Resveratrol attenuates oxidative stress during experimental periodontitis in rats exposed to cigarette smoke inhalation.

OBJECTIVES: This study aimed at investigating the effect of the systemic administration of resveratrol (RESV) on oxidative stress during experimental periodontitis in rats subjected to cigarette smoke inhalation. MATERIAL AND METHODS: Experimental periodontitis (EP) was induced in 26 male Wistar rats by the insertion of a ligature around one of the first mandibular and maxillary molars. The animals were assigned randomly to the following groups: cigarette smoke inhalation (CSI; 3 times/d, 8 minutes/d) + resveratrol (10 mg/Kg), that is, SMK + RESV (n = 13) and cigarette smoke inhalation + placebo, that is, SMK + PLAC (n = 13). The substances were administered daily for 30 days (19 days prior and 11 days following EP induction), and then, the animals were euthanized. The maxillary specimens were processed for morphometric analysis of bone loss, and the tissue surrounding the first maxillary molars was collected for mRNA quantification of Sirtuin 1 (SIRT1) by real-time PCR. The gingival tissues surrounding the mandibular first molars were collected for quantification of superoxide dismutase 1 (SOD1) and nicotinamide adenine dinucleotide phosphatase oxidase (NADPH) using an ELISA assay. RESULTS: Reduced bone loss was demonstrated in animals in the SMK + RESV group as compared to those in the SMK + PLAC (P < 0.05) group on the basis of morphometric analysis. Resveratrol promoted higher levels of SIRT and SOD (P < 0.05) as well as reduced levels of NADPH oxidase (P < 0.05) were found in tissues derived from animals in the SMK + RESV group when compared to those in the SMK + PLAC group. CONCLUSION: Resveratrol is an efficient therapeutic agent that reduces exacerbation of bone loss found in animals with EP that were also exposed to smoke. The results suggest that its effects could be mediated, at least in part, by its antioxidant and anti-inflammatory properties which attenuate the effects of oxidative stress on EP in the presence of cigarette smoke.

RG108 increases NANOG and OCT4 in bone marrow-derived mesenchymal cells through global changes in DNA modifications and epigenetic activation.

Human bone marrow-derived mesenchymal stem cells (hBMSCs) are important for tissue regeneration but their epigenetic regulation is not well understood. Here we investigate the ability of a non-nucleoside DNA methylation inhibitor, RG108 to induce epigenetic changes at both global and gene-specific levels in order to enhance mesenchymal cell markers, in hBMSCs. hBMSCs were treated with complete culture medium, 50 µM RG108 and DMSO for three days and subjected to viability and apoptosis assays, global and gene-specific methylation/hydroxymethylation, transcript levels' analysis of epigenetic machinery enzymes and multipotency markers, protein activities of DNMTs and TETs, immunofluorescence staining and western blot analysis for NANOG and OCT4 and flow cytometry for CD105. The RG108, when used at 50 µM, did not affect the viability, apoptosis and proliferation rates of hBMSCs or hydroxymethylation global levels while leading to 75% decrease in DNMTs activity and 42% loss of global DNA methylation levels. In addition, DNMT1 was significantly downregulated while TET1 was upregulated, potentially contributing to the substantial loss of methylation observed. Most importantly, the mesenchymal cell markers CD105, NANOG and OCT4 were upregulated being NANOG and OCT4 epigenetically modulated by RG108, at their gene promoters. We propose that RG108 could be used for epigenetic modulation, promoting epigenetic activation of NANOG and OCT4, without affecting the viability of hBMSCs. DMSO can be considered a modulator of epigenetic machinery enzymes, although with milder effect compared to RG108.

Smoking habit modulates peri-implant microbiome: A case-control study.

