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1 Background

Peri‐implant diseases are prevalent, with numerous therapies studied in an attempt to combat this condition. The present review aims to systematically evaluate the effectiveness of laser therapy with non‐surgical or surgical therapy in managing peri‐implant mucositis and peri‐implantitis.

2 Methods

An electronic search of three databases and a hand search of peer‐reviewed journals for relevant articles published (in English) from January 1980 to June 2016 were performed. Human clinical trials of ≥ 10 patients with peri‐implant diseases, treated with surgical or non‐surgical approaches and laser therapy, and a follow‐up period of ≥ 6 months, were included. Random‐effects meta‐analyses were performed to analyze weighted mean difference (WMD) and confidence interval for the recorded variables according to PRISMA guidelines. Risk of bias assessment was also performed for randomized controlled trials included.

3 Results

From 22 articles selected, 11 were included in the meta‐analyses. The outcomes of using lasers as a monotherapy could not be evaluated since no controlled studies were identified. Therefore, all reported results were the outcomes of applying lasers as an adjunct to surgical/non‐surgical treatment. For the non‐surgical approach, WMD of probing depth (PD), clinical attachment level (CAL), bleeding on probing (BOP), plaque index (PI), marginal bone level (MBL) and recession (REC) was 0.15 mm (P = 0.50), ?0.10 mm (P = 0.32), 21.08% (P = 0.02), ?0.07 (P = 0.002), ?0.22 mm (P = 0.04) and ?0.11 mm (P = 0.34), respectively. For the surgical approach with a long‐term follow up, WMD of PD, CAL, BOP, and PI was 0.45 mm (P = 0.11), 0.22 mm (P = 0.56), 7.26% (P = 0.76) and ?0.09 (P = 0.84), respectively.

4 Conclusions

Current evidence shows laser therapy in combination with surgical/non‐surgical therapy provided minimal benefit in PD reduction, CAL gain, amount of REC improvement, and PI reduction in the treatment of peri‐implant diseases. Lasers when used as an adjunct to non‐surgical therapy might result in more BOP reduction in the short term. However, current evidence allowed for analysis of only Er:YAG, CO2, and diode lasers. Studies on others failed to have controlled evidence supporting their evaluation.  相似文献   

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Peri‐implantitis is an inflammatory disease of tissues surrounding osseointegrated dental implants. Inflammation affecting soft and hard peri‐implant tissues can cause alveolar bone resorption and subsequent implant loss. Clinical surveillance and early diagnosis are of paramount importance to reduce clinical failures and improve implant survival. Current diagnosis of implants is based on clinical and radiological signs. Molecular tests are an emerging diagnostic methodology, which potentially can help to detect and prevent early peri‐implantitis and monitor the efficacy of therapy as well. A plethora of potential biomarkers are potentially available to support the clinical diagnosis of peri‐implantitis. However, conflicting diagnostic conclusions have been reached, probably related to weak statistical results due to limited sample size or disease heterogeneity. The present paper reviews candidate diagnostic biomarkers for peri‐implantitis, including infective agents, genetic susceptibility factors, and key proteins related to inflammation and tissue remodeling.  相似文献   

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Background : High prevalence rates of peri‐implant diseases have been reported; however, the lack of standardization of definition criteria has lead to variations in the observed estimates. In addition, scarce data are available concerning patient and implant related factors associated to peri‐implantitis. The aim of this study was to determine the prevalence of peri‐implant diseases and their risk indicators at the patient and implant levels. Methods : One hundred forty‐seven patients with 490 dental implants were included. Dental implants were clinically and radiographically evaluated to determine their peri‐implant conditions. Patient‐related conditions and implant and prosthetic‐related factors were recorded. Multivariable Poisson regression was fitted and prevalence ratios (PR) were reported. Results : 85.3% of implants (95%CI 80.2 to 90.4) had mucositis and 9.2% (95%CI 4.7 to 13.7) had peri‐implantitis. 80.9% (95%CI 73.8 to 86.8), and 19.1% (95%CI 12.6 to 25.5) of patients had mucositis and peri‐implantitis. At the patient level, it was observed an increased probability of peri‐implantitis in individuals with pocket depths ≥6 mm (PR = 2.47) and with ≥4 implants (PR = 1.96). Smoking increased the probability of peri‐implantitis by three times (PR = 3.49). The final multilevel Poisson regression model at the implant level indicated that platform switching reduced the probability of peri‐implantitis (PR = 0.18) and implants in function for ≥5 years increased this probability (PR = 2.11). The final model including patient and implant level indicators demonstrated that higher time of function (PR = 2.76) and smoking (PR = 6.59) were associated with peri‐implantitis. C onclusion : Peri‐implant diseases are highly prevalent in the studied sample, and factors associated with the occurrence of peri‐implantitis were presence of pockets ≥6 mm, smoking, time of function, and type of platform.  相似文献   

