Estimation of Bone Loss Biomarkers as a Diagnostic Tool for Peri‐Implantitis

Background: The aims of this study are to estimate the profile of bone loss biomarkers in peri‐implant tissues and to identify potential prognostic biomarkers of peri‐implantitis. Methods: Peri‐implant crevicular fluid samples collected from 164 participants (52 patients with peri‐implantitis, 54 with mucositis, and 58 with healthy peri‐implant tissues) were analyzed using enzyme‐linked immunosorbent assays to evaluate concentrations of the receptor activator of nuclear factor‐κB (RANK), soluble RANK ligand (sRANKL), osteoprotegerin (OPG), cathepsin‐K, and sclerostin. Results: Concentrations of RANK, sRANKL, OPG, and sclerostin were significantly increased in patients with peri‐implantitis compared with patients with healthy peri‐implant tissues. Comparisons between peri‐implantitis and mucositis demonstrated significantly higher values of sclerostin in peri‐implantitis samples. Comparisons between mucositis and healthy peri‐implant tissues showed significantly increased levels of RANK and cathepsin‐K in mucositis. Conclusion: These results are suggestive of a role of sRANKL, OPG, and sclerostin as prognostic biomarkers in peri‐implantitis.     

The evaluation of peri‐implant sulcus fluid osteocalcin,osteopontin, and osteonectin levels in peri‐implant diseases

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 (P > 0.05). Probing depths were not correlated with PISF osteocalcin, osteopontin, and osteonectin levels in the study groups (P > 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.     

Can Peri‐Implant Crevicular Fluid Assist in the Diagnosis of Peri‐Implantitis? A Systematic Review and Meta‐Analysis

Background: A broader understanding of the immune inflammatory profile of peri‐implant diseases could be helpful in the development of host‐targeted preventive and therapeutic strategies. The aim of this study is to answer two clinical questions: 1) whether patients with peri‐implantitis (PP) present higher prevalence of any specific inflammatory cytokine in peri‐implant crevicular fluid (PICF) compared with healthy patients; and 2) whether local inflammation measured in PICF can be used as a predictor for incipient PP. Methods: A systematic review of the literature on the most common cytokines released in PICF in healthy and PP‐affected sites was conducted from 1996 up to and including October 2013 using predefined search strategies. Cross‐sectional and prospective longitudinal studies were considered. Meta‐analyses were done separately for healthy, mucositis (MU), and PP outcomes. Results: Interleukin (IL)‐1β was the most studied cytokine (n = 12), followed by tumor necrosis factor (TNF)‐α (n = 10). Other cytokines were also linked to PP, such as IL‐4, IL‐6, IL‐8, IL‐10, IL‐12, and IL‐17. Statistical differences were revealed when IL‐1β release was compared between healthy implant sites and PP (P = 0.001) or MU sites (P = 0.002), respectively; when PP and MU were compared, no statistical differences could be detected (P = 0.80). For TNF‐α release, significant differences were found between healthy and PP implants (P = 0.02). Conclusions: PICF containing inflammatory mediators, such as IL‐1β and TNF‐α, can be used as additional criteria for a more robust diagnosis of peri‐implant infection. Additionally, once the inflammatory process is installed, no differences were found between peri‐implant MU and PP.     

Longitudinal Comparison of Cytokines in Peri‐Implant Fluid and Gingival Crevicular Fluid in Healthy Mouths

