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The Dental Connection to Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Alyse Shockey, Lisa Marie Samaha, Dawn Ewing
The initial process of periodontal destruction begins silently and characteristically leads to a breech in the sulcular epithelium, even in its early stage, known as gingivitis. This early stage may be devoid of clinical signs or symptoms, although it is representative of an open wound (Figure 7.7).
Odontogenic Tumors
Published in Dongyou Liu, Tumors and Cancers, 2017
Covering the alveolar processes of the maxilla and mandible and finishing at the neck of each tooth, the gingiva (gums) is a mucosal tissue lined with epithelium. The gingival epithelium is divided into the oral, sulcular, and junctional sections. The oral epithelium comprises stratified squamous keratinizing epithelium, which covers the oral and vestibular gingival surfaces. The sulcular epithelium is continuous with the oral epithelium and lines the gingival sulcus. The junctional epithelium lines the dentoepithelial junction at the bottom of the gingival sulcus.
The Adverse Effects of Alcohol and Drug Abuse in the Oral Cavity
Published in John Brick, Handbook of the Medical Consequences of Alcohol and Drug Abuse, 2012
Terry D. Rees, Robert A. Levine
The oral effects of drugs of abuse have not been studied as extensively as the adverse, mental and general, physiologic changes associated with their use. It is well established, however, that chronic use of mood altering drugs may adversely affect one’s compliance with effective oral hygiene practices and routine dental visits. The oral cavity is often the first site of lesions suggestive of HIV infection, diabetes mellitus, venereal diseases, liver disease, and kidney failure, all of which occur at increased frequency among those who abuse drugs or alcohol. Excessive use of illicit drugs may alter host susceptibility to oral infections and delay wound healing. In addition, nutritional deficiencies secondary to drug or alcohol abuse can have a profound effect on oral soft tissues and bone. For example, vitamin B complex (B1, B2, B6, and B12) deficiencies may be associated with a generalized stomatitis, glossitis, gingivitis, and ulcerations with or without manifestations of stomatodynia (burning mouth) (Abrams and Romberg, 1999). Vitamin B12 deficiency may also induce abnormalities of oral epithelial cells leading to epithelial thinning and increased mitotic activity, potentially increasing the risk for epithelial dysplasia or malignant transformation (Mitchell et al., 1986; Theaker, Porter, and Fleming, 1989). Vitamin C (ascorbic acid) deficiency may adversely affect periodontal connective tissues, capillary integrity, and wound healing, resulting in increased severity of gingivitis and periodontitis (Bsoul and Terezhalmy, 2004). This is probably the result of altered immune function, increased permeability of gingival sulcular epithelium, increased levels of tissue metalloproteins, and retention of extracellular fluid as a result of altered capillary permeability. Prolonged ascorbic acid deficiency (scurvy) may result in severe periodontal pathoses including increased tooth mobility, destruction of the periodontal ligament, osseous abnormalities, and, ultimately, exfoliation of the dentition (Leggott et al., 1991; Touyz, 1997). It should be noted that there is no evidence that mild ascorbic acid deficiency initiates periodontitis. However, Nishida et al. (2000) identified a small but statistically significant increase in periodontitis among current and past smokers and smoking may be ubiquitous among those who abuse drugs.
