# Membrane Fluidity and Oxidative Stress in Patients with Periodontitis
## 4 Discussion
### Membrane Fluidity  
To our knowledge, no studies have been reported on the evaluation of MF (\(le/lm\)) in an oral pathology such as periodontitis, although the membrane represents tissue stability, protection, and cellular functionality. The membrane structure depends on phospholipids, cholesterol, and lipid rafts that affect its fluidity. Thus, an increase in lipoperoxidation may modify the functionality of these fatty acids which function as support for the structural integrity of the membrane. Changes in MF alter tissue homeostasis, leading to pathological processes [51; 52]. An analysis of MF (\(le/lm\)) in relation to the PD level revealed a moderate-to-weak positive correlation in patients with periodontitis (\(r<0.5\); Table 2). This result and the reported MDA levels showed similar correlations with PD (Table 2). This similarity was repeated for the MF (\(le/lm\)) and MDA values when Group 2 (PD/CAL \(>5\) mm) was compared with group 1 (PD/CAL \(\leq 5\) mm), as shown in Table 3. These results indicate that the degree of lipid peroxidation influences the MF response of patients with periodontitis. In a previous study, there were higher salivary levels of 8-hydroxyguanosine, a marker of oxidative stress in patients with chronic periodontitis, especially when CAL had a depth greater than 3 mm [50]. On the other hand, the integrity of the connective and epithelium tissues depends on several factors, including the physico-chemical characteristics of intracellular lipids grouped in membrane-lining granules that act as important barriers to the permeability of xenobiotics and pathogens [53; 54]. An analysis of the lipid characteristics in the tissues of 45 patients with oral reactive hyperplasia revealed elevated levels of arachidonic acid, a polyunsaturated fatty acid [55]. This finding is relevant in our work for three reasons, the first being that arachidonic acid is highly vulnerable to oxidation, a deleterious process which affects the fluidity and integrity of the membrane [10; 52]. Secondly, arachidonic acid is a precursor in the synthesis of prostaglandandins (PG-2) and leukotrienes (Tx-2) which induce increased inflammation and tissue damage. Thirdly, with increased inflammation, there are increases in the induction of the enzymatic activities of phospholipases A2 (PLA-2) and lipooxygenase (type 5), which play important roles in increasing MF [9; 13; 52; 55]. Unfortunately, there are no previous studies in the literature on MF in gingival tissue in patients with periodontitis. However, based on the similarity seen in the results of MF (\(le/lm\)) and MDA (Tables 2 and 3), and with the study by [PERSON] et al. (2017), it can be reasonably inferred that MDA levels affected the MF of the patients studied. However, to explain its relationship with PD and CAL, there is a need to study the proportion of polyunsaturated fatty acids in the gingival tissue, quantify the levels of PG and Tx as indices of tissue inflammation, and measure the enzyme activities of PLA-2 and lipoxygenase (type 5) in relation to MF (\(le/lm\)). The increases in ROS and proinflammatory cytokines may be responsible, directly and indirectly, for the destruction of connective tissue and bone resorption through a decoupling mediated by the receptor activator for nuclear factor k B ligand (RANKL)/osteoprotein. In this process, the balance between bone formation and bone resorption is broken, favoring bone loss, a major characteristic feature of periodontitis [56; 57; 58; 59]. Some recently introduced compounds have a significant influence on the oral environment. The use of paraprobiotics [60], probiotics [61; 62], and postbiotics [63] can modify the clinical and microbiological parameters in periodontal patients. Probiotics have been considered the future strategy for achieving a balance in the oral microbiome in the presence of periodontitis, limiting the excessive growth of certain micro-organisms and modulating the inflammatory response to prevent bone loss and control the progression of this pathology [63].