BACKGROUND AND OBJECTIVE: Smoking is a recognized risk factor for peri-implant disease and leads to microbiological changes in mucositis and peri-implantitis. However, there is no knowledge about the impact of smoking in healthy peri-implant tissue. The aim of the study was to evaluate the microbiome in a peri-implant environment in smokers with healthy peri-implant conditions. METHODS: Peri-implant biofilm was collected around single clinically healthy, screwed-retained, teeth-surrounded implants in 12 non-smoker (NSMK) and 12 smoker (SMK) non-periodontitis subjects (no bleeding and probing depth <4 mm). Bacterial DNA was isolated and 16S ribosomal RNA gene libraries were sequenced using pyrosequencing, targeting the V3-V4 region. Datasets were processed using the Quantitative Insights into Microbial Ecology, Greengenes and the Human Oral Microbiome Database databases. RESULTS: An evident difference in the SMK peri-implant microbiome was observed compared to the NSMK microbiome, with a large abundance of species, even with a healthy peri-implant. The SMK core-microbiome showed an abundance of Fusobacterium, Tannerella and Mogibacterium, while the NSMK core revealed an abundance of Actinomyces, Capnocytophaga and Streptococcus, genera that are usually related to periodontal health. The microbiome inter-relationship was shown to be more inter-generic in SMK then in NSMK, indicating different microbiome cohesion. CONCLUSION: Smoking negatively affected the peri-implant microbiome, leading to a disease-associated state, even in clinically healthy individuals.

Occurrence of peri-implant diseases and risk indicators at the patient and implant levels: A multilevel cross-sectional study.

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. CONCLUSION: 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.

Impact of a triclosan-containing toothpaste during the progression of experimental peri-implant mucositis: Clinical parameters and local pattern of osteo-immunoinflammatory mediators in peri-implant fluid.

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. 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. RESULTS: Both groups showed increase in plaque index at implant sites from the 3rd until the 21st day (P < 0.05). Only triclosan treatment was able to avoid an increase in bleeding on probing (BOP) throughout the follow-ups (P > 0.05), whereas a significant intensification in BOP was observed from the 14th day in the placebo-treated sites (P < 0.05). Lower interleukin (IL)-10 concentrations were detected in the placebo group at the 21st day when compared with triclosan-treated implant sites (P < 0.05). IL-10 levels were reduced and IL-1ß concentrations were increased at 21 days when compared with baseline only in placebo-treated sites (P < 0.05). Osteoprotegerin levels significantly increased from the 14th until the 21st day only in triclosan-treated sites (P < 0.05). CONCLUSION: Triclosan-containing toothpaste controls clinical inflammation and interferes positively in the profile of osteo-immunoinflammatory mediators during progression of experimental peri-implant mucositis.

Resveratrol Inhibits Periodontitis-Related Bone Loss in Rats Subjected to Cigarette Smoke Inhalation.

BACKGROUND: Alternative therapeutic approaches have been explored to modulate host response to periodontal disease. Knowledge of new strategies to treat periodontitis is particularly relevant in patients presenting augmented risk to periodontitis, such as smokers. The aim of this study is to investigate the impact of resveratrol (RESV) on progression of experimental periodontitis (EP) in the presence of cigarette smoke inhalation (CSI). METHODS: Rats were assigned to one of three groups: 1) CSI+RESV (n = 20); 2) CSI+placebo (n = 20); and 3) non-CSI (n = 20). CSI was initiated 1 week prior to initiation of RESV or placebo administration (systemically for 30 days) and was continued until the end of the study. EP was induced around the first mandibular and second maxillary molars using ligatures. Specimens from the mandible were processed for morphometric and microcomputed tomography examination of bone volume/levels. Gingival tissues surrounding mandibular molars were collected for quantification of interleukin (IL)-1ß, IL-4, IL-6, IL-17, and tumor necrosis factor-α using an assay system. Additional analyses of immunoinflammatory mediator performance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were performed according to Th cell responses in gingival tissues. Gingival tissues of maxillary molars were subjected to real-time polymerase chain reaction for assessment of osteoprotegrin, runt-related transcription factor-2, receptor activator of nuclear factor-kappa B ligand (RANKL), sclerostin, and Dickkopf Wnt signaling pathway inhibitor 1 levels. RESULTS: Higher linear alveolar bone loss (ABL) and lower interradicular bone density were detected in ligated molars in the CSI+placebo group (P <0.05). IL-4 level was the highest, and Th17/Th2 levels were the lowest in RESV-treated rats compared with placebo rats (P <0.05). RESV reduced expression of messenger RNA for RANKL in animals receiving CSI (P <0.05). CONCLUSION: RESV inhibits EP and CSI-induced supporting ABL and has a beneficial effect on osteo-immunoinflammatory markers.

Periodontitis increases rheumatic factor serum levels and citrullinated proteins in gingival tissues and alter cytokine balance in arthritic rats.

