Journal of Applied Oral Science最新文献

Background: Inflammation, oxidative damage, and adenosine triphosphate (ATP) depletion play a role in the pathogenesis of cisplatin (CIS)-induced oral mucositis.

Objective: The purpose of this research is to examine the impact of ATP against potential oral mucositis development in cisplatin-treated rats. Methodology All rats were randomly assigned to four groups, namely healthy control group (HG), ATP group (ATPG), Cisplatin group (CISG), and ATP + Cisplatin group (ATCS). Firstly, ATP 4 mg/kg was administered via intraperitoneal injection (IP) to both ATPG and ATCS groups. The same volume of normal saline was injected into HG and CISG groups. After 1 h, cisplatin 5 mg/kg was administered via IP to CISG and ATCS groups. The drugs were taken 1x1 for 7 d. Later, tongue tissues were collected from all groups. Biochemical, macroscopic, and histopathological examinations were performed on all tissues.

Results: ATP inhibited cisplatin-induced oxidative damage and pro-inflammatory cytokines levels in tongue tissue. In the CIS group, a significant number of distinct sulcus formations were found in the apex and corpus, as well as a few ulcer foci in the corpus, significant papilla loss, and bleeding. Meanwhile, in the ATP group, a similar appearance to healthy tissue was observed. Histopathologically, it was determined that in cisplatin-aggravated tongue tissue damage, filiform papillae decreased when ATP was administered, and the arrangement and structures of the epithelium, blood capillaries, muscle groups, and adipose cell groups were normal.

Conclusions: Oral mucositis caused by cisplatin is alleviated by ATP. These findings may be useful for developing new therapeutic approaches to prevent or treat mucositis, a side effect so severe that can lead to treatment discontinuation.

Generalized Joint Hypermobility (GJH) is one of the pathophysiological contributing factors for the development of temporomandibular disorders (TMD). There are, however, several counterpoints on the potential relation between TMD and joint hypermobility, especially when considering the temporomandibular joint (TMJ), event known as TMJ hypertranslation. Additionally, there is no consensus regarding the clinical and imaging diagnostic criteria for such condition. Hence, this scoping review addresses the association between GJH, TMJ hypertranslation and TMD, highlighting the lack of consensus concerning TMJ hypertranslation diagnosis. Eligibility criteria included book sections, clinical trials, meta-analyses, multicenter studies, observational studies, and reviews published in English between 1964 and 2024. Bibliographic search was conducted on the PubMed, SciELO, LILACS and Science Direct databases using the following Medical Subjective Headings (MeSH) terms: "temporomandibular joint disorders," "temporomandibular joint," "joint instability" and "joint dislocations." "TMJ hypermobility" and "TMJ subluxation," non-indexed terms, were applied as individual searches in the same databases. Manual search was performed in selected works by cross-referencing the included studies and book sections. Additional search was conducted in the grey literature. All searches were performed from January to June 2024. After selection, 54 texts were included. While some studies suggest that joint hypermobility (generalized or TMJ specific) may be a risk factor for TMD, especially of the intra-articular type, others rule out this association. No consensus on the potential association between joint hypermobility and TMD was achieved due to the diverse methodologies used to define TMJ hypertranslation diagnosis. More robust and controlled studies are needed to establish a diagnostic criteria and, consequently, understanding of its potential repercussions on masticatory structures, as well as management and prevention of the clinical manifestations.

Background: Ionizing radiation directly affects hard dental tissues, compromising the dental structure, which results in damage to dentin collagen fibers and impacts the integrity of the dentin-enamel junction (DEJ).

Objective: To evaluate the effects of radiotherapy on the chemical composition and mechanical properties of human cervical dentin.

Methodology: Ten third molars were divided into control/non-irradiated and irradiated groups (n=5). The irradiated teeth were subjected to in vitro radiotherapy with the following protocol: 1.8 Gy daily, five days per week for eight weeks, totaling 72 Gy. The dentin in the cervical region was evaluated for each group. The chemical composition was assessed using Fourier transform infrared spectroscopy (FTIR) and Raman spectroscopy, focusing on the mineral/matrix ratio (M:M), carbonate/mineral ratio (C:M), and amide I/amide III ratio. Amide I/CH2 ratio was used to assess collagen quality, as amide I reflects protein conformation and hydrogen bonding, while CH2 indicates side-chain vibrations with low sensitivity to molecular orientation. Nanohardness and elastic modulus were evaluated by instrumented indentation. Scanning electron microscopy (SEM) was used to assess the enamel's morphology. Statistical analysis of each parameter was performed using a t-test.

Results: The FTIR analysis showed statistically significant differences in the C:M ratio (p=0.004) and amide I/amide III ratio (p=0.007). Raman spectroscopy revealed significant differences in the M:M ratio (p<0.001), as well as in the amide I/amide III (p<0.001) and amide I/CH2 ratios (p<0.001). Additionally, nanohardness (p=0.04) and the elastic modulus (p=0.003) showed statistically significant differences. SEM images revealed sound dentin shows normal tissue organization, whereas irradiated dentin showed no clear limit between peri and intertubular dentin.