Background: Peri‐implant and gingival tissues provide important sealing and protective functions around implants and teeth, but comparisons of the immunologic responses of these tissues after implant placement have not been conducted. Cytokine levels were measured in peri‐implant crevicular fluid (PICF) and gingival crevicular fluid (GCF) as surrogate measures of immune function at subcrestally placed dental implants and healthy periodontal sites during a 1‐year monitoring period. Methods: A total of 27 dental implants were placed subcrestally in 21 periodontally healthy patients (mean age: 49.0 ± 13.4 years). Repeated clinical and cytokine measurements were obtained over 12 months. GCF and PICF samples were collected and analyzed by cytokine microarray. Data were examined by non‐parametric analysis of variance. Results: Plaque and bleeding indices were similar among all patients (P >0.05) at baseline. During 1 year of monitoring, the mean volumes of PICF and GCF were similar (P >0.05). The levels of interleukin (IL)‐4, ‐6, ‐10, and ‐12p70, tumor necrosis factor‐α, and interferon‐γ in GCF and PICF were not significantly different and did not vary over time (P >0.05). The levels of IL‐1α were higher in GCF than PICF at 1, 2, 6, and 12 months, as were the levels of IL‐8 at 1, 2, 4, 6, and 12 months (P <0.001). Transforming growth factor‐β1 in PICF and GCF exhibited time‐dependent increases, and vascular endothelial growth factor was reduced at 1 year without differences between PICF and GCF (P >0.05). Conclusion: Within the limitations of this study design, it can be concluded that after subcrestal implant placement, the immune response of peri‐implant and periodontal tissues, as assessed by cytokine levels in PICF and GCF, is similar.     

Prevalence and microbiological diversity of Archaea in peri-implantitis subjects by 16S ribosomal RNA clonal analysis

Faveri M, Gonçalves LFH, Feres M, Figueiredo LC, Gouveia LA, Shibli JA, Mayer MPA. Prevalence and microbiological diversity of Archaea in peri‐implantitis subjects by 16S ribosomal RNA clonal analysis. J Periodont Res 2011; 46: 338–344. © 2011 John Wiley & Sons A/S Background and Objective: This study evaluated the prevalence and the molecular diversity of Archaea in the subgingival biofilm samples of subjects with peri‐implantitis. Material and Methods: Fifty subjects were assigned into two groups: Control (n = 25), consisting of subjects with healthy implants; and Test (n = 25), consisting of subjects with peri‐implantitis sites, as well as a healthy implant. In the Test group, subgingival biofilm samples were taken from the deepest sites of the diseased implant. In both groups, subgingival biofilm was collected from one site with a healthy implant and from one site with a periodontally healthy tooth. DNA was extracted and the 16S ribosomal RNA gene was amplified with universal primer pairs for Archaea. Amplified genes were cloned and sequenced, and the phylotypes were identified by comparison with known 16S ribosomal RNA sequences. Results: In the Control group, Archaea were detected in two and three sites of the implant and the tooth, respectively. In the Test group, Archaea were detected in 12, 4 and 2 sites of diseased implants, healthy implants and teeth, respectively. Diseased implants presented a significantly higher prevalence of Archaea in comparison with healthy implants and natural teeth, irrespective of group. Over 90% of the clone libraries were formed by Methanobrevibacter oralis, which was detected in both groups. Methanobacterium congelense/curvum was detected in four subjects from the Test group and in two subjects from the Control group. Conclusion: Although M. oralis was the main species of Archaea associated with both healthy and diseased implant sites, the data indicated an increased prevalence of Archaea in peri‐implantitis sites, and their role in pathogenesis should be further investigated.     

Reversibility of experimental peri-implant mucositis compared with experimental gingivitis in humans

