Abstract
Inflammatory interactions that are uncontrolled integrating innate and adaptive responses leads to a persistent inflammatory response within the periodontal tissues, that constitutes the main hallmark of chronic periodontitis. The interface involving our external environment and the body's internal connective tissue is comprised of the periodontal epithelium, along with other mucosal surfaces. Chronic periodontitis may occur as the consequence of chemical or mechanical environmental stresses that aggravate or exacerbate oral disease. Additionally, chronic periodontitis has also been pertinent to environmental determinants that modulate the host response and systemic health status. When all factors are evaluated, pro-inflammatory processes that include both the environment and the host work together to promote a chronic state of inflammation in the periodontal tissues. This condition can be harmful and eventually result in bone resorption and tooth loss. Periodontal disease is significantly impacted by steroid sex hormones. A steroid sex hormone correlated to periodontal health is estrogen. Considering receptors for estrogen are expressed in the oral cavity's mucosa and periodontium, the overall condition of the oral cavity has a direct association with the hormone's levels. In comparison with premenopausal women, postmenopausal women are more likely to experience periodontitis. This is consistent with investigations showing that postmenopausal women had a significantly greater plaque index than premenopausal and perimenopausal women. It also indicates that postmenopausal women may experience more severe periodontal degeneration in comparison to premenopausal and perimenopausal women. This menopausal symptom, although can occasionally be painless, is an effect of ageing. In general, oral discomfort is experienced among women as they approaches menopause. One of the a multitude low molecular weight byproducts of lipid peroxidation (LPO) is malondialdehyde (MDA), that represents typically quantified as a peroxidation index. MDA has been proven to have substantial pathophysiologic effects. Thiobarbituric acid reactive substances screening is the most frequently employed technique for measuring MDA (TBARS). The quality of TBARS in biological samples is assessed using a range of spectrophotometer tests. Whole saliva is a crucial physiological fluid that is composed of an exceptionally complicated blend of molecules. Immune response fluctuations attributed to psychological stress can enhance the risk of periodontitis. In addition to their diminished capacity to defend themselves, stress also presented an impact in immune response modulation. This mechanism amplifies the organism's susceptibility to inflammatory and psychological disorders. This modulation may facilitate the emergence or progression of periodontal disease, as stressors can exacerbate damage to the tooth's defensive and supporting structures. Material and Methods The research investigated included the recruitment of 64 patients, aged 47 to 55, who had recruited in the Periodontology department at the A. B. Shetty Memorial Institute of Dental Sciences which is located in Deralakatte, Mangalore. Thirty-two postmenopausal women with chronic periodontitis (Group A) and postmenopausal women without chronic periodontitis (Group B) (Healthy subjects) were the two distinct categories of patients. Each participant provided a thorough case history, and unstimulated whole salivary samples were taken in order to measure the levels of malondialdehyde in the saliva. The Perceived Stress Scale questionnaire was used to evaluate each participant's psychological stress. For statistical analysis, the collected data on psychological stress levels, salivary malondialdehyde levels, and their relationships in postmenopausal women with and without chronic periodontitis was submitted. Results: A Mann Whitney U test observed that the mean stress level between the two groups was also statistically significant, and an unpaired t-test showed that the mean value of malondialdehyde among subjects with chronic periodontitis compared to those in a healthy state was statistically significant. Stress and malondialdehyde (MDA) levels showed a weakly positive correlation (r = 0.12) in postmenopausal women with chronic periodontitis patients. By applying the Spearman's rank correlation method, the correlation was not statistically significant (p = 0.517). The multivariate linear regression model suggests that Periodontal probing depth and Stress level may be associated with MDA levels in chronic periodontitis patients, although the statistical significance is borderline when compared to Plaque Index and Clinical attachment loss. Conclusion: This study provides conclusive proof that free radical damage plays a significant etiologic role in postmenopausal women with CP. It showcases how the body's compensating mechanism is partially collapsed due to the unprecedented amount of free radicals and stress yielded during periodontitis and lacks the capacity to combat the increase degeneration of free radicals brought about by post menopause, thereby exacerbates the condition.