Pathway 15-2 Pathogenicity and Virulence Factors

Microbial Pathogenicity and Virulence Factors

• Pathogenicity refers to a microorganism's ability to cause disease.
• Virulence is the degree of pathogenicity.
• Virulence factors are secreted products, structural components, and microbial strategies that contribute to pathogenicity.
• Biofilms are one bacterial strategy that contributes to pathogenicity, offering protection against host defenses, microbial competitors, and antimicrobial agents.
• Primary pathogens routinely cause disease in a specific host, while opportunistic pathogens cause disease only when host defenses are impaired.
• Most bacteria involved in endodontic infections are normal inhabitants of the oral microbiota, becoming opportunistic pathogens when the balance of the host-bacteria relationship is disrupted.
• Bacteria in the forefront of infection must survive host defenses and acquire nutrients to stay alive.
• During pulp necrosis, bacteria colonize necrotic tissue, moving toward the apical part of the canal until it is entirely infected.
• Early colonizers play a crucial role in initiating apical periodontitis and may modify the environment to facilitate the establishment of other bacterial groups.
• Late colonizers may access the canal through coronal exposure or exposed dentin tubules, contributing to a shift in the microbiota.
• Root canals with radiographically detectable apical periodontitis lesions harbor both early and late colonizers.
• Periradicular inflammation can occur before the frontline of intracanal bacterial infection reaches the apical foramen.
• Bacterial virulence factors directly damage host cells or the intercellular matrix, including enzymes, exotoxins, heat-shock proteins, and metabolic end products.
• Bacterial structural components, such as LPS, peptidoglycan, LTA, fimbriae, flagella, outer membrane proteins, and vesicles can directly cause tissue damage by stimulating host immune reactions.
• Inflammatory and noninflammatory host cells release proinflammatory cytokines in response to bacterial components, contributing to bone resorption characteristically observed in apical periodontitis.
• Pus formation in acute apical abscesses is an example of indirect damage, resulting from the destruction of the connective extracellular matrix by oxygen-derived free radicals and lysosomal enzymes released by polymorphonuclear leukocytes.
• Apical periodontitis is a multifactorial disease resulting from the interplay of host and bacterial factors.
• LPS, exclusive to gram-negative bacteria, is detected in high concentrations in canals of teeth with large or symptomatic apical periodontitis and persistent exudation.
• While LPS is a significant virulence factor, other bacterial mediators, such as LTA (exclusive to gram-positive bacteria) and various bacterial secreted products, also contribute to the disease.
• The pathogenesis of apical periodontitis is likely to vary based on the bacterial mediators involved.

Apical Periodontitis

• Apical periodontitis is a multifactorial disease involving host and bacterial interactions.
• Few endodontic pathogens are capable of inducing all the events in the pathogenesis of apical periodontitis.
• The disease process requires an integrated and orchestrated interaction of selected members of the mixed endodontic microbiota and their respective virulence attributes.
• LPS has been found in high concentrations in canals of teeth with large, symptomatic apical periodontitis and persistent exudation.
• Other bacterial mediators likely contribute to the disease, including LTA, which is exclusive to gram-positive bacteria.
• Many bacterial secreted products have been detected in endodontic infections, suggesting that there is no single, stereotyped course of pathogenesis for apical periodontitis.