Periodontal Diseases and Microbiology

The theory that the amount of plaque, not the type of bacteria, determines periodontal disease severity. Harmful products from plaque overwhelm the host's defenses.

The theory that only certain types of bacteria in plaque cause periodontal disease. Pathogenic bacteria trigger tissue destruction.

Bacteria that cause disease, in this case, periodontal disease.

Inflammatory diseases affecting the tissues that support the teeth.

The body's natural defenses against pathogens (bacteria, etc.).

A sticky film of bacteria that forms on teeth.

The observation that periodontal disease can affect some areas of the mouth more severely than others, even among adjacent teeth.

Methods like brushing and flossing to remove plaque.

A form of periodontal disease characterized by rapid bone loss, often in young adults.

The theory that specific bacteria cause periodontal diseases.

Antibiotics for periodontitis may not be effective in the long term and can lead to resistance.

Properties of bacteria that contribute to their ability to cause disease.

The Updated NSPH views plaque as having bacteria that work together through colonization, defense evasion and inflammation to cause and progress disease in individuals.

Microbial species that cannot be grown in laboratories and their roles in periodontal diseases.

Bacteria, viruses and other microorganisms that cause periodontal disease.

Disease results from an imbalance in oral microflora due to ecological stress, leading to enrichment of harmful oral bacteria.

Certain low-abundance pathogens cause disease by altering the normal microbiota's quantity and composition.

The variety of bacteria found in dental plaque.

The ability of a microorganism to cause disease.

The conditions in plaque, influenced by nutrients, pH, and bacteria.

Species that have a large effect on its environment, despite low abundance.

The environment in plaque, partly determined by the host.

Alterations in the types and amounts of bacteria in dental plaque.

A type of lipopolysaccharide (LPS) found in Porphyromonas gingivalis that acts as an agonist of TLR4, activating the immune system.

A type of lipopolysaccharide (LPS) found in Porphyromonas gingivalis that acts as an antagonist of TLR4, inhibiting the immune response.

A source of iron found in gingival crevicular fluid (GCF) that influences the type of LPS Porphyromonas gingivalis produces.

The production of IL-8, a chemokine that attracts neutrophils to fight infection, is blocked by Porphyromonas gingivalis.

The process where Porphyromonas gingivalis blocks the production of IL-8, effectively preventing the recruitment of neutrophils.

Porphyromonas gingivalis interferes with the complement system, a major part of the innate immune response.

Proteinases produced by Porphyromonas gingivalis that cleave complement factors, disrupting the complement system.

A receptor on leukocytes that is activated by Porphyromonas gingivalis through its gingipains, leading to increased inflammation but impaired leukocyte killing.

A specific bacterial species that can cause a major shift in the microbial community, leading to disease, even if they are present in small numbers.

A disease caused by multiple different types of microorganisms working together.

An imbalance in the normal microbial community, often leading to disease.

A keystone pathogen found in the mouth that can manipulate the host's immune system, leading to gum disease.

It uses various strategies to disrupt the host's immune defenses, including manipulating toll-like receptor (TLR) responses, subverting interleukin 8 (IL-8) signaling, and corrupting the complement system.

P. gingivalis alters the way the host's immune system recognizes and responds to bacteria using two types of lipopolysaccharide (LPS) - type I and type II.

P. gingivalis can interfere with the production or function of IL-8, a crucial signaling molecule that attracts immune cells to fight infection.