Prevalence of peri-implantitis after alveolar ridge preservation at periodontitis and nonperiodontitis extraction sites: A retrospective cohort study.

INTRODUCTION: Periodontitis is the main indication for dental extraction and often leads to peri-implantitis (PI). Alveolar ridge preservation (ARP) is an effective means of preserving ridge dimensions after extraction. However, whether PI prevalence is lower after ARP for extraction after periodontitis remains unclear. This study investigated PI after ARP in patients with periodontitis. MATERIALS AND METHODS: This study explored the 138 dental implants of 113 patients. The reasons for extraction were categorized as periodontitis or nonperiodontitis. All implants were placed at sites treated using ARP. PI was diagnosed on the basis of radiographic bone loss of ≥3 mm, as determined through comparison of standardized bitewing radiographs obtained immediately after insertion with those obtained after at least 6 months. Chi-square and two-sample t testing and generalized estimating equations (GEE) logistic regression model were employed to identify risk factors for PI. Statistical significance was indicated by p < 0.05. RESULTS: The overall PI prevalence was 24.6% (n = 34). The GEE univariate logistic regression demonstrated that implant sites and implant types were significantly associated with PI (premolar vs. molar: crude odds ratios [OR] = 5.27, 95% confidence intervals [CI] = 2.15-12.87, p = 0.0003; bone level vs. tissue level: crude OR = 5.08, 95% CI = 2.10-12.24; p = 0.003, respectively). After adjustment for confounding factors, the risks of PI were significantly associated with implant sites (premolar vs. molar: adjusted OR [AOR] = 4.62, 95% CI = 1.74-12.24; p = 0.002) and implant types (bone level vs. tissue level: AOR = 6.46, 95% CI = 1.67-25.02; p = 0.007). The reason for dental extraction-that is, periodontitis or nonperiodontitis-was not significantly associated with PI. CONCLUSION: ARP reduces the incidence of periodontitis-related PI at extraction sites. To address the limitations of our study, consistent and prospective randomized controlled trials are warranted.

Association of Peri-Implant Health Status With COVID-19.

OBJECTIVE: The aim of this research was to evaluate peri-implant health status in patients infected with COVID-19 and control patients (individuals without COVID-19). METHODS: This observational investigation was performed in adults with (test group) and without (control group) COVID-19 infection having at least 1 functional dental implant. Self-reported education status and daily frequency of toothbrushing and flossing was determined. A questionnaire was administered to record demographic data, brushing/flossing frequency, and education status. Periodontal examination comprised full-mouth assessment of clinical attachment loss (CAL), plaque index (PI), probing depth (PD), and gingival index (GI). Peri-implant PD, modified PI, and modified gingival index were recorded. Loss of marginal and crestal bone around teeth and implants was also measured. Significance level was established for P < .05. RESULTS: Seventy-three (41 males) and 71 (44 males) individuals were included in the test and control groups, respectively. Average ages of patients and controls were 44.6 ± 5.2 and 40.1 ± 3.1 years, respectively. University-level education was attained by 52 (75.3%) and 50 (70.4%) individuals in the test and control groups, respectively. Seventy (95.9%) and 68 (95.7%) patients and controls were brushing twice a day. Once-daily interproximal flossing was reported by 44 (60.3%) and 48 (67.6%) individuals in test and control groups. All participants had healthy periodontal and peri-implant tissues. CONCLUSIONS: The study indicated that there are no short-term adverse effects on the peri-implant tissues due to acute COVID-19 infection, and further well-controlled longitudinal studies are needed to evaluate the long-term effect of the infection on these tissues.

Risk indicators of long-term outcome of implant therapy in patients with a history of severe periodontitis or no history of periodontitis: A retrospective cohort study.