Objective: To monitor clinical, microbiological and host‐derived alterations occurring around teeth and titanium implants during the development of experimental gingivitis/mucositis and their respective healing sequence in humans. Material and methods: Fifteen subjects with healthy or treated periodontal conditions and restored with dental implants underwent an experimental 3‐week period of undisturbed plaque accumulation in the mandible. Subsequently, a 3‐week period with optimal plaque control was instituted. At Days 0, 7, 14, 21, 28, 35 and 42, the presence/absence of plaque deposits around teeth and implants was assessed, (plaque index [PlI]) and the gingival/mucosal conditions were evaluated (gingival index[GI]). Subgingival/submucosal plaque samples and gingival/mucosal crevicular fluid (CF) samples were collected from two pre‐determined sites around each experimental unit. CF samples were analyzed for matrix‐metalloproteinase‐8 (MMP‐8) and interleukin‐1beta (IL‐1β). Microbial samples were analyzed using DNA–DNA hybridization for 40 species. Results: During 3 weeks of plaque accumulation, the median PlI and GI increased significantly at implants and teeth. Implant sites yielded a greater increase in the median GI compared with tooth sites. Over the 6‐week experimental period, the CF levels of MMP‐8 were statistically significantly higher at implants compared with teeth (P<0.05). The CF IL‐1β levels did not differ statistically significantly between teeth and implants (P>0.05). No differences in the total DNA counts between implant and tooth sites were found at any time points. No differences in the detection frequency were found for putative periodontal pathogens between implant and tooth sites. Conclusion: Peri‐implant soft tissues developed a stronger inflammatory response to experimental plaque accumulation when compared with that of their gingival counterparts. Experimental gingivitis and peri‐implant mucositis were reversible at the biomarker level. Clinically, however, 3 weeks of resumed plaque control did not yield pre‐experimental levels of gingival and peri‐implant mucosal health indicating that longer healing periods are needed. To cite this article:
Salvi GE, Aglietta M, Eick S, Sculean A, Lang NP & Ramseier CA. Reversibility of experimental peri‐implant mucositis compared with experimental gingivitis in humans.
Clin. Oral Impl. Res. 23 , 2012; 182–190.
doi: 10.1111/j.1600‐0501.2011.02220.x     

Early intervention of peri‐implantitis and periodontitis using a mouse model

1 Background

Peri‐implantitis is an inflammatory response to bacterial biofilm resulting in bone loss and can ultimately lead to implant failure. Because of the lack of predictable treatments available, a thorough understanding of peri‐implantitis's pathogenesis is essential. The objective of this study is to evaluate and compare the response of acute induced peri‐implantitis and periodontitis lesions after insult removal.

2 Methods

Implants were placed in one‐month‐old C57BL/6J male mice eight weeks post extraction of their left maxillary molars. Once osseointegrated, ligatures were placed around the implants and contralateral second molars of the experimental groups. Controls did not receive ligatures. After one week, half of the ligatures were removed, creating the ligature‐retained and ligature‐removed groups. Mice were sacrificed at two time points, 5 and 14 days, from ligature removal. The specimens were analyzed via micro‐computed tomography and histology.

3 Results

By 5 and 14 days after ligature removal, the periodontitis group experienced significant bone gain, whereas the peri‐implantitis group did not. Histologically, all implant groups exhibited higher levels of cellular infiltrate than any of the tooth groups. Osteoclast numbers increased in peri‐implantitis and periodontitis ligature‐retained groups and decreased following insult removal. Collagen was overall more disorganized in peri‐implantitis than periodontitis for all groups. Peri‐implantitis experimental groups revealed greater matrix metalloproteinase‐8 and NF‐kB levels than periodontitis.

4 Conclusions

Implants respond slower and less favorably to insult removal than teeth. Future research is needed to characterize detailed peri‐implantitis disease pathophysiology.     

The Association Between Thalassemia Major and Periodontal Health

Background : The aim of this cross‐sectional study is to compare the local and systemic levels of soluble receptor activator of nuclear factor‐κB ligand (sRANKL), osteoprotegerin (OPG), a proliferation‐inducing ligand (APRIL), B‐cell activating factor (BAFF), interleukin (IL)‐6, and IL‐8 in biofluids of patients with thalassemia major (TM) with or without gingivitis. Methods: Seventy‐seven patients are included in this study (TM, n = 29; systemically healthy, n = 48). Gingival crevicular fluid (GCF), saliva, and serum levels of IL‐6, IL‐8, sRANKL, OPG, BAFF, and APRIL were determined by enzyme‐linked immunosorbent assay. Data were analyzed by appropriate non‐parametric or parametric statistical tests. Results: Median GCF, serum, and saliva levels for BAFF (P <0.001) and IL‐6 and IL‐8 (P <0.005) were higher in TM gingivitis than in systemically healthy gingivitis (P <0.001). GCF, serum, and saliva levels for APRIL, sRANKL, IL‐6, and IL‐8 were higher in TM than in systemically and periodontally healthy comparison groups (P <0.05). Positive correlations were found between bleeding on probing (BOP), plaque index (PI) scores, and GCF APRIL, serum sRANKL, serum OPG, and sRANKL concentrations in TM groups (P <0.05). Several significant positive correlations were found between BOP, PI scores, and biofluid parameters also in systemically healthy groups. Conclusion: TM may have a role in the underlying systemic hematologic condition and potentially affect gingival inflammation via dysregulation of lymphocytes and increased activation of osteoclasts.     

