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PURPOSE: To investigate the influence of different denture-bearing conditions on the masticatory function and patient-reported outcome measures (PROMs) of complete denture wearers. METHODS: Sixty edentulous patients were selected and allocated into two groups according to the American College of Prosthodontics' (ACP) classification: non-atrophic (NAT) (Classes I and II) (n = 24) and atrophic (AT) (Classes III and IV) (n = 36). All patients received new complete dentures (CDs). The objective variables (masticatory performance and swallowing threshold) were assessed as well as the PROMs (oral health-related quality of life (OHIP-EDENT), patient satisfaction) and quality of the prosthesis, at baseline (using the old CD) and after 4 months new prostheses use. Data were analyzed by Mann-Whitney test followed by the Generalized Equations Estimation (GEE), linear regression and Chi-square test. RESULTS: Higher masticatory performance was observed in the NAT group (p < .05) for both time points, baseline and after 4 months. However, compared to baseline, both groups showed significant masticatory improvement after 4 months (p < .05). Satisfaction and overall quality of life improved after 4 months with no difference between groups (p > .05). Regarding the quality of the CD, baseline results were significantly (p < .05) lower in the AT group, but after 4 months, no significant differences were found between groups and in intragroup analysis (p > .05). CONCLUSIONS: The denture-bearing conditions seems to impact masticatory function, but the PROMs are barely affected.

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BACKGROUND: Dipeptidyl peptidase 4 (DPP-4) plays a crucial role in breaking down various substrates. It also has effects on the insulin signaling pathway, contributing to insulin resistance, and involvement in inflammatory processes like obesity and type 2 diabetes mellitus. Emerging effects of DPP-4 on bone metabolism include an inverse relationship between DPP-4 activity levels and bone mineral density, along with an increased risk of fractures. MAIN BODY: The influence of DPP-4 on bone metabolism occurs through two axes. The entero-endocrine-osseous axis involves gastrointestinal substrates for DPP-4, including glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptides 1 (GLP-1) and 2 (GLP-2). Studies suggest that supraphysiological doses of exogenous GLP-2 has a significant inhibitory effect on bone resorption, however the specific mechanism by which GLP-2 influences bone metabolism remains unknown. Of these, GIP stands out for its role in bone formation. Other gastrointestinal DPP-4 substrates are pancreatic peptide YY and neuropeptide Y-both bind to the same receptors and appear to increase bone resorption and decrease bone formation. Adipokines (e.g., leptin and adiponectin) are regulated by DPP-4 and may influence bone remodeling and energy metabolism in a paracrine manner. The pancreatic-endocrine-osseous axis involves a potential link between DPP-4, bone, and energy metabolism through the receptor activator of nuclear factor kappa B ligand (RANKL), which induces DPP-4 expression in osteoclasts, leading to decreased GLP-1 levels and increased blood glucose levels. Inhibitors of DPP-4 participate in the pancreatic-endocrine-osseous axis by increasing endogenous GLP-1. In addition to their glycemic effects, DPP-4 inhibitors have the potential to decrease bone resorption, increase bone formation, and reduce the incidence of osteoporosis and fractures. Still, many questions on the interactions between DPP-4 and bone remain unanswered, particularly regarding the effects of DPP-4 inhibition on the skeleton of older individuals. CONCLUSION: The elucidation of the intricate interactions and impact of DPP-4 on bone is paramount for a proper understanding of the body's mechanisms in regulating bone homeostasis and responses to internal stimuli. This understanding bears significant implications in the investigation of conditions like osteoporosis, in which disruptions to these signaling pathways occur. Further research is essential to uncover the full extent of DPP-4's effects on bone metabolism and energy regulation, paving the way for novel therapeutic interventions targeting these pathways, particularly in older individuals.

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PURPOSE: This study aimed to evaluate the risk of bone loss around single short molar crown-supporting implants in an atrophic mandible. METHODS: Implants of different lengths (L = 4 or 6 mm) and diameters (Ø = 4.1 or 4.8 mm) were placed in the molar area of an atrophic mandible. Additional control mandible models were simulated for 4.1 mm diameter implants (L = 4, 6, 8, and 10 mm). A vertical masticatory load of 200 N was applied to three or six occlusal contact areas (3ca or 6ca) of the prosthetic crown. The bone strain energy density (SED) of 109.6 µJ/mm3 was assumed to be the pathological threshold for cortical bone. The peri-implant bone resorption risk index (PIBRri) was calculated by dividing the maximum SED of the crestal cortical bone by the SED pathological threshold. RESULTS: Increasing the implant length from 4 to 6 mm, implant diameter from 4.1 to 4.8 mm, and number of contact areas from 3 to 6 reduced the SED and PIBRri values by approximately 20%, 35%, and 40%, respectively, when comparing pairs of models that isolated a specific variable. All models with 6ca had a low bone resorption risk (PIBRri<0.8), while the Ø4.1 short implant with 3ca had a medium (0.8≤PIBRri≤1.0) or high (PIBRri>1.0) resorption risk. CONCLUSIONS: Increasing the diameter or occlusal contact area of a 4 mm short implant in an atrophic mandible resulted in reduced bone resorption risks, similar to or lower than those observed in a regular mandible with standard-length implants.

