Pathogenesis of Periodontal Disease 2 hard

The study of the structure and function of the gums' tissues.

Study of the body's defense mechanism against pathogens.

A community of bacteria that adhere to surfaces.

Properties of bacteria that allow them to cause harm.

Inflammation of the gums.

Inflammation of the tissues that support teeth.

Development of periodontal disease.

The body's defense mechanism against disease-causing organisms in the gums.

Occurs 2-4 days after plaque buildup.

Occurs 4-7 days after plaque accumulation, showing mild vasodilation, plasma fluid exudation in gingival sulcus, and increased gingival crevicular fluid, with no obvious clinical changes.

Plaque bacteria release toxins that affect connective tissues.

Immune cells in connective tissue that initiate inflammation by releasing pro-inflammatory cytokines (like histamine and interleukins).

The process where neutrophils move from the bloodstream into the gingival sulcus to fight infection.

Begins 4-7 days after plaque accumulation.

The process where bacteria gather on teeth and gums.

Neutrophils release cytotoxic enzymes that damage collagen fibers supporting the gingiva, leading to spaces in the tissue.

Bacteria in plaque release toxins impacting underlying tissues.

An exaggerated increase in the ability of blood vessels to leak fluids and inflammatory cells into the gingival tissues, furthering the inflammation.

Bacterial toxins lead to changes in the cells at the junction of gums and teeth.

Toxins damage the connective tissue underneath the gums.

Early gum periodontitis stages have noticeable symptoms for the host.

The stage of periodontal disease 21 days after plaque buildup, characterized by immune cell infiltration (plasma cells, B lymphocytes, neutrophils), collagen destruction, and increased blood viscosity.

An irreversible stage of periodontal disease where collagen destruction extends to periodontal ligament and alveolar bone, leading to pocket formation.

The deepened space between the tooth and gum, created by migration of the junctional epithelium into collagen-depleted areas.

A large number of neutrophils, macrophages, B lymphocytes, T lymphocytes and plasma cells are found in all stages of periodontal disease in gingival tissues.

Collagen fibers are degraded by enzymes released by neutrophils and other factors involved in an individuals immune response. This damages the supporting tissues of the teeth causing periodontal pockets.

Substances like matrix metalloproteinases (MMPs), PGE2, and cytokines, derived from both bacteria and the body's immune response, contribute to periodontal tissue destruction.

Initial stages of periodontal disease are reversible using good oral hygiene and treatment that stops immune response and plaque accumulation causing the inflammatory response

The body's protective system that, while initially helpful, can lead to significant tissue destruction if overactive in periodontal disease.

Cytokines like interleukin-1 beta and TNF-alpha, produced by immune cells (T lymphocytes and macrophages), drive inflammation and bone loss in periodontal disease.

Matrix metalloproteinases (MMPs) are enzymes that break down connective tissue, including bone, partly caused by cytokines during periodontal disease.

Cytokines stimulate the transformation of macrophages into osteoclasts, which destroy bone.

21 days after plaque buildup, showing increased inflammatory response, tissue changes, and possible early clinical signs.

A more severe stage of periodontal disease with further tissue destruction, bone loss and clinical signs.

A component of the bacterial outer membrane, which plays an important role in the initiation and progression of periodontitis.

A model illustrating how risk factors, genetics, bacteria, and the host immune response contribute to the development and progression of periodontal disease.

Substances produced by bacteria that contribute to their ability to cause disease in periodontal tissues.