Lipid peroxidation (LPO) participates in the development of various diseases, including periodontitis, and malondialdehyde (MDA) is its terminal product. Therefore, in the present study, salivary and plasma MDA levels in 30 periodontitis patients were compared to those in 20 healthy controls, as well as in relation to periodontal therapy in order to assess its effectiveness. Periodontal status was assessed via plaque index, gingival index, papilla bleeding index, probing depth and clinical attachment level, while salivary and plasma MDA levels were determined by the ELISA method. The periodontitis group had a significantly greater salivary (2.99 pmol/µL) and plasma (0.50 pmol/µL) MDA levels relative to the healthy controls (1.33 pmol/µL and 0.40 pmol/µL, respectively). Three months after the periodontal therapy completion, although salivary MDA levels were significantly lower than those measured at the baseline (p < 0.001), the reduction in plasma MDA was not statistically significant (p > 0.05). These findings indicate that, while inflammatory processes in periodontium may increase local and systemic lipid peroxidation, periodontal therapy can result in a significant decrease in salivary, but not plasma, MDA levels.

Given the posited role of oxidative stress in the pathogenesis of both periodontitis and type 2 diabetes mellitus (T2DM), it may also serve as a link between these highly prevalent chronic inflammatory diseases. This view is supported by an ample body of evidence indicating that the severity and progression of periodontitis is in part driven by diabetes, while periodontal infection may hinder the attainment of adequate glycemic control in diabetic patients. Thus, this review focuses on the potential synergistic interactions along the oxidative stress–inflammation pathway characterizing both conditions. Because periodontitis and T2DM share the same risk factors and compromise patients’ quality of life, to develop effective strategies for combatting both conditions, their mutual influence needs to be explored.

As oxidative stress has been implicated in the pathogenesis of diabetes mellitus and periodontitis, it may serve as a link between these conditions. Therefore, as a part of the present study, salivary lipid peroxidation (LP) in periodontitis patients with and without diabetes mellitus type 2 (DM2) was evaluated, along with the periodontal therapy effectiveness. The study sample comprised of 71 DM2 patients with periodontitis and 31 systemically healthy controls suffering from periodontitis of comparable severity. In all participants, periodontal indices—plaque index (PI), gingival index (GI), papilla bleeding index (PBI), probing pocket depth (PPD), and clinical attachment level (CAL)—were recorded, and salivary LP was measured using a spectrophotometric method prior to treatment initiation and three months post-treatment. At baseline, mean salivary LP in DM2 patients was higher than that measured for the control group, but the difference did not reach statistical significance (p > 0.05), whereas a positive significant correlation was found between PPD and LP in both groups. Three months after nonsurgical periodontal therapy, clinical periodontal parameters and salivary LP levels were significantly reduced in both groups (p < 0.05). These findings indicate that the improvement in clinical periodontal status following nonsurgical periodontal therapy is accompanied by a significant decrease in salivary LP in DM2 patients, suggesting that periodontitis, rather than diabetes, is the primary driver of the elevated salivary LP in this group.

Antioxidant capacity is frequently measured by evaluating superoxide dismutase (SOD) concentration in body fluids. The aim of this study was to compare SOD concentrations in the saliva and plasma of patients with periodontitis to those measured in a group of patients with healthy periodontium, as well as to evaluate the influence of nonsurgical periodontal therapy on salivary and plasma SOD in periodontitis patients. For this purpose, 40 systemically healthy patients aged 30–70 years who had at least 20 teeth were recruited, 20 of whom had periodontitis, and 20 served as healthy periodontitis-free controls. In all participants, periodontal status was assessed via the plaque index (PI), gingival index (GI), papilla bleeding index (PIB), probing depth (PD), and clinical attachment level (CAL), and the SOD concentration in both saliva and plasma was determined by conducting a commercial immunoenzymatic ELISA test. In periodontitis patients, periodontal indices and saliva and blood samples were taken at the beginning of the study, as well as 3 months after periodontal therapy, while in the control group, these data were gathered at the beginning of the study only. SOD values in the saliva of patients with periodontitis (0.244 U/µL) were statistically significantly higher compared with patients with healthy periodontium (0.017 U/µL). Moreover, periodontal therapy led to a statistically significant decrease in this marker in the saliva of patients with periodontitis (p = 0.023), which was comparable with that measured in the control group. On the other hand, no statistically significant differences were noted in plasma SOD values either between the two groups or at follow-up compared with baseline in the group with periodontitis. These findings suggest that the elevated salivary SOD in patients with periodontal disease may represent a mechanism of tissue protection against oxidative stress that occurs in response to periodontal disease.

Chronic periodontitis is a common complication in diabetes. The aim of this study was to evaluate some clinical and microbiological parameters in controlled and uncontrolled type 2 diabetes mellitus (type 2 DM) patients compared to non-diabetic (ND...

The beneficial effect of autologous blood products in the post-extraction period has been proven regarding acceleration of soft tissue healing, pain reduction, swelling and trismus, but data concerning bone healing are contradictory. The objective of this study was to evaluate the effect of L-PRF on bone tissue healing after third mandibular molar extraction. Extractions of bilateral, symmetrical, impacted mandibular molars were performed in 30 patients, in a prospective split-mouth, randomized, double-blind clinical trial. L-PRF was applied to one alveolus, while the other alveolus was left to heal spontaneously. A sample of 60 extraction alveoli (the control and experimental groups, with 30 alveoli each) was analyzed. Two CBCT images were performed immediately after the surgery and eight weeks postoperatively to reconstruct the healing site and analyze the volume of the extraction defect and bone density. The depth of the periodontal pocket on the adjacent tooth was clinically measured 7 days and 8 weeks after extraction. The results show that the minimum and maximum values of the monitored parameters in the alveoli in both the control and experimental groups are within the expected range. Based on p = 0.826 (MANOVA; for I measurement) and p = 0.499 (MANOVA; for II measurement), it was concluded that no significant difference and clearly defined boundary between the groups were observed. Considering that p > 0.1 (VOL, bone density, periodontal pocket) is for both I and II measurement, no significant difference was observed between the groups regarding the wound volume, bone density and periodontal pocket.