Evaluation of milk fat globule-epidermal growth factor–factor VIII and IL-1β levels in gingival crevicular fluid and saliva in periodontal disease and health

Odontology - The aim of this study is to determine the levels of MFG-E8 and interleukin (IL)-1β in saliva and gingival crevicular fluid (GCF) associated with periodontal health and disease....     

Evaluation of the potential dependence of 2D–3D growth rates and structures of polypyrrole films in aqueous solutions of hexafluorates

Polypyrrole hexafluorosilicate, PPYSiF₆, and polypyrrole hexafluoroaluminate, PPYAlF₆, were found to follow the mixed 2DI–3DI kinetic model of electrodeposition in the potentials range (+0.80 V, +0.60 V) and (+0.95 V, +0.55 V) vs. SCE, respectively. The potentiostatic depositions of polypyrrole were performed on polycrystalline gold and on the single layer or bilayer polypyrrole films. Only in the case of the third layer deposition of PPYSiF₆ (on PPYSiF₆) at +0.6 V, the experimental current was found to fit better with the 2DP–3DI model. For electrodeposition of PPYAlF₆ on gold, a slightly better quality fitting with 2DP–3DP or 2DP–3DI kinetic models was observed only for some samples synthesized at 0.55 V. In general, contribution of the 2D structure in the polypyrrole deposits was observed to decrease with an increase of the polarization potential. Conclusions of the mathematical analysis of the current–time functions are in accordance with a texture of the outer surface of the polymer layers visible in SEM micrographs. The apparent rate constants of the lateral and outward growths of polypyrrole increase with potentials in (+0.55, +0.80) V range. Under assumption of the classical electrochemical kinetics law, the anodic transfer coefficients were found lower than 0.5. Values of the outward growth rate constant were of the order of 10⁻⁸–10⁻¹⁰ mol/(s cm²); being approximately one order of magnitude higher for polypyrrole hexafluorosilicate than for polypyrrole hexafluoroaluminate. The lateral growth rates of PPYAlF₆ on gold were found to depend on the electrodeposition potential more significantly than the outward growth rate. An increase in the growth rates with the potential was observed to diminish/vanish at E > +0.80 V, probably due to concurrent degradation processes of polypyrrole chains. The analysis of the deposition currents was done under conditions of the masking double layer currents that were characterized by the relaxation times of the order of seconds or longer.     

Nicotine and lipopolysaccharide stimulate the production of MMPs and prostaglandin E(2) by hypoxia-inducible factor-1α up-regulation in human periodontal ligament cells

Kim Y‐S, Shin S‐I, Kang K‐L, Herr Y, Bae W‐J, Kim E‐C. Nicotine and lipopolysaccharide stimulate the production of MMPs and prostaglandin E₂ by hypoxia‐inducible factor‐1α up‐regulation in human periodontal ligament cells. J Periodont Res 2012; 47: 719–728. © 2012 John Wiley & Sons A/S Background and Objective: Although hypoxia‐inducible factor 1α (HIF‐1α) is up‐regulated in the periodontal pockets of periodontitis patients, the expression and precise molecular mechanisms of HIF‐1α remain unknown in human periodontal ligament cells (PDLCs). The aim of this study was to explore the effects, as well as the signaling pathway, of nicotine and lipopolysaccharide (LPS) on the expression of HIF‐1α and on the production of its target genes, including cyclooxygenase‐2 (COX‐2)‐derived prostaglandin E₂ (PGE₂), MMP‐2 and MMP‐9 in PDLCs. Material and Methods: The expression of COX‐2 and HIF‐1α proteins was evaluated using western blotting. The production of PGE₂ and MMPs was evaluated using enzyme immunoassays and zymography, respectively. Results: LPS and nicotine synergistically induced the production of PGE₂, MMP‐2 and MMP‐9, and increased the expression of MMP‐2, MMP‐9, COX‐2 and HIF‐1α proteins. Inhibition of HIF‐1α activity by chetomin or knockdown of HIF1α gene expression by small interfering RNA markedly attenuated the production of LPS‐ and nicotine‐stimulated PGE₂ and MMPs, as well as the expression of COX‐2 and HIF‐1α. Furthermore, pretreatment with inhibitors of COX‐2, p38, extracellular signal‐regulated kinase, Jun N‐terminal kinase, protein kinase C, phosphatidylinositol 3‐kinase and nuclear factor‐kappaB decreased the expression of nicotine‐ and LPS‐induced HIF‐1α and COX‐2, as well as the activity of PGE₂ and MMPs. Conclusion: These data demonstrate novel mechanisms by which nicotine and LPS promote periodontal tissue destruction, and provide further evidence that HIF‐1α is a potential target in periodontal disease associated with smoking and dental plaque.     

