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Human gingiva. A: Inner gingival epithelium consists of OSE and JE. Bar = 250 m. B: Higher magnification of the JE. Bar = 100 m.
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The continuity of epithelial tissue is collapsed by tooth eruption. The junctional epithelium (JE) is attached to the tooth surface by hemidesmosomes, which constitutes the front-line defense against periodontal bacterial infection. JE constitutively expresses intercellular adhesion molecule-1 (ICAM-1), and neutrophils and lymphocytes penetrate int...
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... gingival epithelium consists of the oral gingival epithelium (OGE), oral sulcular epithelium (OSE), and junc- tional epithelium (JE) (Fig. 1A, B). Among them, the JE attaches to the tooth surface via hemidesmosomes, which forms the front-line of defense against periodontal bacte- rial infection [4,5]. In rodents, the JE is clearly distinguished from OSE (Fig. 2). The JE originates from the enamel organ and constructs the gingival epithelium along with OGE and OSE, which are derived from the oral epithelium [6,7]. The OGE and OSE are keratinized squamous epithelial cells with narrow intercellular space [8,9]. On the contrary, the JE is non-keratinized epithelium and has wide intercellu- lar space (Fig. 3A, B). In addition, many migrating cells such as polymorphonuclear cells (PMNs) and lymphocytes are located within JE [10][11][12][13][14][15] (Fig. 3A, B). The JE shows rapid turnover, which might contribute to its defense against den- tal plaque [16,17]. The structure of the gingival epithelium is maintained by the coordination of epithelial tissues of two different origins. Therefore, the structure, origin, and func- tion of the JE at the dento-gingival junction have been the subject of interest and ...
Citations
... The junctional epithelium (JE), a nonkeratinized epithelium, is a specialized epithelial structure that is in contact with the tooth surface to prevent the invasion of bacteria into the underlying hard and soft tooth-supporting tissues [10,11]. As an epithelial barrier, the JE plays an important role in maintaining gingival and periodontal health [12][13][14]. ...
The junctional epithelium (JE) serves a crucial protective role in the periodontium. High glucose-related aging results in accelerated barrier dysfunction of the gingival epithelium, which may be associated with diabetic periodontitis. Metformin, an oral hypoglycemic therapeutic, has been proposed as a anti-aging agent. This study aimed to clarify the effect of metformin on diabetic periodontitis and explore its mechanism in ameliorating senescence of JE during hyperglycemia. The db/db mice was used as a diabetic model mice and alterations in the periodontium were observed by hematoxylin-eosin staining and immunohistochemistry. An ameloblast-like cell line (ALC) was cultured with high glucose to induce senescence. Cellular senescence and oxidative stress were evaluated by SA-β-gal staining and Intracellular reactive oxygen species (ROS) levels. Senescence biomarkers, P21 and P53, and autophagy markers, LC3-II/LC3-I, were measured by western blotting and quantitative real-time PCR. To construct a stable SIRT1 (Sirtuin 1) overexpression cell line, we transfected ALCs with lentiviral vectors overexpressing the mouse SIRT1 gene. Cellular senescence was increased in the JE of db/db mice and the periodontium was destroyed, which could be alleviated by metformin. Moreover, oxidative stress and cellular senescence in a high glucose environment were reduced by metformin in in-vitro assays. The autophagy inhibitor 3-MA and SIRT1 inhibitor EX-527 could dampen the effects of metformin. Overexpression of SIRT1 resulted in increased autophagy and decreased oxidative stress and cellular senescence. Meanwhile, AMPK (AMP-activated protein kinase) inhibition reversed the anti-senescence effects of metformin. Overall, these results suggest that metformin alleviates periodontal damage in db/db mice and cellular senescence in ALCs under high glucose conditions via the AMPK/SIRT1/autophagy pathway.
... sulcular epithelium (SE) and junctional epithelium (JE) [17]. In humans, the inner epithelium is clearly observed when there is a pathological periodontal pocket [7]. ...
... In the present study, the proliferation rate of peri-implant (inner/outer) epithelium was significantly higher in periodontitis than in peri-implantitis. The JE with rapid turnover [17] originates from the enamel organ and constructs the inner marginal epithelium along with sulcular epithelium, which is derived from the oral epithelium [20] [21]. On the other hand, the inner implant epithelium, which originates from the oral mucosa, has a lower capacity for a proliferative and regenerative mechanism than does the normal inner marginal epithelium [4] [18]. ...
