BackgroundJuvenile idiopathic arthritis (JIA) often affects the temporomandibular joint (TMJ) caused by an abnormal immune system that includes overactive inflammatory processes. Salivary biomarkers may be a powerful tool that can help establishing diagnosis, prognosis and monitor disease progress.ObjectiveThe objective was to investigate biomarkers in parotid saliva and blood plasma in relation to temporomandibular joint (TMJ) magnetic resonance imaging (MRI) findings in patients with JIA and healthy individuals.MethodsForty-five children aged 6 to 16 years with JIA and 16 healthy age- and sex-matched controls were included. Unstimulated parotid saliva samples and venous blood were collected. Biochemical analyses were performed for the cytokine biomarkers. The participants underwent MR imaging of the TMJs, where changes in the inflammatory and the damage domains were assessed.ResultsIn the JIA patients, lower concentrations of IL-6R and gp130 were found in parotid saliva than in plasma. Higher concentrations of IL-6 were found in parotid saliva than in plasma. IL-6, IL-6R and gp130 in parotid saliva explained the presence of bone marrow oedema and effusion in the JIA patients.ConclusionsThis study suggests that the IL-6 family in parotid saliva is associated with TMJ bone marrow oedema and effusion in patients with JIA, suggesting that IL-6 has promising properties as a parotid saliva biomarker for TMJ inflammatory activity. image

Aim

In juvenile idiopathic arthritis (JIA), the temporomandibular joint (TMJ) is a particularly challenging joint to assess both clinically and with imaging. The aim of this article is to investigate TMJ magnetic resonance imaging (MRI) findings in relation to clinical and psychosocial factors in patients with JIA and healthy individuals related to TMJ arthritis in JIA.

Material and methods 

In total, 45 patients (6–16 years) with JIA and 16 healthy age- and sex-matched controls were examined according to the diagnostic criteria for temporomandibular disorders (DC/TMD). The subjects answered questionnaires about psychosocial factors (pain intensity, pain-related disability, depression, stress, catastrophising, pain locations, and jaw function) and underwent bilateral MRI of the TMJ.

Results

There were no significant differences between JIA patients and healthy individuals in any of the TMJ MRI findings. Moderate/severe changes among JIA patients were found only for effusion, synovial thickening, condylar flattening, and erosion, with no moderate/severe changes in healthy individuals. In JIA patients, orofacial pain intensity was related to TMJ bone marrow oedema, and pain in jaw muscles during jaw function was related to TMJ bone marrow oedema and erosion. There were no significant correlations between psychosocial aspects and MRI findings.

Conclusions

This study indicates a substantial overlap of TMJ MRI findings in both the inflammatory domain and the damage domain between JIA patients and healthy individuals. In JIA patients, the inflammatory MRI sign of bone marrow oedema seems to influence orofacial pain intensity.

The aims of this proof-of-concept study were to develop a collecting method for unstimulated parotid saliva in juvenile idiopathic arthritis (JIA) patients and healthy children and to investigate if inflammatory biomarkers could be detected in these samples. Forty-five children with JIA (median age of 12 years and 25th-75th percentile of 10-15 years; 33 girls and 12 boys) and 16 healthy children as controls (median age of 13 years and 25-75th percentile of 10-13 years; 11 girls and 5 boys) were enrolled in this study. Unstimulated parotid saliva was collected with a modified Carlson-Crittenden collector. The salivary flow rate and salivary concentrations of total protein and inflammatory mediators were assessed. The Meso Scale Discovery electrochemiluminescence immunoassay was used for analyzing protein concentrations and the inflammatory biomarkers. Sufficient parotid saliva volumes to be analyzed could be collected with the collection device. JIA patients had a lower sampling saliva volume (p = 0.008) and saliva flow rate (p = 0.039) than controls. The total protein concentrations and inflammatory biomarkers were measured in the last six healthy subjects. The median protein concentration was 1312 mu g/mL (25th percentile: 844 mu g/mL and 75th percentile: 2062 mu g/mL; n = 6) and quantifiable concentrations of 39 inflammatory proteins could be assessed in these samples. In conclusion, this study indicates that the saliva sampling method, as used in the present study, is able to collect sufficient sample volumes in children, and that it is possible to analyze various inflammatory biomarkers in the collected saliva.

