Gingival Epithelium Research Articles

Demineralized freeze-dried bone allograft with Periocol® membrane versus Perioglas® with Periocol® membrane in the treatment of intrabony defects: A case report

Introduction: Intrabony defects associated with periodontal pockets can be successfully treated with bone graft and Guided Tissue Regeneration membrane (GTR). Demineralized freeze-dried bone allograft (DFDBA) consists primarily of collagen including bone growth and differentiation factors like Bone Morphogenetic Proteins. Perioglas® is a bioactive glass that is osteoconductive, composed entirely of elements naturally occurring in the body and bonds directly to the bone and soft tissue. Periocol® is a resorbable Guided Tissue Regenerative (GTR) membrane that delays the apical migration of gingival epithelium by excluding the gingival connective tissue and allows granulation tissue derived from PDL and osseous tissues to repopulate the space adjacent to the denuded root surface. Objective: To compare DFDBA with Periocol® and Perioglas® with Periocol® membrane in the treatment of intrabony defects clinically and radiographically.Methodology: A patient with bilateral intrabony defects was selected. In one site - Open Flap Debridement (OFD) with Perioglas® and Periocol® membrane was placed and on the other site – OFD with DFDBA and Periocol® membrane was placed.Conclusion: DFDBA with Periocol® membrane has shown better results than Perioglas® with Periocol® membrane.

Expression of neurotransmitter receptors in oral keratinocytes and their response to agonists

This study aimed to investigate whether neurotransmitter receptors in the nervous system were also expressed in oral keratinocytes. Expressions of various neurotransmitter receptor genes in immortalized mouse oral keratinocyte (IMOK) cells were examined by reverse transcriptase polymerase chain reaction. IMOK cells expressed calcitonin gene-related peptide (CGRP) receptor subunit genes Ramp1 and Ramp3 and glutamate receptor subunit genes Grina , Gria3 , Grin1 , Grin2a , and Grin2d . Moreover, IMOK cells expressed Adrb2 and Chrna5 that encode beta 2 adrenergic receptor and cholinergic receptor nicotinic alpha 5 for sympathetic and parasympathetic neurotransmitters, respectively. The expression of Bdkrb1 and Ptger4 , which encode receptors for bradykinin and prostaglandin E2 involved in inflammatory responses, was also observed at low levels. Expressions of Ramp1 and Grina in the mouse gingival epithelium were also confirmed by immunohistochemistry. When the function of neurotransmitter receptors expressed on IMOK cells was tested by intracellular calcium response, CGRP, glutamate, and cholinergic receptors did not respond to their agonists, but the bradykinin receptor responded to bradykinin. Collectively, oral keratinocytes express several neurotransmitter receptors, suggesting the potential regulation of oral epithelial homeostasis by the nervous system.

Peripheral odontogenic keratocyst: Clinicopathological and immunohistochemical characterization.

The aim of this study is to present and discuss the salient clinicopathological features, differential diagnosis and epithelial immunohistochemical profile of three additional cases of peripheral odontogenic keratocyst (POKC) and to present a review of the literature. POKC is a locally aggressive odontogenic lesion. The peripheral variant of the odontogenic keratocyst is rare and more frequently located in anterior gingiva. We present the clinicopathological features of 3 new cases of POKC (2 women and 1 man; age range: 14-74years). Immunohistochemical study included CK7, CK14, CK19 and Ki-67, and a systematic review of the literature was performed in PubMed, Scopus and Web of Science databases. All cases were located in the anterior gingiva (2 in maxilla and 1 mandible), and none corresponded to Gorlin-Goltz syndrome. High expression of CK14 was seen in all cases, with CK19 and CK7 been only focally positive. The expression of Ki-67 was located in the basal and parabasal cells in all cases. POKC is a rare gingival lesion that seems to originate from remnants of dental lamina or from the basal cells of the gingival epithelium and present a similar histopathology as compared to intraosseous OKC.

Hyperglycemia accelerates inflammaging in the gingival epithelium through inflammasomes activation.