Analysis of cathepsin-K activity at tooth and dental implant sites and the potential of this enzyme in reflecting alveolar bone loss

Background: Cathepsin‐K is an enzyme involved in bone metabolism which may make this feature important for both natural teeth and dental implants. The aims of the present study are to comparatively analyze the gingival crevicular fluid (GCF)/peri‐implant sulcus fluid (PISF) cathepsin‐K levels of natural teeth and dental implants, and to assess the potential relationship between this biochemical parameter and alveolar bone loss around natural teeth and dental implants. Methods: Probing depth, bleeding on probing, gingival index, and plaque index clinical parameters were assessed, and GCF/PISF samples were obtained from natural teeth/dental implants presenting with either clinical health, gingivitis/peri‐implant mucositis, or chronic periodontitis/peri‐implantitis. Cathepsin‐K activity levels of 42 GCF samples and 54 PISF samples were determined, and marginal bone loss (MBL) measures were calculated from digitalized standardized intraoral periapical radiographs obtained from natural teeth and dental implants by using cemento‐enamel junction and the actual distance between two consecutive threads of the dental implant as reference points for natural teeth and dental implants, respectively. Results: Comparing the natural teeth group with dental implant group with regard to MBL measure, cathepsin‐K activity, and GCF/PISF volume revealed no significant differences. In both natural teeth and dental implant groups, despite higher MBL measures, cathepsin‐K activity, and GCF/PISF volumes with the presence of inflammation, it was the presence of alveolar bone loss that lead to significantly higher values for these parameters. Conclusion: We suggest cathepsin‐K as a biochemical parameter for monitoring periodontal/peri‐implant alveolar bone loss.     

Arginine–Nitric Oxide–Polyamine Metabolism in Periodontal Disease

Background: Arginine is converted to nitric oxide (NO) via NO synthase and to ornithine via arginase. Ornithine decarboxylase (ODC) catalyzes the conversion of ornithine to polyamines. Arginase can inhibit NO production, and NO can inhibit ODC activity as part of an early inflammatory response. This study examines the arginine‐NO‐polyamine pathway alteration in saliva and gingival biopsy samples of patients with gingivitis or periodontitis and healthy controls and evaluates the response to periodontal treatment. Methods: This study includes nine gingivitis patients, 15 chronic periodontitis patients, and 11 healthy age‐matched controls. Periodontal clinical measurements, gingival biopsies, and saliva samples were obtained before treatment (BT) and 1 month after periodontal treatment (AT). Arginase and ODC activities and NO levels were determined spectrophotometrically. Results: The BT salivary and gingival NO levels were found to be highest in the gingivitis group, followed by the healthy and the periodontitis groups, respectively. Salivary NO levels significantly increased in the periodontitis group and decreased in the gingivitis group AT (P <0.05). Gingival NO levels decreased significantly in the periodontitis and the gingivitis groups AT (P <0.05). Arginase levels were detected highest in the gingivitis group and lowest in the periodontitis group, both in saliva and gingiva. Only gingival arginase levels significantly increased AT (P <0.05). ODC activity was highest in saliva, and lowest in the gingiva of the periodontitis patients BT. It was found to be significantly higher in the periodontitis group AT (P <0.05). Conclusions: In this study, regarding arginine‐NO‐polyamine metabolism, gingival tissue seems to be more informative about periodontal pathogenesis than saliva. At early phase of periodontal inflammation, NO arginase and ODC levels were measured as higher than at an established lesion of periodontitis.     