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Bone and dental lesions have been documented in various deer species globally, affecting the efficiency of ingestion and digestion, consequently influencing their general health and leading to a decline in survival and reproductive performance. The present study aimed to characterize bone and dental lesions in the dry skulls of individual deer, estimate the prevalence of these lesions, and assess potential risk factors associated with the development of bone and dental alterations. This study assessed bone and dental lesions in 180 dry skulls of eleven neotropical deer species, originating from both captivity and wildlife conditions, through direct visual inspection. A high prevalence of bone and dental lesions was observed in all analyzed species. Dental calculus was the most common alteration (96.7%), followed by dental wear (71.1%). Animal age positively correlated with most bone and dental alterations, indicating that older animals showed more lesions. Additionally, the prevalence of these alterations was similar between sexes. Moreover, all lesions were more common in captive-bred animals, likely attributed to their older age and a less diverse diet. Blastocerus dichotomus and Mazama americana were most affected by bone resorption and dental trauma and had the highest dental calculus prevalence, along with Subulo gouazoubira and Passalites nemorivagus. All eleven species evaluated in the present study were susceptible to the occurrence of bone and dental lesions. Therefore, monitoring oral health and diet in captivity are fundamental practices for the conservation of these species.

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The aim of this study was to investigate the influence of systemic antibiotic therapy on the development and progression of induced apical periodontitis (AP) in Wistar rats. Fifty-six rats were submitted to pulp exposure of the lower left first molar for the induction of AP. On the same day, intraperitoneal antibiotic therapy was administered once a day, for 15 days, until euthanasia. The groups were formed according to the different treatments (n = 8): C-control; GEN-treated with gentamicin (10 mg/Kg); AC-treated with amoxicillin (100 mg/Kg); MZ-treated with metronidazole (40 mg/Kg); AMP-treated with ampicillin (100 mg/Kg); AMC group-treated with amoxicillin + clavulanic acid (100 mg/kg); CLI-treated with clindamycin (60 mg/kg). After euthanasia, the jaws were collected and processed for (1) histological and histometric analysis using hematoxylin and eosin staining, (2) analysis of collagen fibers using Picrosirius Red staining and (3) bacteriological analysis using Brown-Brenn staining. The data were analyzed statistically (p < 0.05). AP induction was confirmed in all groups. The AMC group had the lower intensity of inflammatory infiltrate (p = 0.028) and less periapical bone resorption compared to control (p = 0.006). Regarding collagen maturation, PSR staining revealed a predominance of mature collagen fibers in all groups. The AC and AMC groups had the lower amount of mature fibers and the highest amount of immature fibers, compared to all other groups (p < 0.001). All groups showed bacterial contamination; however, the AC and AMC groups showed a lower extent of bacterial contamination compared to the control (p < 0.001). It can be concluded that systemic antibiotic therapy influences the development and progression of induced AP.

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INTRODUCTION: This study evaluated the effects of cigarette smoke inhalation (CSI) on apical periodontitis (AP) induced in rats by histometric, immunohistochemical, and microtomographic analysis. METHODS: A total of 32 male Wistar rats were divided into 4 experimental groups (n = 8): control, CSI, AP, and CSI + AP. Rats in the CSI and CSI + AP groups inhaled cigarette smoke by remaining inside a smoking chamber for 8 minutes 3 times a day for 50 days. After 20 days of smoke inhalation, rats in the AP and CSI + AP groups had the pulp of their first right lower molar exposed to induce AP. Blood was collected on day 50 to evaluate nicotine and serum cotinine levels. The animals' mandibles were removed for histologic processing to evaluate bone resorption by histometric, immunohistochemical (receptor activator of nuclear factor kappa B ligand/osteoprotegerin), and microtomographic analysis. The Student t test was applied. RESULTS: Histometric analysis showed a larger area of bone resorption (P < .05) and microtomographic analysis found greater resorption volume (P < .001) for the CSI + AP group compared with the AP group. The CSI + AP group presented a high RANKL immunostaining pattern compared with the AP group (P < .001). CONCLUSIONS: CSI increased bone resorption caused by AP.