Diabetes accelerates inflammaging in various tissue with an increase in senescent cell burden and senescence-associated secretory phenotype (SASP) secretion, which is a significant cause of tissue dysfunction and contributes to the diabetic complications. Recently, inflammasomes are thought to contribute to inflammaging. Here, utilizing diabetic models in vivo and in vitro, we investigated the potential association between hyperglycemia-induced inflammaging and gingival tissue dysfunction and the mechanism underlying inflammasome-associated inflammaging. Gingival epithelium and serum were collected from control and diabetic patients and mice. The expression of p16, p21, and inflammasomes in the gingival epithelium, SASP factors in serum, and the molecular factors associated with gingival epithelial barrier function were assessed. Human oral keratinocyte (HOK) was stimulated with normal and high glucose, and pre-treated with Z-YVAD-FMK (Caspase-1 inhibitor) prior to evaluating cellular senescence, SASP secretion, and inflammasome activation. In vivo, hyperglycemia significantly elevated the local burden of senescent cells in the gingival epithelium and SASP factors in the serum and simultaneously reduced the expression levels of Claudin-1, E-cadherin, and Connexin 43 in the gingival epithelium. Interestingly, the inflammasomes were activated in the gingival epithelium. In vitro, high glucose-induced the inflammaging in HOK, and blocking inflammasome activation through inhibiting Caspase-1 and glucose-induced inflammaging. Hyperglycemia accelerated inflammaging in the gingival epithelium through inflammasomes activation, which is potentially affiliated with a decline in the gingival epithelial barrier function in diabetes. Inflammasomes-related inflammaging may be the crucial mechanism underlying diabetic periodontitis and represents significant opportunities for advancing prevention and treatment options.

SARS-CoV-2 impact on oral health: A general view.

Coronavirus disease 2019 (COVID-19) is a new disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. China reported the first case of COVID-19 in December 2019, and a few months later, the World Health Organization declared it as a pandemic. Oral ulcers in adult patients have been associated with COVID-19. However, no cases have yet been documented in children. The angiotensin-converting enzyme-2 (ACE2) receptor has been identified in tissues of the oral cavity. Studies have identified the tongue as the site with the highest expression of ACE2, and the oral epithelium, gingival epithelium, and salivary glands as sites of lesser extent expression. ACE2 expression is lower in children and varies with age. SARS-CoV-2 in saliva has been identified in various studies, which suggests that this could be a useful sample for diagnosis. However, its presence in saliva would indicate the high risk of contagion of this fluid.

Porphyromonas gingivalis lipopolysaccharide affects oral epithelial connections via pyroptosis

Background/purposePyroptosis is a form of programmed cell death dependent on the activation of caspase-1. Porphyromonas gingivalis (P. gingivalis) is a major pathogenic bacterium in periodontitis and its lipopolysaccharide (LPS) can trigger inflammation. However, whether P. gingivalis-LPS affects epithelial connections or triggers pyroptosis in the gingival epithelium is unknown. Materials and methodsGingival samples from human donors were collected and the expression levels of E-cadherin, nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), caspase-1/4/5, interleukin (IL)-18, and IL-1β were examined. P. gingivalis-LPS was injected into rat gingival sulcus to establish gingivitis models, and the expression levels of E-cadherin, NLRP3, caspase-1/11, IL-18, and IL-1β were compared via immunohistochemistry. The mRNA levels of E-cadherin, caspase-1, IL-18, and IL-1β were evaluated in oral mucosa epithelial cells (OMECs) and rat gingival tissues. ResultsIn the present study, NLRP3 (p < 0.01), caspase-1 (p < 0.01), caspase-4 (p = 0.044), and IL-18 (p = 0.036) expression was greater in the human inflammatory gingival samples, whereas E-cadherin (p = 0.045) had the opposite presentation. Gingivitis models were successfully established in rats with the injection of P. gingivalis-LPS. NLRP3 (p = 0.015), caspase-1 (p < 0.01), caspase-11 (p < 0.01), and IL-18 (p = 0.041) were upregulated, whereas E-cadherin (p = 0.038) expression was decreased. Furthermore, E-cadherin mRNA was decreased while caspase-1, IL-18, and IL-1β mRNA levels were increased. The addition of a caspase-1 inhibitor reversed the expression changes. ConclusionP. gingivalis-LPS may effectively destroy the epithelial connection by triggering pyroptosis.

