AIMS: This study was designed to evaluate the effect of gap width and graft placement on bone healing around implants placed into simulated extraction sockets in the mandibles of four beagle dogs. MATERIALS AND METHODS: Four Ti-Unite implants (13 mm x 3.3 mm) were placed on each side of the mandible. Three implants were surrounded by a 1.35 mm circumferential and a 5 mm deep gap around the coronal portion of the implants. A fourth implant was inserted conventionally into both sides of the mandibles as a positive control. The gaps were filled with either Bio-Oss, autogenous bone or with a blood clot alone. The study design was balanced for animal, side and modality. Ground sections were prepared from biopsies taken at 3 months, and computer-aided histometric measurements of bone/implant contact and area of bone within threads were made for the coronal 5 mm. Data were analysed using analysis of variance. RESULTS: The mean bone/implant contact was 9.8 mm for the control and ranged from 9.3 to 11.3 mm for the three test modalities. The corresponding values for area within threads were 1 mm(2) and 1-1.2 mm(2). Modality had a significant effect on both bone/implant contact (F=16.9; P<0.0001) and area within threads (F=16.7; P<0.0001). CONCLUSION: The results of this study suggest that both autogenous bone graft and Bio-Oss played an important role in the amount of hard tissue fill and osseointegration occurring within marginal bone defects around implants.

OBJECTIVE: (I) To compare the oral microflora at implant and tooth sites in subjects participating in a periodontal recall program, (II) to test whether the microflora at implant and tooth sites differ as an effect of gingival bleeding (bleeding on probing (BOP)), or pocket probing depth (PPD), and (III) to test whether smoking and gender had an impact on the microflora.

MATERIAL AND METHODS: Data were collected from 127 implants and all teeth in 56 subjects. Microbiological data were identified by the DNA-DNA checkerboard hybridization.

RESULTS: PPD> or =4 mm were found in 16.9% of tooth, and at 26.6% of implant sites (P<0.01). Tooth sites with PPD> or =4 mm had a 3.1-fold higher bacterial load than implant sites (mean difference: 66%, 95% confidence interval (CI): 40.7-91.3, P<0.001). No differences were found for the red, orange, green, and yellow complexes. A higher total bacterial load was found at implant sites with PPD> or =4 mm (mean difference 35.7 x 10(5), 95% CI: 5.2 (10(5)) to 66.1 (10(5)), P<0.02 with equal variance not assumed). At implant sites, BOP had no impact on bacterial load but influenced the load at tooth sites (P<0.01).

CONCLUSION: BOP, and smoking had no impact on bacteria at implant sites but influenced the bacterial load at tooth sites. Tooth sites harbored more bacteria than implant sites with comparable PPD. The 4 mm PPD cutoff level influenced the distribution and amounts of bacterial loads. The subject factor is explanatory to bacterial load at both tooth and implant sites.

OBJECTIVE: The purpose of the study was to investigate whether osseointegration can occur on rough implant surfaces that previously had been coated with bacterial biofilm. MATERIALS AND METHODS: The premolars on both sides of the mandible in four beagle dogs were extracted. Following 3 months healing, three titanium implants Ti-Unite, Nobel Biocare were partially inserted in the left side of each mandible. Some threads protruded from the tissues into the oral cavity. Plaque accumulated on the exposed part of the implant. Following a 5-week healing period, the contaminated parts of each implant were treated using three different techniques: (1) swabbing with citric acid for 30 s followed by rinsing with physiological saline, (2) cleansing with a toothbrush and physiological saline for 1 min, and (3) swabbing with 10% hydrogen peroxide for 1 min followed by rinsing with physiological saline. The treated implants and one pristine implant (control) were installed to the full implant length on the contralateral sides of the mandibles. Following 11 weeks of healing, the dogs were sacrificed and biopsies were obtained. Ground sections were prepared for histomorphometric analysis. RESULTS: All treatment modalities were associated with direct bone-to-implant contact on the portion of implant surface previously exposed to the oral environment. CONCLUSIONS: The results demonstrate that rough surfaces, which were plaque contaminated and cleaned by different methods, can re-osseointegrate.

