Bacteria associated with periodontal disease are also increased in health.

BACKGROUND: The objective of this cross-sectional clinical study was to analyze the differences in the microbiome in gingival sulci of adult patients in the presence or absence of chronic periodontitis. MATERIAL AND METHODS: Patients with or without periodontal disease were included in this cross-sectional study. Subgingival biofilm samples were collected and analyzed by 16S massive pyrosequencing. Functional analyses were also performed. RESULTS: A total of 15 phyla, 154 genera and 351 species were detected globally. Differences between disease and non-disease samples were observed in all taxonomical levels which suggest functional profile changes in the community. It was found that the main species associated with non-disease samples were reduced in disease but not completely suppressed. Analysis of the functional potential of the biofilms revealed a significantly higher activity related to endocytosis and phosphatidylinositol signaling in the disease group but lower cell adhesion molecules. CONCLUSIONS: Specific differences between health and disease suggest functional profile changes in the community, although bacteria associated with periodontal disease are also increased in health. Transcriptome studies should be conducted to confirm and deepen metabolic dysfunctions.

Inferior alveolar nerve trajectory, mental foramen location and incidence of mental nerve anterior loop.

OBJECTIVES: Injury of the inferior alveolar nerve (IAN) is a serious intraoperative complication that may occur during routine surgical procedures, such as dental implant placement or extraction of impacted teeth. Thus, the purpose of this study was to analyze the trajectory of the mandibular canal (MC), the location of the mental foramen (MF) and the presence and extension of an anterior loop of the mental nerve (AL). STUDY DESIGN: In this cross-sectional study, a total of 348 CBCTs were analyzed. Distances from MC to the surface of the basal, medial and lateral cortical of the mandible were measured at the level of the second molar, first molar and second premolar. Location of the MF relative to the apices of the premolars, as well as incidence and anterior extent of the AL were also determined. RESULTS: Significant and clinically relevant correlations were found between the position of the MC in women, which was located more caudal (r=-0.219, p=0.007; r=-0.276, p<0.001; right and left, respectively) and lateral (r=-0.274, p=0.001; r=-0.285, p<0.001; right and left, respectively), particularly at the level of the premolars. Additionally, the presence (r=-0.181, p=0.001; r=-0.163, p=0.002; right and left, respectively) and anterior extension (r=-0.180, p=0.009; r=-0.285, p=0.05; right and left, respectively) of the AL was found to be inversely correlated with the age of the patient. CONCLUSIONS: This analysis of a Caucasian population has found that the older the patient, the lower the incidence of the loop and the shorter its anterior extension.

Periostin increases migration and proliferation of human periodontal ligament fibroblasts challenged by tumor necrosis factor -α and Porphyromonas gingivalis lipopolysaccharides.

BACKGROUND: In the chronic established periodontal lesion, the proliferation and migration potential of periodontal ligament (PDL) cells are significantly compromised. Thus, the progressive loss of tissue integrity is favored and normal healing and regeneration compromised. Periostin, a known PDL marker, modulates cell-matrix interactions, cell behavior, as well as the matrix biomechanics and PDL homeostasis. OBJECTIVE: To evaluate whether periostin restores the regenerative potential of PDL cells in terms of proliferation, migration, and activation of survival signaling pathways after being challenged by Porphyromonas gingivalis lipopolysaccharides and tumor necrosis factor alpha α. METHODS: Human PDL (hPDL) cells were cultured under different conditions: control, periostin (50 or 100 ng/mL), and fibroblast growth factor 2 (10 ng/mL) to evaluate cell proliferation (by Ki67), cell migration (by scratch assays) and PI3K/AKT/mTOR pathway activation (by western blot analyses of total AKT, phospho-AKT and PS6). A different set of cultures was challenged by adding tumor necrosis factor alpha α (10 ng/mL) and P. gingivalis lipopolysaccharides (200 ng/mL) to evaluate the effects of periostin as described above. RESULTS: Periostin significantly increased cell proliferation (twofold), migration (especially at earlier time points and low dose) and activation of survival signaling pathway (higher phosphorylation of AKT and PS6). Furthermore, periostin promoted similar cellular effects even after being challenged with proinflammatory cytokines and bacterial virulence factors. CONCLUSION: Periostin acts as an important modulator of hPDL cell-matrix dynamics. It modulates hPDL proliferation, migration and PI3K/AKT/mTOR pathway. It also helps in overcoming the altered biological phenotype that chronic exposure to periodontal pathogens and proinflammatory cytokines produce in hPDL cells.

Periostin is down-regulated during periodontal inflammation.

Periostin, a matricellular adapter protein highly expressed by periodontal ligament fibroblasts, is implicated in the maintenance of periodontal integrity, which is compromised during periodontal diseases. The aim of this study was to explore the influence of chronic periodontal inflammation on tissue periostin levels. Periodontal breakdown was induced in a pre-clinical ligature periodontal inflammatory disease model. Periodontal tissue specimens were harvested at baseline, 2 weeks, and 4 weeks and prepared for histologic, immunofluorescence, and micro-CT examination. Statistical analyses were conducted by Kruskal-Wallis, Mann-Whitney, and Spearman's tests. Periostin detection levels were reduced over time in response to the inflammatory process (1 ± 0.05; 0.67 ± 0.03; 0.31 ± 0.02; p < 0.001; baseline, 2, and 4 weeks, respectively). Simultaneously, alveolar bone loss increased from baseline to the 2- and 4-week time-points (0.40 ± 0.02 mm; 1.39 ± 0.08 mm; 1.33 ± 0.15 mm; p < 0.001), which was inversely correlated with the levels of periostin (ρ = -0.545; p < 0.001). In conclusion, periostin PDL tissue levels significantly decrease under chronic inflammatory response and correlate with the detrimental changes to the periodontium over time.