This study investigated some immunological features by experimental periodontitis (EP) and rheumatoid arthritis (RA) disease interact in destructive processes in arthritic rats. Rats were assigned to the following groups: EP +RA; RA; EP; and Negative Control. RA was induced by immunizations with type-II collagen and a local immunization with Complete Freund's adjuvant in the paw. Periodontitis was induced by ligating the right first molars. The serum level of rheumatoid factor (RF) and anti-citrullinated protein antibody (ACCPA) were measured before the induction of EP (T1) and at 28 days after (T2) by ELISA assay. ACCPA levels were also measured in the gingival tissue at T2. The specimens were processed for morphometric analysis of bone loss, and the gingival tissue surrounding the first molar was collected for the quantification of interleukin IL-1ß, IL-4, IL-6, IL-17 and TNF-α using a Luminex/MAGpix assay. Paw edema was analyzed using a plethysmometer. Periodontitis increased the RF and ACCPA levels in the serum and in the gingival tissue, respectively. Besides, the level of paw swelling was increased by EP and remained in progress until the end of the experiment, when EP was associated with RA. Greater values of IL-17 were observed only when RA was present, in spite of PE. It can be concluded that periodontitis increases rheumatic factor serum levels and citrullinated proteins level in gingival tissues and alter cytokine balance in arthritic rats; at the same time, arthritis increases periodontal destruction, confirming the bidirectional interaction between diseases.

Neuropilin Controls Endothelial Differentiation by Mesenchymal Stem Cells From the Periodontal Ligament.

BACKGROUND: Periodontal ligament (PDL) has been reported to be a source of mesenchymal stem cells (MSCs).New vascular networks from undifferentiated cells are essential for repair/regeneration of specialized tissues, including PDL. The current study aims to determine potential of CD105(+)-enriched cell subsets of periodontal ligament cells (PDLSCs) to differentiate into endothelial cell (EC)-like cells and to give insights into the mechanism involved. METHODS: CD105(+)-enriched PDLSCs were induced to EC differentiation by endothelial growth medium 2 (EGM-2) for 3, 7, 14, and 21 days, with mRNA/protein levels and functional activity assessed by: 1) real-time polymerase chain reaction; 2) Western blotting; 3) fluorescence-activated cell sorting; 4) immunohistochemistry; 5) immunofluorescence; 6) matrigel; and 7) small interfering RNA assays. RESULTS: Data analyses demonstrated that EGM-2 treated PDLSCs presented increased expression of EC markers, including: 1) CD105; 2) kinase domain-containing receptor; and 3) Ulex europaeus agglutinin 1, and were able to form cord/tube-like structures. Gene and protein expression analysis showed that neuropilin 2 (NRP2), a key factor for vascular development, was significantly downregulated during EC differentiation. NRP2 was constitutively expressed in mouse PDL tissues by immunohistochemistry analysis, and NRP2 knockdown in CD105(+)-enriched PDLSCs resulted in increased cord/tube-like structures in a matrigel assay. CONCLUSION: These findings demonstrated the potential of CD105(+)-enriched PDLSCs to support angiogenesis, and NRP2 as a pivotal factor regulating this process.

Current perspective of the impact of smoking on the progression and treatment of periodontitis.

This literature review provides an overview of the current scenario regarding the impact of smoking on the progression and treatment of periodontitis; clinical, microbiological and immunological data from studies from our and other groups are presented. In general, preclinical and clinical data are unanimous in demonstrating that smokers present increased susceptibility, greater severity and faster progression of periodontal disease compared with nonsmokers. The evidence further demonstrates that smokers lose more teeth and have a less favorable response to therapy than do nonsmokers. Although it is well established that smoking significantly impacts on the onset, progression and outcome of periodontal disease, the mechanisms involved remain unclear. More importantly, some of the reported deleterious effects of smoking on periodontal tissues have been reported to be reversible upon participation in smoking-cessation programs. Therefore, clinicians should strongly advise smokers to enroll in cessation strategies, even temporarily, in order to improve the overall outcome.

Characterization of highly osteoblast/cementoblast cell clones from a CD105-enriched periodontal ligament progenitor cell population.

