Pathogenesis of periodontal disease workbook hard

Antibodies, produced locally or systemically, prevent microorganism adherence, recognize and neutralize pathogens, marking them for phagocytosis, and assisting with complement system lysis of bacteria.

Pro-inflammatory cytokines (like IL-1, IL-6, TNF-α) are released in response to pathogens, promoting periodontal tissue destruction. Anti-inflammatory cytokines (like IL-4, IL-10) counteract this effect.

A type of immune response that does not rely on antibodies, rather utilizing T-cell receptors to target and fight pathogens.

Prostaglandins (like PGE2) contribute to periodontitis by promoting bone resorption, chemotaxis, vascular permeability, and dilation.

Matrix metalloproteinases (MMPs) degrade connective tissue. This can result in tissue damage.

The process of displaying antigens on the surface of cells, like Langerhans'/dendritic cells, for T-cells to recognize.

Helper T (TH) cells produce cytokines, assist in B-cell differentiation into plasma cells, and activate macrophages and neutrophils.

A dynamic balance exists between plaque and host defenses in healthy gums and stable gingivitis. Periodontitis disrupts this, favoring tissue damage.

Progression from gingivitis to periodontitis involves a shift from T-cell-dominant to B-cell-dominant immune response, with T-cells having an immunoregulatory role.

Increased plaque levels and virulence (harmfulness) of microbes in dental biofilm are key contributors to periodontal disease.

Cytokines, prostaglandins, and MMPs are chemical messengers regulating inflammation, immune response, and tissue damage in periodontal disease.

Weakened immune defenses provide easier entry for oral bacteria to damage soft tissues and the structures supporting teeth.

T-cells play a regulatory role in the shift from gingivitis to periodontitis, affecting immune responses and disease progression.

Hypotheses on the role of bacteria in periodontal disease are outlined here (detailed explanations are missing).

The table and texts include descriptions of mediators, actions, and factors but their release points are not covered.

Cytokines are chemical messengers that regulate inflammation, immune response and tissue damage in periodontal disease.

Microbial infection causing inflammation, leading to irreversible destruction of periodontal tissues and support structures.

Community of microorganisms in an extracellular matrix on tooth surfaces.

Initial attachment, initial colonization, maturation, and dispersal.

Organic (proteins, glycoproteins, polysaccharides, lipids) and inorganic components (calcium, sodium, phosphorus, potassium).

One or more communities of microorganisms embedded within an extracellular matrix.

Maturation: increased complexity of the biofilm.

Dispersal: parts of the biofilm are released.

Body's defense system against the dental plaque. Includes innate and acquired immunity.

Formation of a biofilm slime layer on teeth or other surfaces.

A biofilm with a mushroom-shaped colony structure.

The tissue covering the free and attached gingiva, keratinized for protection.

Non-keratinized, lines the gingival sulcus, allowing crevicular fluid flow.

Non-keratinized tissue connecting gingiva to tooth, tightly packed with desmosomes.

Bacteria that thrive in environments lacking oxygen.

Specific bacteria species like P. gingivalis, T. denticola, T. forsythia, and A. actinomycetemcomitans.

The body's first response to plaque, involving inflammation, epithelial cells and saliva.

Gingival crevicular fluid flows through semi-permeable tissues.

Tissue damage at the junctional epithelium leads to a periodontal pocket, causing inflammation and lowered protection due to micro-ulcers.

Keratinocytes in the junctional epithelium release cytokines and TNF during the inflammatory response in the gums.

Langerhans' cells, a type of tissue macrophage, release host defenses.

Saliva prevents oral tissue dryness.

Damage to the junctional epithelium weakens the oral tissue's ability to protect against bacteria.

A space or pocket formed between the tooth and gum due to inflammation & tissue destruction.

Cells in the junctional epithelium that release inflammatory proteins during an immune response.

The immune response that is activated when innate immunity fails to eliminate pathogens, highly specific to a particular pathogen, and characterized by immunological memory.

An adaptive immune response where antibodies are produced to target pathogens in body fluids (humours). This responds to extracellular pathogens.

A molecule that triggers an immune response, recognized as foreign by the immune system.

Immune cells that differentiate into plasma cells to produce antibodies targeting a specific antigen.

Specialized B-cells that produce and release antibodies against a specific antigen.

Proteins produced by the immune system that bind to specific antigens, facilitating neutralization, phagocytosis, or complement activation.

Cells that present antigens from pathogens to circulating lymphocytes, triggering the adaptive immune response.

Antimicrobial effect -- Secretory and serum antibody IgA -- influence bacteria attachment improving chances of being swallowed.