Epigenetic changes caused by diabetes and their potential role in the development of periodontitis.

Aims/IntroductionPeriodontal disease, a chronic inflammation induced by bacteria, is closely linked with diabetes mellitus. Many complications associated with diabetes are related to epigenetic changes. However, the exact epigenetic changes whereby diabetes affects periodontal disease remain largely unknown. Thus, we sought to investigate the role of diabetes‐dependent epigenetic changes of gingival tissue in the susceptibility to periodontal disease.Materials and MethodsWe studied the effect of streptozotocin‐induced diabetes in minipigs on gingival morphological and epigenetic tissue changes. Accordingly, we randomly divided six minipigs into two groups: streptozotocin‐induced diabetes group, n = 3; and non‐diabetes healthy control group, n = 3. After 85 days, all animals were killed, and gingival tissue was collected for histology, deoxyribonucleic acid methylation analysis and immunohistochemistry.ResultsA diabetes mellitus model was successfully created, as evidenced by significantly increased blood glucose levels, reduction of pancreatic insulin‐producing β‐cells and histopathological changes in the kidneys. The gingival tissues in the diabetes group presented acanthosis of both gingival squamous epithelium and sulcular/junctional epithelium, and a significant reduction in the number and length of rete pegs. Deoxyribonucleic acid methylation analysis showed a total of 1,163 affected genes, of which 599 and 564 were significantly hypermethylated and hypomethylated, respectively. Immunohistochemistry staining showed that the hypomethylated genes – tumor necrosis factor‐α and interleukin‐6 – were positively expressed under the junctional epithelium area in the diabetes group.ConclusionsDiabetes mellitus induces morphological and epigenetic changes in periodontal tissue, which might contribute to the increased susceptibility of periodontal diseases in patients with diabetes.

The Treponema denticola DgcA protein (TDE0125) is a functional diguanylate cyclase.

Periodontal disease (PD) is a progressive inflammatory condition characterized by degradation of the gingival epithelium, periodontal ligament, and alveolar bone ultimately resulting in tooth loss. Treponema denticola is a keystone periopathogen that contributes to immune dysregulation and direct tissue destruction. As periodontal disease develops, T. denticola must adapt to environmental, immunological and physiochemical changes in the subgingival crevice. Treponema denticola produces bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP), an important regulatory nucleotide. While T. denticola encodes several putative diguanylate cyclases (DGCs), none have been studied and hence the biological role of c-di-GMP in oral treponemes remains largely unexplored. Here, we demonstrate that the T. denticola open reading frame, TDE0125, encodes a functional DGC designated as DgcA (Diguanylate cyclase A). The dgcA gene is universal among T. denticola isolates, highly conserved and is a stand-alone GGEEF protein with a GAF domain. Recombinant DgcA converts GTP to c-di-GMP using either manganese or magnesium under aerobic and anaerobic reaction conditions. Size exclusion chromatography revealed that DgcA exists as a homodimer and in larger oligomers. Site-directed mutagenesis of residues that define the putative inhibitory site of DgcA suggest that c-di-GMP production is allosterically regulated. This report is the first to characterize a DGC of an oral treponeme.

Expression of vitamin D 1α-hydroxylase in human gingival fibroblasts in vivo.

BackgroundVitamin D 1α-hydroxylase CYP27B1 is the key factor in the vitamin D pathway. Previously, we analyzed the expression of CYP27B1 in human gingival fibroblasts in vitro. In the present study, we analyzed the gingival expression of CYP27B1 in vivo.MethodsForty-two patients with periodontitis Stage IV Grade C and 33 controls were recruited. All patients with periodontitis had unsalvageable teeth and part of the wall of the periodontal pocket was resected and obtained after tooth extraction. All controls needed crown-lengthening surgery, and samples of gingiva resected during surgery were also harvested. All the individuals’ gingivae were used for immunohistochemistry and immunofluorescence. In addition, gingivae from seventeen subjects of the diseased group and twelve subjects of the control group were analyzed by real-time PCR.ResultsExpression of CYP27B1 was detected both in gingival epithelia and in gingival connective tissues, and the expression in connective tissues colocalized with vimentin, indicating that CYP27B1 protein is expressed in gingival fibroblasts. The expression of CYP27B1 mRNA in gingival connective tissues and the CYP27B1 staining scores in gingival fibroblasts in the diseased group were significantly higher than those in the control group.ConclusionsExpression of CYP27B1 in human gingival tissues was detected, not only in the fibroblasts of gingival connective tissues, but also in the gingival epithelial cells, and might be positively correlated with periodontal inflammation.