Objectives: The aim of the present study was to evaluate the effects of a novel bone substitute system (Natix®), consisting of porous titanium granules (PTG) and a bovine-derived xenograft (Bio-Oss®), on hard tissue remodelling following their placement into fresh extraction sockets in dogs. Material and methods: Six modalities were tested; Natix® granules with and without a covering double-layered Bio Gide® membrane; Bio-Oss® with and without a covering double-layered Bio Gide® membrane; and a socket left empty with and without a covering double-layered Bio Gide® membrane. Linear measurements, indicative of buccal bone height loss, and an area measurement indicative of buccal bulk bone loss were made. The statistical analysis was based on the Latin Square design with two blocking factors (dog and site). Tukey's post hoc test was used to adjust for multiple comparisons. Results: Histological observation revealed that while bone formed around both the xenograft and the titanium particles, bone was also noted within titanium granules. Of the five modalities of ridge preservation techniques used in this study, no one technique proved to be superior. Conclusion: The titanium granules were observed to have promising osseoconductive properties.

OBJECTIVES: The aim of this study was to identify systemic and local risk indicators associated with peri-implantitis.

MATERIAL AND METHODS: One hundred eighty-three patients treated with 916 osseointegrated titanium implants, in function for at least 1 year, were included in the present study. The implants were installed at the Foundation for Scientific and Technological Development of Dentistry (FUNDECTO) - University of Sao Paulo (USP) - from 1998 to 2012. Factors related to patient's systemic conditions (heart disorders, hypertension, smoking habits, alcoholism, liver disorders, hepatitis, gastrointestinal disease, diabetes mellitus I and II, hyperthyroidism or hypothyroidism, radiation therapy, chemotherapy, menopause, osteoporosis, active periodontal disease, history of periodontal disease and bruxism), implant's characteristics (location, diameter, length, connection, shape, and antagonist), and clinical parameters (wear facets, periodontal status on the adjacent tooth, plaque accumulation on the adjacent tooth, modified plaque index, sulcus bleeding index, probing depth, bleeding on probing, width of keratinized tissue and marginal recession).

RESULTS: An increased risk of 2.2 times for history of periodontal disease (PD), 3.6 times for cemented restorations compared to screw-retained prostheses, 2.4 times when wear facets were displayed on the prosthetic crown and 16.1 times for total rehabilitations when compared to single rehabilitations were found. Logistic regression analysis did not show any association between the implant's characteristics and peri-implantitis.

CONCLUSIONS: A history of periodontal disease, cemented prostheses, presences of wear facets on the prosthetic crown and full mouth rehabilitations were identified as risk indicators for peri-implantitis. Implants' characteristics were not related to the presence of peri-implantitis.

BACKGROUND: Information on bacterial colonization immediately after dental implant insertion is limited.

AIMS: (1) To assess the early colonization on titanium implants immediately after placement and throughout the first 12 post-surgical weeks, (2) to compare the microbiota at interproximal subgingival implant and adjacent tooth sites.

MATERIAL AND METHODS: Subgingival plaque samples from implant and neighbouring teeth were studied by checkerboard DNA-DNA hybridization before surgery, 30 min after implant placement, and 1, 2, 4, 8, and 12 weeks after surgery.

RESULTS: Comparing bacterial loads at implant sites between 30 min after placement with 1-week data showed that only the levels of Veillonella parvula (P<0.05) differed with higher loads at week 1 post-surgically. Week 12 data demonstrated significantly higher bacterial loads for 15/40 species at tooth sites compared with pre-surgery (P-values varying between 0.05 and 0.01). Between the period immediately after surgery and 12 weeks at implant sites, 29/40 species was more commonly found at 12 weeks. Included among these bacteria at implant sites were Porphyromonas gingivalis (P<0.05), Tannerella forsythia, (P<0.01), and Treponema denticola (P<0.001). Immediately post-surgery 5.9% of implants, and 26.2% of teeth, and at week 12, 15% of implants, and 39.1% of teeth harbored Staphylococcus aureus. Comparing tooth and implant sites, significantly higher bacterial loads were found at tooth sites for 27/40 species after 30 min following implant placement. This difference increased to 35/40 species at 12 weeks post-surgically.

CONCLUSIONS: Bacterial colonization occurred within 30 min after implant placement. Early colonization patterns differed between implant and tooth surfaces.

