In the mid‐1990s, early insights about complex diseases, such as periodontitis, led to new conceptual models of the pathogenesis of periodontitis. Soluble RANKL can induce osteoclastogenesis independently of direct contact between infiltrating lymphocytes and osteoclast precursors on the bone surface. These resident periodontal cells detect bacterial PAMP, such as lipopolysaccharide (LPS) , which binds to the Toll-like receptors (TLR4/2), triggering the recruitment of several protein kinases in the cytoplasmic end of the receptors, ultimately causing the activation of proinflammatory transcription factors, such as nuclear factor kappa B (NFκB) and activator protein 1 (AP-1) , which induces the synthesis and release of mediators to trigger the inflammatory response. IL-1 and TNF induce expression of other mediators that amplify the inflammatory response, such as prostaglandins, and lead to production of lytic enzymes and stimulate the production of chemokines. Several studies have shown that also IL-18 can influence the pathogenesis of chronic periodontitis [46–51]. These macrophages may undergo a classical (M1) or alternative (M2) activation. PATHOGENESIS Apical periodontitis may be acute (symptomatic) or chronic (asymptomatic). In contrast, M2 macrophages are induced by Th2 cytokines and secrete high levels of IL-10 and transforming growth factor beta 1 (TGF-β1). Osteoprotegerin (OPG) is a soluble protein that has the ability to block the biological functions of RANKL by competitive inhibition . Le DMA et de l'os minéral naturel ont été utilisés pour traiter des défauts intraosseux chez 11 patients présentant une parodontite chroniqu avancée. In a clear advantage over the body defenses weak ¬ CCW action pathogenic factor in developing chronic fibrosis periodontitis. 1111 /j. 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. Therefore, studies have shown a direct correlation of macrophage infiltration with the severity of periodontal disease , contributing greatly to the intensification of the degradation of the collagen matrix in the connective periodontal tissue [32, 33]. The knowledge of how immune mechanisms and inflammatory responses are regulated is fundamental to understanding the pathogenesis of periodontal disease. IL-18 is a potent proinflammatory cytokine with structural similarity to IL-1β . The alveolar process is dependent on the teeth as they develop and remodel with their formation and eruption. By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers. model of periodontitis pathogenesis to the one illus-trated in Fig. It is generally accepted that periodontitis is initiated by complex and diverse microbial biofilms which form on the teeth, i.e. The initial lesion begins 2–4 days after the accumulation of the microbial plaque. Concepts of the specific mechanisms involved in the disease have evolved with new technologies and knowledge. Inflammation is a physiological response of the innate immune system against several endogenous or exogenous stimuli. 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. Other collagens associated with cementum include type I, III, V, VI, XII, and XIV . 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]. PATHOGENESIS OF CHRONIC PERIODONTITIS. Chronic adult periodontitis is a multifactorial disease. Chronic usage of synthetic chemicals and antibiotics is limited by undesired adverse events to the host. Chronic periodontitis, a common disease of microbial origin, is the major cause of tooth loss in adult humans. In fact, the proper functioning of the periodontium is only achieved through the structural integrity and interaction between its components . The inflammatory response consists of four main components: (1) endogenous or exogenous factors, such as molecular patterns associated with pathogens (PAMP) and damage (DAMP), which are derived from bacteria, viruses, fungi, parasites, and cell damage, as well as toxic cellular components or any other harmful condition; (2) cellular receptors that recognize these molecular patterns (PRR), for example, Toll-like receptors (TLR); (3) proinflammatory mediators, such as cytokines, chemokines, the complement system, etc. Periodontitis is a globally widespread pathology of the human oral cavity. Periodontal disease is an inflammatory disease of the gum caused by a formation of a plaque that triggers immune responses and inflammation leading to the destruction of tissues surrounding and supporting the teeth. 3). Although neither IL-1β nor TNF-α is directly involved in the stimulation of bone resorption, they indirectly promote bone destruction by stimulating sustained inflammation of the periodontal tissue . Likewise, junctional epithelial cells differ considerably from those of the gingival epithelium. The inflammation of periapical tissues is induced by microorganisms residing in the apical root canal, accidental trauma, injury from The association between inflammation and major depression has been supported by the well-known clinical observation that pro-inflammatory cytokines such as interferon (IFN)-α, which is used to treat hepatitis C, renal cancer, and multiple myeloma, and interleukin (IL)-2, which is used to treat renal cancer and angiosarco… Ann R Australas Coll Dent Surg. *Address all correspondence to: firstname.lastname@example.org, Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations. Gingiva is a portion of the oral mucosa covering the tooth-carrying part of the alveolar bone and the cervical neck of the tooth. Pathogenesis of acute (a,b), chronic (c), and cystic (d,e) apical periodontitis (AP) lesions. Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. Current understanding of periodontal disease pathogenesis and targets for host-modulation therapy. Chronic periodontitis, the most common form of periodontitis, causes swelling and redness in the gums. Inflammation begins with an acute pattern; however, it can become chronic by activating the adaptive immune response through cellular and noncellular mechanisms. Periodontitis in the house musk shrew (Suncus murinus): a potential animal model for human periodontal disease. CP is highly prevalent, a ecting about 35% of adults >30 years of age . Type I collagen is the predominant organic component, constituting up to 90% of the organic matrix. Chronic adult periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissue and bone that support teeth. According to the Global Oral Health Programme, conducted by the World Health Organization (WHO), around 5-15% of the global population (34-45 years of age) suffer from severe periodontitis Brief introduction to this section that descibes Open Access especially from an IntechOpen perspective, Want to get in touch? Deo V, Bhongade ML. Subsequently, the established lesion develops within 2–3 weeks. The evolution of this inflammatory response culminates in the destruction of periodontal tissues. Smoking, through dysfunction of antioxidant system, plays an important role in the pathogenesis of inflammatory diseases.The current study aimed at comparing salivary antioxidant capacity in smokers and non-smokers with severe chronic periodontitis.In this case-control study, among patients referred to … Chronic periodontitis (CP; Figure 1) is a multifactorial inflammatory disease associated with dysbiotic dental plaque biofilms and characterized by progressive destruction of the tooth‐supporting structures.1 CP is a major public health problem due to its high prevalence and because it may lead to tooth loss and disability. Contents Pathophysiology Edit Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. It is important to understand that each of the periodontal tissues has a very specialized structure and that these structural characteristics directly define the function. X-ray diagnostics of apical periodontitis. This enables the tooth to maintain its relationship to adjacent and opposing teeth . | The purpose of this chapter is to show the current panorama of the immunological mechanisms involved in the pathogenesis of periodontal disease. Open Access is an initiative that aims to make scientific research freely available to all. Chronic periodontitis (CP) is an inﬂammatory disease of the gingiva, accompanied by the loss of supportive connective tissues, including the periodontal ligament and alveolar bone . Periodontitis is a multifactorial chronic inflammatory oral disease caused by dental plaque (mostly bacterial plaque) biofilm. (c) Bundles of collagen fibers: crestal alveolar fibers (CAF), horizontal fibers (HF), oblique fibers (OF), and apical fibers (AF). DOI: 10. The junctional epithelium is the first periodontal structure to face the bacterial challenge . The alveolar bone, together with the root cementum and the periodontal ligament, constitutes the tooth insertion apparatus, whose main function is to distribute the forces generated by chewing and other contacts . It's usually the result of poor oral hygiene. Clipboard, Search History, and several other advanced features are temporarily unavailable. Periodontitis is a gum infection that can eventually lead to a buildup of gingival crevicular fluid, gum disease, alveolar bone loss and attachment loss of the teeth, meaning they will fall out. Chronic adult periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissue and bone that support teeth. It is generally accepted that periodontitis is initiated by complex and diverse microbial biofilms which form on the teeth, i.e. Alzheimer’s disease has chronic inflammatory components, which can be enhanced by systemic immune activation resulting in inflammation or vice versa. In addition, they can promote the survival, proliferation, and development of B cells into antibody-secreting plasma cells. Login to your personal dashboard for more detailed statistics on your publications. Finally, RANKL can also be secreted by Th17 lymphocytes, which in cooperation with inflammatory cytokines derived from Th1 lymphocytes are capable to tilt bone metabolism favoring bone resorption . 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]. 