Could implant position influence the peri-implant parameters in edentulous mandibles of diabetics rehabilitated with overdentures? A split-mouth randomized study.

This randomized controlled trial assessed the impact of crestal level position of implants installed in type 2 diabetes mellitus (T2DM) patients rehabilitated with overdentures. Twenty-two mandibular edentulous T2DM patients were submitted to implant placement for retention of an overdenture. By means of a split-mouth design, two implants were installed: one at supracrestal level (SL) and one at crestal level (CL). Clinical, immunoenzymatic and tomographic analyses were performed at prosthesis placement (baseline) and after 6, 12 and 24 months following implant loading. Increased peri-implant probing depths were detected in CL implants when compared with SL implants at all time-points (baseline P=0.047; 6 months P=0.014; 12 months P=0.027; 24 months P=0.036). Indeed, augmented clinical attachment levels were also detected in CL implants when compared with SL implants at all time-points (baseline P=003; 6 months P=0.045; 12 months P=0.029; 24 months P=0.026). CL implants demonstrated increased amounts of interleukin-6 (IL-6) at 6 months (P=0.043) and higher IL-17 (P=0.021), IL-21 (P=0.034) and tumour necrosis factor alpha (TNF-α) concentrations (P=0.030) at 24 months in comparison with SL implants. CL group revealed enhanced bone loss from baseline to 6 (P=0.032), 12 (P=0.043) and 24 months (P=0.028) when compared with SL. In conclusion, this study showed that implants placed supracrestally in T2DM patients rehabilitated with overdentures demonstrated lower bone loss and better clinical parameters with beneficial modulation of peri-implant immunoinflammatory biomarkers when compared with implants positioned at crestal level.

Subgingival Host-Microbial Interactions in Hyperglycemic Individuals.

Type 2 diabetes mellitus (T2DM) is an established risk factor for periodontitis, yet its contribution to creating host-bacterial disequilibrium in the subgingival crevice is poorly understood. The present investigation aimed to quantify the impact of hyperglycemia on host-bacterial interactions in established periodontitis and to map shifts in these dynamics following mechanical nonsurgical therapy. Seventeen T2DM and 17 non-T2DM subjects with generalized severe chronic periodontitis were recruited along with 20 periodontally healthy individuals. Subjects with periodontitis were treated with scaling and root planing (SRP). Samples of subgingival biofilm and gingival crevicular fluid were collected at baseline and at 1-, 3-, and 6 mo postoperatively. Correlations were generated between 13.7 million 16S ribosomal DNA sequences and 8 immune mediators. Intermicrobial and host-microbial interactions were modeled using differential network analysis. Periodontal health was characterized by a sparse interbacterial and highly connected cytokine-bacterial network, while both normoglycemics and T2DM subjects with periodontitis demonstrated robust congeneric and intergeneric hubs but significantly fewer cytokine-bacterial connections. Following SRP, the cytokine-bacterial edges demonstrated a 2-fold increase 1 mo postoperatively and a 10-fold increase at 6 mo in normoglycemics. In hyperglycemics, there was a doubling at 1 mo but no further changes thereafter. These shifts accompanied an increasingly sparse interbacterial network. In normoglycemics, the nodes anchored by interleukin (IL)-4, IL-6, and IL-10 demonstrated greatest rewiring, while in hyperglycemics, IL-1ß, IL-6, INF-γ, and IL-17 exhibited progressive rewiring. Thus, the present investigation points to a breakdown in host-bacterial mutualism in periodontitis, with interbacterial interactions rather than host-bacterial interactions primarily determining community assembly. Hyperglycemia further exacerbates this uncoupled mutualism. Our data also demonstrate that while nonsurgical therapy might not consistently alter microbial abundances or lower proinflammatory molecules, it "reboots" the interaction between the immunoinflammatory system and the newly colonizing microbiome, restoring a role for the immune system in determining bacterial colonization. However, this outcome is lower and delayed in hyperglycemics.