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ABSTRACT One of the most common dental procedures is tooth extraction; however, the bone defect resulting from the process is only partially restored, leading to considerable bone loss. To rehabilitate a fully or partially edentulous patient, we must handle these sites with delicate surgical procedures. There is a large literature presenting attempts to overcome the negative effects of a dental extraction, with the aim of reducing tissue volume loss or restoring the alveolar architecture. In this context, Partial Extraction Therapy (PET) represents a subgroup of interventions to prevent bone loss after extraction using the tooth itself to prevent alveolar bone loss. This literature review aims to make a survey of the published articles on PET, with an emphasis on socket shield technique, and to explain the other techniques such as root burial, pontic-shield and proximal socket-shield, their indications and counter indications in order to deepen the knowledge of these techniques. To identify the included or considered studies, we adopted a detailed search strategy for MEDLINE and Cochrane Library focused in the last 31 years, whose language was English, Spanish or Portuguese. This text presents an analysis of current data regarding the alternatives for alveolar preservation and the installation of immediate implants in these areas, presenting the possibility of a different surgical technique. However, due to the immaturity and lack of conclusive scientific evidence regarding the predictability of the procedures, it is considered that the use of the socket shield technique must be done in an extremely cautious way.

RESUMO Um dos procedimentos odontológicos mais comuns é a extração dentária, contudo, , o defeito ósseo decorrente do processo é apenas parcialmente restaurado, levando a uma perda ossea volumétrica consideravel. Para reabilitar um paciente totalmente ou parcialmente desdentado, devemos manusear estes sitios com intervenções cirúrgicas delicadas. Há uma vasta literatura apresentando tentativas de transpor os efeitos negativos de uma extração dentária, com o objetivo de diminuir a perda volumétrica tecidual ou restaurar a arquitetura alveolar. Neste contexto, a Terapia de Extração Parcial (TEP) representa um subgrupo de intervenções para prevenir a perda óssea após exodontia, usando o próprio dente para prevenir a perda óssea alveolar. Essa revisão de literatura tem por objetivo fazer um levantamento dos artigos publicados sobre as TEP, com ênfase na técnica de socket shield, e explanar a cerca das demais técnicas como sepultamento radicular, pontic-shield e proximal socket-shield, suas indicações e contra-indicações, a fim de aprofundar o conhecimento dessas técnicas. Para a identificação dos estudos inclui?dos ou considerados, adotamos a estrate?gia de busca detalhada para os bancos MEDLINE e Biblioteca Cochrane nos u?ltimos 31 anos, cujo idioma fosse o ingle?s, espanhol ou o portugue?s. Este texto, apresenta uma análise de dados atuais a respeito das alternativas para a preservação alveolar e instalação de implantes imediatos nestas áreas, apresentando a possibilidade de uma técnica cirúrgica diferenciada. No entanto, devido a imaturidade e falta de comprovação cientifica contundente a respeito da previsibilidade dos procedimentos, considera-se que o emprego da técnica de socket shield deve ser feito de forma cautelosa.

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Lipoproteins are immunostimulatory bacterial components suggested to participate in inflammation-induced bone loss in periodontal disease through stimulation of osteoclast differentiation. Toll-like receptor 2 activation by Pam2CSK4 (PAM2), known to mimic bacterial lipoproteins, was previously shown to enhance periodontal bone resorption in mice. The anti-inflammatory cytokine interleukin-4 (IL-4) is a known inhibitor of RANKL-induced bone resorption in vitro. Here, we have investigated whether IL-4 could decrease PAM2-induced periodontal bone loss and osteoclastogenesis in vivo. In a model of periodontitis induced by gingival injections of PAM2 in mice, concomitant injections of IL-4 reduced bone loss. Histologically, IL-4 reduced the recruitment of inflammatory cells and the formation of TRAP+ osteoclasts stimulated by PAM2. Mouse bone marrow macrophages (BMMs) and neonatal calvarial osteoblasts were used to assess the effect of IL-4 on PAM2-induced osteoclastogenesis in vitro. In RANKL-primed BMMs stimulated by PAM2 Nfatc1, Ctsk, and Acp5 gene expression was up-regulated and resulted in robust formation of TRAP+ multinucleated osteoclasts, effects which were impaired by IL-4. These effects were mediated by impairment in PAM2-induced c-fos expression. In primary calvarial osteoblast cultures, IL-4 decreased PAM2-induced Tnfsf11 (encoding RANKL) mRNA and enhanced Tnfrsf11b (encoding OPG) expression. Our data demonstrate that the osteoprotective effect by IL-4 on lipoprotein-induced periodontal disease occurs through the inhibition of osteoclastogenesis by three mechanisms, one by acting directly on osteoclast progenitors, another by acting indirectly through decreasing the expression of osteoclast-regulating cytokines in osteoblasts and a third by decreasing inflammation.

