| 1. |
- Björnfot Holmström, Sofia, et al.
(författare)
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MMP-12 and S100s in saliva reflect different aspects of periodontal inflammation
- 2019
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Ingår i: Cytokine. - : Academic Press. - 1043-4666 .- 1096-0023. ; 113, s. 155-161
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Tidskriftsartikel (refereegranskat)abstract
- Matrix metalloproteinase (MMP)-12, S100A8/A9, and S100A12 are involved in innate immune responses. We addressed whether different aspects of oral health and non-disease-related covariates influence their levels in saliva. 436 participants were clinically examined, completed a health questionnaire, and provided stimulated saliva. Salivary levels of MMP-12, S100A8/A9, and S100A12 were determined by enzyme-linked immunosorbent assays. Lower MMP-12 levels were observed in individuals 40-64years old (yo) compared to < 40yo, and higher S100A8/A9 levels were found in individuals > 64yo compared to 40-64yo. Smokers exhibited lower MMP-12 and S100A12 levels compared to non-smokers. All three proteins were elevated in individuals with bleeding on probing (BOP)>20% compared to those with BOP/= 10% gingival pocket depths (PPD)>/=4mm compared to the ones with shallow pockets < 4mm. The extent of alveolar bone loss or presence of manifest caries did not alter any of the markers. MMP-12, S100A8/A9, and S100A12 levels were higher in participants with high periodontal inflammatory burden. All three proteins correlated positively to BOP, PPD, and to several inflammatory mediators. The explanatory variables for MMP-12 in saliva were age, smoking, presence of any tumor, and percentage of PPD>/=4mm. The determinant of salivary S100A8/A9 was percentage of BOP, while S100A12 levels were associated with percentage of BOP and presence of any tumor. Taken together, MMP-12 and the S100/calgranulin levels in saliva reflect different aspects of periodontal inflammation. Smoking and age should be taken into account in further investigation of these proteins as biomarker candidates of periodontal disease.
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| 2. |
- Boström, Elisabeth A., et al.
(författare)
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The Newly Discovered Cytokine IL-34 Is Expressed in Gingival Fibroblasts, Shows Enhanced Expression by Pro-Inflammatory Cytokines, and Stimulates Osteoclast Differentiation
- 2013
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 8:12, s. e81665-
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Tidskriftsartikel (refereegranskat)abstract
- Background: Interleukin-34 (IL-34) is a recently discovered cytokine functionally overlapping macrophage colony stimulating factor (M-CSF), a mediator of inflammation and osteoclastogenesis in bone-degenerative diseases such as rheumatoid arthritis. The objective of this study was to assess the expression of IL-34 in human gingival fibroblasts and investigate if the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and Interleukin-1B (IL-1 beta) modulate its expression, and moreover if IL-34 could contribute to recruitment of bone-resorbing osteoclasts. Methods: IL-34 expression was evaluated in gingival fibroblasts by real time PCR following stimulation by TNF-alpha, IL-1 beta, and treatment with inhibitors of intracellular pathways. The formation of osteoclasts was evaluated by tartrate-resistant acid phosphatase (TRAP) staining of bone marrow macrophages treated with IL-34 or M-CSF in addition to receptor activator of nuclear factor kappa-B ligand (RANKL). Results: IL-34 was expressed in gingival fibroblasts. The expression was enhanced by TNF-alpha and IL-1 beta, regulated by the transcription factor nuclear factor kappa B (NF-kappa B) and activation of c-Jun N-terminal kinase (JNK). Further, IL-34 supports RANKL-induced osteoclastogensis of bone marrow macrophages, independently of M-CSF. Summary: In conclusion, this study shows for the first time IL-34 expression in human gingival fibroblasts, stimulated by TNF-alpha and IL-1 beta, key mediators of periodontal inflammation. Furthermore, IL-34 can be substituted for M-CSF in RANKL-induced osteoclastogenesis. IL-34 may contribute to inflammation and osteoclastogenesis in bone-degenerative diseases such as periodontitis.
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| 3. |
- Lira-Junior, Ronaldo, et al.
(författare)
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Colony stimulating factor-1 in saliva in relation to age, smoking, and oral and systemic diseases
- 2017
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Ingår i: Scientific Reports. - : Nature Publishing Group. - 2045-2322. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- Colony stimulating factor (CSF)-1 is a growth factor that stimulates the survival, proliferation and differentiation of mononuclear phagocytes, which has been implicated in several inflammatory diseases. This study evaluated the possible influence of age, sex, smoking, periodontitis, caries, and several systemic conditions on salivary levels of CSF-1. Four-hundred and forty-one individuals were enrolled in this study. All participants answered a health questionnaire and underwent a comprehensive oral examination. Stimulated saliva was collected and CSF-1 levels were analysed by enzyme-linked immunosorbent assay. Salivary levels of CSF-1 were significantly increased in participants over 64 years old and in non-smoking individuals, whereas no difference was observed between men and women. Individuals having periodontitis and manifest caries had significantly higher levels of CSF-1. Participants with muscle and joint disease exhibited increased CSF-1 levels as compared to those without. Age, smoking, percentage of pockets >= 4 mm, number of manifest caries lesions, and presence of tumor were associated with CSF-1 levels. Salivary levels of CSF-1 are associated with age, smoking, periodontitis, manifest caries, and the presence of muscle and joint diseases and tumors. CSF-1 might be a promising biomarker candidate in saliva of both local and systemic conditions that needs further investigation.
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| 4. |
- Lira-Junior, Ronaldo, et al.