The impact of implant abutment surface treatment with TiO2 on peri-implant levels of angiogenesis and bone-related markers: a randomized clinical trial.

The goal of this randomized, blinded, split-mouth controlled clinical trial was to assess the influence of abutment surface treatment on tissue healing. Fifteen patients received two implants distributed randomly to two groups: test (TiO2 abutment surface), control (standard abutment surface). Levels of epidermal growth factor (EGF), bone morphogenetic protein 9 (BMP-9), endothelin 1 (ET-1), fibroblast growth factor (FGF), placental growth factor (PlGF), and vascular endothelial growth factor (VEGF) were quantified in the peri-implant fluid after 3, 14, 30, and 60 days. Inter-group comparisons indicated higher levels of EGF, BMP-9, ET-1, FGF, and PlGF in the test group after 30days (P<0.05). PlGF levels were also higher in the test group after 60 days. In the test group, intra-group analysis revealed different levels of ET-1 and FGF between days 3 and 30, and days 3 and 60 (P<0.05); furthermore, VEGF levels were significantly higher on day 60 than on day 3 (P <0.05). In the control group, intra-group analysis demonstrated significantly different levels of ET-1, FGF, and PlGF between days 3 and 60 and of PlGF between days 14 and 60 (P<0.05). In conclusion, abutment surfaces treated with TiO2 influenced the levels of angiogenesis and bone-related markers.

Short implants versus bone augmentation in combination with standard-length implants in posterior atrophic partially edentulous mandibles: systematic review and meta-analysis with the Bayesian approach.

The use of short implants as an alternative to bone reconstruction techniques for the placement of standard-length dental implants is a debated topic. The aim of this study was to perform a systematic review and meta-analysis in order to assist in the clinical decision making about the most appropriate approach for the fixed rehabilitation of the posterior atrophic partially edentulous lower jaws. Only randomized trials with at least 1-year follow-up were included. Of the 1024 studies initially retrieved, 14 articles were selected and independently evaluated by two reviewers. Finally, four studies were included, and underwent data extraction and meta-analysis with the Bayesian approach. Both treatment approaches provide high implant survival rate after 1year of function. However, the probability of survival rate of short implants being greater than standard length implants is 84%, and the probability of complications using short implants being greater than standard-length implants is 15.7%. In spite of similar survival rates when the residual bone is sufficient for placement of short implants, the latter should be preferred to augmentation techniques and standard-length implants due to fewer complications, lower morbidity and greater comfort for patients.

Effect of curcumin on bone tissue in the diabetic rat: repair of peri-implant and critical-sized defects.

This study determined the effect of curcumin on bone healing in animals with diabetes mellitus (DM). One hundred rats were divided into five groups: DM+PLAC, DM+CURC, DM+INS, DM+CURC+INS, and non-DM (CURC, curcumin; PLAC, placebo; INS, insulin). Critical calvarial defects were created and titanium implants were inserted into the tibiae. Calvarial defects were analyzed histometrically, and BMP-2, OPN, OPG, RANKL, Runx2, Osx, ß-catenin, Lrp-5, and Dkk1 mRNA levels were quantified by PCR. The implants were removed for a torque evaluation, the peri-implant tissue was collected for mRNA quantification of the same bone-related markers, and the tibiae were submitted to micro-computed tomography. The DM+CURC+INS and non-DM groups exhibited greater closure of the calvaria when compared to the DM+PLAC group (P<0.05). Increased retention of implants was observed in the DM+CURC, DM+CURC+INS, and non-DM groups when compared to the DM+PLAC group (P<0.05). CURC improved bone volume and increased bone-implant contact when compared to DM+PLAC (P<0.05). In calvarial samples, CURC favourably modulated RANKL/OPG and Dkk1 and improved ß-catenin levels when compared to DM+PLAC (P<0.05). In peri-implant samples, Dkk1 and RANKL/OPG were down-regulated and BMP-2 up-regulated by CURC when compared to DM+PLAC (P<0.05). CURC reverses the harmful effects of DM in bone healing, contributing to the modulation of bone-related markers.

