Pathogenesis of Periodontal Disease 2 medium

The study of the microscopic structure of the gums.

The study of how the immune system responds to bacteria in the gums.

A complex community of bacteria that forms on the teeth and gums.

Traits of a bacteria that allow it to cause harm to the host.

Inflammation of the gums, often caused by bacterial infection.

Severe gum disease leading to bone and tissue damage.

The development of periodontal disease from initial lesion to advanced lesion.

How the body's immune response participates to fight against infection in the mouth and gums

Periodontal disease stage starting 2-4 days after plaque buildup.

Bacterial buildup on teeth, triggering periodontal disease.

Periodontal disease stage 4-7 days after plaque accumulation.

Characteristics of the bacteria present during periodontal disease development.

Changes in cells (e.g., inflammation) during the initial/early stages of periodontal disease.

Changes in tissues (e.g., damage) as a result of bacteria invasion during the initial and early stages of periodontal disease.

Noticeable signs of disease, observed and identified by dentists.

Body's reaction to the infection.

Inflammation triggered by plaque accumulation, marked by mild vascular changes and increased gingival crevicular fluid; no significant clinical symptoms in the first 4-7 days.

Immune cells initiating the inflammatory response in connective tissues by releasing pro-inflammatory cytokines that increase vascular permeability, allowing fluid seepage into the gingival crevice.

The process where neutrophils are drawn from the bloodstream to the inflamed gum tissue (gingival crevice).

Increased vascular permeability, extensive migration of inflammatory cells (lymphocytes, macrophages), substantial neutrophil infiltration, collagen destruction, and junctional epithelium proliferation.

Increased gingival bleeding, noticeable inflammation, deeper gingival sulcus, and visible plaque; the gums appear swollen, red, and painful.

Characterized by significant immune cell infiltration (plasma cells, B lymphocytes, neutrophils) and collagen destruction within gingival tissues; reversible.

Cytokines are messengers that signal cells, recruiting more immune cells in periodontal disease, indirectly causing bone loss.

Irreversible stage of periodontal disease, characterized by collagen destruction spreading into the periodontal ligament and alveolar bone, resulting in pocket formation, and further plaque accumulation.

Inflammation, driven by cytokines, recruits immune cells, leading to bone and tissue destruction in periodontitis.

The creation of a deepened space between the teeth and gums, filled with plaque and bacteria due to collagen fiber loss, enabling the progression of the disease.

Cytokines stimulate osteoclasts to break down alveolar bone, contributing to periodontal bone loss.

In advanced lesions, neutrophils are predominant in the junctional epithelium and periodontal pockets; while macrophages, T and B lymphocytes dominate in the underlying connective tissue.

A periodontal lesion 21 days after plaque biofilm accumulation, showing bacterial and immune cell activity.

B lymphocytes mature into plasma cells, which produce antibodies that target bacteria but can also damage healthy periodontal tissues.

A more severe periodontal lesion, later in the disease progression than the established lesion, showing prominent tissue and bone damage.

The multi-step process from biofilm accumulation to severe tissue and bone destruction in periodontitis.

Enzymes released by immune cells that degrade collagen fibers, contributing to tissue destruction in periodontal disease.

A lipid derived from cell membranes, especially macrophages present in periodontal disease, and that plays a significant role in periodontal tissue degradation.

Interleukin-1 beta and TNF-alpha are critical for the inflammatory process in gum disease.

Though an initial inflammatory reaction is set off by plaque, the majority of tissue damage is caused by a severe host immune reaction, not by the bacteria itself.

Clinical signs include bone loss, mobility in teeth, furcations, and periodontal pockets.