Peri-implantitis in partially edentulous patients: association with inadequate plaque control

Objective: The aim of the present study was to describe some clinical periodontal features of partially edentulous patients referred for the treatment of peri‐implantitis. Material and methods: The 23 subjects involved in this study were selected from consecutive patients referred to the department of Periodontology Södra Älvsborgs Hospital, Borås, Sweden, for treatment of peri‐implantitis during 2006. The patients had clinical signs of peri‐implantitis around one or more dental implants (i.e.≥6 mm pockets, bleeding on pockets and/or pus and radiographic images of bone loss to≥3 threads of the implants) and remaining teeth in the same and/or opposite jaw. The following clinical variables were recorded: Plaque Index (PI), Gingival Bleeding Index (GBI) Probing Pocket Depth (PPD), Access/capability to oral hygiene at implant site (yes/no), Function Time. The patients were categorized in the following sub‐groups: Periodontitis/No periodontitis, Bone loss/No bone loss at teeth, Smoker/Non‐smokers. Results: Out of the 23 patients, the majority (13) had minimal bone loss at teeth and no current periodontitis; 5 had bone loss at teeth exceeding 1/3 of the length of the root but not current periodontitis and only 5 had current periodontitis. Six patients were smokers (i.e. smoking more than 10 cig/day). The site level analysis showed that only 17 (6%) of the 281 teeth present had ≥1 pocket of ≥6mm, compared to 58 (53%) of the total 109 implants (28 ITI^® and 81 Brånemark^®); 74% of the implants had no accessibility to proper oral hygiene. High proportion of implants with diagnosis of peri‐implantitis were associated with no accessibility/capability for appropriate oral hygiene measures, while accessibility/capability was rarely associated with peri‐implantitis. Indeed 48% of the implants presenting peri‐implantitis were those with no accessibility/capability for proper oral hygiene (65% positive predict value) with respect to 4% of the implants with accessibility/capability (82% negative predict value). Conclusion: The results of the study indicate that local factors such as accessibility for oral hygiene at the implant sites seems to be related to the presence or absence of peri‐implantitis. Peri‐implantitis was a frequent finding in subjects having signs of minimal loss of supporting bone around the remaining natural dentition and no signs of presence of periodontitis (i.e. presence of periodontal pockets of ≥6 mm at natural teeth). Only 6 of the examinated subjects were smokers. In view of these results we should like to stress the importance of giving proper oral hygiene instructions to the patients who are rehabilitated with dental implant and of proper prosthetic constructions that allow accessibility for oral hygiene around implants.     