Studies have shown similarities in the microflora between titanium implants or tooth sites when samples are taken by gingival crevicular fluid (GCF) sampling methods. The purpose of the present study was to study the microflora from curette and GCF samples using the checkerboard DNA-DNA hybridization method to assess the microflora of patients who had at least one oral osseo-integrated implant and who were otherwise dentate. Plaque samples were taken from tooth/implant surfaces and from sulcular gingival surfaces with curettes, and from gingival fluid using filter papers. A total of 28 subjects (11 females) were enrolled in the study. The mean age of the subjects was 64.1 years (SD+/-4.7). On average, the implants studied had been in function for 3.7 years (SD+/-2.9). The proportion of Streptococcus oralis (P<0.02) and Fusobacterium periodonticum (P<0.02) was significantly higher at tooth sites (curette samples). The GCF samples yielded higher proportions for 28/40 species studies (P-values varying between 0.05 and 0.001). The proportions of Tannerella forsythia (T. forsythensis), and Treponema denticola were both higher in GCF samples (P<0.02 and P<0.05, respectively) than in curette samples (implant sites). The microbial composition in gingival fluid from samples taken at implant sites differed partly from that of curette samples taken from implant surfaces or from sulcular soft tissues, providing higher counts for most bacteria studied at implant surfaces, but with the exception of Porphyromonas gingivalis. A combination of GCF and curette sampling methods might be the most representative sample method.

INTRODUCTION: The assignment for this working group was to update the existing knowledge regarding factors considered being of special relevance for the patient undergoing implant therapy. This included areas where conflicting opinions exists since long or recently has been expressed, like the role of antibiotic prophylaxis in dental implant surgery and peri-implantitis. Also areas with growing interest and concern such as patient-reported outcome measures (PROMs) and health-economy was included in this review.

MATERIALS AND METHODS: The literature in the respective areas of interest (antibiotic prophylaxis, peri-implantitis, patient-reported outcome measurements and health-economic aspects) was searched using different strategies for the different papers. Search strategies ranged from a complex systematic review to systematic- and narrative reviews, depending on subject and available literature. All collected material was critically reviewed. Four manuscripts were subsequently presented for group analysis and discussion and plenum discussions and concensus approval. The selected areas were considered to be of key importance and relevance for the patient undergoing implant therapy.

RESULTS: The results and conclusions of the review process are presented in the respective papers. The group's conclusions, identified knowledge gaps, directions for future research and concensus statements are presented in this article. The following reviews were available for group discussions and the foundation for subsequent plenary sessions: Lund B, Hultin M, Tranaeus S, Naimi-Akbar A, Klinge B. (2015) Perioperative antibiotics in conjunction with dental implant placement. A complex systematic review. Renvert S & Quirynen M. (2015) Risk indicators for peri-implantitis. A narrative review. De Bruyn H, Raes S, Matthys C, Cosyn J. (2015) The current use of patient centered/reported outcomes in implant dentistry. A systematic review. Beikler T & Flemmig T.F. (2015) Economic evaluation of implant-supported prostheses. A narrative review.

OBJECTIVE: The task of this working group was to update the existing knowledge base regarding the prevalence of peri-implant tissue destruction, the role of occlusal overload, and the outcome of non-surgical and surgical treatment.

MATERIALS AND METHODS: The literature was systematically searched and critically reviewed. Four manuscripts were presented in key areas deemed to be essential for the current understanding of the magnitude of the clinical entity peri-implantitis. The role of overload as an etiological component was reviewed. Also available data on the results from non-surgical and surgical interventions for the control of tissue destruction were presented.

RESULTS: The consensus statements following plenary session approval, clinical implications, and directions for future research based on the group discussions are presented in this article. The results and conclusions of the systematic review process are presented by the respective authors in the subsequent papers.

This study investigated whether osseointegration can occur on a surface which had previously been coated with dental plaque. The mandibular premolar regions of four young adult Labrador dogs were used for the study. The lower premolars (P1, P2, P3, and P4) were extracted on either side of the mandibles. Following a 12-week healing period, three 3.75 mm x 13 mm commercially pure titanium implants (Nobel BiocareAB, Gothenburg, Sweden) were partially inserted in one side of each mandible. This resulted in some threads protruding from the tissues into the oral cavity. Plaque was allowed to accumulate on the exposed implant surfaces. Following a 5-week healing period, the contaminated parts of each implant were treated using three different cleaning techniques: (1) swabbing with supersaturated citric acid for 30 s on a cotton pellet followed by rinsing with physiological saline, (2) cleansing with a toothbrush and physiological saline only for 1 min, and (3) swabbing with 10% hydrogen peroxide (H2O2) on a cotton pellet for 1 min followed by rinsing with physiological saline. The treated implants and one previously unused implant (control) were then placed into freshly prepared tapped sites to the full implant length on the contralateral sides of the mandibles. Following 11 weeks of healing, biopsies were obtained and ground sections prepared for histomorphometric analysis. All treatment modalities were associated with direct bone to implant contact on the portion of implant surface previously exposed to the oral environment. In conclusion, The results demonstrate that osseointegration can occur to surfaces that were plaque contaminated and cleaned by different methods.