Salivary levels of IL-1β, IL-6, IL-8, and TNF-α in patients with burning mouth syndrome

Objective

To compare salivary IL-1β, IL-6, IL-8, and TNF-α levels between patients with burning mouth syndrome (BMS) and controls.

Design

Forty female patients with BMS (mean age: 61.6 ± 10.1 years) and 20 female control subjects (mean age: 65.1 ± 9.0 years) were included in the study. Unstimulated (UWS) and stimulated whole saliva samples (SWS) were collected and their flow rates were determined. Salivary IL-1β, IL-6, IL-8, and TNF-α levels and total protein concentration were also determined. Salivary transferrin level was determined to investigate the level of blood contamination in saliva samples. Gingival index of the subjects was also examined. Student's t-test, Pearson's correlation analysis, and analysis of covariance were used.

Results

No significant differences were found in the salivary levels of IL-1β, IL-6, IL-8, and TNF-α in BMS patients compared with controls. Salivary flow rates and their total protein concentrations did not differ significantly between the groups. The levels of salivary cytokines and total protein concentration correlated significantly with the level of blood contamination in both UWS and SWS.

Conclusion

There were no differences in the salivary levels of IL-1β, IL-6, IL-8, and TNF-α in BMS patients compared with controls. Cytokine levels in whole saliva were affected mainly by the amount of blood contamination.     

Immunoexpression of TNF-α and TGF-β in central and peripheral giant cell lesions of the jaws

J Oral Pathol Med (2012) 41 : 194–199 Background: Peripheral giant cell lesion (PGCL) is a reactive process associated with a local irritating factor that shows low recurrence after treatment, especially if the irritating factor is eliminated. On the other hand, central giant cell lesion (CGCL) presents a variable clinical behavior ranging from slow and asymptomatic growth without recurrence to rapid, painful and recurrent growth. Our aim was to compare the immunoexpression of tumor necrosis factor‐alpha (TNF‐α) and transforming growth factor‐beta (TGF‐β) in CGCL and PGCL. Methods: Twenty CGCL and 20 PGCL were selected for analysis of the immunoexpression of TNF‐α and TGF‐β in multinucleated giant cells (MGC) and mononucleated cells (MC). Results: The PGCL showed lightly higher expression of TNF‐α than CGCL. In comparison with PGCL, the CGCL showed higher expression of TGF‐β in MC and MGC (P < 0.05) and in total cells (P < 0.05). Significant positive correlation was found between expressions of TGF‐β and TNF‐α in CGCL (P < 0.05). Conclusions: Our results suggest that, in CGCL, coordinated interactions between TGF‐β and TNF‐α may be important for osteoclastogenesis and bone resorption. PGCL occasionally cause bone resorption but to a lower extent, a fact that might be explained by the lower expression of TGF‐β in these lesions.     

Effects of glucosamine-chondroitin combination on synovial fluid IL-1β, IL-6, TNF-α and PGE2 levels in internal derangements of temporomandibular joint

Background

The aim of the present study was to evaluate the effects of glucosamine-chondroitin sulphate combination on internal derangements of temporomandibular joint in clinical and biochemical manners.

Material and Methods

This randomized clinical study included 31 cases reporting joint tenderness, in which disc displacement was detected on MR imaging. In all patients, synovial fluid sampling was performed under local anesthesia. In the study group, the patients were prescribed a combination of 1500 mg glucosamine and 1200 mg chondroitin sulphate, while patients in the control group were only prescribed 50 mg tramadol HCl (twice daily) for pain control. After 8 weeks, synovial fluid sampling was repeated in the same manner. The levels of pain, maximum mouth opening (MMO), synovial fluid IL-1ß, IL-6, TNF-α and PGE2 measured before and after pharmacological intervention were compared.

