Pathogenesis of periodontitis

Abstract

Periodontitis is an inflammatory disease of the periodontium which is characterized by a progressive destruction of the tissues supporting the tooth. Its primary etiology is an ill-defined series of microbial infections which may be composed of only some of the more than 300 species of bacteria currently recognized in the oral cavity. The disease is currently considered to progress as periodic, relatively short episodes of rapid tissue destruction followed by some repair, and prolonged intervening periods of disease remission. Despite the apparent random distribution of episodes of disease activity, the resulting tissue breakdown exhibits a symmetrical pattern of alveolar bone loss and pocket formation which is common to several forms of periodontitis, although the distribution of the most affected teeth and surfaces may vary among diseases (e.g., juvenile periodontitis versus adult periodontitis or rapidly progressive periodontitis). Several reports have indicated that bacterial cells can be found in the pocket wall of periodontitis lesions. The translocation of bacteria into the tissues from the pocket environment is quite common, as evidenced by the common occurrence of bacteremias in patients with periodontitis following relatively minor events such as chewing and oral hygiene procedures. However, it is important to distinguish between the passive introduction of bacteria into periodontal tissues and frank invasion as might occur in an acute infection, since the pathological implications may be quite different.

Association of Systemic Oxidative Stress with Suppressed Serum IgG to Commensal Oral Biofilm and Modulation by Periodontal Infection

“…It is known that the presence of periodontitis is associated with lower serum concentrations of vitamin C (12), even after adjusting for smoking, suggesting that periodontal disease may pose an oxidative stress that consumes ascorbate. Also, the mucosal tissue wounding associated with deep periodontal pockets has been associated with an increased occurrence of bacteremia (38). In this regard, 8-isoprostane concentrations have been demonstrated to be increased in Helicobacter pylori (H. pylori)-positive subjects (16), noncirrhotic chronic hepatitis C patients (30) and cystic fibrosis patients (15), as well as animal models of endotoxemia (3).…”

“…In this regard, 8-isoprostane concentrations have been demonstrated to be increased in Helicobacter pylori (H. pylori)-positive subjects (16), noncirrhotic chronic hepatitis C patients (30) and cystic fibrosis patients (15), as well as animal models of endotoxemia (3). Because the presence of periodontitis can result in recurring systemic exposure to oral biofilm microorganisms (38), it is conceivable that the resulting low-level bacteremia, endotoxemia, and consequent metabolic stress could contribute to an elevated serum concentration of serum 8-isoprostane.…”

Variabilidad de la síntesis de citoquinas por células dendríticas humanas estimuladas con los distintos serotipos de Aggregatibacter actinomycetecomitans

“…Aunque las bacterias pueden causar dañar a los tejidos, es la respuesta inmune del hospedero la principal causa de la destrucción del aparato de soporte periodontal (3,4) . Estas interacciones (bacteria-hospedero) inducen la síntesis de citoquinas y quimioquinas, las que pueden determinar la destrucción del tejido conectivo y óseo característico de las periodontitis y, eventualmente, pueden llevar a la pérdida de los dientes (5,8) . En las periodontitis, las células dendríticas reconocen las bacterias patógenas del biofilm subgingival, las fagocitan y destruyen, y luego procesan y conjugan sus antígenos a moléculas del complejo mayor de histocompatibilidad (MHC) para presentarlos a los linfocitos TCD4 + y así, iniciar la respuesta inmune adaptativa (9)(10)(11)(12) .…”

Genes and Gene Polymorphisms Associated with Periodontal Diesases

“…Bazı bireyler, bazı dişler veya dişlerin bazı yüzeyleri periodontal hastalıktan daha şiddetli etkilenirken, sağlıklı durum ile hastalığın farklı safhaları aynı hastada ve aynı dişlerde birlikte bulunabilir. 12,13 Epidemiyolojik çalışmalarda erişkin populasyonunun %80-90'ında geçirilmiş veya aktif periodontitise işaret eden klinik ataşman kaybı veya radyografik kemik kaybı görüldüğü, yanı sıra aynı populasyonun ancak %7-15'inin şiddetli ve yaygın periodontitisten etkilendiği bildirilmektedir. [14][15][16][17] Yaygın olarak görülen periodontal hastalıkların etiyolojisinin belirlenmesi ve sınıflan-dırılmasının yanı sıra, hastalığın genetik özel-liklerinin tanımlanması, hastalığın tanı ve tedavisinde de oldukça önemlidir.…”