Peri-implantitis fibroblasts respond to host immune factor C1q

Verardi S, Quaranta M, Bordin S. Peri‐implantitis fibroblasts respond to host immune factor C1q. J Periodont Res 2011; 46: 134–140. © 2010 John Wiley & Sons A/S Background and Objective: Current therapies for peri‐implantitis apply the same clinical protocols as those used for the treatment of periodontitis; however, outcomes remain unpredictable. We hypothesized that resident fibroblasts of the peri‐implantitis stroma and periodontitis stroma differ in their phenotype and response to host immune factors. Fibroblasts are highly heterogeneous and comprise discrete subtypes with the potential of modulating inflammatory activities. The aim of the present study was to characterize the expression of receptors for complement C1q of innate immunity on human peri‐implantitis fibroblasts and investigate effects of C1q on the proinflammatory properties of the cells. Material and methods: Fibroblasts were cultured from gingival tissues exhibiting peri‐implantitis and periodontitis, and from healthy gingivae as a control. Expression of C1q receptors for the collagen (cC1qR) and globular domains (gC1qR) of the protein was determined by flow cytofluorometric analysis (FITC) of specific antibodies bound to the surface of the cells. Secretion of C1q‐inducible proinflammatory mediators was quantified after 24 h incubation using array‐based ELISAs. Results: The percentage of fibroblasts FITC‐positive for cC1qR was 67, 75 and 12% in peri‐implantitis, healthy and periodontitis cultures, respectively, whereas the percentage of gC1qR FITC‐positive fibroblasts was 5, 3 and 59%, respectively. The C1q interactions with peri‐implantitis and healthy fibroblasts increased secretion of the chemokines interleukin‐6 and interleukin‐8 twofold, and monocyte chemoattractant protein‐1 fourfold over baseline values, whereas periodontitis fibroblasts were unresponsive. Complement C1q increased levels of vascular endothelial growth factor sevenfold and transforming growth factor‐β1 12‐fold over baseline values in peri‐implantitis cultures, only. Conclusions: Peri‐implantitis fibroblasts differ from periodontitis fibroblasts in phenotypic expression of cC1qR and function, and from healthy fibroblasts in proinflammatory, angiogenic and fibrogenic function. Peri‐implantitis fibroblasts may represent a novel subtype.     

Composition of supra- and subgingival biofilm of subjects with healthy and diseased implants

Objectives: The purpose of this study was to compare the microbial composition of supra‐ and subgingival biofilm in subjects with and without peri‐implantitis. Material and methods: Forty‐four subjects (mean age 48.9 ± 13.51 years) with at least one implant restored and functional for at least 2 years were assigned to two groups: a peri‐implantitis group (n=22), consisting of subjects presenting peri‐implant sites with radiographic defects >3 mm, bleeding on probing and/or suppuration; and a control group (n=22), consisting of subjects with healthy implants. The clinical parameters evaluated were plaque index, gingival bleeding, bleeding on probing, suppuration, probing depth and clinical attachment level. Supra‐ and subgingival biofilm samples were taken from the deepest sites of each implant and analyzed for the presence of 36 microorganisms by checkerboard DNA–DNA hybridization. Results: Higher mean counts of Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia were observed in the peri‐implantitis group, both supra‐ and subgingivally (P<0.05). The proportions of the pathogens from the red complex were elevated, while host‐compatible beneficial microbial complexes were reduced in diseased compared with healthy implants. The microbiological profiles of supra‐ and subgingival environments did not differ substantially within each group. Conclusion: Marked differences were observed in the composition of supra‐ and subgingival biofilm between healthy and diseased implants. The microbiota associated with peri‐implantitis was comprised of more periodontal pathogenic bacterial species, including the supragingival biofilm.     

On site noninvasive assessment of peri-implant inflammation by optical spectroscopy

Nogueira‐Filho G, Xiang XM, Shibli JA, Duarte PM, Sowa MG, Ferrari DS, Onuma T, de Cardoso LAG, Liu K‐Z. On site noninvasive assessment of peri‐implant inflammation by optical spectroscopy. J Periodont Res 2011; 46: 382–388. © 2011 John Wiley & Sons A/S Background and Objective: Optical spectroscopy has been proposed to measure regional tissue hemodynamics in periodontal tissue. The objective of this study was to further evaluate the diagnostic potential of optical spectroscopy in peri‐implant inflammation in vivo by assessing multiple inflammatory parameters (tissue oxygenation, total tissue hemoglobin, deoxyhemoglobin, oxygenated hemoglobin and tissue edema) simultaneously. Material and Methods: A cross‐sectional study was performed in a total of 64 individuals who presented with dental implants in different stages of inflammation. In brief, visible–near‐infrared spectra were obtained, processed and evaluated from healthy (n = 151), mucositis (n = 70) and peri‐implantitis sites (n = 75) using a portable spectrometer. A modified Beer–Lambert unmixing model that incorporates a nonparametric scattering loss function was employed to determine the relative contribution of each inflammatory component to the overall spectrum. Results: Tissue oxygenation at peri‐implantitis sites was significantly decreased (p < 0.05) when compared with that at healthy sites, which was largely due to an increase in deoxyhemoglobin and a decrease in oxyhemoglobin at the peri‐implantitis sites compared with the mucositis and healthy sites. In addition, the tissue hydration index derived from the optical spectra in mucositis was significantly higher than that in other groups (p < 0.05). Conclusion: In summary, the results of this study revealed that hemodynamic alterations can be detected around diseased peri‐implant sites by optical spectroscopy, and this method may be considered an alternative and feasible approach for the monitoring and diagnosis of peri‐implant diseases.     