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Chronic cases of chikungunya fever represent a public health problem in countries where the virus circulates. The disease is prolonged, in some cases, for years, resulting in disabling pain and bone erosion among other bone and joint problems. As time progresses, tissue damage is persistent, although the virus has not been found in blood or joints. The pathogenesis of these conditions has not been fully explained. Additionally, it has been considered that there are multiple factors that might intervene in the viral pathogenesis of the different conditions that develop. Other mechanisms involved in osteoarthritic diseases of non-viral origin could help explain how damage is produced in chronic conditions. The aim of this review is to analyze the molecular and cellular factors that could be involved in the tissue damage generated by different infectious conditions of the chikungunya virus.

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INTRODUCTION: The aim of this study was to investigate the role of the proinflammatory axis TNF-α-TNFR1 in experimentally induced periapical inflammation and bone resorption in mice. METHODS: After receiving Ethics Committee Approval (2019.1.139.58.0), experimental apical periodontitis was induced by means of inoculating oral microorganisms into the root canals of molars of mice. Genetically deficient tumor necrosis factor-α receptor-1 mice (TNFR1-/-; n = 50) response was compared with that of C57Bl6 wild-type mice (wild-type; n = 50) after 7, 14, 28, and 42 days. The analyses performed were micro-computed tomographic, histopathologic, histomicrobiological, and histometric evaluation, tartrate-resistant acid phosphatase staining, immunohistochemistry, and quantitative reverse transcriptase polymerase chain reaction. Data were analyzed by using one-way analysis of variance, followed by Tukey or Bonferroni tests (α = 5%). RESULTS: TNFR1-/- mice exhibited lower recruitment of neutrophils at 14, 28, and 42 days (P < .05), which resulted in reduced area and volume of apical periodontitis at 42 days (P < .05). The number of osteoclasts was also lower in TNFR1-/- animals at 14 and 42 days (P < .01), along with reduced synthesis of CTSK, MMP-9, and COX-2. Expression of RANKL, but not OPG, was reduced at 14 and 42 days (P < .001). The highest RANKL expression over OPG (ratio > 1) was found in wild-type animals at 7 (P < .0001) and 42 days (P < .001). CONCLUSIONS: Periapical inflammation and bone resorption were exacerbated in wild-type animals compared with TNFR1-/- mice, demonstrating that the TNF-α-TNFR1 signaling pathway mediated catabolic events in bone after root canal contamination.

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BACKGROUND: Pro- and anti-inflammatory cytokines are acknowledged, during inflammatory bone destruction, as key regulators of osteoclast and osteoblast differentiation and activity. However, evidence regarding the exact role of pro- and anti-inflammatory cytokines and osteoclastogenesis-related factors in peri-implant diseases is unclear. We aimed to execute a systematic review and meta-analysis about the pro- and anti-inflammatory cytokines and osteoclastogenesis-related factors levels in peri-implant diseases. METHODS: The focused question was elaborated to summarize the levels of pro-and anti-inflammatory cytokines and osteoclastogenesis-related factors in tissue samples (mRNA) and biofluids (protein levels) of patients with/without peri-implant diseases. Electronic searches of the PubMed, Cochrane Controlled Trials Registry, Web of Science, EMBASE, Scopus and Google scholar databases were conducted for publications up to March 2023. Meta-analysis evaluating the mediator´s levels (protein levels by ELISA) in peri-implant crevicular fluid (PICF) were made. The effect size was estimated and reported as the mean difference. The 95% confidence interval was estimated for each mediator, and the pooled effect was determined significant if two-sided p-values < 0.05 were obtained. RESULTS: Twenty-two publications were included in the systematic review (qualitative analysis), with nine of these subjected to meta-analyses (quantitative analysis). In the qualitative analysis, higher pro-inflammatory cytokines [Interleukin (IL)-1ß, IL-6] and pro-osteoclastogenic mediator [Receptor Activator of Nuclear Factor-Kappa B ligand (RANKL)] levels were observed in PICF of individuals with peri-implant diseases in comparison to healthy individuals. Higher RANKL/osteoprotegerin (OPG) ratios were observed in PICF from individuals with peri-implant diseases in comparison to healthy individuals. Meta-analysis showed higher RANKL levels in diseased groups compared to controls. CONCLUSIONS: The results showed that the levels of IL-1ß, IL-6, IL-10, and RANKL/OPG are not balanced in peri-implant disease, suggesting that these mediators are involved in the host osteo-immunoinflammatory response related to peri-implantitis.