The impact of different torques for the insertion of immediately loaded implants on the peri-implant levels of angiogenesis- and bone-related markers.

The aim of this split-mouth, randomized, double-blind, controlled clinical trial was to evaluate the influence of different insertion torque values for dental implants on bone- and angiogenesis-related marker profiles. Eighteen edentulous patients received dental implants and fixed complete-arch mandibular prostheses. The implants (n=36) were assigned randomly to two groups: reduced torque (n=18), with insertion torque <30Ncm; and conventional torque (n=18), with insertion torque ≥30Ncm. Levels of vascular endothelial growth factor (VEGF), placental growth factor, bone morphogenetic protein 9 (BMP-9), periostin, osteoprotegerin (OPG), and tartrate-resistant acid phosphatase (TRAP) in the peri-implant fluid were quantified at 7, 14, 30, and 120days after implant placement. Inter-group comparisons showed that VEGF and OPG levels were higher in the low-level torque group than in the conventional torque group on days 7 and 30, respectively (P<0.05). BMP-9 and periostin levels were higher in the conventional group than in the low-level torque group on day 120, and TRAP was up-regulated around implants inserted with conventional torque when compared to those inserted with lower-level torque at all time points evaluated (P<0.05). In conclusion, the use of different levels of torque for implantation of immediately loaded implants significantly influenced the levels of bone- and angiogenesis-related markers during early peri-implant repair.

Systemic treatment with resveratrol and/or curcumin reduces the progression of experimental periodontitis in rats.

BACKGROUND AND OBJECTIVE: Periodontitis is a chronic inflammatory disease of periodontal tissues that leads to the destruction of bone and other connective tissues. Resveratrol and curcumin are plant-derived substances with biological properties that may have immunomodulatory properties. This study investigated the effect of continuous administration of resveratrol and curcumin and the association of resveratrol and curcumin on the progression of experimental periodontitis in rats. MATERIAL AND METHODS: Forty Wistar rats were assigned randomly to the following groups: group 1, experimental periodontitis + placebo (PL) (n = 10); group 2, experimental periodontitis + resveratrol (RSV) (n = 10); group 3, experimental periodontitis + curcumin (C) (n = 10); and group 4, experimental periodontitis + resveratrol + curcumin (COMBI) (n = 10). Periodontitis was induced in rats by tying a silk suture, as a ligature, around one of the first molars. Daily administration of the placebo solution, 10 mg/kg of resveratrol, 100 mg/kg of curcumin or 10 mg/kg of resveratrol plus 100 mg/kg of curcumin was carried out from day 0 to day 30. At the end of the relevant experimental periods, rats were killed and the specimens obtained were processed for morphometric analysis of bone loss. Gingival tissues surrounding the first molar were collected for quantification of interleukin (IL)-1ß, IL-4, interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) using a Luminex/MAGPIX assay. RESULTS: Intergroup comparisons of the morphometric outcomes revealed higher bone-loss values in the PL group (p < 0.05) when compared with RSV, C and COMBI groups. There was no difference in bone-loss values among RSV, C and COMBI groups (p > 0.05). The immunoenzymatic assay of the gingival tissue showed a lower concentration of IL-1ß in the COMBI group in comparison with the PL group (p < 0.05). Higher values of IL-4 were demonstrated in groups RSV, C and COMBI in comparison with the PL group (p < 0.05). Only RSV caused a reduction in the levels of IFN-γ (p < 0.05). There was no difference in the concentration of TNF-α amongst the four groups (p > 0.05). CONCLUSION: Resveratrol and curcumin are capable of reducing alveolar bone loss in an animal model of periodontitis. This occurred when these agents were added singly or in combination with one another, but there did not appear to be either synergistic or additive effects.

Impact of smoking on experimental gingivitis. A clinical, microbiological and immunological prospective study.