OBJECTIVE: The aim of this retrospective cohort study was to assess factors associated with peri-implant disease in partially edentulous patients with a history of severe periodontitis or no history of periodontitis. METHODS: Partially edentulous patients with a history of severe periodontitis/without history of periodontitis who received implant surgery within the past 6 to 8 years were recalled. Clinical and radiographic examinations were recorded. Periodontal probing depth, marginal bone loss (MBL) and peri-implantitis were considered as the primary outcome and peri-implant bleeding on probing (BOP) was considered as the secondary outcome. The following criteria were considered as the predictors, as well: history of severe periodontitis, gender, age, smoking, brushing frequency, recall interval, full-mouth plaque score, full-mouth bleeding score, splinted prosthesis, open/tight interproximal contact, width of keratinized mucosa, mucosal thickness, implants placed in the grafted bone and implant type. Univariate and multivariate regression analyses were utilized. RESULTS: A total of 88 patients (186 implants) fulfilled the study. Forty-seven patients (108 implants) had a history of severe periodontitis and 41 patients (78 implants) had no history of periodontitis. There was a higher chance of peri-implantitis in patients with a history of severe periodontitis (OR = 11.13; p = 0.045), implants with lack of peri-implant KM (<2 mm) and implants placed in the grafted bone (OR = 14.94, p < 0.001; OR = 4.93, p = 0.047). The risk of peri-implant MBL ≥3 mm was higher in patients with greater FMBS (OR = 1.20; p < 0.001). The chance of peri-implant BOP was independently higher in patients who brushed their teeth at most once per day (OR = 3.20; p = 0.04), higher FMBS (OR = 1.16; p < 0.001) and irregular recall visits (OR = 15.34; p = 0.001). CONCLUSIONS: Partially edentulous patients with the history of severe periodontitis, lack of peri-implant KM and implants placed in bone-grafted sites expressed higher probability of peri-implantitis. In addition, inadequate frequency of brushing (at most once daily) and irregular recall visits were associated with greater chance of peri-implant BOP.

Does childhood chemotherapy affect mandibular bone structures in a lifetime?

BACKGROUND: Chemotherapy, one of the most important treatment modalities for treating childhood cancers, is a major cause of bone loss in patients and survivors. OBJECTIVES: This study aimed to evaluate mandibular bone structures in childhood cancer survivors (CCSs) by means of fractal dimension (FD) analysis and the Klemetti index (KI), and to compare them with regard to the control group. MATERIAL AND METHODS: In this retrospective study, the panoramic radiographs of 49 CCSs were included as the study group and the panoramic radiographs of 49 cancer-free volunteers were included as the control group. Based on the panoramic radiographs, FD and KI were determined. RESULTS: No significant differences were observed between the study and control groups in terms of mean FD values for regions of interest (ROIs) ROI_1, ROI_2 and ROI_3 (p = 0.750, p = 0.490 and p = 0.910, respectively). The mean FD values for ROI_1 for the study and control groups were 1.08 ±0.18 and 1.07 ±0.14, respectively. The mean FD values for ROI_2 for the study and control groups were 1.11 ±0.13 and 1.09 ±0.13, respectively. The mean FD values for ROI_3 for the study and control groups were 1.15 ±0.14 and 1.15 ±0.15, respectively. Statistically significant differences between the study and control groups were noted only in the distribution of the KI categories (p = 0.015). CONCLUSIONS: Childhood chemotherapy may affect mandibular bone structures during a lifetime. The Klemetti index should be considered a useful clinical diagnostic tool for the examination of mandibular bone structures.

LEVELS OF SMOKING AND PERI­IMPLANT MARGINAL BONE LOSS: A SYSTEMATIC REVIEW AND META-ANALYSIS.

AIM: This systematic review and meta-analysis sought to determine if there was a significantly enhanced risk of peri­implant marginal bone loss (MBL) due to the increased number of cigarettes smoked per day. MATERIALS AND METHODS: Six databases, including Medline, Embase, Cochrane Library, Web of Science, Scopus, and ProQuest, were searched until February, 2021. The search terms "dental implant, oral implant, smoking, smoker, non-smoker, marginal bone loss and crestal bone loss" were used in combination to seek the articles providing data for MBL related to the smoking habit. Articles were excluded if the quantity of cigarettes smoked per day was not reported. Random-effects meta-analyses were used to pool the estimates of mean difference (MD) with 95% confidence intervals (CI). RESULTS: Eight studies were included for qualitative and 5 for quantitative synthesis. The meta-analyses revealed higher levels of MBL in patients who smoked <10 or >10 cigarettes/day than in non-smokers (<10: (MD -0.33, 95% CI -0.69-0.03 and >10: MD -0.58, 95% CI -0.96- -0.19). There was a significant risk of MBL between patients who smoked >10 and <10 cigarettes/day (MD -0.23, 95% CI -0.47-0.01). CONCLUSION: It seems the risk of MBL is steadily increasing as daily smoking increases.