Evaluation of Biochemical Parameters and Local and Systemic Levels of Osteoactive and B‐Cell Stimulatory Factors in Gestational Diabetes in the Presence or Absence of Gingivitis

Background: Gestational diabetes mellitus (GDM) is defined as varying glucose intolerance, with first onset or recognition in pregnancy. This study evaluates clinical and biochemical parameters in a possible association between GDM and gingivitis. Methods: A total of 167 pregnant females was included in the study. There were 101 females with GDM and 66 females without GDM. Subgroups were created according to the presence or absence of gingival inflammation. Plaque index, bleeding on probing, and probing depth were recorded at four sites per tooth. Serum, saliva, and gingival crevicular fluid (GCF) levels of interleukin (IL)‐6, IL‐8, soluble receptor activator of nuclear factor‐kappa B ligand (sRANKL), osteoprotegerin (OPG), B‐cell activating factor (BAFF), and a proliferation‐inducing ligand (APRIL) were determined by enzyme‐linked immunosorbent assay. Data were analyzed by Kruskal‐Wallis and Mann‐Whitney U tests and Spearman correlation analysis. Results: Age and anthropometric indices were higher in the GDM than non‐GDM group (P <0.0001). Clinical periodontal recordings, serum BAFF, IL‐8, and saliva sRANKL levels were higher in the GDM group (P <0.05). Saliva IL‐6 level was higher in the GDM with gingivitis group than non‐GDM with gingivitis group (P = 0.044). Serum and GCF BAFF (P <0.0001), serum, saliva, and GCF APRIL (P <0.0001; P <0.0001; P = 0.032, respectively), GCF OPG (P = 0.036), and serum and saliva sRANKL (P <0.0001) were higher in the GDM with gingivitis group than GDM without gingivitis group. Conclusions: The inflammatory response seems to be more pronounced in females with GDM. The observed increase in both local and systemic levels of inflammatory cytokines may suggest an interaction between gingivitis and GDM.     

Periodontal and peri‐implant diseases: identical or fraternal infections?

Peri‐implant diseases (peri‐implantitis and peri‐implant mucositis) are bacterially driven infections. Peri‐implantitis leads to aggressive bone resorption and eventual loss of the implant. Traditionally, peri‐implantitis was regarded as microbially similar to periodontitis, and translocation of periodontal pathogens into the peri‐implant crevice was considered as a critical factor in disease causation. However, evidence is emerging to suggest that the peri‐implant and periodontal ecosystems differ in many important ways. The purpose of this review is to examine the evidence supporting microbial congruence and discordance in these two communities. Current evidence suggests that osseointegrated implants truly create unique microenvironments that force microbial adaptation and selection. Further studies that revisit the “microbial reservoir” hypothesis and identify species that play an etiologic role in peri‐implant disease and examine their transmission from teeth are needed.     