BACKGROUND: It is known that periodontal ligament (PDL) harbors a heterogeneous progenitor cell population at different stages of lineage commitment. However, characterization of PDL stem cells committed to osteoblast/cementoblast (O/C) differentiation remains to be elucidated. The present study is carried out to isolate single cell-derived, cluster of differentiation (CD)105-positive PDL clones and to characterize the clones that present high potential to differentiate toward O/C phenotype in vitro. METHODS: Isolation of single cell-derived colonies (clones) from a CD105-enriched PDL progenitor cell population was performed by the ring-cloning technique. Cell clones were evaluated for their O/C differentiation potential, metabolic activity, and expression of STRO-1 protein. Additionally, the clones that showed potential to O/C differentiation were characterized by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) for expression of runt-related transcriptor factor 2 (RUNX2), alkaline phosphatase, CD105, and CD166 during osteogenic induction. RESULTS: Six PDL-CD105(+) clones were obtained, three being highly O/C clones (C-O) and three others that did not have the ability to produce mineralized matrix in vitro (C-F). The C-O group showed lower metabolic activity compared with the C-F group, and both cell groups were positively immunostained for STRO-1. qRT-PCR analysis demonstrated an increased expression of transcripts for RUNX2 and CD166 during the maturation of C-O cells toward O/C phenotype. CONCLUSIONS: These results provide evidence that PDL-CD105(+) purified progenitor cells comprise a heterogeneous cell population that presents a cell subset with high O/C potential and, further, that surface antigen CD166 is modulated during the O/C maturation of this cell subset.

Photodynamic therapy during supportive periodontal care: clinical, microbiologic, immunoinflammatory, and patient-centered performance in a split-mouth randomized clinical trial.

BACKGROUND: This study investigates the effect of photodynamic therapy (PDT) as monotherapy during supportive periodontal therapy. METHODS: A split-mouth, randomized controlled trial was conducted in patients with chronic periodontitis (N = 22) presenting at least three residual pockets (probing depth [PD] ≥5 mm with bleeding on probing [BOP]). The selected sites randomly received the following: 1) PDT; 2) photosensitizer (PS); or 3) scaling and root planing (SRP). At baseline and 3 and 6 months, clinical, microbiologic (real-time polymerase chain reaction analyses), cytokine pattern (multiplexed bead immunoassay), and patient-centered (regarding morbidity) evaluations were performed. RESULTS: All therapies promoted similar improvements in clinical parameters throughout the study (P <0.05), except that BOP was not reduced in the PS protocol (P >0.05). Lower levels of Aggregatibacter actinomycetemcomitans were observed in the PDT and SRP protocols at 3 months when compared with the PS protocol (P <0.05). An inferior frequency detection of Porphyromonas gingivalis was observed in the PDT protocol at 3 and 6 months and in the SRP protocol at 6 months from baseline (P <0.05). In addition, PDT protocol presented inferior frequency of P. gingivalis at 3 months when compared with the other therapies (P <0.05). Only patients in the PDT protocol exhibited augmented levels of anti-inflammatory interleukin (IL)-4 and reduced proinflammatory IL-1ß and IL-6 throughout the study (P <0.05). Intergroup analyses showed reduced IL-10 and increased interferon-γ and IL-1ß levels in the PS protocol when compared with the other therapies during follow-ups (P <0.05). No differences in morbidity were observed between the therapies (P >0.05), although the need for anesthesia was higher in SRP-treated sites (P <0.05). CONCLUSION: PDT as an exclusive therapy may be considered a non-invasive alternative for treating residual pockets, offering advantages in the modulation of cytokines.

Esthetic treatment of gingival hyperpigmentation with Nd:YAG laser or scalpel technique: a 6-month RCT of patient and professional assessment.

This double-masked, randomized controlled trial with a split-mouth design aimed to compare patient- and professional-centered outcomes using different therapeutic approaches-neodymium-yttrium aluminum garnet (Nd:YAG) laser or scalpel technique-for gingival depigmentation. Patients presenting bilateral melanin gingival hyperpigmentation and who requested cosmetic therapy were recruited. Contralateral quadrants were randomly assigned to receive Nd:YAG laser (settings: 6 W, 60 mJ/pulse, and 100 Hz) or scalpel technique. Patient morbidity experienced at intratherapy and during the first postoperative week was evaluated. In addition, after 6 months, the cosmetic results achieved for the different therapeutic approaches were evaluated by patients and professionals. The chair time of each technique was also calculated. Patient-oriented outcomes concerning intratherapy morbidity did not demonstrate any differences between groups (p > 0.05), although a higher extent of discomfort/pain was experienced in the side treated by the scalpel technique compared to the Nd:YAG laser procedure during the first posttherapy week (p < 0.05). Regarding to cosmetic outcomes, no differences between techniques were observed for patient and professionals (p > 0.05). Significantly higher chair time was required for the scalpel technique than for the Nd:YAG laser therapy (p < 0.05). The Nd:YAG laser or the scalpel technique may be successfully used for the treatment of melanin gingival hyperpigmentation. However, the use of the Nd:YAG laser has presented advantages in terms of less discomfort/pain during the posttherapy period and a reduction of treatment chair time.