Are partially edentulous patients with a history of severe periodontitis more prone to develop peri-implantitis over the long term?

Aim This study aimed to compare the long-term outcome of implant therapy in partially edentulous patients with severe periodontitis compared to those with no history of periodontitis.Design Retrospective cohort study.Cohort selection Eighty-eight patients (34 men and 54 women; age ranging from 28 to 45 years) with severe periodontitis (47 patients with 108 implants) and no history of periodontitis (41 patients with 78 implants) were included in this institutional study. All these cohorts had received implants 6-8 years previously.Data analysis Probing pocket depth, radiographic marginal bone level and peri-implantitis were the primary outcomes, while bleeding on probing was the secondary outcome. The effect of variables was measured by odds ratio with 95% confidence interval. Both patient-level and implant-level analyses were used to evaluate the association between peri-implantitis and potential risk factors. In addition, the association between probing pocket depth and radiographic marginal bone level with potential risk factors was assessed at implant-level analyses. In contrast, for patient-level data, a positive relationship was assessed with the Chi-square test.Results Patients with a history of severe periodontitis (OR = 11.13; p = 0.045), implants with a lack (<2 mm) of peri-implant keratinised mucosa (OR = 14.94; p <0.001) and implants placed in bone-grafted sites (OR = 4.93; p = 0.047) were associated with greater risk of peri-implantitis, at 6-8 years post-implant placement. The risk of developing radiographic marginal bone level ≥3 mm was significantly greater (OR = 1.20; p <0.001) in patients with higher full-mouth bleeding scores. The chance of peri-implant bleeding on probing was independently and especially higher in patients who brushed their teeth at most once per day (OR = 3.20; p = 0.04), with higher full-mouth bleeding score values (OR = 1.16; p <0.001) and irregular recall visits (OR = 15.34; p = 0.001).Conclusion This retrospective cohort study concluded that partially edentulous patients with a history of severe periodontitis were more prone to develop peri-implantitis at 6-8 years post-implant placement.

Risk factors for developing medication-related osteonecrosis of the jaw when preserving the tooth that can be a source of infection in cancer patients receiving high-dose antiresorptive agents: a retrospective study.

PURPOSE: To retrospectively investigate whether apical lesion, alveolar bone loss, probing pocket depth, or local infectious symptoms were associated with the onset of medication-related osteonecrosis of the jaw (MRONJ) in patients treated with high-dose antiresorptive agents who did not undergo tooth extraction. METHODS: The study included 92 patients receiving high-dose antiresorptive agent therapy who had teeth with apical lesion ≧ 3 mm, alveolar bone loss ≧ 1/2, probing pocket depth ≧ 4 mm, or local infection symptoms such as swelling, pain, and pus discharge, but did not undergo tooth extraction. Univariate and multivariate Cox regression analyses were performed to determine the relationship between each variable and MRONJ onset. RESULTS: MRONJ developed in 15 of 92 patients (35 of 404 teeth) from 74 to 1883 days (median, 383 days) after the first visit. Multiple Cox regression analysis revealed that a lower number of teeth, diabetes, increased leukocyte count, administration of antiresorptive agents for 180 days or more, local infection symptoms, apical lesion ≧ 3 mm, and probing pocket depth ≧ 4 mm were significantly correlated with the development of MRONJ. CONCLUSION: It is recommended that teeth with apical lesion ≧ 3 mm, probing pocket depth ≧ 4 mm, or local infection symptoms are extracted before or as early as possible after beginning of medication in cancer patients receiving high-dose antiresorptive agent therapy to prevent the development of MRONJ.