Results

The reduction in pain levels was significant in both groups. There was no significant difference between two groups in terms of pain reduction. The improvement in MMO was significant in the study group but it was not in the control group. The MMO improvement was significantly higher in the study group compared to the control group. In the study group, significant decrease was observed in PGE2 level, while the decreases in IL-1β, IL-6 and TNF-α levels were not significant. In the control group, no significant decrease was observed in any of the inflammatory cytokines after 8 weeks, moreover IL-1ß and IL-6 levels were increased. Alterations of IL-1ß and IL-6 levels were significant in study group while TNF-α and PGE2 levels were not, compared to control group.

Conclusions

In conclusion, these results might suggest that glucosamine-chondroitin combination significantly increases the MMO and decreases the synovial fluid IL1β and IL6 levels in internal derangements of TMJ compared to tramadol. The modifications of synovial fluid TNF-α and PGE2 levels do not reach statistical significance. This combination also provides efficient pain relief in similar level with tramadol, a narcotic analgesic. Key words: Chondroitin sulphate, glucosamine, internal derangement, TMJ, tramadol.     

Evaluation and comparison of serum vitamin D and calcium levels in periodontally healthy,chronic gingivitis and chronic periodontitis in patients with and without diabetes mellitus – a cross-sectional study

Objective: Limited data are available with respect to the relation of vitamin D and calcium with periodontal infections and type-2 diabetes mellitus (T2DM). The aim of this cross-sectional study was to evaluate the levels of vitamin D and calcium in serum of periodontally healthy, chronic gingivitis and chronic periodontitis patients with and without T2DM.

Material and methods: The study evaluated 100 patients equally divided into five groups (Group I to Group V) according to the inclusion criteria. Clinical parameters and serum 25-hydroxyvitamin D level were assessed. Other laboratory investigations comprised of random blood sugar, glycated haemoglobin and serum calcium.

Results: The probing pocket depth and clinical attachment loss were found to be greater in chronic periodontitis and chronic periodontitis with diabetes mellitus, while the vitamin D and calcium levels were found to be least in these groups. When vitamin D and calcium levels were compared between periodontal disease with diabetes to that of non-diabetics, statistically significant difference were found between the two with p-value of .001 indicating decrease in levels of vitamin D and calcium with increase in RBS and HbA1c values.

Conclusion: Vitamin D and calcium levels are inversely correlated with random blood sugar and glycated haemoglobin and also probing pocket depth and clinical attachment loss, thus contributing towards increase in periodontal disease severity.     

Sodium butyrate induces the production of cyclooxygenases and prostaglandin E₂ in ROS 17/2.8 osteoblastic cells

ObjectiveSodium butyrate (butyric acid; BA) is a major metabolic by-product of the anaerobic periodontopathic bacteria present in subgingival plaque. We examined the effects of BA and/or indomethacin on cell proliferation, the expression of cyclooxygenases (COXs), prostaglandin (PG) receptors (EP1-4), extracellular matrix proteins, such as type I collagen and osteopontin, and PGE₂ production, using ROS17/2.8 cells as osteoblasts.MethodsThe rat clonal cell line ROS 17/2.8 was cultured with 0, 10^?5, 10^?4, and 10^?3 M BA in the presence or absence of 0.5 μM indomethacin, for up to 7 days. The expression of COX-1, COX-2, EP1, EP2, EP3, EP4, type I collagen, and osteopontin was examined at the mRNA and protein levels using real-time PCR and Western blotting, respectively. The amount of PGE₂ in the culture medium was measured by ELISA.ResultsProliferation of ROS 17/2.8 cells was not affected by the addition of BA. However, PGE₂ production and the expression of COX-1 and COX-2 increased with the addition of BA. In contrast, indomethacin, an inhibitor of COX, blocked the stimulatory effect of BA. Furthermore, EP2 expression increased with BA treatment, whereas EP1 expression was not affected and the expression of EP3 and EP4 was not detected. The addition of BA also increased the expression of type I collagen and osteopontin. Indomethacin blocked about 50% of the stimulatory effect of BA on type I collagen, whereas it did not block the effect on osteopontin.ConclusionsThese results suggest that BA induces PGE₂ production by increasing the expression of COX-1 and COX-2 in osteoblasts, and that an autocrine action of the produced PGE₂, via EP1 or BA-induced EP2, is related to an increase in type I collagen expression by BA.     

