{'fraction_non_alphanumeric': 0.02901023890784983, 'fraction_numerical': 0.016211604095563138, 'mean_word_length': 5.306451612903226, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Research progress in secreting sytokines interferon-gamma and interleukin-17 of T helper 1 and 17 cells on periodontitis].

Periodontal disease (PD) is an infection-driven chronic inflammatory disease characterized by the inflammation of tooth-supporting tissues and the destruction of the associated alveolar bone. The immune response of the host to periodontal pathogens infection determines the course and progress of the disease. The effects of secreting cytokines interferon-gamma (IFN-γ) and interleukin-17 (IL-17) of T helper 1 cells (Th1) and T helper 17 cells (Th17) on the development of periodontitis has attracted much attention. IFN-γ is a potential immune-modulatory cytokine and can mediate cellular immune responses by activating various immune cells of the host such as macrophages. As one of the most potential bone physiological regulation mediators, IL-17 is closely related with alveolar bone resorption in periodontitis. This review elaborated the relationship between IFN-γ and IL-17 in the progress of periodontitis, providing new explanations into the development of periodontitis and alveolar bone destruction caused by the host immune response.