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The human genetic variation is a valuable source of information in various fields, including forensic identification. However, not all forensic questions can be answered through genetic examination, and further development in the field of DNA analysis continues to be improved, especially in the field of epigenetics. Understanding epigenetics and its relationship with dental anthropology is believed to be useful for further development of DNA analysis in forensic science, for solving cases through distinctive epigenetic modifications in an individual. The epigenetic approach in the field of forensic dental anthropology has not been widely studied. This brief review aims to analyze the relationship between epigenetics and dental anthropology for the development of the field of forensic dentistry. [ABSTRACT FROM AUTHOR]

Background & Aim: To investigate the potential of cardiovascular disease as risk factor for periodontal disease in the context of current etiology model. Methods: It was used a cross-sectional sample consisting of 374 dentate adults, age >30 years. Subjects were selected from patients attending periodontal care between years 2016-2017 in the Faculty of Dentistry Constanta Romania, South-Eastern Europe. Ethical approval was obtained from the local ethics committee and each patient signed an informed consent form. The self-reported systemic condition was used for the evaluation. In addition, periodontal probing depth (PPD), bleeding on probing (BOP) and CPITN index were used to assess the periodontal involvement. In order to relate systemic status among severity of periodontal disease, all patients were categorized according to their maximum PPD: with PPD of <4 mm (no periodontitis), with PPD of =4 (periodontitis). Data were analyzed using IBM SPSS statistics software version 20. Results: It was found dependent relation between periodontitis and cardiovascular disease (CVD) odds ratio (OR) = 5; 95% confidence interval (CI): 2.41-10.34. No statistical significant relation was found between BOP and CVD (p=0.09). Patients with CVD have higher mean of CPITN score (3,2±0,72) as compared with patients without CVD (2,56±0,85). The presence of CVD and periodontitis were not correlated to sex (÷2 calc = 1.74, df = 1, p = 0.186 > á = 0.05). Conclusions: In this adult population, cardiovascular disease may act as risk factor for periodontal disease, in terms of pocket formation. Those findings fit with the current etiology model, together with other etiological factors. [ABSTRACT FROM AUTHOR]

Periodontitis is a risk factor for coronary heart disease (CHD). Both diseases are an inflammatory diseases and have the same potential pathogenic mechanisms. Interleukin-1β as a pro-inflammatory main cytokine, can be found in this both diseases. Gingival crevicular fluid (GCF) derived from the serum of gingival sulcus, affected by inflammatory mechanism and the amount of this fluid will increase in that situation. Objective: To analyze the relationship of interleukin-1β levels in gingival crevicular fluid (GCF) of CHD and non-CHD patients with periodontal status. Methods: Oral clinical examination (plaque index, bleeding on probing, pocket depth and clinical attachment loss) for 35 subjects with CHD and 35 non CHD were checked, laboratory test to measure the levels of Interleukin-1β was checked with enzyme-linked immunosorbent assay (ELISA). Results: There was no significant differences between interleukin-1β levels in CHD and non-CHD patients (p>0.05); there was no significant difference between the level of Interleukin-1β with periodontal status in CHD and control (non CHD) patients (p>0.05). Conclusions: levels of Interleukin-1β in CHD patients do not have a relationships with plaque index, pocket depth and clinical attachment loss, but has a relationships with bleeding on probing. [ABSTRACT FROM AUTHOR]

Periodontitis is a risk factor for coronary heart disease (CHD). Both diseases are an inflammatory diseases and have the same potential pathogenic mechanisms. Interleukin-1β as a pro-inflammatory main cytokine, can be found in this both diseases. Gingival crevicular fluid (GCF) derived from the serum of gingival sulcus, affected by inflammatory mechanism and the amount of this fluid will increase in that situation. Objective: To analyze the relationship of interleukin-1β levels in gingival crevicular fluid (GCF) of CHD and non-CHD patients with periodontal status. Methods: Oral clinical examination (plaque index, bleeding on probing, pocket depth and clinical attachment loss) for 35 subjects with CHD and 35 non CHD were checked, laboratory test to measure the levels of Interleukin-1β was checked with enzyme-linked immunosorbent assay (ELISA). Results: There was no significant differences between interleukin-1β levels in CHD and non-CHD patients (p>0.05); there was no significant difference between the level of Interleukin-1β with periodontal status in CHD and control (non CHD) patients (p>0.05). Conclusions: levels of Interleukin-1β in CHD patients do not have a relationships with plaque index, pocket depth and clinical attachment loss, but has a relationships with bleeding on probing. [ABSTRACT FROM AUTHOR]