Conclusions: Radiotherapy induced significant changes in dentin composition and mechanical properties, characterized by increased organic content and phosphate levels, reduced carbonate, and decreased nanohardness and elastic modulus. These findings highlight the adverse effects on dentin's structural integrity.

Objective: To evaluate the association between non-syndromic cleft lip with or without cleft palate (NSCL±P) and tooth agenesis (TA), as well as the association of both conditions with polymorphisms in genes encoding growth factors.

Methodology: This cross-sectional study included children with NSCL±P and a control group of children without NSCL±P. Permanent teeth TA (excluding third molars) was evaluated using panoramic radiographs by a trained examiner. Only TA located outside the cleft was considered in the NSCL±P group. Genetic polymorphisms in Transforming Growth Factor Beta 1 (TGFB1)-rs1800470 and rs4803455-Transforming Growth Factor Beta Receptor 2 (TGFBR2)-rs3087465 and rs764522-Epidermal Growth Factor (EGF)-rs4444903 and rs2237051-and Epidermal Growth Factor Receptor (EGFR)-rs2227983- were genotyped by real-time PCR allele discrimination from buccal cell samples. Associations were tested by uni and multivariable Poisson regression models (5% significance level).

Results: A total of 243 children-127 with NSCL±P (mean age = 8.80±2.14 years) and 116 without NSCL±P (mean age = 8.58±2.03 years) were included. TA was more frequent in the NSCL±P group (23.8%) than in the control group (6.2%) (p<0.01). The EGF rs2237051 was significantly associated with NSCL±P, independently of the other variables (PRa=1.41; p=0.042). Regarding TA, only the cleft presence was associated with a higher prevalence of TA regardless of different variables (PRa=3.70; p=0.001). There was no association between TA and the investigated genetic polymorphisms. When TA and NSCL±P were considered together, a borderline association was observed with rs1800470 in TGFB1 (p=0.06).

Conclusion: NSCL±P is associated with TA outside the cleft area. The EGF rs2237051 was associated with NSCL±P. Polymorphisms in genes encoding growth factors are not associated with TA.

Background: The role of human Stem Cells from the Apical Papilla (SCAP) in tissue regeneration has been described, but their impact on modulating the apical inflammatory process by other surrounding cell populations, such as periodontal ligament fibroblasts (PLFs), is unclear. Therefore, we investigated the role of SCAP in the activation of PLFs in vitro.

Methods: Primary SCAP culture was used to obtain conditioned media (CM). A primary human PLF culture was established and stimulated with increasing concentrations of Escherichia coli lipopolysaccharide (LPS) (0.01, 0.1, and 1 µg/mL). At the 24 h time-point, an MTT viability assay was performed, and interleukin (IL)-6 and chemokine (CC-motif) ligand 2 (CCL2) levels were quantified by enzyme-linked immunosorbent assay. Then, PLFs were stimulated with LPS in the presence of SCAP-CM (1:5 dilution) for cell viability assessment and cytokine detection. The following groups were tested: PLF activated with LPS at concentrations of 0.01 and 1 µg/mL with or without SCAP-CM; a group with PLF stimulated by SCAP-CM alone; and a control group (proliferation medium only). The experiments were conducted in triplicate and sextuplicate. Statistical analyses were performed using analysis of variance followed by Tukey's post-hoc test, with statistical significance established at 5% (p=0.05).

Results: The MTT assay showed no cytotoxicity of LPS or SCAP-CM on PLFs (p>0.05). The production of CCL2 and IL-6 significantly increased in the presence of SCAP-CM regardless of the presence of LPS (p<0.0001).

Conclusion: SCAP-CM significantly enhanced the release of proinflammatory cytokines by PLFs in vitro.

Background: This article is derived from Irisvaldo Lima Guedes's Master's dissertation and is available at the address: https://sigaa.ufpi.br/sigaa/public/programa/noticias_desc.jsf?lc=pt_BR&id=370¬icia=519307121 Eugenol has demonstrated efficacy against Candida spp., which is highly prevalent in denture wearers. However, the low water solubility and high volatility limit its application. The encapsulation in nanostructured lipid carriers (NLCs) may be a viable approach for developing new sanitizing agents for denture hygiene.

Objective: To develop a sanitizing dispersion for denture hygiene using nanostructured lipid carriers (NLCs) containing eugenol and to evaluate the efficacy against Candida spp. biofilms.

Methodology: The formulation was prepared using the ultrasonication method and characterized in terms of particle size (PS), polydispersity index (PDI), zeta potential (ZP), and encapsulation efficiency (EE). The minimum inhibitory concentration (MIC) was determined by the broth microdilution method and the antifungal activity was evaluated by four treatment groups (nanostructured formulation containing eugenol (NFE), free eugenol (FE), saline solution (SS), and the drug-free formulation NFW after eight hours of immersion in biofilms of two Candida species (Candida albicans and Candida glabrata) adhered to polymethyl methacrylate resin specimens.