Critical roles of adherens junctions in diseases of the oral mucosa
Published in Tissue Barriers, 2023
Christina Kingsley, Antonis Kourtidis
The gingival epithelium has been extensively studied due to its implication in periodontal disease. The gingival epithelium is composed of keratinizing stratified epithelium and covers the external surface of the gingiva, which surrounds the teeth (Figure 1).6 An important function of the gingival epithelium is to provide the first line of defense in the oral cavity against pathogens.7 There are several components of the gingiva. The attached gingiva is firmly bonded to the connective tissue over the alveolar bone and is separated from the oral mucosa by the mucogingival line (Figure 1). The attached gingiva is located apically to the gingival sulcus, which is the space surrounding each tooth and is lined by the oral sulcular epithelium (Box 1; Figure 1). This epithelium is stratified and non-keratinized.2 The junctional epithelium is a specialized epithelial component. This epithelium is derived from the enamel epithelium and mediates the attachment of the gingival epithelium to the enamel on the tooth surface (Figure 1).8 This is an important function of the junctional epithelium, because it forms a barrier against pathogens passing from the oral cavity into the tissue that supports the tooth.9 Due to its role, the junctional epithelium isan area of extensive study in periodontal disease,10 where tooth mobility and loss are found. In comparison to the gingival epithelium, the junctional epithelium shows no keratinization and exhibits much higher proliferation and turnover rate2,7,8 (Figure 1).
Gingival epithelial barrier: regulation by beneficial and harmful microbes
Published in Tissue Barriers, 2019
Naoki Takahashi, Benso Sulijaya, Miki Yamada-Hara, Takahiro Tsuzuno, Koichi Tabeta, Kazuhisa Yamazaki
Distinct from the oral epithelium, the gastrointestinal epithelium is composed of a simple layer of columnar epithelial cells. Goblet cells are a major secretory cellular lineage in the intestinal epithelium, synthesizing and secreting mucin into the intestinal lumen. Among other lineages of intestinal epithelial cells, enterocytes are involved in nutrient absorption and immunoglobulin secretion, and Paneth cells can synthesize and produce antimicrobial peptides.23 These specialized epithelial cells are efficient physical and chemical barriers against invading microbes. Unlike the gut, the oral epithelium consists of a stratified squamous epithelium which can be subdivided into three components based on cell morphology: oral epithelium (OE), sulcular epithelium (SE), and junctional epithelium (JE).24 The OE is a keratinizing form of epithelium, providing an effective physical barrier against microbial invasion of the underlying gingival connective tissue. In contrast, SE and JE are dominated by a non-keratinized epithelium,25 which suggests that those epithelia are semipermeable and, thus, allow the transport of macro substances from the gingival sulcus into the underlying connective tissue.
aMMP-8 point-of-care - diagnostic methods and treatment modalities in periodontitis and peri-implantitis
Published in Expert Opinion on Therapeutic Targets, 2023
Hanna Lähteenmäki, Tommi Pätilä, C Pirjo Pärnänen, Ismo Räisänen, Taina Tervahartiala, Shipra Gupta, Timo Sorsa
When we talk about oral fluids it includes saliva, mouth rinse, gingival crevicular fluid (GCF), and peri-implant sulcular fluid (PISF). Total saliva is mixed with GCF which originates in periodontal tissue and is excreted from there in the gingival pocket, as well as PISF similarity corresponds dental implants [43–45]. The saliva of an individual can be used as an objective indicator of his/her disease status [3,20,45,46]. It is easily accessible, and the collection is noninvasive. Saliva and its constituents play an important role in the human defense system by breaking down bacteria, viruses and other pathogens [47]. GCF and PISF are a source of nutrients for microorganisms in biofilms. Biofilm on the surface of the teeth or implant and in the gingival pockets is characterized by proteolytic and often obsessively anaerobic species. Interactions between microbes are a prerequisite for the concerted catabolism of host proteins and glycoproteins. From this follows that some microorganisms weaken the host’s defenses by releasing certain molecules [48,49]. GCF/PISF excretion increases in an inflammatory situation, and its composition is similar to that of an inflammatory fluid. GCF/PISF levels of cytokines in healthy sites have been detected to be lower than those in diseased sites [50]. When pathogenic microbes enter the mouth, the host response is immediately activated to interrupt the progression of pathogen to the tissue [51]. If the defenses fail and the microbes in the metabolic process can penetrate the sulcular epithelium, inflammation of the gums begins [51]. The mouth rinse represents an initiated inflammatory state, in fact, we analyze the GCF with the mouth rinse [52–54].