Titanium nanoparticles potentially affect gingival tissue through IL-13α2 receptor expression.

To determine the effects of titanium nanoparticles, that may have been scattered after dental implant placement, on gene and promoter expression, and gingival tissue. Ca9-22 cell lines were used as gingival epithelial cells to assess the effects of titanium dioxide nanomaterials as titanium nanoparticles. Cells were cocultured with or without titanium dioxide nanomaterials prior to gene and promoter expression analysis. Expression of interleukin-13α2 receptor was investigated using real-time quantitative reverse-transcription polymerase chain reaction and immunofluorescence staining. Additionally, the enhanced messenger ribonucleic acid (mRNA) expression of transforming growth factor β1 was analyzed using the same method. Titanium dioxide nanomaterials affected gene and promoter expression in Ca9-22 cells: among the 160 upregulated genes, the upregulation of IL13RA2, which encodes interleukin-13α2 receptor, was the highest (8.625 log2 fold change). Immunofluorescence staining confirmed the increased expression of interleukin-13α2 receptor, which enhanced transforming growth factor β1 expression by stimulation with interleukin-13. Titanium dioxide nanomaterials applied on the gingival epithelium around the dental implant may increase interleukin-13α2 receptor expression. In turn, this can enhance the secretion of transforming growth factor β1, which is known to promote the differentiation of osteoclasts involved in bone resorption, and potentially affect gingival tissue.

Gingival Depigmentation

Gingival hyperpigmentation is the condition where melanin deposition occurs in the suprabasal cell layers of the gingival epithelium. Gingival hyperpigmentation is a multifactorial benign condition which causes esthetic concern to the person. Melanin is a nonhemoglobin-derived pigment formed by melanocytes, which are dendritic cells of neuroectodermal origin in the basal and spinous layers. Melanin is a brown-colored pigment, and it is the result of endogenous pigmentation. The deposition of melanin pigment darkens the color of the gingiva. Many individuals visit the dentist or periodontist to seek the treatment of hyperpigmentation of the gingiva. Gingival pigmentation is usually considered as a genetic factor and affects different races differently. Various treatment modalities are available to remove gingival hyperpigmentation which includes scalpel technique, abrasion using diamond bur, laser therapy, electrosurgery, cryotherapy, chemical cauterization, depigmentation followed by gingival autografts, or platelet-rich fibrin. The present case report describes the case of gingival hyperpigmentation managed by scalpel technique and abrasions by diamond bur which is a simple and a cost-effective technique with satisfactory results.

Amlodipine-induced gingival hyperplasia

Drug-induced gingival hyperplasia is the increased growth of gingival epithelium and submucosa which may cause bleeding and loss of teeth. Certain anticonvulsant, immunosuppressive, and antihypertensive drugs are the underlying cause in most cases. Among them, cases due to amlodipine are very rare. Here, we discuss the topic along with a case of gingival overgrowth induced by amlodipine. A 51-year-old female presented with gingival overgrowth. She was on amlodipine because of primary hypertension. She had gingival hyperplasia increasingly growing in the last few months. Her antihypertensive regimen was changed with cessation of amlodipine. This study suggests that amlodipine may lead to gingival hyperplasia.