Results: The nanoparticles of NFE showed a particle size of 199.5±2.55 nanometers (nm) as measured by DLS, high homogeneity (0.07±0.02), an EE of 83.07±0.23, and a negative ZP (-25.86±0.65). The MICs of FE for Candida albicans and Candida glabrata were up to 10 times (64 µg/mL) and eight times (128 µg/mL) higher, respectively, than the MICs of NFE (6 µg/mL and 16 µg/mL). The biofilms of these microorganisms showed a significant reduction after immersion in NFE compared to the other tested groups (FE, NBF, and SS) (P<0.0001).

Conclusion: The NFE demonstrated fungicidal activity against the isolated strains and significantly reduced Candida biofilms, thus showing promising performance for the sanitization of dentures over eight hours.

Background: Circadian rhythm disorders and NF-κB are closely linked and can exacerbate periodontitis. However, the mechanisms via which circadian rhythm-related genes influence periodontitis are not yet fully understood.

Objective: We investigated the effect of brain and muscle Arnt-like protein-1 (BMAL1) on the NF-κB pathway and downstream inflammatory factors on periodontitis. In this study, Bmal1 homozygous knockout and periodontitis mouse models were established.

Methodology: Bone marrow-derived macrophages (BMDMs) from Bmal1-/- mice were cultured and stimulated with lipopolysaccharides. Bone resorption was detected using micro-computed tomography and histological analyses. Gene and cytokine expression was assessed using quantitative reverse-transcription PCR and ELISA. The nuclear translocation of p65 was detected using immunofluorescence.

Results: Our findings indicate that Bmal1 knockout exacerbates periodontitis severity in mice by activating the NF-κB signaling pathway with increased nuclear translocation of p65 (p<0.05), as well as increased expression of Il-1b, Il-6, and Tnfα (p<0.01), along with decreased Nr1d1 expression (p<0.05) in BMDMs under inflammation.

Conclusion: The results highlight the protective role of Bmal1 in periodontitis and suggest its potential link to the circadian clock's influence on the disease.

[This corrects the article doi: 10.1590/1678-7757-2024-0245].

Objective: This study evaluated whether hypoglycemic drug metformin enhances the anti-cancer effects of cisplatin in YD-9 cells.

Methodology: YD-9 cells, derived from oral mucosal squamous cell carcinoma of oral mucosa, were used to assess the combined effects of metformin and cisplatin by means of MTT assay, live and dead cell staining, and colony formation assays to evaluate cell viability and proliferation. Reactive oxygen species level was measured using a Muse cell analyzer. Apoptosis, epithelial-mesenchymal transition, and related molecular pathways were analyzed by western blot. Wound healing assays and Transwell migration assays examined cell migration, whereas monophosphate-activated protein kinase inhibitor Compound C, was utilized to investigate the AMPK pathway.

Results: Sequential treatment of YD-9 cells with metformin and cisplatin resulted in decreased cell viability and proliferation, increased ROS levels, and elevated apoptosis compared with the individual drugs. Moreover, the treatment inhibited EMT, wound healing, and cell migration. These results correlated with increased AMPK phosphorylation, a key regulator of cellular energy homeostasis. Introduction of Compound C pre-treatment upregulated N-cadherin and α-smooth muscle actin along with enhanced cell migration.

Conclusion: This study found synergism in anti-cancer effects between metformin and cisplatin. Additionally, introduction of Compound C confirmed that EMT inhibition is AMPK dependent. These findings indicate the potential use of metformin as an adjunct drug in anti-cancer treatments, warranting further investigation.

Objective: This study evaluated the effect of Stemregen® nutritional supplement on inflammation and resorption in apical periodontitis using a rat model.

Methodology: Rats were divided in three groups: negative control (n=7), positive control (n=10), and Stemregen® (Stem) (n=10). Apical periodontitis was induced in the positive control and Stem groups, and all rats were sacrificed on the 30th day. Serum phosphorus (P), calcium (Ca), and alkaline phosphatase (ALP) were analyzed. Histopathological assessments measured osteoblastic and osteoclastic activity, inflammation, fibrosis, and abscess density. Immunohistochemical analyses evaluated RANKL, TRAP, and OPG levels.

Results: Results showed significantly lower osteoblastic activity in the negative control compared to Stem and positive control groups (p=0.005). Osteoclastic activity was higher in the positive control (p=0.032). Inflammation and abscess formation were reduced in the Stem group compared to the positive control (p<0.001). OPG levels were lower in the negative control compared to the other groups (p=0.005).

Conclusion: Stemregen® effectively reduced inflammation and bone destruction, suggesting potential benefits for apical periodontitis management, though further research is needed.