Gram-positive bacteria cell wall-derived lipoteichoic acid induces inflammatory alveolar bone loss through prostaglandin E production in osteoblasts.

Periodontitis is an inflammatory disease associated with severe alveolar bone loss and is dominantly induced by lipopolysaccharide from Gram-negative bacteria; however, the role of Gram-positive bacteria in periodontal bone resorption remains unclear. In this study, we examined the effects of lipoteichoic acid (LTA), a major cell-wall factor of Gram-positive bacteria, on the progression of inflammatory alveolar bone loss in a model of periodontitis. In coculture of mouse primary osteoblasts and bone marrow cells, LTA induced osteoclast differentiation in a dose-dependent manner. LTA enhanced the production of PGE2 accompanying the upregulation of the mRNA expression of mPGES-1, COX-2 and RANKL in osteoblasts. The addition of indomethacin effectively blocked the LTA-induced osteoclast differentiation by suppressing the production of PGE2. Using ex vivo organ cultures of mouse alveolar bone, we found that LTA induced alveolar bone resorption and that this was suppressed by indomethacin. In an experimental model of periodontitis, LTA was locally injected into the mouse lower gingiva, and we clearly detected alveolar bone destruction using 3D-µCT. We herein demonstrate a new concept indicating that Gram-positive bacteria in addition to Gram-negative bacteria are associated with the progression of periodontal bone loss.

Mice lacking PLAP-1/asporin counteracts high fat diet-induced metabolic disorder and alveolar bone loss by controlling adipose tissue expansion.

Adipose tissue fibrosis with chronic inflammation is a hallmark of obesity-related metabolic disorders, and the role of proteoglycans in developing adipose tissue fibrosis is of interest. Periodontal disease is associated with obesity; however, the underlying molecular mechanisms remain unclear. Here we investigated the roles of periodontal ligament associated protein-1 (PLAP-1)/asporin, a proteoglycan preferentially and highly expressed in the periodontal ligament, in obesity-related adipose tissue dysfunction and adipocyte differentiation. It was found that PLAP-1 is also highly expressed in white adipose tissues. Plap-1 knock-out mice counteracted obesity and alveolar bone resorption induced by a high-fat diet. Plap-1 knock-down in 3T3-L1 cells resulted in less lipid accumulation, and recombinant PLAP-1 enhanced lipid accumulation in 3T3-L1 cells. In addition, it was found that primary preadipocytes isolated from Plap-1 knock-out mice showed lesser lipid accumulation than the wild-type (WT) mice. Furthermore, the stromal vascular fraction of Plap-1 knock-out mice showed different extracellular matrix gene expression patterns compared to WT. These findings demonstrate that PLAP-1 enhances adipogenesis and could be a key molecule in understanding the association between periodontal disease and obesity-related metabolic disorders.

Imaging Microstructural Damage and Alveolar Bone Loss in Rats Systemically Exposed to Methylmercury: First Experimental Evidence.

The alveolar bone is an important mineralized structure of the periodontal support apparatus, and information about the methylmercury (MeHg) effects on the structural integrity is scarce. Therefore, this study aimed to investigate whether systemic, chronic, and low-dose exposure to MeHg can change the alveolar bone microstructure of rats. Adult Wistar rats (n = 30) were exposed to 0.04 mg/kg/day of MeHg or vehicle through intragastric gavage. The animals were euthanized after 60 days, and blood samples were collected for trolox equivalent antioxidant capacity (TEAC), glutathione (GSH), lipid peroxidation (LPO), and comet assays. The mandible of each animal was collected and separated into hemimandibles that were used to determine the total Hg level in the bone and to analyze microstructural damage and alveolar bone loss in terms of trabecular number (Tb.N), trabecular thickness (Tb.Th), bone volume fraction (BV/TV), and exposed root area of the second molars. MeHg exposure triggered oxidative stress in blood represented by lower levels of GSH and TEAC and the increase in LPO and DNA damage of the blood cells. High total Hg levels were found in the alveolar bone, and the microstructural analyses showed a reduction in Tb.N, Tb.Th, and BV/TV, which resulted in an increase in the exposed root area and a decrease in bone height. Long-term MeHg exposure promotes a systemic redox imbalance associated with microstructural changes and alveolar bone loss and may indicate a potential risk indicator for periodontal diseases.