OBJECTIVE: The present study assessed the effect of smoking on clinical, microbiological and immunological parameters in an experimental gingivitis model. MATERIAL AND METHODS: Twenty-four healthy dental students were divided into two groups: smokers (n = 10); and nonsmokers (n = 14). Stents were used to prevent biofilm removal during brushing. Visible plaque index (VPI) and gingival bleeding index (GBI) were determined 5- on day -7 (running phase), baseline, 21 d (experimental gingivitis) and 28 d (resolution phase). Supragingival biofilm and gingival crevicular fluid were collected and assayed by checkerboard DNA-DNA hybridization and a multiplex analysis, respectively. Intragroup comparison was performed by Friedman and Dunn's multiple comparison tests, whereas the Mann-Whitney U-test was applied for intergroup analyses. RESULTS: Cessation of oral hygiene resulted in a significant increase in VPI, GBI and gingival crevicular fluid volume in both groups, which returned to baseline levels 7 d after oral hygiene was resumed. Smokers presented lower GBI than did nonsmokers (p < 0.05) at day 21. Smokers had higher total bacterial counts and higher proportions of red- and orange complex bacteria, as well as lower proportions of Actinomyces spp., and of purple- and yellow-complex bacteria (p < 0.05). Furthermore, the levels of key immune-regulatory cytokines, including interleukin (IL)-8, IL-17 and interferon-γ, were higher in smokers than in nonsmokers (p < 0.05). CONCLUSION: Smokers and nonsmokers developed gingival inflammation after supragingival biofilm accumulation, but smokers had less bleeding, higher proportions of periodontal pathogens and distinct host-response patterns during the course of experimental gingivitis.

Alcohol intake may impair bone density and new cementum formation after enamel matrix derivative treatment: histometric study in rats.

BACKGROUND AND OBJECTIVE: Alcohol intake may interfere with bone metabolism; however, there is a lack of information about the outcomes of regenerative approaches in the presence of alcohol intake. Enamel matrix derivative (EMD) has been used in periodontal regenerative procedures resulting in improvement of clinical parameters. Thus, the aim of this histomorphometric study is to evaluate the healing of periodontal defects after treatment with EMD under the influence of alcohol intake. MATERIAL AND METHODS: Twenty Wistar rats were randomly assigned to two groups: G1 = alcohol intake (n = 10) and G2 = non-exposed to alcohol intake (n = 10). Thirty days after initiation of alcohol intake, fenestration defects were created at the buccal aspect of the first mandibular molar of all animals from both groups. After the surgeries, the defects of each animal were randomly assigned to two subgroups: non-treated control and treated with EMD. The animals were killed 21 d later. RESULTS: G1 showed less defect fill for non-treated controls. Bone density (BD) and new cementum formation were lower for G1 when compared to G2, for EMD-treated and non-treated sites. EMD treatment resulted in greater BD and new cementum formation in both groups and defect fill was not significantly different between groups in the EMD-treated sites. The number of tartrate-resistant acid phosphatase-positive osteoclasts was significantly higher in G1 when compared to G2 and in EMD-treated sites of both groups. CONCLUSION: Alcohol intake may produce a significant detrimental effect on BD and new cementum formation, even in sites treated with EMD. A limited positive effect may be expected after EMD treatment under this condition.

Impact of type 2 diabetes on the gene expression of bone-related factors at sites receiving dental implants.

This study evaluated the influence of type 2 diabetes mellitus (T2DM) on the gene expression of bone-related factors in alveolar bone tissue from sites designated to receive dental implants. Bone biopsies were harvested from sites of planned implants for 19 systemically healthy patients and 35 patients with T2DM (17 with better-controlled T2DM (glycated haemoglobin (HbA1c) levels ≤8%) and 18 with poorly controlled T2DM (HbA1c levels >8%)). The mRNA levels of tumour necrosis factor alpha, transforming growth factor beta, receptor activator of the nuclear factor kappa B ligand (RANKL), osteoprotegerin (OPG), runt-related transcription factor 2, alkaline phosphatase, bone sialoprotein (BSP), type I collagen (COL-I), and osteocalcin were evaluated by quantitative real-time polymerase chain reaction. T2DM up-regulates RANKL levels and the ratio of RANKL/OPG, whereas it down-regulates COL-I and BSP expression (P<0.05). Higher mRNA levels of RANKL/OPG were observed in the poorly controlled T2DM patients compared to those with better-controlled T2DM and systemically healthy patients (P<0.05). A lower amount of COL-I and BSP was detected in the biopsies from individuals with poorly controlled T2DM compared to systemically healthy patients (P<0.05). In conclusion, RANKL, RANKL/OPG, COL-I, and BSP are negatively affected in diabetics. Additionally, the patient's glycaemic status appears to modulate bone-related genes in a different manner.