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Objective: The main objective of this systematic review is to compare the effects of treatment of peri‐implant infection between animal and human studies. Material and methods: A literature search was conducted using the Medline, Cochrane Central Register of Controlled Trials, and Latin American and Caribbean Health Sciences Literature databases up to and including May 2008. In addition, bibliographies of systematic reviews on peri‐implant diseases were searched manually. Non‐surgical and surgical treatments of peri‐implantitis/mucositis in animal models or human studies were compared. Meta‐analysis was conducted to investigate the difference between the reported treatment effects in animal and human studies. Changes in probing pocket depth (PPD) and probing attachment level (PAL) from baseline measurements were used as measures of outcome. Single‐level and multilevel meta‐regression analysis was performed by taking into account the different follow‐up times of the studies included. Results: The single‐level and multilevel random‐effects meta‐analysis showed that the difference in PPD reduction [0.31 mm, 95% confidence interval (CI): ?0.27, 0.88] and in PAL gain (0.21 mm, 95% CI: ?0.47, 0.88) between animal and human studies was not statistically significant. The random‐effects meta‐regression suggested that studies with longer follow‐up times revealed greater PPD reduction (0.25 mm per month, 95% CI: 0.14, 0.35). However, when the different follow‐up times were taken into account, these differences became greater. Substantial heterogeneity between studies was found in the meta‐analyses (I2=97.6% for animal studies and 99.9% for human studies). Conclusion: There was great heterogeneity between human and animal studies in terms of study designs and treatment procedures. Therefore, the results from this meta‐analysis should be interpreted with caution. Heterogeneity between studies and its causes merit further investigations. To cite this article:
Faggion CM Jr, Chambrone L, Gondim V, Schmitter M, Tu Y‐K. Comparison of the effects of treatment of peri‐implant infection in animal and human studies: systematic review and meta‐analysis.
Clin. Oral Impl. Res. 21 , 2010; 137–147.
doi: 10.1111/j.1600‐0501.2009.01753.x  相似文献   

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1 Background

This study evaluated the influence of a triclosan‐containing toothpaste in the profile of osteo‐immunoinflammatory mediators in peri‐implant crevicular fluid (PICF) and in clinical parameters during progression of peri‐implant mucositis.

2 Methods

Twenty‐two clinically healthy patients with an implant‐supported single‐unit crown were enrolled in this double‐blind, randomized, crossover study carried out in two phases of 21 days each. During an experimental 3‐week period of undisturbed plaque accumulation in the implants, patients were randomly assigned to use three times/day: triclosan (n = 11), triclosan/copolymer/fluoride toothpaste; or placebo (n = 11), fluoride toothpaste. After a professional prophylaxis, a washout period of 30 days was established. Clinical parameters and 15 osteo‐immunoinflammatory mediators in the PICF were evaluated at baseline and at 3, 7, 14, and 21 days.

3 Results

Both groups showed increase in plaque index at implant sites from the 3rd until the 21st day (< 0.05). Only triclosan treatment was able to avoid an increase in bleeding on probing (BOP) throughout the follow‐ups (> 0.05), whereas a significant intensification in BOP was observed from the 14th day in the placebo‐treated sites (< 0.05). Lower interleukin (IL)‐10 concentrations were detected in the placebo group at the 21st day when compared with triclosan‐treated implant sites (< 0.05). IL‐10 levels were reduced and IL‐1β concentrations were increased at 21 days when compared with baseline only in placebo‐treated sites (< 0.05). Osteoprotegerin levels significantly increased from the 14th until the 21st day only in triclosan‐treated sites (< 0.05).

4 Conclusion

Triclosan‐containing toothpaste controls clinical inflammation and interferes positively in the profile of osteo‐immunoinflammatory mediators during progression of experimental peri‐implant mucositis.  相似文献   

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1 Background

Peri‐implant mucositis is an inflammation of the soft tissues surrounding an implant. Peri‐implantitis refers to a process characterized by peri‐implant bone loss along with an inflammation of the soft tissues. Osteocalcin, osteopontin, and osteonectin proteins are related to bone remodeling. The aim of the present study was to investigate peri‐implant sulcus fluid (PISF) osteocalcin, osteopontin, and osteonectin levels in peri‐implant mucositis and peri‐implantitis.

2 Methods

Fifty‐two implants with peri‐implantitis, 46 implants with peri‐implant mucositis, and 47 control implants were included in the study. Clinical parameters including probing depth, modified sulcus bleeding index and modified plaque index were recorded. PISF osteocalcin, osteopontin, and osteonectin levels were analyzed by ELISA kits.

3 Results

There were no significant differences in PISF osteocalcin, osteopontin, and osteonectin total amounts between healthy controls, peri‐implant mucositis and peri‐implantitis groups (> 0.05). Probing depths were not correlated with PISF osteocalcin, osteopontin, and osteonectin levels in the study groups (> 0.05).

4 Conclusions

Soft tissue inflammation around dental implants does not cause a change in osteocalcin, osteopontin, and osteonectin levels in PISF. Also, peri‐implantitis does not seem to give rise to an increase in PISF levels of osteocalcin, osteopontin, and osteonectin.  相似文献   

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