... Histologically, the gingiva is made up of the epithelium and the lamina propria (Fig. 2). The gingival epithelium consists of the oral gingival epithelium (OGE), oral sulcular epithelium (OSE), and junctional epithelium (JE) (Nakamura, 2018). The OGE and OSE are constructed from keratinized squamous epithelial cells with narrow intercellular spaces and therefore form a strong barrier to the penetration of microorganisms into the gingival lamina propria. ...
Periodontitis is a chronic infectious and inflammatory disease of periodontal tissues estimated to affect 70 – 80 % of all adults. At the same time, periodontium, the site of periodontal pathologies, is an extraordinarily complex plexus of soft and hard tissues, the regeneration of which using even the most advanced forms of tissue engineering continues to be a challenge. Nanotechnologies, meanwhile, have provided exquisite tools for producing biomaterials and pharmaceutical formulations capable of elevating the efficacies of standard pharmacotherapies and surgical approaches to whole new levels. A bibliographic analysis provided here demonstrates a continuously increasing research output of studies on the use of nanotechnologies in the management of periodontal disease, even when they are normalized to the total output of studies on periodontitis. The great majority of biomaterials used to tackle periodontitis, including those that pioneered this interesting field, have been polymeric. In this article, a chronological review of polymeric nanotechnologies for the treatment of periodontitis is provided, focusing on the major conceptual innovations since the late 1990s, when the first nanostructures for the treatment of periodontal diseases were fabricated. In the opening sections, the etiology and pathogenesis of periodontitis and the anatomical and histological characteristics of the periodontium are being described, along with the general clinical manifestations of the disease and the standard means of its therapy. The most prospective chemistries in the design of polymers for these applications are also elaborated. It is concluded that the amount of innovation in this field is on the rise, despite the fact that most studies are focused on the refinement of already established paradigms in tissue engineering rather than on the development of revolutionary new concepts.
... Attached gingiva can withstand deformative forces from mastication because of its structure that consists of highly keratinized stratified squamous epithelium with more abundant collagenous fibers within the connective tissue layer. This results in higher stiffness and resistance to mechanical stress compared to alveolar and buccal mucosa, which have a larger proportion of non-keratinized epithelial tissue [21,22]. Goktas et al. [6] found that the biomechanical behavior of oral soft tissues is a function of their structure and location. ...
A new design of an alveolar distractor using nickel–titanium (NiTi) open-coil springs was developed and investigated to produce distraction forces against the tensile forces of porcine attached gingiva to simulate human gingiva. We subjected 15 mm long NiTi open-coil springs (Highland and ORMCO) with three levels of forces (light, medium and heavy) to mechanical testing in a 37 ± 1 °C water bath. Ten strips of porcine mandibular attached gingiva were subjected to tensile tests to determine the resistance force. The forces from the springs were compared with the tensile forces from the porcine attached gingiva. Data between groups were analyzed with independent-samples T-tests (p-value < 0.05). The tensile strength and the Young modulus were greater in buccal compared to lingual porcine attached gingiva. Compared to other spring dimensions and companies, forces generated from 0.014 × 0.036″ ORMCO springs were the highest and could overcome the tensile resistance from porcine attached gingiva over the longest distraction range of 1.6 mm. This preliminary in vitro study introduced a new design of an alveolar distractor incorporated with NiTi open-coil springs that could generate light and continuous forces to overcome the resistance from porcine attached gingiva.
... Cells isolated from other areas of the mouth, such as the papillary layer and junctional epithelium, lack the ability to differentiate into ameloblasts and so cannot secrete amelogenin or transport minerals. As a result, new strategies for cell modeling are needed to reconstruct tooth enamel [Nakamura, 2018]. ...
Enamel tissue, the hardest body tissue, which covers the outside of the tooth shields the living tissue, but it erodes and disintegrates in the acidic environment of the oral cavity. On the one hand, mature enamel is cell-free and, if damaged, does not regenerate. Tooth sensitivity and decay are caused by enamel loss. On the other hand, the tissue engineering approach is challenging because of the unique structure of tooth enamel. To develop an exemplary method for dental enamel rebuilding, accurate knowledge of the structure of tooth enamel, knowing how it is created, and how proteins interact in its structure is critical. Furthermore, novel techniques in tissue engineering for using stem cells to develop enamel must be established. This article aims to discuss current attempts to regenerate enamel using synthetic materials methods, recent advances in enamel tissue engineering, and the prospects of enamel biomimetics to find unique insights into future possibilities for repairing enamel tissue, perhaps the most fascinating of all tooth tissues.