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La enfermedad periodontal es una de las principales causas de pérdida dentaria. Clínicamente, esta patología, mediada por la desregulación del sistema inmune producto de una disbiosis ocurrida en el surco gingival, inicia con la inflamación de la encía y evoluciona con el daño irreversible de los tejidos que rodean el diente. El hueso alveolar es uno de los tejidos afectados esta patología, esto debido a la activación de osteoclastos por la sobreexpresión de la proteína RANKL en el huésped. El propósito de este trabajo es determinar el nivel de sobreexpresión de RANKL, en un modelo de células tumorales U2OS, frente a la infección con Porphyromonas gingivalis y Prevotella intermedia. Para identificar el nivel de RANKL, se definieron cuatro grupos: Un grupo control, no tratado; Grupo PG, tratado con P. gingivalis; Grupo PI, tratado con P. Intermedia; y un grupo PG+PI, tratado con ambas bacterias. El nivel relativo de la proteína RANKL fue determinado en el sobrenadante y en los extractos celulares de manera independiente, mediante la técnica Western blot. En sobrenadantes, el grupo PG mostró mayores niveles de RANKL comparados con PI (p < 0,05). En extractos celulares los niveles fueron mayores en el grupo PG+PI (p < 0,05). El grupo PI mostró los niveles más bajos de RANKL. La infección polimicrobiana resulta en una mayor expresión de RANKL en células tumorales U2OS, mientras que frente a la infección P. gingivalis, se observó mayor cantidad de RANKL soluble.

SUMMARY: Periodontal disease is one of the main causes of tooth loss. Clinically, this pathology, mediated by the deregulation of the immune system due to a dysbiosis occurred in the gingival sulcus, begins with the inflammation of the gum and evolves with the irreversible damage of the tissues that surround the tooth. Alveolar bone is one of the most affected tissues by this disease, due to the activation of osteoclasts by the upregulation of RANKL in the host. The aim of this study is to determine the increase of RANKL, in a U2OS tumor cells model, inoculated with Porphyromonas gingivalis and Prevotella intermedia. To identify the level of RANKL, four groups were defined: A control group, not treated; PG group, treated with P.gingivalis; PI group, treated with P. intermedia; and a PG+PI group, treated with both bacteria. The relative level of RANKL was determined in the supernatant and cell extracts independently, using the Western blot technique. In supernatants, the PG group showed higher RANKL levels compared to PI (p < 0.05). In cell extracts the levels were higher in the PG+PI group (p < 0.05.). The PI group showed the lowest levels of RANKL.Polymicrobial infection results in a greater expression of of soluble RANKL was observed.

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OBJECTIVES: The aim of this study was to evaluate the potential protective effect of Chromobacterium violaceum and violacein against periodontitis, in experimental models. MATERIALS AND METHODS: A double-blind experimental study on the exposure to C. violaceum or violacein in experimentally ligature-induced periodontitis, as preventive factors against alveolar bone loss by periodontitis. Bone resorption was assessed by morphometry. Antibacterial potential of violacein was assessed in an in vitro assay. Its cytotoxicity and genotoxicity were evaluated using the Ames test and SOS Chromotest assay, respectively. RESULTS: The potential of C. violaceum to prevent/limit bone resorption by periodontitis was confirmed. Daily exposure to 106 cells/ml in water intake since birth and only during the first 30 days of life significantly reduced bone loss from periodontitis in teeth with ligature. Violacein extracted from C. violaceum was efficient in inhibiting or limiting bone resorption and had a bactericidal effect against Porphyromonas gingivalis in the in vitro assay. CONCLUSIONS: We conclude that C. violaceum and violacein have the potential to prevent or limit the progression of periodontal diseases, in an experimental model. CLINICAL RELEVANCE: The effect of an environmental microorganism with potential action against bone loss in animal models with ligature-induced periodontitis represents the possibility of understanding the etiopathogenesis of periodontal diseases in populations exposed to C. violaceum and the possibility of new probiotics and antimicrobials. This would imply new preventive and therapeutic possibilities.