DNA methylation levels of SOCS1 and LINE-1 in oral epithelial cells from aggressive periodontitis patients.

OBJECTIVE: DNA methylation has been shown to be critical in the regulation of inflammatory genes. Infections are able to trigger susceptibility to disease and it can be considered as potential epimutagenic factors in reshaping the epigenome. Therefore, what would be the DNA methylation status in cells present in an infected and inflamed oral environment? The aim was to verify the DNA methylation pattern in oral epithelium cells from aggressive periodontitis (AgP) patients in a specific gene involved in the inflammation control, as suppressor of cytokine signalling (SOCS)1 and in a broader way through long interspersed nuclear element (LINE)-1. DESIGN: Genomic DNA from oral cells of 30 generalized AgP patients and 30 healthy patients were purified and modified by sodium bisulfite. DNA methylation patterns were analyzed using combined bisulfite restriction analysis (COBRA) for SOCS1 and LINE-1. RESULTS: An overall scenario of demethylation was seen for both groups, whereas the healthy group presented a higher percentage of demethylation (p<0.001), also presenting the majority of total demethylated samples (83.3% versus 70.8% in the AgP group). Total LINE-1 methylation or at each specific loci presented significant differences amongst groups. CONCLUSION: Epithelial cells, present in an infected and inflamed oral environment, show different DNA methylation status from those present in a healthy oral environment, regarding the SOCS1 and LINE-1. In addition, the investigation allows detecting alterations in the DNA in a non-limited manner, since the results observed might reflect a generalized condition of the oral epithelial cells, besides reflecting the condition of the gingival epithelium cells.

Resveratrol improves bone repair by modulation of bone morphogenetic proteins and osteopontin gene expression in rats.

This study investigated the effect of resveratrol on bone healing and its influence on the gene expression of osteogenic markers. Two calvarial defects were created and one screw-shaped titanium implant was inserted in the tibia of rats that were assigned to daily administration of placebo (control group, n=15) or 10mg/kg of resveratrol (RESV group, n=15) for 30 days. The animals were then sacrificed. One of the calvarial defects was processed for histomorphometric analysis and the tissue relative to the other was collected for mRNA quantification of bone morphogenetic protein (BMP)-2, BMP-7, osteopontin (OPN), bone sialoprotein (BSP), osteoprotegrin (OPG), and receptor activator of NF-κB ligand (RANKL). Implants were removed by applying a counter-torque force. Histomorphometric analysis revealed higher remaining defect in the calvarial defects of the control group than the RESV group (P=0.026). Resveratrol increased the counter-torque values of implant removal when compared to control therapy (P=0.031). Gene expression analysis showed a higher expression of BMP-2 (P=0.011), BMP-7 (P=0.049), and OPN (P=0.002) genes in the RESV group than in the control group. In conclusion, resveratrol improved the repair of critical-sized bone defects and the biomechanical retention of implants. Indeed, this natural agent may up-regulate the gene expression of important osteogenic markers.

Cigarette smoke inhalation increases the alveolar bone loss caused by primary occlusal trauma in a rat model.