TNF-alpha TGF-beta2 and IL-1beta levels in gingival and peri-implant crevicular fluid before and after de novo plaque accumulation

Aims: The aim of this split‐mouth study was to investigate levels of tumour necrosis factor alpha (TNF‐α), transforming growth factor beta (TGF‐β2) and interleukin‐1 beta (IL‐1β) in gingival crevicular fluid (GCF) and peri‐implant crevicular fluid (PICF) after a 21‐day‐period of de novo plaque accumulation in the same patient. Material and Methods: In 25 patients, samples of GCF and PICF were collected in the sulcus of the tooth and of the implant after professional hygiene. After the no‐hygiene phase (21 days), second samples of GCF and PICF were taken. Third samples were collected after 69 days of re‐establishment oral hygiene techniques. The crevicular fluids were used to determine the volume and the levels of TNF‐α, TGF‐β2 and IL‐1β. Results: The volume of the crevicular fluids increased significantly after 21 days of plaque accumulation around teeth and implants and decreased significantly by 69 days. TNF‐α and TGF‐β2 did not change significantly among the three different samples. A significant increase of IL‐1β was observed after plaque accumulation around the teeth GCF, whereas in the PICF the increase was not statistically significant. Conclusions: These data suggest that increased volumes of GCF and PICF could be useful markers of early inflammation in gingival and peri‐implant tissues. In the presence of de novo plaque, implants showed lower, and nearly significant, levels of IL‐1β compared with teeth.     

Increased Levels of Dissolved Titanium Are Associated With Peri‐Implantitis – A Cross‐Sectional Study

Background: Peri‐implantitis represents a disruption of the biocompatible interface between the titanium dioxide layer of the implant surface and the peri‐implant tissues. Increasing preclinical data suggest that peri‐implantitis microbiota not only triggers an inflammatory immune response but also causes electrochemical alterations of the titanium surfaces, i.e., corrosion, that aggravate this inflammatory response. Thus, it was hypothesized that there is an association between dissolution of titanium from dental implants, which suggests corrosion, and peri‐implantitis in humans. The objective of this study is to compare levels of dissolved titanium in submucosal plaque collected from healthy implants and implants with peri‐implantitis. Methods: Submucosal plaque from 20 implants with peri‐implantitis and 20 healthy implants was collected with sterile curets from 30 participants. Levels of titanium were quantified using inductively coupled plasma mass spectrometry and normalized for mass of bacterial DNA per sample to exclude confounding by varying amounts of plaque per site. Statistical analysis was performed using generalized estimated equations to adjust for clustering of implants per participant. Results: Implants with peri‐implantitis harbored significantly higher mean levels of titanium (0.85 ± 2.47) versus healthy implants (0.07 ± 0.19) after adjusting for amount of plaque collected per site (P = 0.033). Conclusions: Greater levels of dissolved titanium were detected in submucosal plaque around implants with peri‐implantitis compared with healthy implants, indicating an association between titanium dissolution and peri‐implantitis. Factors triggering titanium dissolution, as well as the role of titanium corrosion in the peri‐implant inflammatory process, warrant further investigation.     

Investigation of the Association Between Cement Retention and Prevalent Peri‐Implant Diseases: A Cross‐Sectional Study

Background: The aim of this study is to examine the association between retention type (cement‐retained versus screw‐retained restorations) and prevalence of peri‐implant diseases in a German university‐treated population. Methods: Data were analyzed from individuals that underwent clinical and radiographic peri‐implant examinations as part of a university‐based cross‐sectional study from September 2011 to October 2012. Results: Data from 139 individuals (mean age: 57.59 years) having 394 implants were analyzed: 192 implants supporting single crowns and 202 fixed partial dentures. Overall, 11.9% of the participants had peri‐implantitis, whereas 68.9% had peri‐implant mucositis. Crude odds ratios (95% confidence intervals) for peri‐implantitis and peri‐implant mucositis for cement‐ versus screw‐retained restorations were 1.43 (0.45, 4.60) and 0.89 (0.53, 1.48), respectively. Results remained non‐significant in multivariable models adjusting for type of restoration and smoking (all P values >0.50). There was also no effect of splinting restorations on disease prevalence in adjusted analyses (P values >0.32). Conclusions: In this university‐treated sample, there is no association between the type of prosthesis retention and peri‐implant diseases. Current findings show that, when appropriate selection and removal of cement is performed, cement retention is not a risk indicator for peri‐implant diseases.