Binge-Like Exposure During Adolescence Induces Detrimental Effects in Alveolar Bone that Persist in Adulthood.

BACKGROUND: Alcohol (EtOH) intake during adolescence has become an important public health issue. Although the detrimental effects of EtOH intake on the musculoskeletal system are well known, only a few studies have investigated its impact on the stomatognathic system of adolescents. This study aimed to investigate the effect of EtOH binge drinking on the alveolar bone and the long-term consequences after abstinence. METHODS: Adolescent female Wistar rats (35 days old) were exposed to 4 cycles of EtOH binge drinking (3 g/kg/d; 3 days On-4 days Off) or distilled water (control group). Alveolar bone micromorphology and vertical bone distance were evaluated at 1, 30, and 60 days after that last EtOH intake through X-ray computed microtomography. The mineral:matrix ratio was assessed through Raman spectroscopy. RESULTS: A decrease in both trabecular thickness and volume ratio, and an increase in trabecular separation were observed at the 1-day evaluation (immediate withdrawal). After 30 and 60 days, the alveolar bone parameters were found similar to control, except for the mineral:matrix ratio in the long-term abstinence. CONCLUSIONS: EtOH binge drinking during adolescence results in alveolar bone damage that may persist in adulthood, even after abstinence.

Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS.

Conventional treatments for chronic periodontitis are less effective in controlling inflammation and often relapse. Therefore, it is necessary to explore an immunomodulatory medication as an adjuvant. Ginsenoside Rb3 (Rb3), one of the most abundant active components of ginseng, has been found to possess anti-inflammatory and immunomodulatory properties. Here, we detected the anti-inflammatory effect of Rb3 on Porphyromonas gingivalis LPS-stimulated human periodontal ligament cells and experimental periodontitis rats for the first time. We found that the expression of pro-inflammatory mediators, including IL-1ß, IL-6 and IL-8, upregulated by lipopolysaccharide (LPS) stimulation was remarkably downregulated by Rb3 treatment in a dose-dependent manner at both transcriptional and translational levels. Network pharmacological analysis of Rb3 showed that the mitogen-activated protein kinase (MAPK) signaling pathway had the highest richness and that p38, JNK, and ERK molecules were potential targets of Rb3 in humans. Western blot analysis revealed that Rb3 significantly suppressed the phosphorylation of p38 MAPK and p65 NF-κB, as well as decreased the expression of total AKT. In experimental periodontitis rat models, reductions in alveolar bone resorption and osteoclast generation were observed in the Rb3 treatment group. Thus, we can conclude that Rb3 ameliorated Porphyromonas gingivalis LPS-induced inflammation by inhibiting the MAPK/AKT/NF-κB signaling pathways and attenuated alveolar bone resorption in experimental periodontitis rats.

Positive Correlation between Activated CypA/CD147 Signaling and MMP-9 Expression in Mice Inflammatory Periapical Lesion.

