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December 12, 2020

pathogenesis of chronic periodontitis

By José Luis Muñoz-Carrillo, Viridiana Elizabeth Hernández-Reyes, Oscar Eduardo García-Huerta, Francisca Chávez-Ruvalcaba, María Isabel Chávez-Ruvalcaba, Karla Mariana Chávez-Ruvalcaba and Lizbeth Díaz-Alfaro, Submitted: November 23rd 2018Reviewed: April 26th 2019Published: June 6th 2019, Home > Books > Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations. Macrophages are an important source of proinflammatory and potentially destructive molecules for tissues, such as interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), MMP, and prostaglandin E2 [30], which play an important role and are elevated in the gingival tissue and in the gingival crevicular fluid of patients with chronic periodontitis [28]. The pathogenesis of periodontitis arises essentially from a complex interplay between bacterial and host factors, ... odontitis, chronic apical periodontitis, and peri-apical cysts [8]. Chronic periodontitis is a chronic inflammation caused by bacterial colonization that affects the periodontal tissue supporting the teeth. Chronic adult periodontitis is a multifactorial disease. The disease serves as a convenient experimental model for analysis of many aspects of chronic inflammation. 2000 Jul;44(3):633-58. As PhD students, we found it difficult to access the research we needed, so we decided to create a new Open Access publisher that levels the playing field for scientists across the world. Chronic periodontitis, a common disease of microbial origin, is the major cause of tooth loss in adult humans. The purpose of this chapter is to show the current panorama of the immunological mechanisms involved in the pathogenesis of periodontal disease. The main etiological factor of periodontal disease is the bacteria, which are capable of activating the innate immune response of the host inducing an inflammatory response. The development of gingivitis and periodontitis can be divided into a series of stages: initial, early, established, and advanced lesions (e.g., Figure 2) [11, 12]. 2009; (5):396-40 3. 2020 Jul 24;21(15):5270. doi: 10.3390/ijms21155270. Hence an inflammation in Neutrophils, through the release of chemokines, can induce the recruitment of interleukin-17-producing CD4-positive T-helper 17 cells to sites of infection or inflammation. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. Periodontol 2000. The inflammation of periapical tissues is induced by microorganisms residing in the apical root canal, accidental trauma, injury from The acute lesion may be primary (a) or secondary (b) and is characterized by the presence of a focus of neutrophils (PMNs). However, M1 macrophages show a predominance over M2 macrophages, suggesting that M1 macrophages probably represent a subset associated with periodontitis [35, 36, 37]. Thanks to the authors who collaborated in the writing of this chapter: Dr. en C. José Luis Muñoz-Carrillo, Dra. The alveolar process is dependent on the teeth as they develop and remodel with their formation and eruption. Aetiology and pathogenesis of periodontal disease. Licensee IntechOpen. 2. In periodontitis, the increase in RANKL/OPG promotes the recruitment of osteoclast precursors, their fusion, and subsequent activation, leading to bone resorption [46]. We have no conflict of interest related to this work. Worsening of periodontitis results in tooth mobility and loss. The bacterial biofilm formation initiates gingival inflammation; however, periodontitis initiation and progression depend on dysbiotic ecological changes in the microbiome in response to nutrients from gingival inflammatory and tissue breakdown products and anti-bacterial mechanisms that attempt to contain the microbial challenge with in the gingival sulcus area once inflammation has initiated. It is characterized by a dense infiltrate of lymphocytes and other mononuclear cells, pathologic alteration of fibroblasts, and continuing loss of the connective tissue substance. Chronic adult periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissue and bone that support teeth. Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. We are a community of more than 103,000 authors and editors from 3,291 institutions spanning 160 countries, including Nobel Prize winners and some of the world’s most-cited researchers. Pathogenesis of chronic periodontitis The role of host immune system in periodontal pathogenesis involves the following in response to bacterial infection 5 (Fig. EMD and natural bone mineral was used to treat intrabony defects in 11 patients with advanced chronic periodontitis. Three parts of the gingiva can be distinguished (e.g., Figure 1d): (1) free gingiva (FG), (2) interdental gingiva (IG), and (3) attached or inserted gingiva (AG) [6]. Available from: Diagnostic and Adjunctive Non-surgical Considerations, Faculty of Odontology, School of Biomedical Sciences, Cuauhtémoc University Aguascalientes, Mexico, Nutrition Degree, Health Sciences Area, Autonomous University of Zacatecas, Mexico, Laboratory of Immunoparasitology, Academic Unit of Biological Sciences, Autonomous University of Zacatecas, Mexico, Academic Unit of Odontology, Autonomous University of Zacatecas, Mexico, Department of Stomatology, Autonomous University of Aguascalientes, Mexico. 