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Osteoclasts play a key role in the regulation of bone mass and are highly active metabolically. Here we show that a metabolic reprogramming toward the hexosamine biosynthetic pathway (HBP) is required not only for osteoclast differentiation but also to determine the bone resorption mode during physiological and pathological bone remodeling. We found that pharmacological inhibition of O-GlcNAc transferase (OGT) significantly reduced protein O-GlcNAcylation and osteoclast differentiation. Accordingly, genetic deletion of OGT also inhibited osteoclast formation and downregulated critical markers related to osteoclasts differentiation and function (NFATc1, αvintegrin, cathepsin K). Indeed, cells treated with OSMI-1, an OGT inhibitor, also reduced nuclear translocation of NFATc1. Furthermore, the addition of exogenous N-acetylglucosamine (GlcNAc) strongly increased osteoclast formation and demineralization ability. Strikingly, our data show for the first time that O-GlcNAcylation facilitates an aggressive trench resorption mode in human cells. The incubation of osteoclasts with exogenous GlcNAc increases the percentage of erosion by trench while having no effect on pit resorption mode. Through time-lapse recording, we documented that osteoclasts making trenches moving across the bone surface are sensitive to GlcNAcylation. Finally, osteoclast-specific Ogt-deficient mice show increased bone density and reduced inflammation-induced bone loss during apical periodontitis model. We show that osteoclast-specific Ogt-deficient mice are less susceptible to develop bacterial-induced periapical lesion. Consistent with this, Ogt-deleted mice showed a decreased number of tartrate-resistant acid phosphatase-positive cells lining the apical periodontitis site. In summary, here we describe a hitherto undiscovered role of the HBP/O-GlcNAcylation axis tuning resorption mode and dictating bone resorption outcome.

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Cinnamaldehyde is a natural product with anti-inflammatory and immune-modulatory properties, known to regulate host responses to bacterial stimuli. This study aimed to investigate the effects of cinnamaldehyde on ligature-induced periodontitis in rats, and its impact on the modulation of human peripheral blood mononuclear cells (PBMC). Male Wistar rats were assigned into three groups:i) control: no ligature + vehicle; ii) ligature: ligature + vehicle; and iii) ligature + cinnamaldehyde (50 mg/kg); all treatments by daily oral gavage. After 14 days of induced periodontitis, the hemimandibles were collected for bone loss evaluation. The gingival levels of IL-1ß, MMP-9 and iNOS mRNA were evaluated. Nitric oxide (NO) was measured in both rat saliva and plasma. PBMC were stimulated with Aggregatibacter actinomycetemcomitans (Aa) in the presence or absence of cinnamaldehyde (5, 20 e 40 µM), and cytokine production was quantified in cell supernatant. Proliferating lymphocytes were taken for flow cytometer reading, while culture supernatants were used for IFN-γ and IL-10 assessment. The ligature group had both increased alveolar bone loss and gingival expression of IL-1ß, MMP-9 and iNOS compared to the control group. All parameters were attenuated by cinnamaldehyde treatment. Lower salivary but not plasma NO was detected in the cinnamaldehyde compared to the ligature group. Aa-stimulated PBMCs treated with cinnamaldehyde produced less IL-1ß; the compound also attenuated lymphocyte proliferation in a dose-dependent manner, as well as cell IL-10 production. Cinnamaldehyde treatment reduced periodontal bone loss, and downregulated key inflammatory mediators and human PBMC responses, pointing to novel potential therapeutic effects of this compound.

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The aim was to characterise the endocannabinoid system (ECS) in the dental pulp of teeth at different stages of eruption. Pulp of: erupted premolars (EPM), third molars in pre-eruptive (PThM), intraosseous (IThM) and eruptive stages (EThM) (n = 12 each group) were used. Messenger RNA expression of components of the ECS as cannabinoid receptors (CBr1 and CBr2), and anandamide synthetizing (NAPE-PLD) and degradation (FAAH) enzymes were measured by RT-PCR. Data were analysed using Student's t-test for comparisons between two groups and one-way analysis of variance and Tukey's post-test for multiple comparisons (statistical significance: p < 0.05). mRNA expression of CBr2, NAPE-PLD and FAAH was similar in the studied stages, was lower in IThM than in PThM and EThM, and the lowest in EThM (p < 0.01); of note, CBr2 mRNA expression was not detected in EThM. CBr1 mRNA did not differ significantly between IThM and PThM but was lower in EThM (p < 0.01). The absence of CBr2 and presence of CBr1 in EThM suggest the involvement of the ECS via CBr1 as a mediator of tooth and bone tissue homeostasis during tooth eruption.