OBJECTIVES: Interleukin (IL)-1alpha, IL-1beta and their natural specific inhibitor IL-1 receptor antagonist (IL-1ra) play a key role in the regulation of the inflammatory response in periodontal tissues. Polymorphisms in the IL-1 gene cluster have been associated with severe adult periodontitis. We aimed to investigate the IL-1 gene cluster polymorphisms in patients with peri-implantitis.

MATERIAL AND METHODS: The study included 120 North Caucasian individuals. A total of 71 patients (mean age 68 years, 76% smokers) demonstrating peri-implantitis at one or more implants as evidenced by bleeding and/or pus on probing and bone loss amounting to >3 threads on Brånemark implants and 49 controls (mean age 66 years, 45% smokers) with clinical healthy mucosa and no bone loss around the implants were recruited for the study. The titanium implants, ad modum Brånemark, had been in function for at least 2 years. Mouthwash samples were collected and used for genotyping of the bi-allelic polymorphisms IL-1A(-889), IL-1B(+3953), IL-1B(-511) and a variable number of tandem repeat IL-1RN gene polymorphisms using PCR technique.

RESULTS: Significant differences were found in the carriage rate of allele 2 in the IL-1RN gene between peri-implantitis patients and controls (56.5% vs. 33.3%, respectively; odds ratios (OR) 2.6; 95% confidence interval (CI) 1.2-5.6; P=0.015). Logistic regression analysis taking smoking, gender and age into account confirmed the association between the IL-1RN allele 2 carriers and peri-implantitis (OR 3; 95% CI 1.2-7.6; P=0.02).

CONCLUSIONS: Our results provide evidence that IL-1RN gene polymorphism is associated with peri-implantitis and may represent a risk factor for this disease.

INTRODUCTION: The remit of this working group (4) was to update existing knowledge on the effects of implant surface topography, composition and design on bone integration and re-osseointegration. MATERIAL AND METHODS: Based on five narrative reviews that were performed following a defined search strategy, clinical implications as well as suggestions for further research have been formulated. RESULTS: The results and conclusions of the review processes in the following papers together with the group consensus, clinical implications and directions for future research are presented: 1. Effects of titanium surface topography on bone integration. 2. Effects of implant surface coatings and composition on bone integration (two reviews). 3. Effects of different implant surfaces and designs on marginal bone level alterations. 4. Re-osseointegration onto previously contaminated implant surfaces.

Objective This study was designed to evaluate the effect of surface contamination on osseointegration of dental implants surrounded by a circumferential bone defect and to compare osseointegration around Osseotite (R) with that around Nanotite (TM) implants. Materials and methods The premolars on both sides of the mandible in four beagle dogs were extracted. Following 4 months healing, two Nanotite (TM) implants and two Osseotite (R) implants were partially inserted in the left side of each mandible. Some threads protruded from the tissues into the oral cavity. Following a 5 week healing period, the implants were removed and the contaminated part of each implant was cleaned. They were then installed to the full implant length on the contra lateral side of the mandibles. The coronal 5 mm of each implant was surrounded by 1 mm circumferential bone defect. Following 12 weeks of healing period, the dogs were sacrificed and biopsies were obtained. Ground sections were prepared for histomorphometric analysis. Results All implants were associated with direct bone-to-implant contact on the portion of the implant surface contaminated previously and surrounded by bone defect. Nanotite (TM) implants performed better than Osseotite (R) implants. Conclusions The results demonstrated that implant surfaces, which were contaminated previously and were surrounded by bone defects, can osseointegrate. To cite this article:Mohamed S, Polyzois I, Renvert S, Claffey N. Effect of surface contamination on osseointegration of dental implants surrounded by circumferential bone defects.

OBJECTIVES: To assess the microbiological outcome of local administration of minocycline hydrochloride microspheres 1 mg (Arestin) in cases with peri-implantitis and with a follow-up period of 12 months.

MATERIAL AND METHODS: After debridement, and local administration of chlorhexidine gel, peri-implantitis cases were treated with local administration of minocycline microspheres (Arestin). The DNA-DNA checkerboard hybridization method was used to detect bacterial presence during the first 360 days of therapy.

