Biomaterial Database

Bacterial pathogenesis and mediators in apical periodontitis. 2007

José F Siqueira, and Isabela N Rôças

Department of Endodontics, Estácio de Sá University, Rio de Janeiro, RJ, Brazil. jf_siqueira@yahoo.com

Apical periodontitis is a group of inflammatory diseases caused by microorganisms (mainly bacteria) infecting the necrotic root canal system. The pathogenesis of different types of apical periodontitis and even the same type in different individuals is unlikely to follow a stereotyped fashion with regard to the involved bacterial mediators. Disease pathogenesis is rather complex and involves a multitude of bacteria- and host-related factors. This review article discusses the bacterial pathogenesis of acute and chronic apical periodontitis, with the main focus on the bacterial mediators conceivably involved in the different stages of the infectious process, including secreted products (enzymes, exotoxins, N-formyl-methionyl-leucyl-phenylalanine peptides, heat-shock proteins and metabolic end-products) and structural components (lipopolysaccharide, peptidoglycan, lipoteichoic acid, lipoproteins, fimbriae, flagella, outer membrane proteins and vesicles, DNA, and exopolysaccharides). Knowledge of the bacterial factors involved in the pathogenesis of apical periodontitis is important to the understanding of the disease process and to help establishing proper therapeutic measures to inactivate this bacterial "artillery".

UI	MeSH Term	Description	Entries
D008070	Lipopolysaccharides	Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)	Lipopolysaccharide,Lipoglycans
D010485	Periapical Periodontitis	Inflammation of the PERIAPICAL TISSUE. It includes general, unspecified, or acute nonsuppurative inflammation. Chronic nonsuppurative inflammation is PERIAPICAL GRANULOMA. Suppurative inflammation is PERIAPICAL ABSCESS.	Periodontitis, Acute Nonsuppurative,Periodontitis, Apical,Acute Nonsuppurative Periodontitides,Acute Nonsuppurative Periodontitis,Apical Periodontitides,Apical Periodontitis,Nonsuppurative Periodontitides, Acute,Nonsuppurative Periodontitis, Acute,Periapical Periodontitides,Periodontitides, Acute Nonsuppurative,Periodontitides, Apical,Periodontitides, Periapical,Periodontitis, Periapical
D002908	Chronic Disease	Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).	Chronic Condition,Chronic Illness,Chronically Ill,Chronic Conditions,Chronic Diseases,Chronic Illnesses,Condition, Chronic,Disease, Chronic,Illness, Chronic
D003790	Dental Pulp Necrosis	Death of pulp tissue with or without bacterial invasion. When the necrosis is due to ischemia with superimposed bacterial infection, it is referred to as pulp gangrene. When the necrosis is non-bacterial in origin, it is called pulp mummification.	Dental Pulp Autolysis,Dental Pulp Gangrene,Necrosis, Dental Pulp,Pulp Gangrene,Pulp Mummification,Pulp Necrosis,Autolysis, Dental Pulp,Gangrene, Dental Pulp,Necroses, Pulp,Pulp Autolysis, Dental,Pulp Gangrene, Dental,Pulp Necroses,Pulp Necrosis, Dental,Autolyses, Dental Pulp,Dental Pulp Autolyses,Dental Pulp Necroses,Gangrene, Pulp,Gangrenes, Pulp,Mummification, Pulp,Mummifications, Pulp,Necroses, Dental Pulp,Necrosis, Pulp,Pulp Autolyses, Dental,Pulp Gangrenes,Pulp Mummifications,Pulp Necroses, Dental
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000208	Acute Disease	Disease having a short and relatively severe course.	Acute Diseases,Disease, Acute,Diseases, Acute
D001419	Bacteria	One of the three domains of life (the others being Eukarya and ARCHAEA), also called Eubacteria. They are unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. Bacteria can be classified by their response to OXYGEN: aerobic, anaerobic, or facultatively anaerobic; by the mode by which they obtain their energy: chemotrophy (via chemical reaction) or PHOTOTROPHY (via light reaction); for chemotrophs by their source of chemical energy: CHEMOLITHOTROPHY (from inorganic compounds) or chemoorganotrophy (from organic compounds); and by their source for CARBON; NITROGEN; etc.; HETEROTROPHY (from organic sources) or AUTOTROPHY (from CARBON DIOXIDE). They can also be classified by whether or not they stain (based on the structure of their CELL WALLS) with CRYSTAL VIOLET dye: gram-negative or gram-positive.	Eubacteria
D001424	Bacterial Infections	Infections by bacteria, general or unspecified.	Bacterial Disease,Bacterial Infection,Infection, Bacterial,Infections, Bacterial,Bacterial Diseases
D018836	Inflammation Mediators	The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).	Mediators of Inflammation,Mediators, Inflammation
D037521	Virulence Factors	Those components of an organism that determine its capacity to cause disease but are not required for its viability per se. Two classes have been characterized: TOXINS, BIOLOGICAL and surface adhesion molecules that effect the ability of the microorganism to invade and colonize a host. (From Davis et al., Microbiology, 4th ed. p486)	Pathogenicity Factor,Pathogenicity Factors,Virulence Factor,Factor, Pathogenicity,Factor, Virulence,Factors, Pathogenicity,Factors, Virulence