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A infecção endodôntica ocorre a após contaminação do tecido pulpar levando à uma colonização bacteriana dos canais radiculares resultando em uma resposta inflamatória dos tecidos periapicais e formação de uma lesão periapical, a periodontite apical (PA). O tabagismo, por sua vez, tem impactos prejudiciais à saúde oral e sistêmica sendo considerado um importante fator de risco para as doenças periodontais. Este trabalho tem por finalidade investigar a influência do tabagismo no desenvolvimento da periodontite apical em ratos. Trinta e dois ratos machos Wistar foram divididos em 4 grupos experimentais (n=8): Controle (sem periodontite apical induzida e sem inalação da fumaça do cigarro); FU (com inalação a fumaça do cigarro); PA (com periodontite apical induzida); FU+PA (com inalação a fumaça do cigarro e periodontite apical induzida). Para a inalar a fumaça do cigarro, grupo de cinco animais permaneceram em uma câmara de tabagismo inalando a fumaça de 10 cigarros por 8 minutos, três vezes ao dia, durante 50 dias. Decorridos 20 dias de inalação de fumaça do cigarro, foi realizada a cirurgia para indução da periodontite apical nos animais do grupo PA e FU+PA, no primeiro molar inferior direto, o qual permaneceu aberto na cavidade bucal por 30 dias. Nesses 30 dias subsequentes da indução da PA, os animais do grupo FU+PA e FU continuaram com a inalação a fumaça do cigarro. No 50º dia, os animais foram eutanasiados e coletados amostras de tecido hematológico para avalição dos níveis séricos de nicotina, cotinina, fosfatase alcalina, cálcio, fósforo, série vermelha e série branca. As hemimandibula removidas foram escaneadas em microtomógrafo para avaliar o volume da destruição óssea e processadas histologicamente para avaliação do perfil inflamatório e expressão das citocinas IL-6, IL-1ß, TNF-α e dos marcadores do metabolismo ósseo RANKL e OPG. Os dados foram tabulados e aplicados os testes estatísticos de Mann-Whitney para os dados não paramétricos e teste t para os dados paramétricos, a um nível de significância de P< 0.05. Com relação a análise histológica o grupo FU+PA apresentou infiltrado inflamatório mais intenso em relação aos demais grupos (P< 0,05). As citocinas pró-inflamatórias IL-6, IL-1ß, TNF-α apresentaram alto padrão de imunomarcação para o grupo FU+PA (P< 0,05). A análise histométrica mostrou maior área de reabsorção óssea no grupo FU+PA, assim como na análise microtomográfica (P< 0,05). As citocinas RANKL esteve mais expressa no grupo FU+PA (P< 0,05) e OPG teve maior expressão no grupo PA (P< 0,05). Na análise hematológica houve um aumento na concentração de hemácias, hemoglobina e leucócitos para o FU+PA (P< 0,05). Os níveis séricos de cálcio foram menores no FU+PA (P> 0,05), a fosfatase alcalina e o cálcio se manteve constante em todos os grupos experimentais (P> 0,05). A concentração sérica de nicotina e cotinina no grupo FU e FU+PA foram compatíveis com fumante humano(AU)

Endodontic infection occurs mainly after pulp tissue contamination by a carious process, leading to bacterial colonization of root canal system and inflammatory response of periapical tissues, followed by formation of apical periodontitis (AP). It is widely known that smoking has harmful impacts on oral and systemic health and is considered a risk factor for periodontal diseases. The objective of this research was to investigate the influence of smoking on the development of AP in rats. Thirty-two male Wistar rats were divided into 4 experimental groups (n = 8): C - Control (no induced AP and no cigarette smoke inhalation); CSI (cigarette smoke inhalation); AP (induced apical periodontitis); CSI + AP (cigarette smoke inhalation and induced apical periodontitis). To inhale cigarette smoke, group with five animals remained in a smoking chamber inhaling smoke from 10 cigarettes for 8 minutes, three times daily, for 50 days. After 20 days of cigarette smoke inhalation, pulp chamber access was performed to induce apical periodontitis in the first mandibular right molar, which remained with pulp chamber exposed to oral cavity for 30 days in animals in the AP and CSI + AP group. During these 30 days after the AP induction, animals in the CSI + AP and CSI group continued to inhale cigarette smoke. On the 50th day, animals were euthanized and blood sample collected to assess serum levels of nicotine, cotinine, alkaline phosphatase, calcium, phosphorus, red series and white series. The hemimandibles were removed and scanned in microtomograph to assess bone volume and histologically processed to assess inflammatory profile and expression of cytokines IL-6, IL-1ß, TNF-α and bone metabolism markers RANKL and OPG. Data were tabulated and statistically analyzed using Mann-Whitney tests for nonparametric data and analysis of variation test for parametric data, with a significance level of P< 0.05. Regarding histological analysis, CSI+AP group showed more intense inflammatory infiltrate compared to other groups (P < 0.05). Histometric analysis showed a larger area of bone resorption in the CSI + AP group, also observed in the microtomographic analysis (P< 0.05). Group CSI+AP had elevated pro-inflammatory cytokines IL-6, IL-1ß, TNF-α expression (P< 0.05). The RANKL cytokines were also more expressed in the CSI+AP group (P< 0.05), while OPG was more expressed in the AP group (P< 0.05). The hematological analysis revealed an increase in the concentration of red blood cells, hemoglobin, and leukocytes for CSI+AP (P< 0.05). Serum calcium levels were lower in CSI+AP (P> 0.05), and alkaline phosphatase and calcium remained constant in all experimental groups (P> 0.05). The serum concentrations of nicotine and cotinine in the CSI and CSI+AP group were compatible with human smokers(AU)

