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Background: Monocyte chemoattractant protein-1 (MCP-1), macrophage migration inhibitory factor (MIF), and fractalkine are chemokines that are expressed by a variety of cell types to regulate macrophage inflammatory response. The aim of the study was to examine the effects of periodontitis and rheumatoid arthritis (RA) on their serum and salivary concentrations.Methods: Adults with either periodontitis (P, n = 21), or with rheumatoid arthritis (RA, n = 23), or with both diseases (RA+P, n = 23) were included in the study. Systemically and periodontally healthy individuals (n = 22) served as controls. Saliva and serum samples were collected from all participants before the medical and periodontal examinations. Salivary and serum MCP-1, MIF, and fractalkine concentrations were measured by the Luminex technique. Total salivary protein levels were determined by the Bradford assay.Results: Salivary MCP-1, MIF, and fractalkine concentrations were elevated in both RA groups (RA+P and RA) in comparison with systemically healthy controls. As related to total salivary protein levels, higher MCP-1 (P = 0.003) and fractalkine (P = 0.045) concentrations were found in controls compared with the P group. In serum, MCP-1 concentrations in the RA+P group were higher (P = 0.003) than those of group P. Elevated serum fractalkine concentrations were observed in both periodontitis groups (RA+P, P = 0.014; and P, P = 0.013) compared with controls.Conclusions: In RA, MCP-1, MIF, and fractalkine concentrations are elevated in saliva. These chemokines may disrupt oral macrophage responses and potentially take part in the interaction between periodontitis and RA. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Craniomandibular Disorders is the property of Quintessence Publishing Company Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Craniomandibular Disorders is the property of Quintessence Publishing Company Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A questionnaire survey concerning all members of the Psoriasis Society of the Greater Helsinki area was carried out to investigate associations between craniomandibular disorders (CMD) and psychosocial problems in psoriasis. Of the psoriatic members 1,517 responded (85%); 1,050 had skin symptoms (psoriasis; P) and 400 had skin and joint symptoms (psoriasis with arthralgia or arthritis; PA). Subjects in the P-group and the PA-group who belonged to the dysfunction group (symptoms of CMD and discomfort of CMD) had poorer general health, suffered more often from stress and somatic problems, and used more drugs than did those in respective orthofunction groups. The present results support the current view that the etiology of CMD is multifactorial, and CMD may be an expression of various pathological disorders. [ABSTRACT FROM AUTHOR]

Background: Interleukin (IL)-23-induced T helper (Th) 17 pathway is involved in the pathogenesis of periodontal disease. This study's aim is to determine levels of IL-1β, IL-17A, IL-23, and lipopolysaccharide (LPS) in saliva, and to examine whether their salivary concentrations are associated with periodontal health status.Methods: Saliva samples originated from 220 participants; 76 had generalized periodontitis (GP) and 65 had localized periodontitis (LP), whereas 79 without periodontitis were used as controls. Cytokine analyses were performed by a flow cytometry-based technique and LPS analyses from pellet by commercially optimized assay coupled with chromogenic substrate.Results: Salivary concentrations of IL-17A and IL-23 were elevated significantly in patients with LP compared with controls and patients with GP. Salivary IL-1β concentrations were significantly higher in patients with GP than in patients with LP, whereas no difference was found between LP and control groups. Significant correlation was found between concentrations of IL-17A and IL-23 or IL-1β. LPS concentrations did not have significant associations with any of the tested ILs.Conclusion: Elevated salivary IL-1β concentrations are related to GP, whereas distinct elevation and reduction profiles of IL-17A and IL-23 are detected in saliva of patients with LP and GP. [ABSTRACT FROM AUTHOR]

Background: In the present study, the expression and localization of three epithelial peptides (human β-defensin [hBD]-2 and -3, and cathelicidin [LL-37]) are studied in an organotypic dento-epithelial (OD-E) model exposed to Fusobacterium nucleatum (Fn) biofilm.Methods: Biofilm of Fn ATCC 25586 or AHN 9508 were produced by culturing each strain on semipermeable membranes. The OD-E model was constructed by seeding keratinocytes on fibroblast-containing collagen gels and by placing dentin pieces on the top. A 3-day-old biofilm was placed on the top of the OD-E and the coculture was incubated for 5 hours or 24 hours. Production of epithelial antimicrobial peptides was determined immunohistochemically.Results: After 5 hours of incubation, the biofilm of each Fn strain stimulated expression of hBD-2 and -3. hBD-2 was localized on superficial layers and hBD-3 on basal cell layers of the epithelium and dento-epithelial junctions, whereas LL-37 was only weakly expressed. After 24 hours, hBD-2 expression was extended toward basal cell layers of the epithelium. In contrast, hBD-3 expression extended toward superficial layers of the epithelium. In the case of Fn AHN 9508 biofilm, LL-37 was localized in the cell layers of the dento-epithelial junction.Conclusion: In our OD-E model, epithelial antimicrobial peptide responses to Fn biofilms have distinct regulation and localization characteristics, resembling those known to occur in the gingival epithelium in vivo. [ABSTRACT FROM AUTHOR]