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. Periodontol 2000. Periodontal diseases in children and adolescents. During the initial lesion, an acute exudative vasculitis in the plexus of the venules lateral to the junctional epithelium, migration of polymorphonuclear (PMN) cells through the junctional epithelium into the gingival sulcus, co-exudation of fluid from the sulcus, and the loss of perivascular collagen were observed. 2020 Jun 3;11:1108. doi: 10.3389/fimmu.2020.01108. Presented by : RICHA sharma 2. These recent concepts suggest that neutrophils could contribute to periodontitis not only by initiating the lesion but also by participating in its progression, by recruiting T-helper 17 cells or promoting the accumulation of B cells and plasma cells in the established and advanced lesions. Pathogenesis of chronic periodontitis The role of host immune system in periodontal pathogenesis involves the following in response to bacterial infection 5 (Fig. The alarming rise in the prevalence of periodontitis has led to the development of innovative diagnostic techniques. 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. Inflammation is a protective response, characterized by its cardinal signs, such as redness, swelling, heat, pain, and disrupted function . Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. The pathogenesis of periodontitis arises essentially from a complex interplay between bacterial and host factors, ... odontitis, chronic apical periodontitis, and peri-apical cysts . Front Immunol. 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. as periodontal disease, periodontal syn dromes, pyorrhoea alveolaris, or chronic periodontitis. By Javier González-Ramírez, Nicolás Serafín-Higuera, Marina Concepción Silva Mancilla, Gustavo Martínez-Coronilla, Jesús Famanía-Bustamante and Ana Laura López López. Periodontitis accounts for a substantial proportion of edentulism and masticatory dysfunction, results in significant dental care costs, and has a plausible negative impact on general health . Ana Paula De Souza, Aline Cristiane Planello, Marcelo Rocha Marques, Daniel Diniz De Carvalho, Sergio Roberto Peres Line, High-throughput DNA analysis shows the importance of methylation in the control of immune inflammatory gene transcription in chronic periodontitis, Clinical Epigenetics, 10.1186/1868-7083-6-15, 6, 1, (2014). Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? 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 . The periodontal ligament contains progenitor cells that can differentiate into osteoblasts for the maintenance and repair of the alveolar bone. 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. 3, 4 Subgingival bacteria are the main factor responsible for chronic periodontitis. In the presence of a microbial challenge, the host responds with immediate inflammatory and immune response in order to control the challenge . Innate and adaptive immune response during periodontal disease (description in the text). 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 . Licensee IntechOpen. The composition of cementum contains about 50% mineral (substituted apatite) and 50% organic matrix. Chronic adult periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissue and bone that support teeth. This leads to the activation of several key molecular pathways, which ultimately activate host-derived proteinases that enable loss of marginal periodontal ligament fibers, apical migration of the junctional epithelium, and allows apical spread of the bacterial biofilm along the root surface . A keratinized stratified squamous epithelium protects the lamina propria of the gingiva on its masticatory surfaces and a nonkeratinized epithelium protects the lamina propria on its crevicular and junctional surfaces [6, 9]. Introduction. 2. 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 . J Clin Periodontol. dental plaque. 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. We have no conflict of interest related to this work. The structural features of the early lesion are consistent with those expected in some form of cellular hypersensitivity, and a mechanism of this kind may be important in the pathogenesis. Periodontitis is defined as a chronic inflammatory disease that affects the tooth-supporting tissues and bacterial deposits play an essential role in the pathogenesis of this condition 18, 22, 25). 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 periodontal inflammation models, macrophages share properties of both M1 and M2. The most common periodontal diseases are gingivitis and periodontitis, whose main characteristic is inflammation. The gums will pull back from the teeth and eventually teeth will loosen and fall out. Numerous studies have examined the role of the genetic factors in the etiology of periodontitis. The periodontal ligament is the soft and specialized connective tissue situated between the cementum covering the root of the tooth and the bone forming the socket wall (alveolodental ligament) . Substituted apatite ) and 50 % organic matrix R. 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