Periodontitis aggressive

Aggressive periodontitis occurs in less than 0.1% of the US population. ANUG is a form of aggressive periodontitis in which stress hormones may overactivate TLRs to PAMPs around and within cells at the base of gingival sulci. The junctional epithelium fragments and its cells release their contents necrosis). The necrotic cell contents induce a massive release of pro-inflammatory cytokines that cause apoptosis of adjacent cells and a heavy infiltrate of leukocytes from more distant cells. Neutrophils and monocytes invade and destroy the surrounding periodontal attachment and alveolar bone. 

Aa leukotoxin lyses leukocytes (neutrophils, monocytes, and macrophages) on contact, whereas Cdt kills lymphocytes whose surface antigen receptor has bound to an antigen, or macrophages whose Macl integrin has bound to one of its many ligands (Sect. 13.2.4). In LAP, antibodies that bind to both these toxins appear in the blood and they may facilitate 

As noted above, proteins B and D are encoded downstream of the acylase (protein C) and the leukotoxin (protein A) genes and their expression is attenuated in comparison with upstream-encoded proteins. The amounts of proteins B and D are reduced compared with 

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Araya, A.V. et al., Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-lbeta, IL-6 and PGE2 secretion in whole blood from type 1 diabetes mellitus patients with or without aggressive periodontitis, Eur. Cytokine Netw., 14, 128, 2003. 

Unknown genes on chromosome 12 Ehlers-Danlos syndrome - type VIII Aggressive periodontal disease... 

EDS VIII is associated with aggressive periodontal disease. It may be caused by a mutation in one or more genes other than the collagen gene (COL2A1) on chromosome 12. Individuals resemble Marfan s syndrome (Table 6.1), but have normal teeth. They display excessive bleeding around the knees and fragile skin, hallmarks of vascular EDS. 

Periodontal disease describes a mixture of diseases in which the periodontal attachment is destroyed, resulting in loose teeth that may exfoliate. Periodontitis is divided into chronic and aggressive forms that are localized or generahzed (affect few or many teeth). Chronic periodontitis is very common (Sects. 13.1.2-13.4.3), whereas aggressive periodontitis is rare (Chap. 14). The collagen fibers of the gingiva and periodontium are described in Chap. 3 (Sect. 3.1.5), and its epithelial cover in Chap. 5 (Sect. 5.2.3). 

By contrast, in necrosis, severe physical, chemical, or bacterial damage causes a cell membrane to burst, releasing apoptotic mediators (Sect. 13.4.3) and proinflammatory cytokines into the stroma (Sect. 13.2.2). The cytosolic enzymes continue to make lactic acid in the absence of mitochondrial function, making the necrotic environment strongly acidic and activating lysosomal enzymes (Sect. 13.2.1) to digest the released cytosolic contents. Necrosis is discussed in relation to aggressive periodontitis (Chap. 14). 

G.C. Armitage, M.P. Cullinan, Comparison of the clinical features of chronic and aggressive periodontitis, Periodontology 53 (2000) 12-27. 

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