These immunosuppressive effects facilitate microbial persistence, promote inflammatory responses, and contribute to tissue degradation within the periodontium, ultimately playing a significant role in the initiation and progression of periodontal disease.32 Furthermore, periodontal tissues express glucocorticoid receptors that are responsive to cortisol released via the hypothalamic-pituitary-adrenal (HPA) axis. Here, NR3C1 is linked to periodontal disorder.