RESULTS: At Day 10, lower bacterial loads for 6/40 individual bacteria including Actinomyces gerensceriae (P<0.1), Actinomyces israelii (P<0.01), Actinomyces naeslundi type 1 (P<0.01) and type 2 (P<0.03), Actinomyces odontolyticus (P<0.01), Porphyromonas gingivalis (P<0.01) and Treponema socranskii (P<0.01) were found. At Day 360 only the levels of Actinobacillus actinomycetemcomitans were lower than at baseline (mean difference: 1x10(5); SE difference: 0.34x10(5), 95% CI: 0.2x10(5) to 1.2x10(5); P<0.03). Six implants were lost between Days 90 and 270. The microbiota was successfully controlled in 48%, and with definitive failures (implant loss and major increase in bacterial levels) in 32% of subjects.

CONCLUSIONS: At study endpoint, the impact of Arestin on A. actinomycetemcomitans was greater than the impact on other pathogens. Up to Day 180 reductions in levels of Tannerella forsythia, P. gingivalis, and Treponema denticola were also found. Failures in treatment could not be associated with the presence of specific pathogens or by the total bacterial load at baseline. Statistical power analysis suggested that a case control study would require approximately 200 subjects.

Objectives: This study was designed to evaluate the effect of gap width and graft placement on bone healing around implants placed in simulated extraction sockets of various widths in four Labrador dogs. Materials and Methods: Five Osseotite (R) implants per dog were placed in the mandible of four dogs. Two implants were inserted into sites with a 2.37 mm and two with a 1 mm gap present between the implants and bone around the coronal 6 mm of the implants in each dog. For one of each gap sizes, the gap was filled with Bio-Oss (R), and the other two with blood alone. A fifth implant was inserted without a gap and used as a control. Ground sections were prepared from biopsies taken at 4 months and histometric measurements of osseointegration and bone between the threads made for the coronal 6 mm. Results: The medians for osseointegration ranged from 5.2 mm for control to 1-2.6 mm for the test modalities. There were significant differences for linear measurements of osseointegration ((2)(chi) 18.27; df 4; P = 0.0011) and bone area within threads (chi(2) 23.4; df 4; P = 0.0001) between test modalities. Conclusions: The results suggest that the wider the gap around the implants, the less favourable the histological outcome at short time intervals following treatment. They also infer that bone grafting with anorganic bovine bone xenograft seems to lead to a more favourable histological outcome for wider circumferential defects but not for narrower defects.

OBJECTIVES: Retrospectively, we assessed the likelihood that peri-implantitis was associated with a history of systemic disease, periodontitis, and smoking habits.

METHODS: Data on probing pocket depth (PPD), bleeding on probing (BOP), and radiographic bone levels were obtained from individuals with dental implants. Peri-implantitis was defined as described by Sanz & Chapple 2012. Control individuals had healthy conditions or peri-implant mucositis. Information on past history of periodontitis, systemic diseases, and on smoking habits was obtained.

RESULTS: One hundred and seventy-two individuals had peri-implantitis (mean age: 68.2 years, SD ± 8.7), and 98 individuals (mean age: 44.7 years, SD ± 15.9) had implant health/peri-implant mucositis. The mean difference in bone level at implants between groups was 3.5 mm (SE mean ± 0.4, 95% CI: 2.8, 4.3, P < 0.001). A history of cardiovascular disease was found in 27.3% of individuals with peri-implantitis and in 3.0% of individuals in the implant health/peri-implant mucositis group. When adjusting for age, smoking, and gender, odds ratio (OR) of having peri-implantitis and a history of cardiovascular disease was 8.7 (95% CI: 1.9, 40.3 P < 0.006), and odds ratio of having a history of periodontitis was 4.5 (95% CI 2.1, 9.7, P < 0.001). Smoking or gender did not significantly contribute to the outcome.

CONCLUSIONS: In relation to a diagnosis of peri-implantitis, a high likelihood of comorbidity was expressed by a history of periodontitis and a history of cardiovascular disease.