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Los antiinflamatorios no esteroideos (AINE) son un grupo de fármacos que han sido comúnmente prescritos por sus propiedades antiinflamato- rias, antipiréticas y analgésicas, mismas que se deben a la inhibición de la formación de prostaglandinas. Este mecanismo ha sido ampliamente respaldado en la literatura; sin embargo, en la actualidad poco se co- noce sobre las propiedades adicionales de estos medicamentos como el efecto antirresortivo y antimicrobiano. La función antirresortiva se debe principalmente al bloqueo de la producción de prostaglandinas en específico la PGE2, que posee gran potencial osteoclastogénico, esencial para la aparición de lesiones periapicales; asimismo, la acción antimicrobiana de los AINE está relacionada con la afectación directa de la perpetuación de biopelícula, potencian la acción de los antibióticos, entre otros. Dichos efectos combinados podrían contribuir en la cura- ción de lesiones periapicales. El objetivo de este estudio es recopilar información actualizada sobre estas funciones agregadas de los AINE, con el fin de dar a conocer a los profesionales estos beneficios en la terapéutica de las lesiones periapicales (AU)

Non-steroidal anti-inflammatory (NSAIDs) are a group of drugs that have been commonly prescribed for their anti-inflammatory, antipyretic and analgesic properties, which are due to the inhibition of prostaglandin formation. This mechanism has been widely supported in the literature; however, currently little is known about the additional properties of these drugs such as the antiresorptive and antimicrobial effect. The antiresorptive function is mainly due to the blockage of prostaglandin production, specifically PGE2, which has great osteoclastogenic potential, and is essential for the appearance of periapical lesions; likewise, the antimicrobial action of NSAIDs is related to the fact that they directly affect the perpetuation of biofilms, enhance the action of antibiotics, among others. These combined effects could contribute to the healing of periapical lesions. The aim of this study is to gather updated information on these added functions of NSAIDs, in order to inform professionals about these benefits in the therapy of periapical lesion (AU)

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INTRODUCTION: To evaluate, by cone-beam computed tomography (CBCT), the change in thickness and height of the alveolar bone and interdental septum in the anterior mandible after orthodontic treatment for dental crowding using tooth extraction. MATERIAL AND METHODS: The sample consisted of 48 mandibular incisors from adult patients who presented with Class I malocclusion and required orthodontic treatment with the extraction of mandibular premolars. CBCT images were taken before starting the treatment (T1) and three months after treatment (T2). The following measurements were evaluated: width and height of the alveolar bone and the interdental septum, the distance between the cementoenamel junction and the bone ridges (F-CEJ-MBC and L-CEJ-MBC), as well as the vertical positioning and inclination of the incisor, using the Lingual Plane as the reference point. The paired Student's t-test and Pearson correlation were used with a significance level of 5%. RESULTS: A significant increase was observed in the distance L-CEJ-MBC, which shows the appearance of bone dehiscence. The degree of dental crowding was not a risk factor for the development of dehiscence. The decrease in the incisor inclination and intrusion was related to the formation of dehiscence on the lingual surface. CONCLUSION: The variation in the incisor's inclination and intrusion during the treatment of dental crowding using tooth extraction are related to the formation of bone dehiscence on its lingual surface.

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OBJECTIVE: The objective of this study was to summarize and compare the local and systemic impact of different models of experimental periodontitis in mice. DESIGN: After defining the PICO strategy, was performed a search for articles in English following the PRISMA guidelines in PubMed, Embase, Scopus, Web of Science, Cochrane and LILACS databases. The search strategy provided 8815 articles from which were selected experimental studies comparing the local and/or systemic effects of two or more models for the induction of periodontitis in mice according to the inclusion and exclusion criteria. RESULTS: After selection, 7 articles that met the inclusion criteria for the review. Were analyzed differences between the following experimental models of periodontitis in mice: ligature, gavage, injection of bacteria, ligation embedded in bacteria and association between them. CONCLUSION: Although most experimental models of periodontitis are efficient in causing alveolar bone loss, there are differences in their characteristics. In ligature, an acute process is established and the host tends to repair itself, decreasing the significance of this loss over time. In models where bacterial challenge is added bone loss appears to be significant with longer induction time, indicating the presence of a chronic condition. Regarding systemic outcomes, gavage showed greater potential for modulating the host's response with systemic inflammatory changes, proving to be more promising between periodontitis and chronic systemic diseases.

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