The mesenchymal stem cells of dental pulp (DPSCs) were isolated and characterized for the first time more than a decade ago as highly clonogenic cells that were able to generate densely calcified colonies. Now, DPSCs are considered to have potential as stem cell source for orthopedic and oral maxillofacial reconstruction, and it has been suggested that they may have applications beyond the scope of the stomatognathic system. To date, most studies have shown that, regardless of their origin in third molars, incisors, or exfoliated deciduous teeth, DPSCs can generate mineralized tissue, an extracellular matrix and structures type dentin, periodontal ligament, and dental pulp, as well as other structures. Different groups worldwide have designed and evaluated new efficient protocols for the isolation, expansion, and maintenance of clinically safe human DPSCs in sufficient numbers for various therapeutics protocols and have discussed the most appropriate route of administration, the possible contraindications to their clinical use, and the parameters to be considered for monitoring their clinical efficacy and proper biological source. At present, DPSC-based therapy is promising but because most of the available evidence was obtained using nonhuman xenotransplants, it is not a mature technology.
Background: Oxidative stress (OxS) has recently been linked with osteoporosis; however, we do not know the influence of OxS as an independent risk factor for this disease.
Our findings suggest that the depletion of estrogen in postmenopause could cause oxidative stress in addition to the known symptoms.
BackgroundMenopause is the onset of aging in women. During this process, some women experience physical changes that may impact upon their psychological and social status, also affecting their quality of life. Furthermore, several psychological changes following menopause have been shown to act as pro-oxidant, but the association between the psychological status that modify the quality of life and oxidative stress in postmenopausal women is still unclear. The aim of this study was to determinate the relationship between oxidative stress with psychological disturbances, low self-esteem, depressive mood and anxiety, and quality of life in the postmenopausal women.MethodsWe carried out a cross-sectional study with101 premenopausal and 101 postmenopausal women from Mexico City. As markers of oxidative stress we measured plasma lipoperoxide levels, erythrocyte superoxide dismutase and glutathione peroxidase activities, and total antioxidant status. We calculate a stress score as global oxidative stress status, with cut-off values for each parameter; this score range from 0 to 6, representing the severity of markers modifications. All the women were rated using the Coopersmith Self-Esteem Inventory, the Zung Self-Rating Anxiety and the Zung Self-Rating Depression Scales, and the WHO Quality of Life-brief.ResultsThe postmenopausal women with low quality of life in the WHO Quality of Life-brief and their subscales had higher stress score compared with premenopausal women with high quality of life (p < 0.05). We found a positive correlation among lipoperoxide levels and Zung Self-Rating Anxiety and Zung Self-Rating Depression score (r = 0.226 and r = 0.173, respectively, p < 0.05), and a negative correlation with WHO Quality of Life-brief scores (r = −0.266, p < 0.01) in postmenopausal women. Multiple linear regression analysis revealed that average lipoperoxide levels increase by 0.0007 μmol/L for every 1-point increase in the Coopersmith Self-Esteem Inventory and by 0.001 μmol/L for every 1-point decrease in the WHO Quality of Life-brief, after adjusted for pro-oxidant factors. Zung Self-Rating Anxiety and Zung Self-Rating Depression Scales scores also contribute to increase lipoperoxides levels, but not significant.ConclusionOur findings suggest that oxidative stress is increased in postmenopausal women with psychological disturbances and low quality of life.
Periodontitis is a chronic disease that begins with a period of inflammation of the supporting tissues of the teeth table and then progresses, destroying the tissues until loss of the teeth occurs. The restoration of the damaged dental support apparatus is an extremely complex process due to the regeneration of the cementum, the periodontal ligament, and the alveolar bone. Conventional treatment relies on synthetic materials that fill defects and replace lost dental tissue, but these approaches are not substitutes for a real regeneration of tissue. To address this, there are several approaches to tissue engineering for regenerative dentistry, among them, the use of stem cells. Mesenchymal stem cells (MSC) can be obtained from various sources of adult tissues, such as bone marrow, adipose tissue, skin, and tissues of the orofacial area. MSC of dental origin, such as those found in the bone marrow, have immunosuppressive and immunotolerant properties, multipotency, high proliferation rates, and the capacity for tissue repair. However, they are poorly used as sources of tissue for therapeutic purposes. Their accessibility makes them an attractive source of mesenchymal stem cells, so this review describes the field of dental stem cell research and proposes a potential mechanism involved in periodontal tissue regeneration induced by dental MSC.
