Important oxidative stress associated with alveolar bone loss biomarkers can be detected in saliva of patients with periodontal disease.

Oral lichen planus (OLP) is a relatively common disorder whose cause is still unknown. Oral cancer is preceded in most cases by pre malignant lesions-leukoplasia, submucous fibrosis and lichen planus. Free radicals and reactive oxygen species play important roles in both pathogenesis of lichen planus and carcinogenesis. Thus monitoring systemic and saliva compounds important for the antioxidant defence (oxidative balance) could be important for the clinician's treatment strategy. Thorough medical management and early active treatment are necessary to improve symptoms and might also be a relevant prevention strategy from squamous cell carcinoma risk, although data to fully support this statement still need investigation. The principal aim of this study was to determine the systemic uric acid, GGT, and albumin levels as well as the levels of uric acid and albumin in 20 patients diagnosed with lichen planus and 20 controls. Extensive medline search failed to reveal any study of this type. Our results showed a significant decrease of saliva (p < 0.005) uric acid and an increase in serum gamma glutamyl transpherase (GGT) (p < 0.01) as well as in the total antioxidant capacity of saliva in patient group with respect to the control one. The preliminary conclusion of our study is that uric acid, the most important salivary antioxidant and GGT could be considered in the future as useful markers of oxidative stress for elaboration of treatment strategy and monitoring.

There are few reports concerning the potential for clinical application of oxidative stress (OS) and collagen degradation markers in oral lichen planus (OLP) patients. We investigated the possibility of using some disease-related biomarkers in saliva and serum of OLP patients. Our study included 30 patients with OLP and 30 controls. We evaluated serum and salivary OS biomarkers including 8-OHdG, MDA, uric acid, TAC and GPx. We also investigated collagen degradation markers such as CTX I and MMP-8. We found significantly increased salivary levels of MMP-8 and CTX I in the OLP group compared to controls and significant differences between the OLP and control groups in serum and saliva for 8-OHdG, MDA (significantly increased), uric acid, TAC and GPx (significantly reduced). Currently there are no criteria for evaluating which OLP patients have a greater risk of malignant transformation. In addition to clinical surveillance, the serum and salivary biomarkers that we evaluated may be useful biomarkers for monitoring OLP patients in the future.

Periodontitis represents a complex inflammatory disease that compromises the integrity of the tooth-supporting tissue through the interaction of specific periodontal pathogens and the host’s immune system. Experimental data help to outline the idea that the molecular way towards periodontitis initiation and progression presents four key steps: bacterial infection, inflammation, oxidative stress, and autophagy. The aim of this review is to outline the autophagy involvement in the pathogenesis and evolution of periodontitis from at least three points of view: periodontal pathogen invasion control, innate immune signaling pathways regulation and apoptosis inhibition in periodontal cells. The exact roles played by reactive oxygen species (ROS) inside the molecular mechanisms for autophagy initiation in periodontitis still require further investigation. However, clarifying the role and the mechanism of redox regulation of autophagy in the periodontitis context may be particularly beneficial for the elaboration of new therapeutic strategies.

Saliva is the first biological fluid that inhaled cigarette smoke (CS) encounters. CS contains several carcinogens known to initiate and promote tumourigenesis and metastasis. One of the aims of this study was to establish if glutathione peroxidase and gamma-glutamyltranspherase (GGT) could be used as possible markers for evaluating the oral oxidative stress caused by smoking. The effect of CS on free radical generation was investigated using two methods. Using different assays, different antioxidants present in saliva may be evidenced due to the different principles on which they are based. Our results indicate that exposure to CS caused a statistically significant decrease of both salivary glutathione peroxidase (p < 0.01) and salivary GGT (p < 0.01). We also found that exposure to CS caused a statistically significant decrease of salivary total antioxidant status (p < 0.01). Such decreases may have a consistent role in the mechanisms by which the toxic effects of CS initiate oral inflammatory diseases, promote precancerous transformations, and destroy the oral cavity homeostasis. Therefore the evaluation of total antioxidant capacity of saliva is important but it must be done together with the evaluation of salivary specific markers of oxidative stress, such as uric acid, albumin and possibly, GGT.