There is a strong association between periodontal disease and atherosclerotic cardiovascular disorders. A key event in the development of atherosclerosis is accumulation of modified lipoproteins within the arterial wall. We hypothesise that patients with periodontitis have an altered lipoprotein profile towards an atherogenic form. Therefore, the present study aims at identifying modifications of plasma lipoproteins in periodontitis. Lipoproteins from ten female patients with periodontitis and gender- and age-matched healthy controls were isolated by density-gradient ultracentrifugation. Proteins were separated by 2D gel-electrophoresis and identified by map-matching or by nano-LC followed by MS. Apolipoprotein (Apo) A-I (ApoA-I) methionine oxidation, Oxyblot, total antioxidant capacity and a multiplex of 71 inflammation-related plasma proteins were assessed. Reduced levels of apoJ, phospholipid transfer protein, apoF, complement C3, paraoxonase 3 and increased levels of alpha-1-antichymotrypsin, apoA-II, apoC-III were found in high-density lipoprotein (HDL) from the patients. In low-density lipoprotein (LDL)/very LDL (VLDL), the levels of apoL-1 and platelet-activating factor acetylhydrolase (PAF-AH) as well as apo-B fragments were increased. Methionine oxidation of apoA-I was increased in HDL and showed a relationship with periodontal parameters. alpha-1 antitrypsin and alpha-2-HS glycoprotein were oxidised in LDL/VLDL and antioxidant capacity was increased in the patient group. A total of 17 inflammation-related proteins were important for group separation with the highest discriminating proteins identified as IL-21, Fractalkine, IL-17F, IL-7, IL-1RA and IL-2. Patients with periodontitis have an altered plasma lipoprotein profile, defined by altered protein levels as well as post-translational and other structural modifications towards an atherogenic form, which supports a role of modified plasma lipoproteins as central in the link between periodontal and cardiovascular disease (CVD).

Background

The aim of this study was to investigate relations between psychosocial factors, signs and symptoms of orofacial pain and jaw dysfunction in patients with juvenile idiopathic arthritis (JIA).

Methods

Forty-five patients with JIA (median age 12 years) and 16 healthy matched controls (median age 13 years) were examined according to the diagnostic criteria for temporomandibular disorders (DC/TMD). The subjects answered the DC/TMD questionnaires regarding psychosocial factors (pain intensity, pain–related disability, depression, stress, catastrophizing, pain locations and jaw function).

Results

JIA patients with orofacial pain had higher degree of stress, depression, catastrophizing and jaw dysfunction compared to subjects without. In turn, these factors were associated with orofacial pain intensity. Also, patients with orofacial pain had higher systemic inflammatory activity.

Conclusions

Orofacial pain in patients with JIA is associated with stress, psychological distress, jaw dysfunction and loss of daily living activities. Pain intensity seems to be the major pain aspect related to these factors. In addition, systemic inflammatory activity appears to be an important factor contributing to orofacial pain in JIA.

Porphyromonas gingivalis (P. gingivalis) is a major etiological agent associated withperiodontitis. This study aims to develop antibodies to P. gingivalis in vitro for real-time detection of bacteria in clinical samples. Lymphocytes were isolated from wholeblood of patient treated for periodontitis and were stimulated with P. gingivalis ATCC33277. B-cell maturation to long-living antibody secreting-plasma cells was studiedusing flow cytometry and immunofluorescence staining. The antibodies developedin vitro were immobilized onto a CM-5 sensor chip of a biosensor to detect the pres-ence of P. gingivalis in the gingival crevicular fluid of patients with periodontitis com-pared to periodontally healthy controls (n = 30). Surface plasmon resonance (SPR)analysis was performed to evaluate specific interactions of bacteria in samples withthe immobilized antibodies. The results of SPR analysis were compared to the detec-tion of P. gingivalis in the samples using DNA–DNA checkerboard hybridizationtechnique. A clear and distinct change in lymphocyte morphology upon stimulationwith P. gingivalis was observed. Anti-P. gingivalis antibodies secreted by CD38+plasma cells showed the presence of all the four IgG subclasses. The results ofDNA–DNA checkerboard analysis were in agreement with that of SPR analysis forthe detection of P. gingivalis in patient samples. Furthermore, incubation with anti-P. gingivalis attenuated the bacterial response in SPR. The in vitro method for antibodyproduction developed during this study could be used for an efficient real-time detec-tion of periodontitis, and the attenuating effects of in vitro antibodies suggest their rolein passive immunization to prevent periodontitis and their associated risk factors.

Background: High levels of hepatocyte growth factor (HGF), a healing factor with regenerative and cytoprotective effects, are associated with inflammatory diseases, including periodontitis. HGF biologic activity requires binding to its receptors, the proto-oncogene c-Met and heparan sulfate proteoglycan (HSPG). This study investigates HGF expression and its relationship to subgingival microbiota in medically healthy individuals with and without periodontitis.

Methods: Saliva, gingival crevicular fluid (GCF), and blood samples from 30 patients with severe periodontitis and 30 healthy controls were analyzed for HGF concentration using enzyme-linked immunosorbent assay and binding affinity for HSPG and c-Met using surface plasmon resonance. The regenerative effects of saliva from three patients and controls were analyzed in an in vitro model of cell injury. Subgingival plaques were analyzed for the presence of 18 bacterial species.

Results: Patients with periodontitis showed higher HGF concentrations in saliva, GCF, and serum (P <0.001); however, the binding affinities for HSPG and c-Met were reduced in GCF and saliva (P <0.002). In contrast to the controls, saliva from patients showed no significant regenerative effect over time on gingival epithelial cells. Compared with controls, patients had a higher prevalence of periodontally related bacteria.