AIMS: To assess the impact of different implant systems on the clinical conditions and the microbiota at implants, and whether the presence of bacteria at tooth sites was predictive of the presence at implant sites. MATERIALS AND METHODS: Subjects with either AstraTech or Brånemark in function for 7 years were enrolled. Sub-gingival bacterial samples at tooth and implant sites were collected with sterile endodontic paper points, and analyzed by the checkerboard DNA-DNA hybridization method (40 species). RESULTS: Fifty-four subjects, 27 supplied with AstraTech (n=132 implants) and 27 with Brånemark (n=102) implants, were studied. Test tooth sites had significantly less evidence of bleeding on probing (P<0.001) and presence of plaque (P<0.001) than implant test sites. Implant sites presented with deeper probing pocket depth than tooth sites (mean difference: 1.1 mm, standard error of differences: 0.08, 95% confidence intervals (CI): 0.9-1.3, P<0.001). Tannerella forsythia (P<0.05), Capnocytophaga sputigena (P<0.05), Actinomyces israelii (P<0.05) and Lactobacillus acidophilus (P<0.05) were found at higher levels at tooth surfaces. No differences in bacterial load for any species were found between the two implant systems. The odds of being present/absent at tooth and implants sites were only significant for Staphylococcus aureus [odds ratio (OR): 5.2 : 1, 95% CI: 1.4-18.9, P<0.01]. CONCLUSIONS: After 7 years in function, implants presented with deeper probing depths than teeth. S. aureus was commonly present at both teeth and implants sites. S. aureus at tooth sites was predictive of also being present at implant sites.

Material and methods Articles on surgical treatment of peri-implantitis in humans published up to December 2011 were included. Results Twenty-six studies were selected, thus limiting the available evidence. There is marked heterogeneity between study designs and case definitions for peri-implantitis in the studies cited, limiting the generalization of the reported results. Adjunctive systemic antibiotics were used in most studies, but no study evaluated the adjunctive benefit of systemic antibiotics. Access flap surgery, removal of granulation tissue and implant surface decontamination has been demonstrated to decrease plaque index, BOP, suppuration, probing depths and to arrest bone loss for 58% of implant sites over 5 years. Laser treatment of the exposed implant surface during surgery was not shown to be beneficial. Available data indicate that it is possible to obtain defect fill of peri-implantitis defects following surgical-treatment modalities with concomitant placement of bone or bone substitutes in such defects. However, there is lack of evidence that placement of membranes in addition to grafting procedures provides any additional defect fill. Conclusions Surgical therapy for treating peri-implantitis is a predictable method for treating peri-implant disease and patients receiving this therapy have benefited from it in the short term.

Objectives The aim of this review was to search the literature for the existing evidence of re-osseointegration after treatment of peri-implantitis at contaminated implant surfaces. Material and Methods A search of PubMed as well as additional hand search of articles were conducted. Publications and articles accepted for publication up to November 2008 were included. Results A total of 25 animal studies fulfilled the inclusion criteria for this review. Access surgery with closed healing has been observed to positively influence the rate of re-osseointegration when compared with non-surgical decontamination of the implant surface with open healing. Open debridement including surface decontamination may result in re-osseointegration and this integration was more pronounced on rougher than on smooth implant surfaces. The adjunctive use of regenerative procedures resulted in varying amounts of re-osseointegration. Conclusions Re-osseointegration is possible to obtain on a previously contaminated implant surface and can occur in experimentally induced peri-implantitis defects following therapy. The amount of re-osseointegration, varied considerably within and between studies. Implant surface characteristics may influence the degree of re-osseointegration. Surface decontamination alone can not achieve substantial re-osseointegration on a previously contaminated implant surface. No method predictably accomplished complete resolution of the peri-implant defect.

Aim: To examine the existing evidence in identifying risk indicators in the etiology of peri-implantitis. Material and methods: A literature search was performed in MEDLINE via PubMed database of the US National Library of Medicine, for articles published until October 2014 using Medical Subject Heading search terms + free text terms and in different combinations. Results: The microbiota associated with peri-implantitis is complex, demonstrating differences and similarities to the one seen at periodontitis sites. Plaque accumulation at dental implants triggers the inflammatory response leading to peri-implant mucositis/peri-implantitis. Individuals with a history of periodontal disease and smokers have an increased risk of developing peri-implantitis. There is some evidence to support the role of genetic polymorphism, diabetes, and excess cement as risk indicators for the development of peri-implantitis. There is also evidence to support that individuals on regular maintenance are less likely to develop peri-implantitis and that successful treatment of periodontitis prior to implant placement lowers the risk of peri-implantitis. Conclusions: Plaque accumulation at implants will result in the development of an inflammation at implants. A history of periodontal disease, smoking, excess cement, and lack of supportive therapy should be considered as risk indicators for the development of peri-implantitis.