Photodynamic therapy in the treatment of class II furcation: a randomized controlled clinical trial.

AIM: To investigate the effect of photodynamic therapy (PDT) as adjunct to mechanical therapy in furcations. MATERIALS AND METHODS: A double-blind, parallel, randomized controlled clinical trial was conducted in subjects presenting class II furcations. The subjects were randomly allocated to a test (PDT; n = 16) or control group (non-activated laser/only photosensitizer; n = 21). At baseline, 3 and 6 months, clinical, microbiological and cytokine pattern evaluation was performed. Clinical attachment level was defined as the primary outcome variable. RESULTS: Clinical parameters improved after both therapies (p < 0.05) with no differences between groups at any time point (p > 0.05). At 6 months, real-time PCR evaluation showed a decrease in Porphyromonas gingivalis and Tannerella forsythia only in the PDT group (p < 0.05) with no inter-group differences. Regarding cytokines, IL-4 and IL-10 levels increased in both groups at 6 months. GM-CSF, IL-8, IL-1ß and IL-6 levels decreased only in the PDT group after 3 months (p < 0.05). At 3 months, inter-group analyses showed that GM-CSF, IFN-γ, IL-6 and IL-8 levels were lower in the PDT group. At 6 months, lower IL-1ß levels were also observed in the PDT group (p < 0.05). CONCLUSION: Photodynamic therapy did not promote clinical benefits for class II furcations; however, advantages in local levels of cytokines and a reduction in periodontopathogens were demonstrated.

Novel ALPL genetic alteration associated with an odontohypophosphatasia phenotype.

Hypophosphatasia (HPP) is an inherited disorder of mineral metabolism caused by mutations in ALPL, encoding tissue non-specific alkaline phosphatase (TNAP). Here, we report the molecular findings from monozygotic twins, clinically diagnosed with tooth-specific odontohypophosphatasia (odonto-HPP). Sequencing of ALPL identified two genetic alterations in the probands, including a heterozygous missense mutation c.454C>T, leading to change of arginine 152 to cysteine (p.R152C), and a novel heterozygous gene deletion c.1318_1320delAAC, leading to the loss of an asparagine residue at codon 440 (p.N440del). Clinical identification of low serum TNAP activity, dental abnormalities, and pedigree data strongly suggests a genotype-phenotype correlation between p.N440del and odonto-HPP in this family. Computational analysis of the p.N440del protein structure revealed an alteration in the tertiary structure affecting the collagen-binding site (loop 422-452), which could potentially impair the mineralization process. Nevertheless, the probands (compound heterozygous: p.[N440del];[R152C]) feature early-onset and severe odonto-HPP phenotype, whereas the father (p.[N440del];[=]) has only moderate symptoms, suggesting p.R152C may contribute or predispose to a more severe dental phenotype in combination with the deletion. These results assist in defining the genotype-phenotype associations for odonto-HPP, and further identify the collagen-binding site as a region of potential structural importance for TNAP function in the biomineralization.

Clinical and microbiological changes after minimally invasive therapeutic approaches in intrabony defects: a 12-month follow-up.

OBJECTIVES: This 12-month randomized, controlled trial evaluated the clinical effects and microbiological changes of minimally invasive nonsurgical and surgical approaches for the therapy of intrabony defects. MATERIALS AND METHODS: Twenty-nine subjects with intrabony defects in single-rooted tooth were randomly assigned to; (1) minimally invasive nonsurgical technique (MINST) or (2) minimally invasive surgical technique (MIST). Quantities of Aggregatibacter actinomycetemcomitans, Tannerella forsythia, and Porphyromonas gingivalis, determined by using real-time PCR, were evaluated at baseline, 3, 6, and 12 months after the treatments. Clinical recordings--probing depth (PD), position of the gingival margin (PGM), and relative clinical attachment level (RCAL)--were obtained at baseline and 12 months post-therapy. The primary outcome variable of the study was RCAL. RESULTS: Both treatment modalities resulted in an improvement in all clinical recordings, with significant PD reductions (p < 0.05), RCAL gains (p < 0.05), and no change in the PGM (p > 0.05) after 12 months in both MINST and MIST groups. No clinical differences were observed between groups (p > 0.05). Regarding the microbiological outcomes, at the re-examinations, a significant decrease was observed for T. forsythia and P. gingivalis when compared with baseline (p < 0.05) for both treatments. The amount of A. actinomycetemcomitans did not reduced decrease throughout the study (p > 0.05). Intergroup differences in the microbiological assay were not found at any time point (p > 0.05). CONCLUSIONS: Both MINST and MIST provided comparable clinical results and microbiological changes in the treatment of intrabony defects over 12 months follow-up. CLINICAL RELEVANCE: This randomized, controlled, parallel trial revealed that both therapeutic modalities may promote clinical and microbiological benefits at 12 months post-therapy.