(författare)
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S100A12 Expression Is Modulated During Monocyte Differentiation and Reflects Periodontitis Severity
- 2020
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Ingår i: Frontiers in Immunology. - : Frontiers Media S.A.. - 1664-3224. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- S100A12 is a calcium-binding protein of the S100 subfamily of myeloid-related proteins that acts as an alarmin to induce a pro-inflammatory innate immune response. It has been linked to several chronic inflammatory diseases, however its role in the common oral immunopathology periodontitis is largely unknown. Previous in vitro monoculture experiments indicate that S100A12 production decreases during monocyte differentiation stages, while the regulation within tissue is poorly defined. This study evaluated S100A12 expression in monocyte subsets, during monocyte-to-macrophage differentiation and following polarization, both in monoculture and in a tissue context, utilizing a three-dimensional co-culture oral tissue model. Further, we explored the involvement of S100A12 in periodontitis by analyzing its expression in peripheral circulation and gingival tissue, as well as in saliva. We found that S100A12 expression was higher in classical than in non-classical monocytes. S100A12 expression and protein secretion declined significantly during monocyte-to-macrophage differentiation, while polarization of monocyte-derived macrophages had no effect on either. Peripheral monocytes from periodontitis patients had higher S100A12 expression than monocytes from controls, a difference particularly observed in the intermediate and non-classical monocyte subsets. Further, monocytes from periodontitis patients displayed an increased secretion of S100A12 compared with monocytes from controls. In oral tissue cultures, monocyte differentiation resulted in increased S100A12 secretion over time, which further increased after inflammatory stimuli. Likewise, S100A12 expression was higher in gingival tissue from periodontitis patients where monocyte-derived cells exhibited higher expression of S100A12 in comparison to non-periodontitis tissue. In line with our findings, patients with severe periodontitis had significantly higher levels of S100A12 in saliva compared to non-periodontitis patients, and the levels correlated to clinical periodontal parameters. Taken together, S100A12 is predominantly secreted by monocytes rather than by monocyte-derived cells. Moreover, S100A12 is increased in inflamed tissue cultures, potentially as a result of enhanced production by monocyte-derived cells. This study implicates the involvement of S100A12 in periodontitis pathogenesis, as evidenced by increased S100A12 expression in inflamed gingival tissue, which may be due to altered circulatory monocytes in periodontitis.
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| 5. |
- Lira-Junior, Ronaldo, et al.
(författare)
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Salivary microbial profiles in relation to age, periodontal, and systemic diseases
- 2018
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 13:3
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Tidskriftsartikel (refereegranskat)abstract
- Background Analysis of saliva is emerging as a promising tool to diagnose and monitor diseases which makes determination of the salivary microbial profile in different scenarios essential. Objective To evaluate the effects of age, periodontal disease, sex, smoking, and medical conditions on the salivary microbial profile. Design A randomly selected sample of 441 individuals was enrolled (51% women; mean age 48.5 +/- 16.8). Participants answered a health questionnaire and underwent an oral examination. Stimulated saliva was collected and the counts of 41 bacteria were determined by checkerboard DNA-DNA hybridization. Results Elderly participants (>64 years old) presented a significant increase in 24 out of 41 bacterial species compared to adults (<= 64 years old). Eubacterium nodatum, Porphyromonas gingivalis, and Tannerella forsythia were significantly higher in participants with generalized bone loss compared to without. Males and non-smokers had higher bacteria counts in saliva. Individuals having mental disorders or muscle and joint diseases showed significantly altered microbial profiles whereas small or no differences were found for subjects with high blood pressure, heart disease, previous heart surgery, bowel disease, tumors, or diabetes. Conclusion Age, periodontal status, sex, smoking, and certain medical conditions namely, mental disorders and muscle and joint diseases, might affect the microbial profile in saliva.
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| 6. |
- Silbereisen, Angelika, et al.
(författare)
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Association of salivary TREM-1 and PGLYRP1 inflammatory markers with non-communicable diseases.
- 2023
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Ingår i: Journal of Clinical Periodontology. - : John Wiley & Sons. - 0303-6979 .- 1600-051X. ; 50:11, s. 1467-1475
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Tidskriftsartikel (refereegranskat)abstract
- AIM: Triggering receptor expressed on myeloid cells 1 (TREM-1) and peptidoglycan recognition protein 1 (PGLYRP1) are elevated in biofluids in the presence of various inflammatory conditions. This cross-sectional study aimed to evaluate the effect of age, sex, smoking and different oral and systemic non-communicable diseases on the levels of TREM-1 and PGLYRP1 in saliva.MATERIALS AND METHODS: In total, 445 individuals (mean age 48.7 ± 16.9 years, female:male 51%:49%) were included. All provided self-reported information on smoking and systemic diseases and whole stimulated saliva. Periodontal and cariological parameters were recorded. Salivary levels of TREM-1, PGLYRP1 and total protein were measured using commercially available assays.RESULTS: Salivary TREM-1 levels were significantly higher in stages III-IV periodontitis compared to other periodontal diagnoses (p < .05). Smoking, bleeding on probing (BOP), percentage of pockets ≥4 mm and the number of manifest caries were associated with TREM-1 (p < .05), while sex, BOP, number of manifest caries and muscle and joint diseases were associated with PGLYRP1 (p < .05).CONCLUSIONS: Salivary TREM-1 is associated with periodontitis and caries, while PGLYRP1 is associated with gingival inflammation and caries. Additionally, TREM-1 levels are modified by smoking, while PGLYRP1 is modified by sex and muscle and joint diseases. TREM-1 and PGLYRP1 in saliva could serve as potential biomarkers for detecting and monitoring non-communicable diseases.
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