Conclusions: Higher circulatory HGF levels indicate a systemic effect of periodontitis. However, the HGF biologic activity at local inflammation sites was reduced, and this effect was associated with the amount of periodontal bacteria. Loss of function of healing factors may be an important mechanism in degenerative processes in periodontally susceptible individuals.

Background: This study examines whether preceding assessment of periodontal status in patients with established coronary artery disease (CAD) can predict future CAD endpoints (myocardial infarction, new revascularization procedure, or CAD-related death) during 8-year follow-up and whether the changes in periodontal status over time differ in patients with CAD compared with healthy controls. Methods: In 2003, periodontal status was examined in 161 patients with CAD who underwent percutaneous coronary intervention or coronary artery bypass graft due to significant stenosis in the coronary arteries and 162 controls without CAD. Eight years later, 126 patients with CAD (102 males and 24 females, mean age: 68 -8.9 years) and 121 controls (101 males and 20 females, mean age: 69 -9.0 years) were reexamined periodontally. A standard classification of periodontal disease in three groups (mild, moderate, and severe) was used. CAD endpoints during follow-up were obtained by review of medical records. CAD as cause of death was confirmed from the Swedish Cause of Death Register. Results: No significant differences were found among patients with CAD, with or without CAD-related endpoints at 8-year follow-up, and severity of periodontitis at baseline (P = 0.7). CAD did not influence the incidence or severity of periodontitis. Significant differences were found at the final examination in periodontitis prevalence and severity (P = 0.001), number of teeth (P = 0.006), probing depth 4 to 6 mm (P = 0.016), bleeding on probing (P = 0.001), and radiographic bone level (P = 0.042) between CAD patients and controls, all in favor of controls. Conclusions: The study results did not show a significant association during 8 years among CAD endpoints and periodontal status at baseline. The progression of periodontitis was low in both groups, although the higher proportion of individuals with severe periodontitis among patients with CAD compared with controls remained unchanged over the 8-year follow-up. Further long-term prospective studies are needed to show whether periodontitis can be considered a risk or prognostic factor for CAD, in terms of endpoints including myocardial infarction, new revascularization procedure, and CAD-related death.

The aim of this study was to evaluate the long term outcome of furcation involved molars in a population treated for periodontal disease. Initially, the study sample was 147 referred periodontal patients. Periodontal treatment consisted of oral hygiene instructions, supra- and subgingival scaling and periodontal surgery. After treatment 99 patients participated in a two year study on root caries. The patients got maintenance treatment every third to fourth month during 2 years. At the end of that study the patients were periodontally healthy and were referred back for supportive treatment to the referring dentist. Thirteen to 16 years after periodontal treatment 81 patients were still alive and 64 accepted a re-examination. At the start of the observation period the remaining 64 patients had in total 1537 teeth. During the 13 to 16 year follow up 217 teeth were lost. The number of molars at baseline was 361. The number of furcation involvement with different degrees were; 267 (0), 67 (I), 25 (II) and 2 (III) respectively. Totally 69 molars were lost during follow up. The proportion of molar loss according to the degree of furcation involvements 0 to III at baseline were 15%, 29%, 40% and 100% respectively. It was a significant greater risk of loosing an initially furcation involved molar than a single rooted tooth (pandlt;0.0001). The risk of loosing an initially furcated molar increased with the degree of furcation involvement (degree I; pandlt;0.05, degree II; pandlt;0.01). I N CONCLUSION: During a long term observation period molars with furcation involvements are more frequently lost than not furcation involved molars. However, two thirds are still in function 13 to 16 years after treatment which indicate that molars with furcation involvements might survive long after periodontal treatment.

Hepatocyte growth factor (HGF) is an angiogenic, cardioprotective factor important for tissue and vascular repair. High levels of HGF are associated with chronic inflammatory diseases, such as coronary artery disease (CAD) and periodontitis, and are suggested as a marker of the ongoing atherosclerotic event in patients with CAD. Periodontal disease is more prevalent among patients with CAD than among healthy people. Recent studies indicate a reduced biological activity of HGF in different chronic inflammatory conditions. Biologically active HGF has high affinity to heparan sulfate proteoglycan (HSPG) on cell-membrane and extracellular matrix. The aim of the study was to investigate the serum concentration and the biological activity of HGF with ELISA and surface plasmon resonance (SPR), respectively, before and at various time points after percutaneous coronary intervention (PCI) in patients with CAD, and to examine the relationship with periodontal condition. The periodontal status of the CAD patients was examined, and the presence of P. gingivalis in periodontal pockets was analyzed with PCR. The HGF concentration was significantly higher, at all time-points, in patients with CAD compared to the age-matched controls (P< 0.001), but was independent of periodontal status. The HGF concentration and the affinity to HSPG adversely fluctuated over time, and the biological activity increased one month after intervention in patients without periodontitis. We conclude that elevated concentration of HGF but with reduced biological activity might indicate a chronic inflammatory profile in patients with CAD and periodontitis.