dental pulp dendritic cells

Macrophages

Mast cells

neutrophils

odontoblast

Outflow of dentinal fluid and intratubular immunoglobulin deposits

neuropeptides

Cytokines and chemokines

B lymphocytes

T lymphocytes

It begins with the innate immune response and continues to develop and activate the adaptive immune response, including humoral responses and cellular responses, causing typical inflammatory changes, and inflammatory damage such as necrosis may occur.

Distributes various immune cells, such as Langerhans cells, macrophages, neutrophils, NK cells, mast cells and eosinophils, as well as the cytokines and chemokines they secrete.

The proportions of T and B cells are different, but both cellular and humoral immunity are involved in the disease process.

Th1-type immune responses are involved in all stages, Th2-type plays an important role in lesions dominated by B cells and plasma cells, and Th17 plays an important role in exacerbating inflammatory responses.

Some of the chronic inflammatory lesions are dominated by humoral immune responses, and important immune regulatory factors are detected. Regulatory T lymphocytes balance the inflammatory response in periapical lesions.

It is mainly mediated by various types of hypersensitivity reactions, including types 1 and 2. There is also delayed hypersensitivity.

Produce toxic factors and other direct damage

Induces host local and systemic immune responses to produce indirect immunopathological damage

Promote tissue cell apoptosis

A few Gram-negative anaerobic bacteria, including Porphyromonas gingivalis, Sodium forsythiana, and Aggregatibacter actinomycetemcomitans, are related to the occurrence and development of periodontal disease.

neutrophils

Macrophages

Early periodontal lesions are characterized by the presence of T lymphocytes and macrophages, while a large number of B lymphocytes and plasma cells appear in established and advanced periodontal lesions.

The progression of periodontal lesions is related to the imbalance of T cell immune regulation.

The important mechanism of T cells' destructive effect on periodontal tissue is the production of cytokines.

The body's susceptibility to infectious diseases is also one of the important factors affecting the occurrence and development of periodontal disease.

After 2 to 4 days of plaque accumulation, the host's protective inflammation against plaque antigens is dominated by chemotactic phagocytosis.

After 4 to 7 days of plaque accumulation, a large number of dense lymphocyte infiltrates appear, with T cells accounting for the majority, and some B cells, macrophages and mast cells.

Within 2 to 3 weeks of plaque accumulation, neutrophil exudation and plasma cell infiltration increased significantly, and the scope expanded to the perivascular and collagen fiber bundles deep in the connective tissue.

High concentrations of IgG, IgA, IgE, complement and a large number of polymorphonuclear granulocytes appear in the gingival crevicular fluid, and a large number of lymphocytes, plasma cells and macrophages infiltrate in the connective tissue.