Oxidative stress (OS) is the imbalance between oxidant and antioxidant molecules, in favor of oxidants, that causes aging and disease. Many studies have been published that demonstrate the relationship between OS and human health and disease; however, the following questions arise: (i) how are we sure that the OS is present in a biological process? (ii) Is the OS reported in the different investigations equivalent? (iii) What are the best oxidant and antioxidant markers for OS diagnosis? (iv) Can we establish the types and the intensity of the OS? (v) Does OS index could be useful for research and/or application in clinical medicine? In this regard, several indexes have been proposed to measure OS in humans relative to the state of health and disease, among which the following can be highlighted: Oxidative Stress Index (OSI), Tiol Ratios (-SH/TT, -SS/-SH, and-SS/TT), Glutathione Ratio (GSSG/GSH), Oxidative Stress Score (OSS), and OXY-index. Therefore, the aim of this review is to present the state of the art of knowledge about OS indexes for diagnosis of health or disease in humans. We searched for articles in English or Spanish in the PubMed/MEDLINE and Scopus electronic databases published up until May 2019. The keywords used were “oxidative stress,” “index,” and “oxidative stress index.” It was identified 11479 records in both databases, and 490 articles were analyzed. Our review suggests that all indexes analyzed allow diagnose and differentiate the OS related to human health and disease. Also, the studies on OSI, Oxy-score, and OSS indexes have proven to be reliable, practical, and with clinical utility. However, it is necessary to continue with longitudinal studies, especially assess the usefulness of the indexes in the clinical prognosis, and make comparative studies between the different indexes.
MENDOZA-NÚÑEZ, V.M., RUIZ-RAMOS, M., SÁNCHEZ-RODRÍGUEZ, M.A., RETANA-UGALDE, R. and MUÑOZ-SÁNCHEZ, J.L. Aging-Related Oxidative Stress in Healthy Humans. Tohoku J. Exp. Med., 2007, 213 (3), 261-268 Oxidative stress has been reported to increase with aging; however, the scientifi c evidence is controversial. We therefore aimed to analyze the relationship between aging and some markers of oxidative stress. A crosssectional and comparative study was carried out in a sample of 249 healthy subjects: (i) 25-29 years (n = 22); (ii) 30-39 years (24); (iii) 40-49 years (30); (iv) 50-59 years (48); (v) 60-69 years (60), and (vi) 70 years (65). We measured lipoperoxides and total antioxidant status in plasma and superoxide dismutase and glutathione peroxidase activities in erythrocytes. There was an age-related increase in lipoperoxides, which was evident in the comparison of the group of 25-29 years (0.22 ± 0.11 μ mol/l) with the group of 60-69 years (0.38 ± 0.18 μ mol/l, p < 0.01) and 70 years (0.42 ± 0.19, p < 0.001). Conversely, the total antioxidant status showed an age-related decrease (25-29 years, 1.4 ± 0.31 mmol/l vs 60-69 years, 1.1 ± 0.21 and 70 years, 1.1 ± 0.22, p < 0.05 for each). In erythrocytes, glutathione peroxidase activity showed an age-related decrease (25-29 years, 7,966 ± 1,813 UI/l vs 60-69 years, 6,193 ± 2,235 and 70 years, 6,547 ± 2,307, p < 0.001 for each), whereas superoxide dismutase activity was similar in all age groups. Importantly, there was no age-related change in oxidative stress markers in subjects of < 60 years. These fi ndings suggest that age of 60 years may be associated with increased oxidative stress.aging; oxidative stress; superoxide dismutase; lipoperoxides; antioxidant enzymes
Alpha-lipoic acid (ALA) has been used as a dietary supplement at different doses in patients with diabetes mellitus type 2 (T2DM) due to its antioxidant, anti-inflammatory, and hypoglycemic effects. However, the reports on the effects of ALA are controversial. For this reason, the purpose of the present study was to determine the effect of 600 mg/day of ALA on the markers of oxidative stress (OxS) and inflammation and RAGE in older adults with T2DM. A quasiexperimental study was carried out with a sample of 135 sedentary subjects (98 women and 37 men) with a mean age of 64±1 years, who all had T2DM. The sample was divided into three groups: (i) experimental group (EG) with 50 subjects, (ii) placebo group (PG) with 50 subjects, and control group (CG) with 35 subjects. We obtained the following measurements in all subjects (pre- and posttreatment): glycosylated hemoglobin (HbA1c), receptor for advanced glycation end products (RAGE), 8-isoprostane, superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant status (TAS), and inflammatory (CRP, TNF-α, IL-6, IL-8, and IL-10) markers. Regarding the effect of ALA on HbA1c, a decrease was observed in the EG (baseline 8.9±0.2 vs. posttreatment 8.6±0.3) and the PG (baseline 8.8±0.2 vs. posttreatment 8.4±0.3) compared to the CG (baseline 8.8±0.3 vs. six months 9.1±0.3) although the difference was not statistically significant (p<0.05). There was a statistically significant decrease (p<0.05) in the blood concentration of 8-isoprostane in the EG and PG with respect to the CG (EG: baseline 100±3 vs. posttreatment 57±3, PG: baseline 106±7 vs. posttreatment 77±5, and CG: baseline 94±10 vs. six months 107±11 pg/mL). Likewise, a statistically significant decrease (p<0.05) in the concentration of the RAGE was found in the EG (baseline 1636±88 vs. posttreatment 1144±68) and the PG (baseline 1506±97 vs. posttreatment 1016±82) compared to CG (baseline 1407±112 vs. six months 1506±128). A statistically significant decrease was also observed in all markers of inflammation and in the activity of SOD and GPx in the CG with respect to the EG and PG. Our findings suggest that the administration of ALA at a dose of 600 mg/day for six months has a similar effect to that of placebo on oxidative stress, inflammation, and RAGE in older adults with T2DM. Therefore, higher doses of ALA should be tried to have this effect. This trial is registered with trial registration number ISRCTN13159380.
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