Aim To investigate pathways between unhealthy and healthy dietary patterns and periodontitis in adolescents (18–19 years of age). Materials and Methods This population‐based study (n = 2515) modelled direct and mediated pathways (via biofilm and obesity) from patterns of healthy diet (fruits, fibre, vegetables, and dairy) and unhealthy diet (sugars, snacks, and salty/fast foods) with initial periodontitis (bleeding on probing [BoP], probing depth [PD] ≥ 4 mm, clinical attachment loss [CAL] ≥ 4 mm), moderate periodontitis (BoP, PD ≥ 5 mm, and CAL ≥ 5 mm), and European Federation of Periodontology and the American Academy of Periodontology (EFP‐AAP) periodontitis definitions, adjusting for sex, socio‐economic status, smoking, and alcohol, through structural equation modelling (α = 5%). Results Higher values of healthy diet were associated with lower values of initial periodontitis (standardized coefficient [SC] = −0.160; p < .001), moderate periodontitis (SC = −0.202; p < .001), and EFP‐AAP periodontitis (p < .05). A higher value of unhealthy diet was associated with higher values of initial periodontitis (SC = 0.134; p = .005) and moderate periodontitis (SC = 0.180; p < .001). Biofilm mediated the association between higher values of unhealthy diet and all periodontal outcomes (p < .05). Conclusions Our findings suggest that both healthy and unhealthy dietary patterns may contribute to reduced or increased extent and severity of periodontitis by local and systemic mechanisms, preceding the effect of other established causes such as smoking and obesity, in younger population.

Aim: To evaluate the association between low bone mineral density (BMD) and severe periodontitis at the end of the second decade of life.Materials and methods: This population-based study analysed 2032 youngers (18-19 years old) of the RPS cohort. BMD of lumbar spine (BMD-LS) and of the whole body (BMD-WB) were assessed by dual x-ray emission densitometry. Low BMD-LS (Z-score ≤ À2) and low BMD-WB (Z-score ≤ À1.5) were correlated with severe periodontitis. The extent of periodontal disease was also evaluated as the following outcomes: proportions of teeth affected by clinical attachment loss ≥5 mm and probing depth ≥5 mm. Multivariate models by sex, education, family income, risk of alcohol dependence, smoking, plaque, bleeding index, and body mass index were estimated through logistic regression (binary outcomes) and Poisson regression (continuous outcomes).Results: The prevalence of severe periodontitis was 10.97%. Low BMD-LS (odds ratio [OR] = 2.08, confidence interval [CI] = 1.12-3.85, p = .01) and low BMD-WB (OR = 1.34, CI = 1.001-1.81, p = .04) were associated with severe periodontitis in the final multivariate models. Low BMD-LS and BMD-WB were also associated with a greater extent of periodontitis (p < .05).Conclusions: Low BMD was found to be associated with the severity and extent of periodontitis in adolescents. Adolescents at peak bone mass age presenting low BMD are more likely to be affected by severe periodontitis.

Aim: To investigate the association between increased serum markers of iron (ferritin and transferrin saturation) and the severity and extent of periodontitis in postmenopausal (PM) women.Materials and Methods: Data from 982 PM women participating in NHANES III were analysed. Exposures were high ferritin (≥300 μg/ml) and transferrin saturation (≥45%). The primary outcome was moderate/severe periodontitis defined according to Centers for Disease Control and Prevention and the American Academy of Periodontology. The extent of periodontitis was also assessed as outcome: proportion of sites affected by clinical attachment loss ≥4 mm and probing depth ≥4 mm. Crude and adjusted prevalence ratio (PR) and mean ratio (MR) were estimated using Poisson regression. Results:The prevalence of moderate/severe periodontitis was 27.56%. High ferritin was associated with moderate/severe periodontitis in the crude (PR 1.55, p = .018) and in the final adjusted model (PR 1.53, p = .008). High ferritin and transferrin saturation levels were associated with a higher proportion of sites with clinical attachment loss ≥4 mm (p < .05). Conclusions:The increasing serum iron markers seem to contribute to periodontitis severity and extent in PM women.

Aim To investigate the association among iron overload, periodontal status, and periodontitis progression rate in sickle cell anaemia (SCA). Materials and Methods This case series evaluated 123 patients. Clinical attachment level (CAL) and probing depth (PD) were evaluated at six sites per tooth. Alveolar bone loss was estimated using periapical radiography. Study outcomes were periodontal status (measured as number of sites with CAL of ≥3 mm, CAL of ≥5 mm, PD of ≥4 mm, and PD of ≥6 mm) and periodontitis progression rate (determined as ratio of alveolar bone loss to age). Serum transferrin saturation and ferritin levels were obtained from medical records. Poisson regression was performed to estimate associations. Covariables included in the adjusted models (comorbidities, skin colour, socioeconomic class, and vaso‐occlusive crisis) were defined by DAGs. Results Serum transferrin saturation level revealed a significant positive association with the number of sites with CAL of ≥3 mm, CAL of ≥5 mm, PD of ≥4 mm, and PD of ≥6 mm. Patients with serum transferrin saturation level of >45% were 1.93 times more likely to have rapid periodontitis progression. Conclusion High serum transferrin saturation level is associated with a greater extent of periodontitis and rapid periodontitis progression in SCA.