... The epithelium attaches to the tooth and the implant surface via hemidesmosomes and extra cellular matrix (ECM) called the internal basal lamina. 7,8 Laminin-332, composed of α3, β3, and γ2 chains, is an important adhesion protein localized in the basal lamina. 9 Another important part in hemidesmosomes is integrin α6β4, which penetrate through cell membrane and binds to basal lamina protein laminin-332. ...
An adequate mucosal attachment is important when it comes to preventing peri‐implant inflammation. The aim of this study was to compare epithelial cell adhesion and adhesion protein expression on in sol TiO2‐coated and non‐coated zirconia and titanium alloy surfaces. Fifty‐six zirconia and titanium discs were cut, and half of them were coated with bioactive TiO2‐coating. To study the epithelial cell attachment, human gingival keratinocytes were cultivated on discs for 1, 3, 6, and 24 h. The cell proliferation was detected by cultivating cells for 1, 3, and 7 days. In addition, the levels of adhesion proteins laminin y2, integrin α6, β4, vinculin, and paxillin were detected with Western Blot method. Furthermore, high‐resolution imaging of the actin cytoskeleton and focal adhesion proteins was established. Longer‐term cell culture (1–7 days) revealed higher cell numbers on the coated zirconia and titanium discs compared to non‐coated discs. The difference was statistically significant (p < .05) after 24 h on coated zirconia and after 3 and 7 days on coated titanium discs compared to non‐coated discs. Clear induction in the protein levels of laminin y2 and integrin α6 were detected on both coated samples, meanwhile integrin β4 were clearly induced on coated titanium alloy. The microscope evaluation showed significantly increased cell spreading on the coated discs. According to this study, the in sol induced TiO2‐coating increases keratinocyte attachment and the expression of adhesion proteins on coated zirconia and titanium in vitro. Consequently, the coating has potential to enhance the mucosal attachment on implant surfaces.
... Hence for protecting from loss of adhesion, laminin-5 derived peptides have been used. This particular laminin isoform was selected as it is the only laminin isoform expressed in the basal lamina of the dento-gingival interface 56,57 . Multilayered Polyelectrolyte Films (MPF's) were used to trigger cell activation or control cell adhesion. ...
Tissue specificity is the essential need of the hour to cut down clinical abnormalities. Allowing desired drug concentration to reach the target site is the current trend of the drug delivery system. Laminin is an active component of the basal lamina and present in most cells and organs has shown great utility in this case. It is a heterotrimeric glycoprotein containing an α-chain, a β-chain, and a γ-chain and found in different isoforms. Laminin influences cell differentiation, migration, adhesion, neurite outgrowth, and angiogenesis. The active peptides screened from the whole-length laminin have been incorporated to develop targeted or tissue-specific approaches. This is because full-length laminin has many active sites and triggers various downstream signaling and functions. Laminin-derived peptides along with various carriers or vectors ensure specific binding to target tissues. The particular therapeutic or diagnostic agent is successfully targeted to the diseased site because of the affinity of peptide sequence towards the cell membrane receptors. Promising applications of laminin-derived peptides are observed in diagnostics, therapy, chemotherapy, and gene therapy. It helps in tumor imaging, delivers cancer therapeutics, and serves as a biomarker. Implant surfaces coated with laminin-derived peptides enhance attachment and biocompatibility and decreases peri-implant inflammation. Having able to influence angiogenesis, it has been found to serve the purpose in the tissue healing process too. Many other effective applications of laminin-derived peptides might be developed with advancing days, but to date, it accounts as one of the promising theranostic approaches.
... The JE is non-keratinized, has large intercellular spaces, and adheres to the tooth surface through hemidesmosomes; therefore, the JE differs from the OGE in terms of histology and morphology 34 . Using a bioengineered tooth technique, we demonstrated that the JE of the transplanted teeth is derived from an odontogenic epithelium different from the OGE 35 . ...
The junctional epithelium (JE) is an epithelial component that attaches directly to the tooth surface and performs the unique function of protecting against bacterial infections; its destruction causes inflammation of the periodontal tissue and loss of alveolar bone. A recent study that used the single-color lineage tracing method reported that JE is maintained by its stem cells. However, the process by which individual stem cells form the entire JE around a whole tooth remains unclear. Using a 4-color lineage tracing method, we performed a detailed examination of the dynamics of individual stem cells that constitute the entire JE. The multicolor lineage tracing method showed that single-color areas, which were derived from each cell color, replaced all the constituent JE cells 168 d after the administration of tamoxifen. The horizontal section of the first molar showed that the single-color areas in the JE expanded widely. We detected putative stem cells at the external basal layer farthest from the enamel. In this study, JE cells that were supplied from different stem cells were visualized as individual monochromatic regions, and the JE around the first molar was maintained by several JE-specific stem cells. These findings indicated that the JE consisted of several cell populations that were supplied from their multiple stem cells and could help to explore the mechanisms involved in periodontal tissue homeostasis.
