Although recent short-term cross-sectional studies have revealed that chronic periodontitis (CP) may be a risk factor for increased cognitive impairment in patients with Alzheimer’s disease (AD), systematic reviews and long-term longitudinal studies have provided less clear evidence regarding the relationship between CP and AD. Therefore, we conducted a retrospective cohort study using the National Health Insurance Research Database (NHIRD) of Taiwan to determine whether patients with CP are at increased risk of developing AD. We conducted a retrospective matched-cohort study using the NHIRD of Taiwan. We identified 9291 patients newly diagnosed with CP between 1997 and 2004. A total of 18,672 patients without CP were matched to the patient cohort according to sex, age, index year, co-morbidity and urbanisation level. Cox proportional hazards regression analyses were performed to evaluate the subsequent risk of AD. Patients with CP had a higher prevalence of hyperlipidaemia, depression, traumatic brain injury and co-morbidities, as well as higher urbanisation levels, than those in the unexposed cohort (all p < 0.01). At the final follow-up, totals of 115 (1.24%) and 208 (1.11%) individuals in the CP exposed and unexposed groups, respectively, had developed AD. Patients with 10 years of CP exposure exhibited a higher risk of developing AD than unexposed groups (adjusted HR 1.707, 95% CI 1.152–2.528, p = 0.0077). Our findings demonstrate that 10-year CP exposure was associated with a 1.707-fold increase in the risk of developing AD. These findings highlight the need to prevent progression of periodontal disease and promote healthcare service at the national level.

Background:  Platelet‐rich fibrin (PRF) prepared by Choukroun’s technique is derived from an autogenous preparation of concentrated platelets without any manipulation. PRF was found to increase osteoblast growth and proliferation. However, the underlying mechanisms are not yet completely understood. This study aimed to determine the effects of PRF on cell attachment, proliferation, phosphorylated Akt, heat shock protein 47 (HSP47) and lysyl oxidase (LOX) expression on human osteoblasts.Methods:  Blood collection was carried out from 10 healthy volunteers. Cell attachment and proliferation were measured by colorimetric assay with WST‐1 and alamar blue in human osteoblast cell line U2OS cells, respectively. Western blot was employed to evaluate the expression of p‐Akt, HSP47 and LOX.Results:  PRF alone was found to stimulate U2OS cell attachment compared with untreated controls (p < 0.05). PRF was found to increase osteoblast proliferation during a 5‐day incubation period (p < 0.05). PRF was found to increase Akt phosphorylation in a time‐dependent manner (p < 0.05). Collagen‐related proteins HSP47 and LOX were significantly elevated by stimulation with PRF compared with untreated controls (p < 0.05).Conclusions:  It is suggested that PRF is capable of increasing osteoblast attachment, proliferation and simultaneously upregulating collagen‐related protein production. These actions in combination would effectively promote bone regeneration.

Background: The cause−effect relation between periodontal inflammatory disease (PID) and Parkinson’s disease (PD) remains uncertain. The purpose of our study was to investigate the association between PID and PD. Methods: We conducted a retrospective matched-cohort study by using Taiwan’s National Health Insurance Research Database. We identified 5,396 patients with newly diagnosed PID during 1997–2004 and 10,792 cases without PID by matching sex, age, index of year (occurrence of PID), and comorbidity. Cox proportional hazard regression was used to evaluate the risk of subsequent PD. Results: At the final follow-up, a total of 176 (3.26%) and 275 (2.55%) individuals developed PD in the case and control groups, respectively. Patients with PID have a higher risk of developing PD (adjusted hazard ratio = 1.431, 95% CI [1.141–1.794], p = 0.002). Discussion: Our results show that PID is associated with an increased risk of developing PD. Whilst these findings suggest that reducing PID may modify the risk of developing PD, further study will be needed.