AIM: Cyclophilin A (CypA)/CD147 signaling plays critical roles in the regulation of inflammation and bone metabolism. This study aimed to investigate the participation of CypA/CD147 in mice periapical lesions progression and its relationship with bone resorption. METHODOLOGY: Periapical lesions were induced by pulp exposure in the first lower molars of 40 C57BL/6J mice. The mice were sacrificed on days 0, 7, 14, 21, 28, 35, 42, and 49. Mandibles were harvested for X-ray imaging, microcomputed tomography scanning, histologic observation, immunohistochemistry, enzyme histochemistry, and double immunofluorescence analysis. Western blot was employed to further detect the related molecular signaling pathways in LPS-stimulated RAW 264.7 cells treated with CypA inhibitor. RESULTS: The volume and area of the periapical lesions increased from day 0 to day 35 and remained comparably stable until day 49. Immunohistochemistry demonstrated that the CypA expression levels also increased from day 0 to day 35 and decreased until day 49, similar to CD147 expression (R 2 = 0.4423, P < 0.05), osteoclast number (R 2 = 0.5101, P < 0.01), and the expression of osteoclastogenesis-related matrix metalloproteinase 9 (MMP-9) (R 2 = 0.4715, P < 0.05). Serial sections further confirmed the colocalization of CypA and CD147 on osteoclasts with immunohistochemistry. And the distribution of CypA-positive or CD147-positive cells was positively correlated with the dynamics of MMP-9-positive cells by using immunofluorescence analysis. Furthermore, CD147 and MMP-9 expression in RAW 264.7 cells were both downregulated with CypA inhibitor treatment (P < 0.05). CONCLUSIONS: The present study reveals the positive correlation of CypA/CD147 signaling and osteoclast-related MMP-9 expression in mice inflammatory periapical lesions progression. Therefore, intervention of CypA/CD147 signaling could probably provide a potential therapeutic target for attenuating inflammatory bone resorption.

Porphyromonas gingivalis lipopolysaccharide-induced periodontitis and serum amyloid-beta peptides.

OBJECTIVE: The aim of this investigation was to determine the circulating levels of amyloid beta (Aß) peptides using the Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) model to induce periodontitis. METHODS: Experimental periodontitis was induced in 6 male Sprague-Dawley rats. Alveolar bone loss was measure by micro computed tomography. Serum concentrations of Aß1-40 and Aß1-42 prior to periodontal induction, at 24 h, 7, 14, and 21 days the last injection of Pg-LPS. RESULTS: The distance between the cemento-enamel junction and the bone crest (i.e., alveolar bone loss) was significantly higher at the end of periodontal induction compared to baseline (2.92 ± 0.29 mm vs. 3.8 ± 0.28 mm, P < 0.001). Periodontitis evoked a slight acute elevation of Aß1-40 serum levels that were maintained during the whole experiment. Aß1-42 peptide levels peak at the end of the study. A positive strong correlation was observed between alveolar bone loss and Aß1-40 serum levels at 7 days (r = 0.695, P = 0.012) and as well as with serum Aß1-42 concentrations at 21 days (r = 0.968, P = 0.002). CONCLUSIONS: Periodontitis induced Pg-LPS produced increased serum levels of Aß peptides. Further studies are needed to confirm our results and to investigate the mechanisms by which periodontitis could be associated with an overexpression of Aß.

Inhibitory Effects of Standardized Boesenbergia pandurata Extract and Its Active Compound Panduratin A on Lipopolysaccharide-Induced Periodontal Inflammation and Alveolar Bone Loss in Rats.

Periodontitis, an inflammatory disease of the gingival tissue, triggered by microbial-derived elements, such as lipopolysaccharide (LPS), collapses the periodontal tissues and resorbs the alveolar bone. This study evaluated the inhibitory effects of standardized Boesenbergia pandurata extract (BPE) and panduratin A (PAN) on periodontitis-induced inflammation and alveolar bone loss. Sprague-Dawley rats with LPS-induced periodontitis were orally administered BPE (50 and 200 mg/kg/day) and PAN (20 mg/kg/day) for 8 days. Histological analysis revealed that BPE- and PAN-administered groups showed decreased cell infiltration and alveolar bone resorption. Furthermore, the BPE and PAN significantly alleviated the mRNA and protein expression levels of nuclear factor kappa B (NF-κB), interleukin-1ß, matrix metalloproteinase (MMP)-2, and MMP-8. BPE and PAN also inhibited the expression of nuclear factor of activated T cells, cytoplasmic 1, c-Fos, and ostoclastogenesis-related enzymes, including cathepsin K and tartrate-resistant acid phosphatase (ALP). BPE and PAN not only upregulated the osteoblastogenesis-associated markers, such as collagen type I (COL1A1) and ALP, but also increased the ratio of osteoprotegerin to receptor activator of NF-κB ligand. Collectively, BPE and PAN efficiently prevent destruction of periodontal tissues and stimulating the loss of alveolar bone tissues, strongly indicative of their potential as natural antiperiodontitis agents.