Studies have suggested an important role of dyslipidemia, a condition with alterations in blood lipid levels, in promoting an additional effect on periodontal breakdown. Thus, this study aimed to explore the theoretical pathways associated with dyslipidemia and periodontitis. We used data from 11,917 US adults with complete periodontal examinations participating in the Third National Health and Nutrition Examination Survey (NHANES III). Our hypothesis was tested using structural equation modelling (SEM). Dyslipidemia was defined according to the National Cholesterol Education Program (NCEP-ATP III) and periodontitis as a latent variable reflecting the shared variance of the number of surfaces with periodontal pocket depth [PPD] = 4 mm, PPD = 5 mm, PPD ≥ 6 mm, clinical attachment level [CAL] = 4 mm, CAL = 5mm, CAL ≥ 6 mm, and furcation involvement. The model also considered distal determinants (age, sex, and socioeconomic status) and proximal determinants (HbA1c, smoking and alcohol consumption, and obesity). The model showed sufficient global fit (Root Mean Squared Error of Approximation = 0.04, 90%CI = 0.04–0.05, Tucker–Lewis Index = 0.93, Comparative Fit Index = 0.95). Age, sex, socioeconomic status, obesity, and smoking were directly associated with periodontitis (p < 0.01). Dyslipidemia revealed a significant direct effect on periodontitis (standardized coefficient [SC] = 0.086, SE 0.027; p < 0.01), also mediated via an indirect pathway through HbA1c (SC = 0.021; SE 0.010; p = 0.02) and obesity (SC = 0.036; SE 0.012; p < 0.01) and resulted in a total effect on periodontitis. Dyslipidemia was associated with periodontitis through a direct pathway and indirectly through HbA1c and obesity in the US population. These results support the need for a multi-professional approach to tackling oral and noncommunicable diseases (NCDs), directed at their common risk factors.

Periodontitis is a common finding among people with diabetes mellitus (DM) and has been cited as a DM complication. Whether and how periodontitis relates to other diabetes-related complications has yet to be explored. This study aims to examine the clustering of periodontitis with other diabetes-related complications and explore pathways linking diabetes-related complications with common risk factors. Using data from participants with DM across 3 cycles of the National Health and Nutrition Examination Survey (NHANES) ( n = 2,429), we modeled direct and indirect pathways from risk factors to diabetes-related complications, a latent construct comprising periodontitis, cardiovascular diseases, proteinuria, and hypertension. Covariates included age, sex, socioeconomic status (SES), smoking, physical activity, healthy diet, alcohol consumption, hemoglobin A1c (HbA1c), dyslipidemia, and body mass index (BMI). Sensitivity analyses were performed considering participants with overweight/obesity and restricting the sample to individuals without DM. Periodontitis clustered with other diabetes complications, forming a latent construct dubbed diabetes-related complications. In NHANES III, higher HbA1c levels and BMI, older age, healthy diet, and regular physical activity were directly associated with the latent variable diabetes-related complications. In addition, a healthy diet and BMI had a total effect on diabetes-related complications. Although sex, smoking, dyslipidemia, and SES demonstrated no direct effect on diabetes-related complications in NHANES III, a direct effect was observed using NHANES 2011–2014 cycles. Sensitivity analysis considering participants with overweight/obesity and without DM showed consistent results. Periodontal tissue breakdown seems to co-occur with multiple diabetes-related complications and may therefore serve as a valuable screening tool for other well-known diabetes-related complications.

The objective of this case report was to describe the retreatment of an immature upper right central incisor in a 20-year-old female patient after unsuccessful endodontic treatment, who had probable clinical-radiographic diagnosis of a large periapical inflammatory cyst and persistent fistula. After removing the root canal filling material, disinfection of the root canal system, and successive intracanal medication changes over 60 days, the fistula remained active. Therefore, parendodontic surgery was performed. The root canal system was obturated, the periapical cyst was surgically enucleated, and retro-obturation with mineral trioxide aggregate was performed. We used the guided tissue regeneration technique with a xenograft and resorbable membrane. On histopathological examination, we observed bacterial colonies present in the lumen of the cystic lesion. Clinical evaluation, periapical radiograph, and cone-beam tomography confirmed complete healing of the periapical area of the affected tooth. The treatment success was verified by periapical healing over a follow-up period of 21 months.

This report describes the oral manifestations of renal tubular acidosis (RTA) associated with secondary rickets and discusses the biological plausibility of these findings. The characteristic electrolyte changes during RTA or genetic mutations that trigger RTA may be responsible for impaired amelogenesis, dental malocclusion, impacted teeth, and absent lamina dura. This report reinforces the possibility of an association between RTA and the oral manifestations described.