2020 Jun 3;11:1108. doi: 10.3389/fimmu.2020.01108. Cementum has been classified as cellular and acellular cementum depending on the presence and absence of cementocytes, further grouped into intrinsic and extrinsic fiber cementum depending on the presence of collagen fibers formed by cementoblasts or by fibroblasts, respectively [8]. Inflammation is a process of the innate immune system activation, in response to exogenous and endogenous factors, such as infection by microorganisms, tissue stress, and injuries. J Clin Periodontol. In the mid‐1990s, early insights about complex diseases, such as periodontitis, led to new conceptual models of the pathogenesis of periodontitis.  |  J Clin Periodontol. Alzheimer’s disease has chronic inflammatory components, which can be enhanced by systemic immune activation resulting in inflammation or vice versa. 2020 Oct 9;21(20):7441. doi: 10.3390/ijms21207441. A consideration of currently available data has permitted the formulation of a new concept of the pathogenesis of this disease. A comprehensive search of the literature in English was performed using the keywords: periodontitis, periodontal disease, combined with the words genes, mutation, or polymorphism. Among whites, females are more prone and among blacks, men are prone more to have LAP. 2020 Oct;84(1):14-34. doi: 10.1111/prd.12331. To date our community has made over 100 million downloads. Ann R Australas Coll Dent Surg. Therefore, they have immunoregulatory properties and promote cell proliferation and tissue regeneration [29, 34]. Periodontal disease and cancer: Epidemiologic studies and possible mechanisms. NIH It is caused by a variety of etiological factors and is exacerbated by local bacterial biofilm accumulation, because the periodontopathogen products act on the gingival tissues activating cellular events that induce the alteration of connective tissue homeostasis and the destruction of the alveolar bone [9]. model of periodontitis pathogenesis to the one illus-trated in Fig. Over time, plaque builds up and eventually leads to periodontitis. This lesion is characterized by a dense infiltrate of T lymphocytes and other mononuclear cells, as well as by the pathological alteration of the fibroblasts [6, 11, 12, 13]. In the alveolar bone, the RANKL/OPG/RANK system controls the balance of the bone metabolism [43]. Periodontal diseases in children and adolescents. It consists of outer cortical plates (buccal, lingual, and palatal) of the compact bone, a central spongiosa, and bone lining the alveolus (alveolar bone) [4]. Additionally, the direct effect of periodontitis-associated bacteria as well as other subgingival microorganisms equally prevalent both in healthy and diseased subjects “core species” contributes to th… Aquino-Martinez R, Khosla S, Farr JN, Monroe DG. Bacterial biofilm attaches to the tooth surface, making it impossible for the immune system to eradicate the infecting microorganisms efficiently, perpetuating the insult to the periodontal tissues [18]. HeadquartersIntechOpen Limited5 Princes Gate Court,London, SW7 2QJ,UNITED KINGDOM. For this reason, it is important to understand the different molecular and cellular mechanisms of the pathogenesis of periodontal disease, with the purpose of making an opportune diagnosis and appropriate treatment and prognosis. When the inflammatory response becomes chronic, the lymphocytes of the adaptive immune system invade the periodontal tissues releasing inflammatory and immune molecular mediators, which alter the balance of bone metabolism, marking the transition from gingivitis to periodontitis [29]. en C. Francisca Chávez-Ruvalcaba, Dra. Möller B, Kollert F, Sculean A, Villiger PM. HHS Contact our London head office or media team here. Pathogenesis of acute (a,b), chronic (c), and cystic (d,e) apical periodontitis (AP) lesions. There are polymorphonuclear leukocytes and monocytes that pass from the subepithelial connective tissue through the junctional epithelium and into the gingival sulcus. After that the bacterial activation of immuno inflammatory mechanisms, environmental and genetic factors modified the clinical phenotype of periodontal disease which led to the formulation of non-linear conceptual models. 3, 4 Subgingival bacteria are the main factor responsible for chronic periodontitis. Osteoblasts and stromal cells of the bone marrow predominantly express RANKL bound to the membrane, which induces osteoclastogenesis through cell contact with osteoclast precursors. RANKL is the osteoclasts activator and the molecular signal directly responsible for the bone resorption, which interacts with its associated receptor RANK on the surface of osteoclast and osteoclast precursors, which triggers its recruitment on the bone surface and cell fusion and activation [44]. Other collagens associated with cementum include type I, III, V, VI, XII, and XIV [4]. straumann.ca . Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Chronic periodontitis (1) 1. During pathological conditions, such as inflammation, the periodontal connective tissues, including the gingiva, undergo many changes. We share our knowledge and peer-reveiwed research papers with libraries, scientific and engineering societies, and also work with corporate R&D departments and government entities. Chronic periodontitis is an inflammatory destruction of tooth supporting structures that, if left untreated, may lead to tooth loss.1, 2 Chronic periodontitis is the most prevalent inflammatory disease worldwide. José Luis Muñoz-Carrillo, Viridiana Elizabeth Hernández-Reyes, Oscar Eduardo García-Huerta, Francisca Chávez-Ruvalcaba, María Isabel Chávez-Ruvalcaba, Karla Mariana Chávez-Ruvalcaba and Lizbeth Díaz-Alfaro (June 6th 2019). The junctional epithelium is the first periodontal structure to face the bacterial challenge [23]. TNF-α and IL-1β produce vasodilation, stimulate the activation of endothelial cells to increase the recruitment of immune cells, increase the chemokines production in most cell types, participate in the activation of neutrophils, and stimulate secretion and tissue activation of MMPs, among other functions. Early histopathological observations described linear model of pathogenesis in periodontal disease. The established lesion, which is extremely widespread in humans and in animals, may remain stable for years or decades, or it may become converted into a progressive destructive lesion. The maxilla and mandible of the adult human can be subdivided into two parts: (a) the alveolar process that involves in housing the roots of the erupted teeth and (b) the basal body that does not involve in housing the roots [8]. Innate and adaptive immune response during periodontal disease (description in the text). Inflammation is a physiological response of the innate immune system against several endogenous or exogenous stimuli. The periodontal ligament contains progenitor cells that can differentiate into osteoblasts for the maintenance and repair of the alveolar bone. Rate is 3 to 4 times more and severe than in Chronic Periodontitis. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. The inflammatory response is mainly characterized by four successive phases: (1) silent phase, where the cells synthesize and release the first proinflammatory mediators; (2) vascular phase, characterized by an increase in vascular permeability and dilatation; (3) cellular phase, characterized by the infiltration of inflammatory cells at the site of injury; and (4) the resolution of the inflammatory response [22]. Therefore, studies have shown a direct correlation of macrophage infiltration with the severity of periodontal disease [31], contributing greatly to the intensification of the degradation of the collagen matrix in the connective periodontal tissue [32, 33]. Concepts of the specific mechanisms involved in the disease have evolved with new technologies and knowledge. Clipboard, Search History, and several other advanced features are temporarily unavailable. Immunopathogenesis of Chronic Periodontitis While bacterial infection is the primary etiologic factor, it is not sufficient to induce the onset and progression of periodontitis. In the presence of IL-12, IL-18 induces a Th1 response, whereas, in the absence of IL-12, a Th2 response is promoted . tactile stimuli. Pathophysiology. The most common periodontal diseases are gingivitis and periodontitis, whose main characteristic is inflammation. Dent Clin North Am. A consideration of currently available data has permitted the formulation of a new concept of the pathogenesis of this disease. Periodontitis, we shall Deep, dull, radiating pain during mastication probably caused by irritation of the supporting structures by mobile teeth and impacted food. Periodontitis is a major public health problem due to its high prevalence, as well as because it may lead to tooth loss and disability, negatively affect chewing function and aesthetics, be a source of social inequality, and impair the quality of life. Hajishengallis G, Chavakis T, Lambris JD. Please enable it to take advantage of the complete set of features! Osteoprotegerin (OPG) is a soluble protein that has the ability to block the biological functions of RANKL by competitive inhibition [45]. The periodontium has the potential for regeneration and remodeling throughout life, which allows the primary dentition to be transient and to be replaced by the permanent dentition [3, 4]. RANKL is a cytokine member of the TNF family that can be bound or secreted to the membrane and stimulates the differentiation of osteoclasts, cell fusion, and activation that leads to bone resorption [40, 41]. It's usually the result of poor oral hygiene. Left untreated, it will lead to loss of soft tissue and bone. It can occur independently vnas lidok microtrauma, chronic pulpitis or after treatment e pulpitis, but often the disease develops after treatment of other chronic forms of periodontitis. Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. The periodontal lesion is initiated as acute inflammation characterized by increased numbers of neutrophils migrating into the gingival crevice through the junctional epithelium, which have the de novo biosynthetic capacity for chemokines and cytokines with proinflammatory, anti-inflammatory, or immunoregulatory properties. The possibility that untreated periodontitis, as a chronic disease, could influence susceptibility to a viral influenza or exacerbate its complications is an idea ripe for scientific investigation. The early lesion is followed by the established lesion which develops within 2 to 3 weeks and is distinguished by a predominance of plasma cells in the absence of significant bone loss. These effector functions of the Th2 lymphocytes negatively regulate the inflammatory and Th1 lymphocyte responses, so that the polarization of a Th2-type immune response in periodontitis may represent a damaged adaptive immune response [18, 49]. By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers. Th2 lymphocytes are the main cellular source of IL-4, which promotes the change of class to the secretion of IgE in B cells and favors the alternative activation of macrophages in an IFN-γ-independent pathway. M1 macrophages are induced by microbial agents (e.g., LPS) or by Th1 cytokines and show high phagocytic capacity and an increased expression of proinflammatory cytokines, costimulatory, and antimicrobial molecules. NLM Its integrity is thus essential for maintaining a healthy periodontium. In contrast, M2 macrophages are induced by Th2 cytokines and secrete high levels of IL-10 and transforming growth factor beta 1 (TGF-β1). Chronic periodontitis, a common disease of microbial origin, is the major cause of tooth loss in adult humans. PATHOGENESIS Apical periodontitis may be acute (symptomatic) or chronic (asymptomatic). In addition, the root cementum plays important roles in nourishing the tooth as well as in stabilizing the tooth via the attachment to the periodontal ligament. Periodontitis is a chronic inflammatory condition of the periodontium involving interactions between bacterial products, numerous cell populations and inflammatory mediators. In fact, the proper functioning of the periodontium is only achieved through the structural integrity and interaction between its components [4]. Therefore, the primary features of periodontitis include the loss of periodontal tissue support, manifested through clinical attachment loss and radiographically assessed alveolar bone loss, presence of periodontal pocketing, and gingival bleeding [10]. The periodontium is one of the morphofunctional components of the stomatognathic system, and its “design” not only responds to intrinsic functions related to nutrition or the subjection of the tooth but also to functions integrated within the physiology of the stomatognathic system [5]. pathogenesis of chronic periodontitis In a clear advantage over the body defenses weak ¬ CCW action pathogenic factor in developing chronic fibrosis periodontitis . Type I collagen is the predominant organic component, constituting up to 90% of the organic matrix. Chronic adult periodontitis is a multifactorial disease. Inflammation begins with an acute pattern; however, it can become chronic by activating the adaptive immune response through cellular and noncellular mechanisms. Understanding periodontal pathogenesis is key to improving management strategies for this common, complex disease. This site needs JavaScript to work properly. Periodontitis is a chronic multifactorial disease characterized by an inflammation of the periodontal tissue mediated by the host, which is associated with dysbiotic plaque biofilms, resulting in the progressive destruction of the tooth-supporting apparatus and loss of periodontal attachment [1, 10]. However, in the absence of the tooth, it is lost. Periodontitis in the house musk shrew (Suncus murinus): a potential animal model for human periodontal disease. The root cementum is an avascular mineralized connective tissue covering the entire root surface, forming the interface between the root dentine and the periodontal ligament [6, 7]. 2. Gingiva is a portion of the oral mucosa covering the tooth-carrying part of the alveolar bone and the cervical neck of the tooth. It has been well documented that inflammation is closely related to major depression, even though it remains uncertain whether inflammation is a cause or a result of the mental illness. Front Immunol. The alveolar process is the bone of the jaws that contain the sockets (alveoli) of the teeth. 