BACKGROUND AND OBJECTIVE: Occlusal trauma (OT) and smoking are both factors that alter alveolar bone metabolism and therefore could synergistically act on alveolar bone loss. The aim of this experimental study was to evaluate the influence of short-term cigarette smoke inhalation (CSI) on inter-radicular alveolar bone loss promoted by primary OT in a rat model. MATERIAL AND METHODS: Forty-eight animals were randomly assigned to one of three groups based on treatment type: OT + CSI (n = 16), animals were exposed to CSI three times per day, for 8 min per exposure, and they concomitantly received unilateral vertical augmentation creating an occlusal interference inducing experimental OT; OT (n = 16), animals received only unilateral vertical augmentation; negative control (NC; n = 16), animals maintained for equal periods to achieve periodontal baseline values of periodontal ligament dimension. Each group was divided into two subgroups (n = 8) based on treatment length: 7 or 14 d. RESULTS: After 7 d, the OT + CSI group exhibited significantly higher bone loss compared to the NC group (p = 0.0022). After 14 d, the OT (p < 0.0001) and OT + CSI (p < 0.0001) groups presented significantly higher bone loss compared to the NC group, and OT + CSI resulted in significantly higher bone loss than OT alone (p = 0.0241). The number of tartrate-resistant acid phosphatase-positive cells on the linear surface of the bone crest after 7 d was significantly higher in the OT + CSI group as compared to the NC and OT groups (p < 0.0001 and p = 0.0045, respectively) and remained significantly higher in the OT + CSI group after 14 d, compared to the OT group (p < 0.0001). CONCLUSION: Short-term CSI increases early bone loss in association with OT after 7 d, and this worsens in severity after 14 d of exposure.

Release of bone markers in immediately loaded and nonloaded dental implants: a randomized clinical trial.

The aim of this study was to compare the release of bone markers during osseointegration of immediately loaded and nonloaded implants. Forty patients who were indicated for rehabilitation with dental implants randomly received either implant and prosthesis placement within 72 hours (group IM) or implant insertion and no prosthesis placement (group NL). Peri-implant crevicular fluid was collected immediately after implant insertion and 7, 15, 30, 60, 90, and 120 days after surgery and levels of osteoprotegerin, transforming growth factors, osteocalcin, osteopontin, and parathyroid hormone were evaluated using Luminex assay. Bleeding index and peri-implantar sulcus depth were also evaluated. The data were compared using statistical tests (α = 5%). No statistical difference was found regarding demographic and clinical parameters (p > .05). Transforming growth factors, osteoprotegerin, osteopontin, and parathyroid hormone presented an earlier release peak in group IM than in NL group (p < .05). Osteocalcin achieved higher levels in group IM versus group NL between 7 and 30 days of evaluation (p < .05). It may be concluded that earlier loading positively modulates bone mediators release around immediately loaded implants when compared with nonloaded dental implants.

Subgingival biodiversity in subjects with uncontrolled type-2 diabetes and chronic periodontitis.

BACKGROUND AND OBJECTIVE: There is a bidirectional relationship between periodontal disease and type-2 diabetes mellitus (DM). Inflammatory mediators may negatively affect glycemic control, and increased glucose levels and resultant glycation end-products may alter the host response against bacterial infection. However, no agreement has been reached regarding the effect of DM on periodontal subgingival microbiota. Therefore, the purpose of the present study was to compare the subgingival biodiversity in deep periodontal pockets of subjects with chronic periodontitis and either uncontrolled type-2 diabetes or no diabetes using 16S rRNA gene cloning and sequencing. MATERIAL AND METHODS: Twelve subjects with uncontrolled type-2 diabetes (glycated hemoglobin > 8%) and eleven nondiabetic subjects presenting severe and generalized chronic periodontitis were selected. Subgingival biofilm from periodontal pockets > 5 mm were assessed using the 16S rRNA gene cloning and sequencing technique. RESULTS: Significant differences were observed in subgingival microbiota between diabetic and nondiabetic subjects. Diabetic subjects presented higher percentages of total clones of TM7, Aggregatibacter, Neisseria, Gemella, Eikenella, Selenomonas, Actinomyces, Capnocytophaga, Fusobacterium, Veillonella and Streptococcus genera, and lower percentages of Porphyromonas, Filifactor, Eubacterium, Synergistetes, Tannerella and Treponema genera than nondiabetic individuals (p < 0.05). Moreover, some phylotypes, such as Fusobacterium nucleatum, Veillonella parvula, V. dispar and Eikenella corrodens were detected significantly more often in diabetic subjects than in nondiabetic subjects (p < 0.05). CONCLUSION: Subjects with uncontrolled type-2 diabetes and chronic periodontitis presented significant dissimilarities in subgingival biodiversity compared with nondiabetic subjects.