Effect of scaling and root planing on interleukin-1β, interleukin-8 and MMP-8 levels in gingival crevicular fluid from chronic periodontitis patients

Konopka ?, Pietrzak A, Brzezińska‐B?aszczyk E. Effect of scaling and root planing on interleukin‐1β, interleukin‐8 and MMP‐8 levels in gingival crevicular fluid from chronic periodontitis patients. J Periodont Res 2012; 47: 681–688. © 2012 John Wiley & Sons A/S Background and Objective: There are few data concerning the effect of scaling and root planing on the levels of immune and inflammatory mediators in gingival crevicular fluid from patients with chronic periodontitis. Therefore, in this study the influence of scaling and root planing was determined on amounts of interleukin (IL)‐1β, IL‐8 and MMP‐8 in gingival crevicular fluid from patients with chronic periodontitis, in relation to clinical parameters. Material and Methods: A total of 51 patients were enrolled in this study. The study population consisted of 30 patients with generalized advanced chronic periodontitis, while 21 periodontally healthy subjects were recruited for the control group. The clinical parameters included approximal plaque index, gingival index, pocket depth and clinical attachment loss. The amounts of IL‐1β, IL‐8 and MMP‐8 in gingival crevicular fluid were measured by ELISA. Periodontal parameters as well as gingival crevicular fluid humoral factor amounts were evaluated in the control group and in chronic periodontitis patients at baseline and at 1 and 4 wk after scaling and root planing treatment. Results: At baseline, there were significant differences between control subjects and chronic periodontitis patients in terms of clinical attachment loss, pocket depth, gingival index (p < 0.001) and approximal plaque index (p < 0.01). The amounts of IL‐1β, MMP‐8 (p < 0.001) and IL‐8 (p < 0.01) in gingival crevicular fluid were significantly lower in healthy subjects than in chronic periodontitis patients. Scaling and root planing led to improvement in all examined clinical parameters, apart from clinical attachment loss. Periodontal treatment also resulted in a significant decrease in the amounts of IL‐1β, IL‐8 and MMP‐8 in comparison to baseline, especially 4 wk after scaling and root planing (p < 0.001); however, the amounts of these humoral factors were still higher than those in control group. Conclusion: Our observations indicated that short‐term nonsurgical therapy resulted in a significant improvement in periodontal indices and in a marked decrease of IL‐1β, IL‐8 and MMP‐8 gingival crevicular fluid levels. Nevertheless, no significant correlations were found between clinical parameters and amounts of humoral factors after therapy.     

The effect of menopause on the relationship between hyperlipidemia and periodontal disease via salivary 8-hydroxy-2′-deoxyguanosine and myeloperoxidase levels

Objective: Impairment of the lipid metabolism could affect the periodontal disease; increased oxidative stress may have a role in this relationship. The aim of the present study was to evaluate the role of menopause in the relationship between hyperlipidemia and periodontal disease via oxidative stress markers in saliva.

Materials and methods: Sixty-seven women were enrolled in the study and divided into four groups as systemically healthy and premenopause (C) (n?=?18), hyperlipidemia and premenopause (H) (n?=?16), systemically healthy and postmenopause (M) (n?=?17), and hyperlipidemia and postmenopause (MH) (n?=?16). Sociodemographics, periodontal and metabolic parameters, and saliva oxidative markers (myeloperoxidase [MPO] and 8-hydroxy-2′-deoxyguanosine [8-OHdG]) were evaluated.

Results: Menopause and/or hyperlipidemia were associated with an increase in all evaluated periodontal parameters. Saliva 8-OHdG and MPO levels were higher in menopausal groups (M and MH). Multivariate linear regression analyses revealed that hyperlipidemia was related to an increase in periodontal parameters. Salivary oxidative stress markers and periodontal parameters were also positively associated with menopause and hyperlipidemia.

Conclusion: Saliva 8-OHdG and MPO levels may indicate that the relationship between periodontal disease and hyperlipidemia is aggravated by menopause.