... The gingival epithelium consists of the junctional epithelium (JE) originating from the enamel organ during tooth eruption, oral gingival epithelium (OGE), and oral sulcular epithelium (OSE) originating from the oral epithelium (Matsson et al. 1979;Nanci and Bosshardt 2006). The OGE and OSE are keratinized squamous epithelia, while the JE is composed of non-keratinized epithelial cells with wider intercellular space compared with the first two (Matsson et al. 1979;Squier 1981;Nakamura 2018), making JE the weakness zone of the periodontium. JE attaches to the tooth surface via hemidesmosomes and contacts close to the underlying connective tissue through epithelial spikes, sealing the interspaces around the teeth. ...
... There are four intercellular protein complexes, including tight junctions (TJs), adherens junctions (AJs), desmosomes, and gap junctions. Many polymorphonuclear cells (PMNs) and lymphocytes can be observed within the JE (Nakamura 2018;Soda et al. 2019), together with inflammatory factors, endotoxin, and metabolite of bacteria, destroying the periodontal tissue during inflammation, which leads to the migration of JE, the formation of the periodontal pocket, and eventually tooth loss (Vicencio et al. 2020). ...
Junctional epithelium (JE) attaching to the enamel surface seals gaps around the teeth, functioning as the first line of gingival defense. Runt-related transcription factor 2 (Runx2) plays a role in epithelial cell fate, and the deficiency of Runx2 in JE causes periodontal destruction, while its effect on the barrier function of JE remains largely unexplored. In the present study, hematoxylin–eosin (H&E) staining revealed the morphological differences of JE between wild-type (WT) and Runx2 conditional knockout (cKO) mice. We speculated that these changes were related to the down-regulation of E-cadherin (E-cad), junctional adhesion molecule 1 (JAM1), and integrin β6 (ITGB6) in JE. Moreover, immunohistochemistry (IHC) was conducted to assess the expressions of these proteins. To verify the relationship between Runx2 and the three above-mentioned proteins, human gingival epithelial cells (HGEs) were cultured for in vitro experiment. The expression of Runx2 in HEGs was depleted by lentivirus. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were adopted to analyze the differences in mRNA and protein expressions. Taken together, Runx2 played a crucial role in maintaining the structure and function integrality of JE via regulating the expressions of E-cad and JAM1.
... The coronal (upper) end of the crevice in Figure 3 is open to saliva, but its base is sealed by junctional epithelium (JE), also called the epithelial attachment [25]. The dentally and stromally attached cells of JE maintain a proliferative phenotype that renews the entire JE in about a week [25][26][27]. During this time, the older progeny differentiates into unattached squamous cells that make up the central portion of the JE, a region of loose intracellular junctions containing few desmosomes, as well as a few adherens and gap junctions. ...
Periodontal disease is a common, bacterially mediated health problem worldwide. Mastication (chewing) repeatedly traumatizes the gingiva and periodontium, causing traces of inflammatory exudate, gingival crevicular fluid (GCF), to appear in crevices between the teeth and gingiva. Inadequate tooth cleaning causes a dentally adherent microbial biofilm composed of commensal salivary bacteria to appear around these crevices where many bacteria grow better on GCF than in saliva. We reported that lysine decarboxylase (Ldc) from Eikenella corrodens depletes the GCF of lysine by converting it to cadaverine and carbon dioxide. Lysine is an amino acid essential for the integrity and continuous renewal of dentally attached epithelium acting as a barrier to microbial products. Unless removed regularly by oral hygiene, bacterial products invade the lysine-deprived dental attachment where they stimulate inflammation that enhances GCF exudation. Cadaverine increases and supports the development of a butyrate-producing microbiome that utilizes the increased GCF substrates to slowly destroy the periodontium (dysbiosis). A long-standing paradox is that acid-induced Ldc and butyrate production support a commensal (probiotic) microbiome in the intestine. Here, we describe how the different physiologies of the respective tissues explain how the different Ldc and butyrate functions impact the progression and control of these two chronic diseases.