Background: The present study evaluates the survival capability of Fusobacterium nucleatum strains in an aerobic environment and compares the invasive capability of F. nucleatum in biofilm and planktonic forms in an organotypic cell culture (OCC) model.Methods: Biofilms of F. nucleatum American Type Culture Collection (ATCC) 25586 or Anaerobe Helsinki Negative (AHN) 9508 were produced by culturing on semipermeable membranes on brucella agar plates. The oxygen tolerance of the F. nucleatum strains was examined by incubating 3-day-old anaerobically grown biofilms in an aerobic environment (CO(2) [5% in air] incubator) for an additional 48 hours. The OCC model was constructed by seeding keratinocytes on a fibroblast-containing collagen gel. In invasion assays, a 3-day-old anaerobically grown biofilm (and planktonic bacteria in solution as the control) was placed upside down on the top of OCC and incubated under 5% CO(2) for 24 hours. Invasion of the bacteria and morphologic changes in OCC were assessed using hematoxylin and eosin, Ki-67, and periodic acid-Schiff stainings.Results: In biofilms, both F. nucleatum strains continuously increased their cell numbers in an aerobic environment for 48 hours. After incubating the bacterial biofilm in contact with the OCC model, F. nucleatum AHN 9508 was able to pass through the epithelial/basement membrane barrier and invade the collagen matrix. The invasiveness of biofilm F. nucleatum ATCC 25586 was limited to the epithelium. Cytotoxic effects and invasiveness of F. nucleatum on the OCC were much stronger when the bacteria were in biofilms than in the planktonic form.Conclusion: Biofilm formation regulates the survival and invasiveness of F. nucleatum in an aerobic environment. [ABSTRACT FROM AUTHOR]

Background: A dual relationship between glycemic status and bone remodeling was suggested recently. The present study aimed to 1) analyze salivary levels of receptor activator for nuclear factor κ-B ligand (RANKL), osteoprotegerin, osteocalcin, and osteopontin as potential biomarkers of alveolar bone loss and 2) determine whether the glycemic status affects the relationship between bone remodeling markers and periodontal status.Methods: Salivary levels of RANKL, osteoprotegerin, osteocalcin, osteopontin, and serum glycosylated hemoglobin A1c, insulin, and glucose were analyzed in 220 participants divided into four groups according to their periodontal health status: 1) 79 participants had at least 14 teeth with probing depth (PD) ≥4 mm (generalized periodontitis [GP]); 2) 65 participants had either two or seven teeth with PD ≥4 mm (two groups of localized periodontitis [LP1 and LP2, respectively]); and 3) 76 participants had no teeth with PD ≥4 mm (non-periodontitis control group).Results: Salivary concentrations of RANKL, osteocalcin, and osteopontin were higher, and osteoprotegerin was lower in females than in males. Salivary osteoprotegerin concentrations were higher in the GP and LP2 groups than in the control group, whereas RANKL, osteocalcin, and osteopontin were not related with periodontal status. Salivary osteopontin correlated positively with serum and salivary insulin. The association observed between increased osteoprotegerin concentrations and periodontitis was lost after salivary insulin was included into the analyses as a confounding factor.Conclusions: Salivary concentrations of bone markers are either affected by glycemic status or detected at very low levels. These factors hinder their use as salivary biomarkers of periodontitis. [ABSTRACT FROM AUTHOR]

Background: A deeper understanding of periodontitis pathophysiology is central to future development of novel biomarkers and therapeutics. The following is reported here: 1) an in silico network model of interactions among cell adhesion molecules and a network-focused microarray analysis of the corresponding genes in periodontitis; 2) analysis of secretions of adhesion molecules in gingival tissue samples from patients with periodontitis and healthy controls; and 3) effect of the human neutrophilic peptide-1 (HNP-1) on epithelial adhesion molecules.Methods: The network model identified 85 nodes in relation to the interactions of adhesion molecules. Subsequently, the relative gene expression was overlaid on the network model. Differential gene expression was analyzed, and false discovery rate control was performed for statistical assessment of the microarray data. Both tissue and cell culture samples were immunostained for desmocollin (DSC)2, occludin (OCLN), desmoglein (DSG)1, tight junction protein 2, and gap junction protein α.Results: The differential gene expression analysis revealed that the epithelial adhesion molecules were significantly lower in abundance in individuals with periodontitis than controls. In contrast, the genes for leukocyte adhesion molecules showed a significant upregulation. Immunostainings revealed elevated secretions of both DSG1 and OCLN in periodontitis. An in vitro model suggested reduced DSC2 and OCLN secretions in the presence of HNP-1.Conclusions: Gene expression of gingival adhesion molecules in periodontitis is regulated by leukocyte transmigration, whereas the neutrophilic antimicrobial peptide HNP-1 is noted as a putative regulator of epithelial adhesion molecules. These observations contribute to the key mechanisms by which future biomarkers might be developed for periodontitis. [ABSTRACT FROM AUTHOR]