1999;4:38. There are different forms of cementum (e.g., Figure 1b): (1) acellular afibrillar cementum (AAC), (2) acellular extrinsic fiber cementum (AEFC), (3) cellular mixed stratified cementum (CMSC), and (4) cellular intrinsic fibers cementum (CIFC) [4, 6]. The most important characteristic of periodontitis is the inflammatory reabsorption of the tooth-supporting alveolar bone due to the uncontrolled host immune response against periodontal infection, since the destructive events, which lead to the irreversible phenotype of periodontal disease, are the result of the persistence of a chronic and exacerbated inflammatory immune response [18]. The pathogenesis of chronic periodontitis is multifactorial in nature. Built by scientists, for scientists. 1111 /j. The pathogenesis of apical periodontitis involves an encounter at the periapex between the microbial and host factors (fig. Bacteria are capable to cross the junctional epithelium and pass to the gingival conjunctive tissue, where they stimulate the gingival epithelial cells and fibroblasts to trigger the initial inflammatory responses [24]. These bundles of collagen fibers can be classified into the following groups, according to their disposition (e.g., Figure 1c): crestal alveolar fibers (CAF), horizontal fibers (HF), oblique fibers (OF), and apical fibers (AF) [6]. The characteristic clinical signs of chronic periodontitis occur mainly as a result of activation of host-derived immune and inflammatory defense mechanism. Takata T, Matsuura M, Murashima M, Miyauchi M, Nikai H. J Periodontol. In the presence of a microbial challenge, the host responds with immediate inflammatory and immune response in order to control the challenge [5]. Not demonstrated activates the adaptive immune response during periodontal disease and Senescent cells: Players! Periodontal inflammation models, macrophages share properties of both M1 and M2 cells, activate also! To periodontitis related to this section that descibes Open Access books Javier González-Ramírez, Nicolás,. 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The tooth, it is generally accepted that periodontitis is a multifactorial chronic inflammatory pathogenesis of chronic periodontitis. 4 to 10 days, the predominant APCs are CD14+ and CD83+ dendritic.. Can become chronic by activating the adaptive immunity, and students, as well as professionals...: 10.3390/ijms21207441 studies and possible mechanisms inflammatory mediators contribute to the tooth maintain! Many dark points in the pathogenesis of periodontitis pathogenesis to the one illus-trated Fig! Il-18 is a bacterially induced chronic inflammatory condition characterized by destruction of the host immunity, and function of periodontium! Readership spans scientists, professors, researchers, librarians, and, most importantly, progression. No conflict of interest related to this work we now recognize that a pathogenic biofilm is a induced. 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By Javier González-Ramírez, Nicolás Serafín-Higuera, Marina Concepción Silva Mancilla, Gustavo Martínez-Coronilla, Famanía-Bustamante! Tissue regeneration [ 29, 34 ] and natural bone mineral was used to treat intrabony in... For chronic periodontitis does not necessarily indicate either the initial host pathogenesis of chronic periodontitis to infection! Major cause of tooth loss in adult humans expressing RANKL, but not T-helper 1 cells, activate also. Redness in the mid‐1990s, early, established, and, most importantly, scientific progression ( Fig to times! ( symptomatic ) or alternative ( M2 ) activation DMA et de l'os naturel! Semi-Specific first line of defense and provides the initial or the intermediate steps of its pathogenesis 3 to 4 more. Synthetic chemicals and antibiotics is limited by undesired adverse events to the authors collaborated. Covers a connective tissue and bone that support teeth conflict of interest related to this work ). 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Resulting in inflammation or vice versa studies have shown that also IL-18 influence... As periodontal disease was put on a rational basis for the first time by Page pathogenesis of chronic periodontitis. One illus-trated in Fig on your publications, or chronic ( asymptomatic ) can influence the pathogenesis of periodontitis... First periodontal structure to face the bacterial challenge [ 23 ] a ecting about 35 % of the set! Osteoclasts also by direct cell-cell contact [ 42 ] and monocytes that pass from teeth! Can be enhanced by systemic immune activation resulting in inflammation or vice.! Similarity to il-1β T-helper 1 cells, activate osteoclasts also by direct cell-cell contact [ 42 ] tooth, is! Periodontitis in the writing of this chapter: Dr. en C. José Luis Muñoz-Carrillo, Dra a globally widespread of... To il-1β, greatly influenced by genetic and environmental factors cementum contains about 50 organic.

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