Human placental extract a miracle that heals the wound faster

Introduction: Human placental extract gel contains extract of human placenta and total nitrogen not more than 0.25% w/w. It is natural vitamins, peptides, nucleotides and amino acid gel. It enhances wound healing significantly; increases collagen synthesis and improves tensile strength of healing tissue. It brings about maximum increases in the percent of DNA, total protein and epithelialisation. It also has anti-inflammatory and analgesic effects. Aim and Objective: Clinical and histological evaluation of depigmented gingival epithelium on application of human placental extract gel. Material and Method: 10 healthy patients in the age group of 18-35 yrs. who were indicated for depigmentation procedure were selected for the study. Depigmentation was done with scalpel technique on maxillary and mandibular anterior region. In group A human placental extract gel was applied on the wound and non-eugenol pack was placed whereas group B was covered with non-eugenol pack only. Wound Healing index and Visual Analogue Score was assessed after 7 and 15 days. Epithelisation of wound was assessed by using toluidine blue after 7 days of surgery. Result: Application of human placental extract gel showed a statistically significant improvement clinically and histologically. Conclusion: Application of human placental extract can be a successful approach to protect the raw wound area of depigmented gingiva with better patient comfort and faster healing. Introduction: In today's era, increased aesthetic concerns have increased the number of patients receiving gingival depigmentation surgeries to create an aesthetically pleasing appearance of gingiva. Human placental extract gel contains extract of human placenta and total nitrogen not more than 0.25% w/w. It is natural vitamins, peptides, nucleotides and amino acid gel. It enhances wound healing significantly; increases collagen synthesis and improves tensile strength of healing tissue. It brings about maximum increases in the percent of DNA, total protein and epithelialisation. It also has anti-inflammatory and analgesic effects. Aim and Objective: Clinical and histological evaluation of depigmented gingival epithelium on application of human placental extract gel. Material and Method: 10 healthy patients in the age group of 18-35 yrs. who were indicated for depigmentation procedure were selected for the study. Depigmentation was done with scalpel technique on maxillary and mandibular anterior region. In group A human placental extract gel was applied on the wound and non-eugenol pack was placed whereas group B was covered with non-eugenol pack only. Wound Healing index and Visual Analogue Score was assessed after 7 and 15 days. Epithelisation of wound was assessed by using toluidine blue after 7 days of surgery. Result: Application of human placental extract gel showed a statistically significant improvement clinically and histologically. Conclusion: Application of human placental extract can be a successful approach to protect the raw wound area of depigmented gingiva with better patient comfort and faster healing.

Efficacy of glycine powder air-polishing in supportive periodontal therapy: a systematic review and meta-analysis.

PurposeThis systematic review and meta-analysis was conducted to assess the effects of glycine powder air-polishing (GPAP) in patients during supportive periodontal therapy (SPT) compared to hand instrumentation and ultrasonic scaling.MethodsThe authors searched for randomized clinical trials in 8 electronic databases for relevant studies through November 15, 2019. The eligibility criteria were as follows: population, patients with chronic periodontitis undergoing SPT; intervention and comparison, patients treated by GPAP with a standard/nozzle type jet or mechanical instrumentation; and outcomes, bleeding on probing (BOP), patient discomfort/pain (assessed by a visual analogue scale [VAS]), probing depth (PD), gingival recession (Rec), plaque index (PI), clinical attachment level (CAL), gingival epithelium score, and subgingival bacteria count. After extracting the data and assessing the risk of bias, the authors performed the meta-analysis.ResultsIn total, 17 studies were included in this study. The difference of means for BOP in patients who received GPAP was lower (difference of means: −8.02%; 95% confidence interval [CI], −12.10% to −3.95%; P<0.00001; I2=10%) than that in patients treated with hand instrumentation. The results of patient discomfort/pain measured by a VAS (difference of means: −1.48, 95% CI, −1.90 to −1.06; P<0.001; I2=83%) indicated that treatment with GPAP might be less painful than ultrasonic scaling. The results of PD, Rec, PI, and CAL showed that GPAP had no advantage over hand instrumentation or ultrasonic scaling.ConclusionsThe findings of this study suggest that GPAP may alleviate gingival inflammation more effectively and be less painful than traditional methods, which makes it a promising alternative for dental clinical use. With regards to PD, Rec, PI, and CAL, there was insufficient evidence to support a difference among GPAP, hand instrumentation, and ultrasonic scaling. Higher-quality studies are still needed to assess the effects of GPAP.

NETs Are Double-Edged Swords with the Potential to Aggravate or Resolve Periodontal Inflammation.