PDT in non-surgical treatment of periodontitis in HIV patients: a split-mouth, randomized clinical trial.

BACKGROUND AND OBJECTIVE: The aim of this study was to evaluate the clinical and microbiological effect of photodynamic therapy (PDT) in the non-surgical treatment of periodontitis in HIV patients. METHODS: Twelve HIV patients from the CEAPE/UNIP, Brazil, with periodontitis were included in this 6-month, split-mouth, double-blind, controlled clinical trial. Patients were placed in the following groups: Group SRP-scaling and root planning with an ultrasonic device (SRP); and Group SRP + PDT-SRP associated with a course of PDT with a diode laser with a wavelength of 660 nm and 0.03 W power associated with methylene blue 0.01% lasting 133 seconds. All clinical measurements (periodontal probing depth (PPD), gingival recession (GR), clinical attachment level (CAL), full-mouth plaque index (FMPI), bleeding score (FMBS)), and microbiological parameters (detection of Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Aggregatibacter actinomycetemcomitans (Aa)) were assessed at baseline and at 45 days, and 3 and 6 months after therapy. The ANOVA/Tukey was used for statistical analysis (α = 5%). RESULTS: There were no differences in any of the investigated parameters observed at baseline in the two groups (P > 0.05). Moreover, participants in the SRP + PDT group presented a higher PPD reduction and CAL gain than those in the SRP group at 45 days and 3 and 6 months. At 6 months, sites receiving SRP + PDT showed a significant PPD reduction of 1.4 ± 0.5 mm, while those in the SRP group showed a 0.3 ± 0.8 mm reduction (P < 0.05). The CAL gain at the sixth month was 1.3 ± 0.5 mm and 0.2 ± 0.7 mm for participants in the SRP + PDT and SRP groups, respectively (P < 0.05). Microbiologically, both therapies presented a reduction in the detection of Pg, Tf, and Aa, and there was no difference between them (P > 0.05). CONCLUSION: We concluded that PDT therapy used adjunctively to SRP could promote additional benefits in the treatment of HIV-associated periodontitis.

Impact of supragingival therapy on subgingival microbial profile in smokers versus non-smokers with severe chronic periodontitis.

BACKGROUND: The aim of this study was to assess subgingival microbiological changes in smokers versus non-smokers presenting severe chronic periodontitis after supragingival periodontal therapy (ST). METHODS: Non-smokers (n=10) and smokers (n=10) presenting at least nine teeth with probing pocket depth (PPD) (≥5 mm), bleeding on probing (BoP), and no history of periodontal treatment in the last 6 months were selected. Clinical parameters assessed were plaque index (PI), BoP, PPD, relative gingival margin position (rGMP) and relative clinical attachment level (rCAL). Subgingival biofilm was collected before and 21 days after ST. DNA was extracted and the 16S rRNA gene was amplified with the universal primer pair, 27F and 1492R. Amplified genes were cloned, sequenced, and identified by comparison with known 16S rRNA sequences. Statistical analysis was performed by Student's t and Chi-Square tests (α=5%). RESULTS: Clinically, ST promoted a significant reduction in PI and PPD, and gain of rCAL for both groups, with no significant intergroup difference. Microbiologically, at baseline, data analysis demonstrated that smokers harbored a higher proportion of Porphyromonas endodontalis, Bacteroidetes sp., Fusobacterium sp. and Tannerella forsythia and a lower number of cultivated phylotypes (p<0.05). Furthermore, non-smokers featured significant reductions in key phylotypes associated with periodontitis, whereas smokers presented more modest changes. CONCLUSION: Within the limits of the present study, ST promoted comparable clinical improvements in smokers and non-smokers with severe chronic periodontitis. However, in smokers, ST only slightly affected the subgingival biofilm biodiversity, as compared with non-smokers.