Perinatal periodontal disease reduces social behavior in male offspring.

OBJECTIVE: Our objective was to verify whether prenatal maternal periodontitis is a risk factor for the development of central nervous system disorders in rats. METHODS: Periodontitis was induced by placing a ligature around the upper and lower first molars in 9 female Wistar rats (experimental group); 9 rats were left unligated (control group). The maternal general activity in an open field was observed on gestational day (GD) 0, GD 4, and GD 14, and the maternal performance was assessed on the second day after birth. The pups' play behavior was assessed on postnatal day 30. The relative level of reelin was measured in the frontal cortex by real-time PCR analysis. RESULTS: The results showed that, compared with the control group, (1) the general activity in female rats with periodontitis was decreased, (2) the maternal performance of these rats was not modified by periodontitis, (3) the play behavior of pups from dams with periodontitis was decreased, and (4) there were no differences in the frontal cortex reelin levels of pups from dams with periodontitis. CONCLUSIONS: We conclude that pre- and postnatal periodontitis induces maternal sickness behavior and reduces the pups' play behavior without interference with frontal cortex reelin expression.

Effect of autologous bone marrow-derived cells associated with guided bone regeneration or not in the treatment of peri-implant defects.

This study investigated the effect of bone marrow-derived cells associated with guided bone regeneration in the treatment of dehiscence bone defects around dental implants. Iliac-derived bone marrow cells were harvested from dogs and phenotypically characterized with regard to their osteogenic properties. After teeth extraction, three implant sites were drilled, dehiscences created and implants placed. Dehiscences were randomly assigned to: bone marrow-derived cells, bone marrow-derived cells+guided bone regeneration, and control (no treatment). After 3 months, implants with adjacent tissues were processed histologically, bone-to-implant contact, bone fill within the threads, new bone area in a zone lateral to the implant, new bone height, and new bone weight at the bottom of the defect were determined. Phenotypic characterization demonstrated that bone marrow-derived cells presented osteogenic potential. Statistically higher bone fill within the threads was observed in both bone marrow-derived cells+guided bone regeneration bone marrow-derived cell groups compared with the control group (P<0.05), with no difference between the groups treated with cells (P>0.05). For the other parameters (new bone area, bone-to-implant contact, new bone height and new bone weight), only the bone marrow-derived cells+guided bone regeneration group presented higher values compared with the non-treated control (P<0.05). Bone marrow-derived cells provided promising results for peri-implantar bone regeneration, although the combined approach seems to be relevant, especially to bone formation out of the implant threads.

Impact of Porphyromonas gingivalis inoculation on ligature-induced alveolar bone loss. A pilot study in rats.

BACKGROUND AND OBJECTIVE: Periodontitis is a polymicrobial infection characterized by the loss of connective tissue attachment, periodontal ligament and alveolar bone. The aim of this study was to evaluate the impact of Porphyromonas gingivalis inoculation on the ligature-induced alveolar bone loss (ABL) model in rats. MATERIAL AND METHODS: Forty male Wistar rats were randomly assigned to the following groups: G1, control (n = 10); G2, ligature-induced ABL (n = 15); and G3, ligature-induced ABL + P. gingivalis inoculation (n = 15). Rats in G2 and G3 were killed 15, 21 and 30 d after ligature placement, and the following parameters were assessed: microbiological load; ABL; and interleukin (IL)-1ß (Il1beta)/Il1ra, Il6/Il10 and Rankl/osteoprotegerin (Opg) mRNA ratios in the gingival tissues, as determined by quantitative PCR. RESULTS: Microbiological analyses demonstrated that rats in G1, G2 and G3 were positive for the presence of bacteria (determined using PCR amplification of the 16S gene), but that only the treatment sites of rats in G3 were positive for P. gingivalis at all time-points investigated. Histometrically, significant bone loss (p<0.001) was observed for both ligated groups (G2 and G3) compared with the nonligated group (G1), with higher ABL observed for G2 at all the experimental time-points. Furthermore, gene-expression analysis demonstrated that the presence of P. gingivalis in the dentogingival area significantly decreased the Il1ß/Il1ra, Il6/Il10 and Rankl/Opg mRNA ratios compared with ligature alone. CONCLUSION: Within the limits of this pilot study, it was concluded that inoculation of P. gingivalis affected the ligature-induced ABL model by the induction of an anti-inflammatory and antiresorptive host response.

