###### Abstract  
Background: Human beta-defensins (hBDs) are small cationic peptides of the epithelium with broad antimicrobial and immune response-regulatory activities. hBDs are also related to oncogenesis, and their secretion profiles are affected by radiotherapy treatment. The present study aimed to investigate the oral cavity hBD 1-3 levels in head and neck cancer patients and its relation to radiotherapy treatment. Methods: Sixteen head and neck cancer patients (all with a history of smoking) were included in this study. Periodantal parameters were measured before radiotherapy, and medical information was collected from registries. Oral rinses of the patients were collected before radiotherapy; on the 1 st, 3 rd, and 6 th weeks of radiotherapy; and the 1 st month following the end of radiotherapy. hBD 1-3 levels were measured using ELISA. Results: Oral hBD-1 levels increased during radiotherapy at week 6 (\(p\) = 0.019). hBD-1 levels returned to pretreatment levels after the end of radiotherapy. No significant change was detected for hBD-2 or hBD-3 levels during or after radiotherapy. Conclusions: The constant expression of hBD-1, which is distinct from the infection and inflammation-dependent expression profiles of hBD-2 and hBD-3, may explain why this peptide is the only one affected by radiotherapy. human beta-defensins; radiotherapy; head and neck cancer +
Footnote †: journal: Medical  
fully understood. Periodontally healthy individuals generally produce hBD-1 and hBD-2 in the granular and spinous layers of the stratified squamous epithelium of the gingiva. hBD-2 is generally observed in the superficial layers of the epithelium, which indicates its interactions with oral microflora [4]. Similarly, hBD-3 is usually found in both the undifferentiated basal lamina of the stratified squamous epithelium and the junctional epithelium. In individuals with periodontal disease, hBD-3 can also be detected in the spinous and outermost layers of the gingival epithelium. It is thought that hBD-3 plays a role in facilitating communication between the gingival epithelium and connective tissue, as well as in linking innate and acquired immunity [4; 5; 6]. It is worth noting that the antimicrobial activity of hBDs may vary depending on the type of microorganism and the specific conditions under which they are tested. Some studies have suggested that hBDs may be more effective against certain types of bacteria than others, and the exact mechanisms with which they exert their antimicrobial activity are not fully understood [4; 5; 6; 7]. Studies have shown that hBDs may play a role in immunomodulation in inflammatory processes. This immunomododulation has the ability to modulate both natural immunity and acquired immunity [11]. During the active stage of the disease, there is a greater abundance of immunological disturbance caused by hBDs, which is associated with the disruption of the numbers and function of peri- and intra-follicular inflammatory cells [12]. In terms of function, hBDs play a role in regulating the chemotactic activity of various innate immune cells and stimulating the release of various cytokines [13]. These findings imply that there is a complex interplay between the host's defense mechanisms and their role in maintaining bacterial balance and responding to pathogens [12; 14]. Cancer pathophysiology has been shown to be influenced by hBDs. [12; 15; 16; 17; 18; 19]. Some studies have suggested that hBDs may have anti-tumor properties, including the inhibition of the growth and proliferation of cancer cells and the migration and invasion of breast cancer cells, as well as reducing the formation of new blood vessels, which is an important step in the development and progression of cancer [12; 17; 18]. However, other studies have suggested that hBDs may also have pro-tumorigenic properties, meaning that they may promote the development of cancer by stimulating the growth and proliferation of certain cancer cells such as cervical cancer [20; 21].