Periodontitis is a general term for diseases characterised by inflammatory destruction of tooth-supporting tissues, gradual destruction of the marginal periodontal ligament and resorption of alveolar bone. Early-onset periodontitis is due to disturbed neutrophil extracellular trap (NET) formation and clearance. Indeed, mutations that inactivate the cysteine proteases cathepsin C result in the massive periodontal damage seen in patients with deficient NET formation. In contrast, exaggerated NET formation due to polymorphonuclear neutrophil (PMN) hyper-responsiveness drives the pathology of late-onset periodontitis by damaging and ulcerating the gingival epithelium and retarding epithelial healing. Despite the gingival regeneration, periodontitis progression ends with almost complete loss of the periodontal ligament and subsequent tooth loss. Thus, NETs help to maintain periodontal health, and their dysregulation, either insufficiency or surplus, causes heavy periodontal pathology and edentulism.

Expression profile of macrophage migration inhibitory factor in periodontitis

ObjectiveMacrophage migration inhibitory factor (MIF) is a pivotal mediator of host innate immunity and influences the development of several inflammatory diseases. The role of MIF in periodontitis is unclear. MethodsEighteen periodontally healthy volunteers and 18 patients with stage III or IV periodontitis were enrolled. Blood samples and gingival tissues were collected from all individuals. The serum concentrations of MIF and MCP-1 were measured by ELISA. The protein and mRNA levels of MIF and MCP-1 in gingival tissue were evaluated by immunohistochemical staining and quantitative PCR. The levels of secreted MIF and MCP-1, as well as their mRNA levels, were determined by ELISA and quantitative PCR in oral epithelial cells infected with Porphyromonas gingivalis. ResultsAfter adjusting for age, the level of MCP-1 was significantly higher in the serum and gingival tissue of periodontitis patients, as well as in infected epithelial cells. The serum concentration of MIF was increased in periodontitis patients (15.25 ± 2.16 ng/mL, P < 0.05) compared to healthy controls (10.43 ± 1.02 ng/mL). Increased MIF immunoreactivity was found in gingival epithelial tissue but not in the gingival connective tissue of periodontitis patients. The secretion of MIF was 3.82-fold higher in the supernatant of infected cells than in the supernatant of control (P < 0.01). No increase in the MIF mRNA level was found in either gingival tissue or epithelial cells. ConclusionsBased on our limited evidence, we showed the level of MIF was related to periodontal conditions. P. gingivalis may contribute to the development and progression of periodontitis through MIF.

Gingival epithelium attachment to well- or partially cured resin composites.

Ideal restoration material for caries would allow attachment of gingival epithelia. The attachment of epithelial cells to specimens of the 4 most commercially used well- or partially-cured resin composites, with and without TEGDMA, was assessed. Effects of resin composite on the Ca9-22 gingival epithelial cell-line were assessed by measuring the cytotoxicity, viability and gene expression for attachment, apoptosis, ROS-production, pro-inflammatory cytokines, and matrix metalloproteinases. As controls, cells on tissue culture plastic or bovine tooth enamel specimens were used. Significantly less cell attachment was measured on freshly made resin-composite specimens. Concomitantly, significantly higher cytotoxicity was measured in the presence of freshly made resin-composite specimens. However, after 8 d of leakage, the cell attachment to and cytotoxicity of the resin composite was comparable to bovine tooth enamel. Significantly higher expressions of IL6, MMP2, BCL6 and ITGA4 were measured in cells attached to resin-composite surfaces than controls. There were no significant differences between the results using different conditions of resin composite, with or without TEGDMA and well or partially cured. Less cell attachment and presence of more inflammatory markers were observed on all freshly-made resin-composite surfaces. However, after a leakage period attachment of cells to the resin composite improved to the level of natural tooth materials such as enamel. This indicated that the negative effects of resin composites on epithelial cells might be transient.

Repurposing Napabucasin as an Antimicrobial Agent against Oral Streptococcal Biofilms.