Objectives: To assess the microbiota at implants diagnosed with peri-implantitis, implant mucositis, or being clinically healthy. Material and methods: Clinical and microbiological data were collected from 213 subjects (mean age: 65.7 +/- 14) with 976 implants in function (mean: 10.8 years, SD +/- 1.5). Forty species were identified by the checkerboard DNA-DNA hybridization method. Results: Implant mean % plaque score was 41.8 +/- 32.4%. Periodontitis defined by bone loss was found in 44.9% of subjects. Implant mucositis was diagnosed in 59% and peri-implantitis in 14.9% of all cases. Neisseria mucosa, Fusobacterium nucleatum sp. nucleatum, F. nucleatum sp. polymorphum, and Capnocytophaga sputigena dominated the implant sub-mucosal microbiota and the sub-gingival microbiota at tooth sites. Implant probing pocket depth at the implant site with the deepest probing depth was correlated with levels of Eikenella corrodens (r=0.16, P < 0.05), the levels of F. nucleatum sp. vincentii (r=0.15, P < 0.05), Porphyromonas gingivalis (r=0.14, P < 0.05), and Micromonas micros (r=0.17, P=0.01). E. corrodens was found in higher levels at implants with mucositis compared with implant health (P < 0.05). Subjects who lost teeth due to periodontitis had higher yields of F. nucleatum sp. vincentii (P < 0.02) and N. mucosa (P < 0.05). Independent of implant status subjects with teeth had higher levels of P. gingivalis (P < 0.05), and Leptotrichia buccalis (P < 0.05). Conclusions: At implant sites studied, few bacteria differed by whether subjects were dentate or not or by implant status.

Objectives: To report a follow-upof patients following the surgical anti-infective treatment of peri-implantitis and to identify possible risk indicators for the progression of disease during supportive peri-implant therapy. Material and Methods: Following peri-implant surgery, 41 patients (213 implants) were enrolled in a supportive peri-implant therapy. At the 2-year follow-up, two groups of patients were identified, with or without residual peri-implant pockets (responding and non-responding group). Eighteen patients (85 implants) of the non-responding group were followed for further 8 years. Results: At the 2-year examination, 73 of the 117 treated implants (62.4%) presented healthy peri-implant condition, while 44 (37.6%) presented persisting peri-implantitis associated with substantial bone loss before treatment. The 10-year examination of the non-responding group revealed that 1) 84% of the implants that regained health following surgery remained healthy during the entire observation period; 2) 66% of the implants with residual pockets following surgery maintained stable peri-implant condition; and 3) 29% of all treated implants showed disease progression, and 11 of those were extracted. Presence of pockets at 3–4 sites of the implants was identified as risk indicator for progression of peri-implantitis. Conclusion: The peri-implant health achieved following therapy was maintained formost of the implants during the follow-up. Residual pockets were a frequent finding at implants with substantial bone loss before treatment. Presence of pockets around the entire circumference of the implants resulted as a risk indicator for further disease progression. The probability of progression of peri-implant disease increased with increased observation time.

AIM: To study whether cytokine levels and bacterial counts in p atients with peri-implantitis reflect clinical treatment outcome following non-surgical management.

MATERIALS AND METHODS: Luminex magnet bead technology and checkerboard DNA-DNA hybridization were used to assess treatment outcome after treatment at the implant with the most severe peri-implantitis in 41 participants.

RESULTS: Study group mean age was 40.3 years (SD ± 9.9). Stable treatment outcome after 6 months (no further bone loss, probing pocket depth decrease ≥0.5 mm, no bleeding/suppuration) was identified in 9 of 41 (22%) participants. Peri-implant crevicular fluid (PICF) levels were also lower for Il-1β (P < 0.01), and with trends of lower cytokine levels in PICF for TNF-α (P = 0.071), PDGFBB (P = 0.071), as well as for VEGF (vascular endothelial growth factor) (P = 0.071), and bacterial counts for Actinomyces israelii, Aggregatibacter actonomycetemcomitans (Y4), Campylobacter gracilis, Echerichia coli, Fusobacterium periodonticum, Leptotrichia buccalis, Parvimonas micra, Staphylococcus haemolyticus, Streptococcus anginosus, and Tannerella forsythia. Increasing levels of IL-1 β and S. aureus (r(2)  = 0.856) were found only at implants with non-stable outcome. A reduction of PICF levels for selected cytokines and bacteria studied had a sensitivity of 0.77, and a specificity of 0.80 against the clinical outcome as gold standard. Data analysis failed to differences in treatments (PerioFlow(®) versus YAG: ER laser) for changes in the expression of cytokines and bacteria studied.

