CCL28, IL-8, IL-1β and TNF-α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.

As a result of the observed vascular and cell activity changes that occur within patients diagnosed with DM, periodontal diseases become more severe. These changes hinder the migration and the ability of chemotactic factors and leukocytes to protect periodontal tissues from the effects of microorganisms. In order to eliminate microorganisms, the epithelial cells in patients with DM may release more hBD-1 and hBD-3 into the gingival crevicular fluid. Determining the amount of hBD-1 and hBD-3 in the gingival crevicular fluid of patients with and without DM will help to elucidate the relationship among hBD-1, hBD-3, DM and periodontal disease.

Epithelial cells in contact with microorganisms release LL-37 and hBD-2 to eliminate them. The release response of LL-37 and hBD-2 formed against microorganisms can change depending on factors such as smoking, which activates the nicotinic receptors present on epithelial surfaces. This interaction can increase the release of LL-37 and hBD-2. Smoking may also affect the capillary tissues and reduce leukocytic chemotaxis. The increased number of colonized microorganisms may lead to higher levels of LL-37 and hBD-2 release in the tissues of smokers than in non-smokers.

An increased adrenomedullin level was found in individuals with chronic periodontitis and also in individuals with diabetes mellitus. It is thought that the effect of diabetes mellitus on the pathogenesis of chronic periodontitis could have been achieved through antimicrobial peptides such as adrenomedullin, or that increased adrenomedullin was released in individuals with diabetes mellitus in order to ensure no further periodontal tissue loss.

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