, the presence of BOP, and suppuration should be assessed regularly for the diagnosis of peri-implant diseases. Radiographs are required to evaluate supporting bone levels around implants. The review identified strong evidence that poor oral hygiene, a history of periodontitis and cigarette smoking, are risk indicators for peri-implant disease. Future prospective studies are required to confirm these factors as true risk factors.

Adjunctive local antibiotic therapy in the treatment of peri-implantitis II: clinical and radiographic outcomes.

AIM: To monitor over 12 months clinical and radiographic changes occurring after adjunctive local delivery of minocycline microspheres for the treatment of peri-implantitis. MATERIAL AND METHODS: In 25 partially edentulous subjects, 31 implants diagnosed with peri-implantitis were treated. Three weeks after oral hygiene instruction, mechanical debridement and local antiseptic cleansing using 0.2% chlorhexidine gel, baseline (Day 0) parameters were recorded. Minocycline microspheres (Arestin) were locally delivered to each implant site with bone loss and a probing pocket depth (PPD) >or=5 mm. Rescue therapy with Arestin was allowed at Days 180 and 270 at any site exhibiting an increase in PPD>or=2 mm from the previous visit. The following clinical parameters were recorded at four sites/implant at Day 0, 10, 30, 60, 90, 180, 270 and 360: PPD, clinical attachment level (CAL), bleeding on probing (BOP) and plaque index (PlI). RESULTS: Six implants in six subjects were either rescued or exited because of persisting active peri-implantitis. Successful implants showed a statistically significant reduction in both PPD and percentage of sites with BOP between baseline and Day 360 (P<0.05). At mesial implant sites, the mean PPD reduction amounted to 1.6 mm (95% CI: 0.9-2.2 mm, P<0.001) and was accompanied by a statistically significant reduction of the BOP value (P<0.001). Binary regression analysis showed that the clinical parameters and smoking history could not discriminate between successfully treated and rescued or exited implants at any observation time point. CONCLUSION: Non-surgical mechanical treatment of peri-implantitis lesions with adjunctive local delivery of microencapsulated minocycline led to positive effects on clinical parameters up to 12 months.

Association between periodontal and peri-implant conditions: a 10-year prospective study.

OBJECTIVES: The aims of this study were to (1) compare prospectively the clinical and radiographic changes in periodontal and peri-implant conditions, (2) investigate the association of changes in periodontal parameters and peri-implant conditions over a mean observation period of 10 years (8-12 years) after implant installation, and (3) evaluate patient risk factors known to aggravate the periodontal conditions for their potential influence on the peri-implant tissue status. MATERIALS AND METHODS: Eighty-nine partially edentulous patients with a mean age of 58.9 years (28-88 years) were examined at 1 and 10 years after implant placement. The patients contributed with 179 implants that were placed after comprehensive periodontal treatment and restored with crowns or fixed partial dentures. One hundred and seventy-nine matching control teeth were chosen as controls. Also, the remaining teeth (n=1770) in the dentitions were evaluated. Data on smoking habits and general health aspects were collected at 1 and 10 years as well. RESULTS: At 10 years, statistically significant differences existed between implants and matching control teeth with regard to most of the clinical and radiographic parameters (P<0.01) with the exception of plaque index (PII) and recession. Multiple regression analyses were performed to associate combinations of periodontal diagnostic parameters to the peri-implant conditions: probing attachment level (PAL) at implants at 10 years was associated with implant location, full-mouth probing pocket depth (PPD) and full-mouth PAL (P=0.0001, r2=0.36). PPD at implants at 10 years correlated to implant location, full-mouth PPD and full-mouth PAL (P<0.001, r2=0.47). Marginal bone level at implants at 10 years was significantly associated to smoking, general health condition, implant location, full-mouth PAL and change over time in full-mouth PPD (P<0.001, r2=0.39). CONCLUSIONS: These results present evidence for the association between periodontal and peri-implant conditions and the changes in these tissues over 10 years in partially edentulous patients.

Antimicrobial treatment of peri-implant diseases.

PURPOSE: To review the literature on the treatment of peri-implant diseases. Specific emphasis was placed on the use of antimicrobial therapy, defined as local or systemic administration of antiseptic and/or antibiotic agents. MATERIALS AND METHODS: A search of MEDLINE, the Cochrane Controlled Trials Register, and The Cochrane Health Group Specialized Register was conducted, and articles published in English until July 31, 2003, were included. The results of experimental animal studies and human research are presented. RESULTS: A variety of antimicrobial treatment regimens in combination with nonsurgical or surgical debridement with and without regenerative therapy were reported. Use of antimicrobials varied between studies with respect to type of drug, dosage, delivery system, duration, and commencement of antibiotic administration. Patient compliance and adverse effects related to the antimicrobials were mostly not mentioned. DISCUSSION: While the majority of the case reports and studies presented showed positive outcomes following antimicrobial treatment, there were no non-medicated controls included, so the relative effect of the antimicrobial agent(s) cannot be evaluated. CONCLUSIONS: Although antimicrobials are widely used for the treatment of peri-implant diseases, evidence of their benefit is limited, and randomized, controlled human trials should be initiated where ethically possible. In addition, prospective cohort studies designed to monitor consecutive cases treated using specific treatment protocols are required.

Long-term implant prognosis in patients with and without a history of chronic periodontitis: a 10-year prospective cohort study of the ITI Dental Implant System.

AIM: The aim of this 10-year study was to compare the failure, success and complication rates between patients having lost their teeth due to periodontitis or other reasons. MATERIAL AND METHODS: Fifty-three patients who received 112 hollow screw implants (HS) of the ITI Dental Implant System were divided into two groups: group A - eight patients with 21 implants having lost their teeth due to chronic periodontitis; group B - forty five patients with 91 implants without a history of periodontitis. One and 10 years after surgical placement, clinical and radiographic parameters were assessed. The incidences of peri-implantitis were noticed over the 10 years of regular supportive periodontal therapy. RESULTS: Success criteria at 10 years were set at: pocket probing depth (PPD)