Objectives Disruption of microbial biofilms is an effective way to control dental caries. Drug resistance and side effects of the existing antimicrobials necessitate the development of novel antibacterial agents. The current study was aimed at investigating the antibacterial activities of the repurposed natural compound napabucasin against oral streptococci. Methods The minimum inhibitory concentration, minimum bactericidal concentration, minimum biofilm inhibition concentration, and minimum biofilm reduction concentration of Streptococcus mutans, Streptococcus gordonii, and Streptococcus sanguinis were examined by a microdilution method. Cytotoxicity of napabucasin against human oral keratinocytes, human gingival epithelia, and macrophage RAW264.7 was evaluated by CCK8 assays. The dead/live bacterium and exopolysaccharide in the napabucasin-treated multispecies biofilms were evaluated by confocal laser scanning microscopy. Microbial composition within the napabucasin-treated biofilms was further visualized by fluorescent in situ hybridization and qPCR. And the cariogenicity of napabucasin-treated biofilms was evaluated by transverse microradiography. Results Napabucasin exhibited good antimicrobial activity against oral streptococcal planktonic cultures and biofilms but with lessened cytotoxicity as compared to chlorhexidine. Napabucasin reduced the cariogenic S. mutans and increased the proportion of the commensal S. gordonii in the multispecies biofilms. More importantly, napabucasin significantly reduced the demineralization capability of biofilms on tooth enamels. Conclusion Napabucasin shows lessened cytotoxicity and comparable antimicrobial effects to chlorhexidine. Repurposing napabucasin may represent a promising adjuvant for the management of dental caries.

Expression of caveolin-1 in tooth germ, ameloblastoma and ameloblastic carcinoma.

Background The caveolin-1 protein (structural component of membrane caveolae) plays important roles in several biological functions, such as endocytosis, cell adhesion, and cell signaling. However, this protein has been associated with mechanisms of tumorigenesis in several neoplasms. The expression patterns and roles of caveolin-1 in the oral epithelium and in embryonic and odontogenic tumor tissues are still unclear. Material and Methods The expression of caveolin-1 was evaluated in samples of the normal gingival epithelium (n=7), human tooth germ (TG) (n=12), ameloblastoma (AM) (n=83), and ameloblastic carcinoma (AC) (n=9) by immunohistochemistry. Additionally, AM samples were analyzed by qRT-PCR and Western blot. Results Most TG (91.7%), AM (73.5%) and AC (100%) samples showed diverse patterns of immunohistochemical positivity for caveolin-1, while only one gingival sample was positive. The transcript levels of cav-1 were significantly upregulated by 14.9-fold in AM tissue (P = 0.0014) compared to those in normal gingival epithelial tissue, as shown by qRT-PCR. Presence of caveolin-1 protein was confirmed by Western blot analysis. The caveolin-1 immunoexpression patterns throughout the stages of TG show its importance during odontogenesis. Conclusions The overexpression of caveolin-1 in AM and AC compared to its expression in normal gingival epithelium (adult tissue) suggests a possible role of caveolin-1 in protumoral events, but due to the similar immunoexpression observed in AM and AC, caveolin-1 may not necessarily participate in the malignant transformation process. However, future studies are needed to clarify and confirm these hypotheses. Key words:Ameloblastoma, ameloblastic carcinoma, caveolin-1, immunohistochemistry, real-time polymerase chain reaction.

IMMUNOHISTOCHEMICAL EVALUATION OF β DEFENSINS ON INDUCED PERIODONTITIS IN RATS

Abstract . Background: The health of the gingival tissue has an important effect on the general health. Defensins are proteins found in humans as well as other vertebrates. They have antibacterial, antiviral and antifungal functions. Objectives: The purpose of the present study was to assess expression of beta defensin on the gingival epithelium in rats. Methods and materials: A 30 adult Sprague-Dawley male rats were randomly divided into 3 equal groups (n=10), 5 rats for experimental study and other fives as control within each group. Ligatures were placed in the inferior frontal group which acted as a gingival irritant. Scarifications were done after 3 days, one week and two weeks alternative. The levels of defensins were tested in the gingival tissue of all rats. Results: the expression of β defensin 2 showed that there is a statistically significant difference in immunolocalization of Defensin-2 percentage between the 1st group (after 3 days) and control one (P ≤ 0.05), while there is a highly statistical difference when comparing both the 2nd (after 1 week) and third group (after 2 weeks) versus control group (P ≤ 0.01). Conclusions: From the present work, it may assume that, the rat model may be a good system for experimental analysis of the innate immune response to the bacteria in the oral cavity, as well as the potential role of β -defensins in the host response to colonization