Harrison's Principles of Internal Medicine. 31(5):396-401. As this persistent inflammation continues, periodontal ligaments break down and destruction of the local alveolar bone occurs. Triratana T, Rustogi KN, Volpe AR, et al. Measuring the pocket depth of the groove between your gums and your teeth by inserting a dental probe beside your tooth beneath your gum line, usually at several sites throughout your mouth. Periodontal disease and coronary heart disease risk. A consideration of currently available data has permitted the formulation of a new concept of the pathogenesis of this disease. The recognition of pathogenic microorganisms and the recruitment of effector cells (e.g., neutrophils) and molecules (e.g., the complement system) are central to effective innate immunity. 5(2):150-5. Interaction between bacteria and keratinocytes results in the upregulation of IL-8 and ICAM-1 expression in the gingival epithelium, thereby stimulating neutrophil migration into the tissues and the gingival sulcus [89, 90]. Gingivitis. [Medline]. 3(1):62-75. Elias-Boneta AR , Toro MJ , Noboa J , Romeu FL , Mateo LR , Ahmed R , et al. Various studies using the experimental gingivitis model showed 13% of all individuals representing a “resistant” group [9, 11, 12]. Clinical gingival health is generally associated with an inflammatory infiltrate and a host response consistent with homeostasis. Microbiological understandings and mysteries of noma (cancrum oris). Available from: Immune responses in periodontal pathogenesis, College of Dentistry, Jazan University, Kingdom of Saudi Arabia, Sree Mookambika Institute of Dental Sciences, India. Periodontitis Increases the Risk of a First Myocardial Infarction: A Report From the PAROKRANK Study. The most common type of gingivitis involves the marginal gingiva and is brought on by the accumulation of microbial plaques in persons with inadequate oral hygiene. Recent publications show several cases in areas such as Nigeria, where ANUG and noma were observed in children younger than 14 years. 2004 Spring. /viewarticle/939330 Immune responses in periodontal pathogenesis. Chronic gingivitis leads to tooth loss. Zimmer S, Kolbe C, Kaiser G, et al. Gingivitis refers to the inflammation of soft tissues, surrounding the teeth. 78(2):349-54. [Experience with clindamycin in stomatologic diseases]. [3, 4, 5, 6] Elevated levels of chronic inflammation (eg, C-reactive protein) have been shown to fall after treatment of periodontal disease. J Clin Periodontol. 199-200. Understanding the disease processes is important for the development of improved treatment strategies. Perez A, Wagner AM, Carreras G, et al. The accumulation of these defense cells and the extracellular release of their destructive enzymes cause destruction of collagen and subsequent proliferation of the junctional epithelium leading to vasodilatation, increased vascular permeability, and hyperplastic gingival tissues. When Toll-like receptors bind pathogen-associated molecular patterns, a series of intracellular events are initiated, leading to the production of cytokines, chemokines, and antimicrobial peptides (AMPs) [64]. PGE2 induces the secretion of MMPs, as well as osteoclastic bone resorption, and it contributes significantly to the alveolar bone loss seen with all forms of periodontitis [100]. Cytokines are produced by resident cells, such as epithelial cells and fibroblasts, by phagocytes (neutrophils and macrophages) in the acute and early chronic phases of inflammation, and by immune cells (lymphocytes) in established and advanced lesions [69]. 2007 Nov. 154(5):830-7. The classic studies of Page and Schroeder [6] described the basic understanding of histologic changes that occur in the gingival tissues as the initial, early, established, and advanced gingival lesions. Gingivitis: a prelude to periodontitis?. 'Etiology and Pathogenesis of Periodontal Disease' represents a new concept in periodontology with its pronounced focus on understanding through knowledge rather than presenting the present valid answers. In other words, the initial lesion corresponds to the histologic picture that is evident in clinically healthy gingival tissues. Innate immunity reflects the capacity of the host to defend against infectious attacks. Initial, early, established, and advanced lesions of the development of gingivitis and periodontitis. With time, lesions become chronic and are characterized by the presence of plasma cells and B lymphocytes. Oral soft tissue manifestations and CD4 lymphocyte counts in HIV-infected children. 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