The expression of β-defensin-3 is related to periodontitis and diabetes mellitus, and the latter two are associated with each other. Patients with periodontitis exhibit reduced expression of β-defensin-3 in gingival crevicular fluid. Moreover, the expression level of β-defensin-3 is negatively correlated with the severity of periodontal inflammation and the number of total periodontopathogens. Non-periodontopathic bacteria, such as Streptococcus gordonii, Streptococcus sanguinis, and Veillonella atypica, can up-regulate the expression of β-defensin-3. Orange complex bacteria, including Prevotella intermedia and Fusobacterium nucleatum, can efficiently induce production of β-defensin-3, whereas red complex bacteria, such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, exhibit suppressive effects. The increased expression of β-defensin-3 in periodontally healthy tissues is important to maintain periodontal homeostasis because of its functions, such as antimicrobial activity, immunoregulation, and promotion of cell proliferation and growth. In diabetic wounds, β-defensin-3 is inadequately expressed because of the high-glucose environment that impairs the body’s immune responses. Further studies must elucidate the possible adverse reaction and biological function of β-defensin-3, as well as its mechanism in infectious diseases.