Influence of nicotine on orthodontic tooth movement: A systematic review of experimental studies in rats.

OBJECTIVE: The objective of this systematic review was to assess the impact of nicotine administration on orthodontic tooth movement (OTM). METHODS: A systematic search was conducted in PubMed, Scopus, EMBASE, MEDLINE (OVID) and Web of Knowledge databases and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. Studies evaluating the influence of nicotine on OTM, and with the presence of a control group (OTM without nicotine administration), were included. Quality assessment of the selected studies was performed following the Animal Research Reporting in Vivo Experiment (ARRIVE) guidelines. RESULTS: Six of the initially identified 108 articles fulfilled the inclusion criteria and were selected. All included studies were performed in male rats, which underwent OTM with or without nicotine administration. Since there was a variation among the included studies regarding nicotine dosage and the duration and magnitude of force application during OTM only a qualitative analysis could be performed. The studies reported that nicotine administration accelerated OTM by inducing alveolar bone resorption around the moving teeth. It was also found that nicotine increased root resorption during experimental OTM. More standardized animal research or clinical studies are warranted to further evaluate the impact of nicotine on OTM. CONCLUSIONS: On an experimental level, nicotine exposure in rats jeopardizes OTM by increasing alveolar bone loss and root resorption. From a clinical perspective, further studies are needed to assess the impact of habitual use of tobacco products on OTM.

Spontaneous alveolar bone loss after 4NQO exposure in Wistar rats.

OBJECTIVE: This study evaluated the effect of an experimental carcinogenic, 4-Nitroquinoline 1-oxide (4NQO), in the spontaneous alveolar bone loss (ABL) in an animal model. DESIGN: Twenty-two male Wistar rats were included in this study. They were randomly divided into two groups: the control group (n = 10) received food and water ad libitum, and the test group (n = 12) receive the same food; however, 25 ppm of 4NQO was diluted in the drinking water. All animals were euthanized after 20 weeks, and the tongues were removed and analyzed macroscopically to determine the presence of oral mucosal lesions. All specimens were paraffin-embedded and histological sections were obtained. The microscopic analysis was based on routine procedure (haematoxylin and eosin stain). The analysis of spontaneous ABL was performed by a calibrated examiner using standardized photographs and imaging software. Differences in spontaneous ABL were assessed among the three resulting groups: control, 4NQO with oral squamous cell carcinoma (OSCC), and 4NQO without OSCC. RESULTS: In the 4NQO-treated group, nine animals developed OSCC. The animals in the 4NQO with OSCC group presented significantly more spontaneous ABL (0.65 ±â€¯0.21 mm) than the control group (0.34 ±â€¯0.05) (p < 0.001). The animals in the 4NQO without OSCC group showed a mean spontaneous ABL of 0.47 ±â€¯0.13 mm, which was not statistically significant different when compared to the control group (p = 0.096). CONCLUSIONS: It was concluded that the presence of OSCC enhanced spontaneous ABL in Wistar rats when compared to control animals. Additionally, it was shown that, solely, administration of 4NQO may not be considered responsible for alveolar bone destruction.

Low-level laser and antimicrobial photodynamic therapy on experimental periodontitis in rats submitted to chemotherapy by 5-fluorouracil.