Aim: To investigate the potential systemic risk factors for periodontal disease in a population from Constanta, Romania. Method: A cross-sectional sample consisting of 740 dentate adults 18-85 years of age (mean 39,9±17,89) were selected from patients attending dental clinics of Constanta Faculty between 2012-2013. The charts of patients were examined to determine patient's self-reported systemic condition: diabetes, cardiovascular pathology. In addition, periodontal probing depth (PPD) and bleeding on probing (BOP) was used to assess the periodontal status. Ethical approval was obtained from the local ethics committee and each patient signed an informed consent. For the purpose of this study and in order to relate systemic status among severity of periodontal disease, all patients were categorized according to their maximum PPD: with PPD of <3.5 mm (no periodontitis), with PPD of =3.5 but not exceeding 6 mm (periodontitis with moderate pockets), or =6 mm (periodontitis with deep pockets). Results: It was found dependent relation between BOP and cardiovascular disease (CVD) (p=0.001), odds ratio (OR)=2.65, 95% confidence interval (CI) for OR: 1.43- 4.91. CVD was also associated with the presence of periodontitis (p<0.001), OR=6.82, 95% CI for OR: 3.91-11.91. Self-reported diabetes was associated with the risk for periodontal disease (p <0.001), relative risk RR=2.31, 95% CI for RR: 1.94-2.76. The relative risk for deep pockets formation in diabetic patients is 1.43, 95% CI for RR: 1.10-1.87. BOP was also associated with diabetes (p=0.008). No significant relation of dependence was found between CVD and deep pocket formation (p=0.437). Conclusion: Cardiovascular disease and diabetes are both risk factors for periodontal disease in terms of bleeding on probing in this adult population. Diabetes increases also the risk for deep pocket formation, which can aggravate the evolution of periodontal disease. [ABSTRACT FROM AUTHOR]

Aim: The present study assesses the percentages of cases with deep pockets attributable to cigarette smoking in an adult urban population from Constanta. Methods: A randomly-selected sample comprising 483 dentate individuals from 528 eligible individuals for the survey was chosen among patients addressing for dental treatment in Constanta Dental Faculty. A full-mouth clinical examination was performed and an interview using a structured written questionnaire was undertaken. A multivariate analysis for complex surveys was performed, and adjusted for age, gender, plaque index and dental calculus index. The null hypothesis was no significant clinical differences regarding plaque deposits, calculus accumulation and pocket depth between smokers and non-smokers. Results: Overall, 47% of this adult population, or 219 individuals have been exposed to cigarette smoking. In the youngest age group, under 35 years old, 55% are current smokers, the highest prevalence of smoking compared with the other age groups. The mean age of the study group is 38,39 years (SD 17,78), with a mean of 43,39 years (SD 19,43) in non-smokers group and 32,20 years (SD 13,32) in the smokers group. Positive differences were found between plaque depositions in smokers, which exhibit higher plaque accumulation (P=0,0095) compared with non-smokers. Significant statistical differences (Wilcoxon test) were found between levels of calculus accumulation in total study group smokers compared with non-smokers P=0,0034, the smoking habit being associated with higher calculus accumulation. The periodontal disease attributable fraction (AF) for the whole study group is 46,24%, with the value of 38,54% in adults <35 years old. The population attributable risk (PAR) to develop deep pockets due to smoking is higher in individuals 35-44 years old (0,11) as compared with other age groups. The population attributable fraction (PAF) has highest value in individuals 35-44 years old (55,65%). Conclusion: Cigarette smoking was associated with plaque and calculus accumulations, deep pocket formation and adult periodontitis in this study population, and a significant percentage of cases could have been prevented if smoking cessation interventions had been implemented. [ABSTRACT FROM AUTHOR]