Clinical and patient-centered outcomes after minimally invasive non-surgical or surgical approaches for the treatment of intrabony defects: a randomized clinical trial.

BACKGROUND: The present study aims to compare the performance of minimally invasive non-surgical and surgical approaches for the therapy of intrabony defects. METHODS: Twenty-nine patients who presented with intrabony defects were randomly assigned to: 1) a minimally invasive non-surgical technique (MINST) group, or 2) minimally invasive surgical technique (MIST) group. The chair time of each therapeutic procedure was calculated. The probing depth (PD), position of the gingival margin (PGM) and relative clinical attachment level (RCAL) were evaluated at 3 and 6 months after treatments. The patient perception of discomfort/pain experienced during and after therapy and patient satisfaction regarding treatments were also evaluated. RESULTS: Significant PD reductions, RCAL gains, and no changes in the PGM were obtained at 3 and 6 months in MINST and MIST groups (P <0.05). No differences were observed between groups at any time points (P >0.05). Patient-oriented outcomes did not demonstrate differences between therapeutic approaches (P >0.05). Significant higher chair times were required in the MIST group than in the MINST group (P <0.05). CONCLUSIONS: Minimally invasive non-surgical and surgical approaches were successfully used for the treatment of intrabony defects and achieved periodontal health in association with negligible morbidity and suitable patient satisfaction. However, non-surgical therapeutic modality presented an advantage in terms of a reduction of treatment chair time.

The role of enamel matrix derivative protein in minimally invasive surgery in treating intrabony defects in single-rooted teeth: a randomized clinical trial.

BACKGROUND: This study investigates the impact of enamel matrix derivative (EMD) proteins on the outcome of a minimally invasive surgical technique (MIST) for the treatment of intrabony defects. METHODS: Thirty patients who presented with intrabony defects were randomly assigned to treatment with: 1) MIST plus EMD or 2) MIST alone. Probing depth (PD), position of the gingival margin (PGM), and relative clinical attachment level (RCAL) were evaluated at 3 and 6 months after treatment. Radiographs and markers in gingival crevicular fluid associated with periodontal regeneration were also evaluated. RESULTS: Significant PD reductions, RCAL gains, and no changes in PGM were obtained at 3 and 6 months in both groups. Clinical and radiographic evaluations and levels of mediators of wound healing did not present differences between therapies at any time. CONCLUSION: The use of EMD did not provide superior benefits on the outcome of the minimally invasive surgical approach for the treatment of intrabony defects.

The impact of cigarette smoke inhalation on the outcome of enamel matrix derivative treatment in rats: histometric analysis.

BACKGROUND: Tobacco use is the most significant risk factor of periodontal disease. Clinical evidence has demonstrated that tobacco may negatively influence the results after surgical and non-surgical periodontal therapy. Enamel matrix derivative (EMD) have been used in periodontal regenerative procedures resulting in improvement of clinical parameters. The effect of EMD in the presence of tobacco compounds is unclear. Thus, the aim of the present study is to evaluate the impact of cigarette smoke inhalation (CSI) on the results of EMD treatment. METHODS: Twenty-two Wistar rats were assigned to two groups: Group 1, CSI (n = 11); Group 2, non-exposed (n = 11). Thirty days after initiation of CSI, fenestration defects were created at the buccal aspect of the first mandibular molar. The study followed a split-mouth design. After the surgeries the defects were randomly assigned to two subgroups: non-treated control and treated with EMD. The animals were sacrificed 21 days later and the percentage of defect fill, density of newly formed bone, and new cementum formation were histometrically assessed. The number of osteoclasts was determined by tartrate-resistant acid phosphatase. RESULTS: CSI was associated with less bone density compared to the non-exposed group. EMD provided an increased defect fill and new cementum formation in both groups. The number of tartrate-resistant acid phosphatase-positive osteoclasts was significantly higher in the CSI non-treated control group compared to the non-treated control of the non-exposed animals. CONCLUSIONS: EMD may provide increased defect fill and cementum formation in the presence or absence of CSI. However, tobacco smoke produced a detrimental effect on bone healing when density of newly formed bone was considered.