PURPOSE: The aim of this study was to evaluate the effects of low-level laser therapy (LLLT) and antimicrobial photodynamic therapy (aPDT) as adjuvant to mechanical treatment of experimental periodontitis (EP) in adult rats submitted to 5-fluorouracil (5-FU) chemotherapy. METHODS: EP was induced through ligature around the left mandibular first molar for 7 days. The ligature was removed and the animals separated into groups: EP, no treatment; 5FU, systemic administration of 5-FU (80 and 40 mg/kg); 5FU/scaling and root planing (SRP), systemic application of 5-FU and SRP; 5FU/SRP/LLLT, systemic application of 5-FU, SRP, and LLLT (660 nm, 0.035 W; 29.4 J/cm2); and 5FU/SRP/aPDT, systemic application of 5-FU, SRP, and aPDT (methylene blue irrigation and LLLT). The animals were euthanized 7, 15, and 30 days after treatments. Histological sections from mandibles were processed for histomorphometric and immunohistochemical analysis (TRAP, RANKL, OPG, TNF-α, IL-6, IL-10). The alveolar bone loss (BL) area in the furcation region of the mandibular first molar was analyzed histometrically. RESULTS: There was less bone loss in 5FU/SRP/aPDT compared with 5FU at 7 days (p < 0.05). The immunohistochemical analysis showed no significant difference for TRAP and osteoprotegerin, but lower RANKL immunolabeling was observed in the 5FU/SRP/LLLT and 5FU/SRP/aPDT groups compared with the 5FU group at 15 days. There was lower TNF-α and IL-6 immunolabeling in the 5FU/SRP/LLLT and 5FU/SRP/aPDT groups and higher IL-10 immunolabeling in 5FU/SRP/aPDT at 30 days. CONCLUSION: LLLT and aPDT adjuvant to SRP minimized the effects of 5-FU on periodontal disease. Furthermore, aPDT promoted greater benefits in bone loss control and inflammatory response.

The Impact of Residual Subgingival Cement on Biological Complications Around Dental Implants: A Systematic Review.

OBJECTIVES: To perform a systematic review on the impact of residual subgingival cement on peri-implant diseases and crestal bone loss. MATERIAL AND METHODS: MEDLINE, SCOPUS, ISI Web of Knowledge and Cochrane Central Register of Controlled Trials (CENTRAL) databases were used to identify articles published without time limits. RESULTS: A total of 6 articles were selected for a total of 389 patients (687 implants). The studies were heterogeneous and had a moderate-to-high risk of bias, but met the inclusion criteria. Four of 6 studies were published by the same research group and assessed similar populations over time. A positive relationship between residual cement and peri-implant inflammation was observed. Data on peri-implant probing depths and crestal bone loss were reported in 1 study. CONCLUSION: Residual subgingival cement seems to be strongly associated with peri-implant mucositis which is a risk factor for increased probing depths crestal bone loss and peri-implantitis. Zinc oxide eugenol cements should be preferred to resin cements especially in patients with a history of periodontitis.

Adipokine Chemerin Bridges Metabolic Dyslipidemia and Alveolar Bone Loss in Mice.

Chemerin is an adipokine that regulates adipogenesis and metabolic functions of mature adipocytes mainly through the activation of chemokine-like receptor 1 (CMKLR1). Elevated levels of chemerin have been found in individuals with obesity, type 2 diabetes, and osteoporosis. This adipokine was identified as an inflammatory and metabolic syndrome marker. Considering that the association between metabolic syndrome and bone health remains unclear, the present study aimed to clarify the role of chemerin in the pathophysiology of bone loss induced by dyslipidemia, particularly modulating osteoclastogenesis. In vitro analyses showed a downregulation of CMKLR1 at the early stage of differentiation and a gradual increase at late stages. Strikingly, chemerin did not modify osteoclast differentiation markers or osteoclast formation; however, it increased the actin-ring formation and bone resorption activity in mature osteoclasts. The increased bone resorption activity induced by chemerin was effectively inhibited by CMKLR1 antagonist (CCX832). Chemerin boosting mature osteoclast activity involves ERK5 phosphorylation. Moreover, two models of dyslipidemia (high-fat diet [HFD]-treated C57/BL6 and db/db mice) exhibited significantly increased level of chemerin in the serum and gingival tissue. Morphometric analysis showed that HFD-treated and db/db mice exhibited increased alveolar bone loss compared to respective control mice, which was associated with an up-regulation of chemerin, CMKLR1 and cathepsin K mRNA expression in the gingival tissue. The treatment of db/db mice with CCX832 effectively inhibited bone loss. Antagonism of chemerin receptor also inhibited the expression of cathepsin K in the gingival tissue. Our results show that chemerin not only increases osteoclasts activity in vitro, but also that increased level of chemerin in dyslipidemic mice plays a critical role in bone homeostasis. © 2016 American Society for Bone and Mineral Research.