CONCLUSIONS: At 6 months, clinically stable treatment outcome of peri-implantitis is associated lower levels of putative pathogens total bacterial load with ≥30% reduction of IL1-β, L-6, and VEGF levels in PICF.

AIMS: (i) To assess the pattern of early bacterial colonization on titanium oral implants after installation, at 12 weeks and at 12 months, (ii) to compare the microbiota at submucosal implant sites and adjacent subgingival tooth sites and (iii) to assess whether or not early colonization was predictive of 12-month colonization patterns.

MATERIAL AND METHODS: Submucosal/subgingival plaque samples from 17 titanium oral implants and adjacent teeth were analyzed by checkerboard DNA-DNA hybridization 30 min, 12 weeks and 12 months after implant installation.

RESULTS: At 12 months, none of the inserted implants had been lost or presented with signs of peri-implantitis. The distribution of sites at implants and teeth with bleeding on probing varied between 2% and 11%. Probing pocket depths < or =3 mm were found at 75% of implant sites. At 12 months, the sum of the bacterial counts of 40 species was statistically significantly higher at tooth compared with implant sites (mean difference: 34.4 x 10(5), 95% confidence interval -0.4 to 69.4, P<0.05). At 12 months, higher individual bacterial counts at tooth sites were found for 7/40 species compared with implant sites. Detection or lack of detection of Staphylococcus aureus at implant sites at 12 weeks resulted in the highest positive (e.g. 80%) and negative (e.g. 90%) predictive values, respectively. Between 12 weeks and 12 months, the prevalence of Tannerella forsythia increased statistically significantly at implant sites (P<0.05). Lack of detection of Porphyromonas gingivalis at 12 weeks yielded a negative predictive value of 93.1% of this microorganism being undetectable at implant sites at 12 months.

CONCLUSIONS: Within the limits of this study, the findings showed (i) a few differences in the prevalence of bacterial species between implant and adjacent tooth sites at 12 months and (ii) high positive and negative predictive values for selected bacterial species.

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.

OBJECTIVES: To report a follow-up of patients following the surgical anti-infective treatment of peri-implantitis and to identify possible risk indicators for the progression of disease during supportive peri-implant therapy.

MATERIAL AND METHODS: Following peri-implant surgery, 41 patients (213 implants) were enrolled in a supportive peri-implant therapy. At the 2-years follow up, two groups of patients were identified, with or without residual peri-implant pockets (responding and non-responding group). Eighteen patients (85 implants) of the non-responding group were followed for further 8 years.

RESULTS: at the 2-years examination, 73 of the 117 treated implants (62.4%) presented healthy peri-implant condition, while 44 (37.6%) presented persisting peri-implantitis associated with substantial bone loss before treatment. The 10-years examination of the non-responding group revealed that 1) 84% of the implants that regained health following surgery remained healthy during the entire observation period; 2) 66% of the implants with residual pockets following surgery, maintained stable peri-implant condition; 3) 29% of all treated implants showed disease progression and 11 of those were extracted. Presence of pockets at 3 - 4 sites of the implants were identified as risk indicator for progression of peri-implantitis.

CONCLUSION: The peri-implant health achieved following therapy was maintained for most of the implants during the follow up. Residual pockets were a frequent finding at implants with substantial bone loss before treatment. Presence of pockets around the entire circumference of the implants resulted as a risk indicator for further disease progression. The probability of progression of peri-implant disease increased with increased observation time.

The effect of bone morphogenetic protein on supracrestal bone growth around partially inserted implants in a dog model is described. The lower premolar teeth (P1, P2, P3 and P4) were extracted on both sides of the mandible in six dogs. At a surgical exposure 12 weeks later, two 10-mm turned titanium implants were partially inserted, approximately 15 mm apart, in the areas of the P1 and P3 in each side of the mandible, allowing five threads to protrude from the bone crest. A titanium mesh was fastened to the coronal aspect of the two fixtures and the space beneath the mesh was filled with bone morphogenetic protein (S300 BMP) in combination with an insoluble bone matrix carrier, or with the carrier alone. The mesh was covered with an ePTFE membrane. Thus, a space for potential bone formation was created between the two implants. The surgical flaps were coronally positioned and secured with vertical mattress sutures. After 16 weeks of healing, biopsy specimens were retrieved and examined histologically. Bone was not formed around the protruding implants or in the created space between the implants in any case. The carrier was incompletely resorbed. We conclude that supracrestal bone growth beyond the crestal limit with or without BMP in such a large space as in this experimental design may not be possible.