Impact of smoking on inflammation: overview of molecular mechanisms.

BACKGROUND: Inflammation is a critical component of normal tissue repair, as well as being fundamental to the body's defense against infection. Environmental factors, such as smoking, have been reported to modify the host response and hence modify inflammation progression, severity and outcome. Therefore, a comprehensive understanding of the molecular mechanisms by which smoking affects inflammation is vital for preventive and therapeutic strategies on a clinical level. AIM: The purpose of the present article is to review the potential biological mechanisms by which smoking affects inflammation, emphasizing recent developments. RESULTS: Smoking is reported to effect a number of biological mediators of inflammation through its effect on immune-inflammatory cells, leading to an immunosuppressant state. Recent evidence strongly suggests that the molecular mechanisms behind the modulation of inflammation by smoking mainly involve the nuclear factor-kappa B (NF-kB) family, through the activation of both an inhibitor of IkB kinase (IKK)-dependent and -independent pathway. In addition to NF-kB activation, a number of transcriptional factors including GATA, PAX5 and Smad 3/4, have also been implicated. CONCLUSION: Multiple mechanisms may be responsible for the association of smoking and inflammation, and the identification of potential therapeutic targets should guide future research.

Levels of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, inflammatory cytokines and species-specific immunoglobulin G in generalized aggressive and chronic periodontitis.

BACKGROUND AND OBJECTIVE: Aggressive periodontitis pathogenesis still is not completely understood in the literature regarding the relationship between microbial and inflammatory aspects. So this study aimed to compare microbial and inflammatory patterns in the gingival crevicular fluid of generalized aggressive and chronic periodontitis patients. MATERIAL AND METHODS: Forty aggressive and 28 chronic periodontitis patients were selected. Biofilm and gingival crevicular fluid were collected from a deep pocket (periodontal probing depth >7 mm) and a moderate pocket (periodontal probing depth = 5 mm) of each patient, and microbiological and immunoenzymatic assays were performed. Real-time PCR was used to determine quantities of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. Enzyme-linked immunosorbent assay (ELISA) was employed to determine gingival crevicular fluid levels of interleukin-1beta, interferon-gamma, prostaglandin E(2) and interleukin-10. In addition, immunoglobulin G (IgG) levels against A. actinomycetemcomitans and P. gingivalis lipopolysaccharide were also determined by ELISA. Analysis of variance/Tukey test, Mann-Whitney U-test and the Pearson correlation test were used to determine differences and correlations between variables analysed (alpha = 5%). RESULTS: Patients suffering from generalized aggressive periodontitis had their mouth colonized by higher amounts of A. actinomycetemcomitans and P. gingivalis than chronic periodontitis patients. Conversely, the gingival crevicular fluid levels of IgG against both pathogens were statistically inferior in aggressive periodontitis patients (p < 0.05). With regard to gingival crevicular fluid levels of cytokines, aggressive periodontitis patients presented reduced levels of interleukin-10 (p < 0.05). CONCLUSION: In comparison to chronic periodontitis, generalized aggressive periodontitis patients have an imbalance in the host response, with reduced levels of interleukin-10 and IgG, and increased periodontal pathogens.