Oral health problems are associated with malnutrition in hospitalised adult patients.

BACKGROUND & AIMS: Hospitalised patients are especially vulnerable to malnutrition, which is associated with an increased risk of complications, leading to longer hospital stays, increased healthcare costs, and with a potentially negative effect on the prognosis. Poor oral health may make food intake difficult and contribute to poor nutritional status. The aim of the present cross-sectional study was to assess the occurrence of poor oral health and malnutrition in adult hospitalised patients, and further to investigate associations between oral health problems and malnutrition. METHODS: The Patient-Generated Subjective Global Assessment (PG-SGA) determined the patients' nutritional status. The oral health condition was evaluated according to the Revised Oral Assessment Guide-Jönköping (ROAG-J) and unstimulated salivary flow rate. Clinical information was collected from medical records. RESULTS: The study population included 118 patients from 15 somatic and 3 psychiatric wards at a University Hospital in Norway. Nearly half the patients (46%) were categorised as malnourished and in need of symptom alleviation or nutritional intervention. Malnutrition was found in all diagnostic conditions. According to ROAG-J, at least one oral health problem was identified in 93% of the patients. Severe oral health problems were more frequent in malnourished patients. Overall, both the number and total score of oral health problems were associated with malnutrition (OR 1.57, 95% CI 1.20-2.06 and OR 1.47, 95% CI 1.17-1.83, respectively). Of specific oral health items, problems with lips and mucous membranes were significantly associated with malnutrition. One-fifth of all patients had hyposalivation, but this was not associated with malnutrition. CONCLUSIONS: Oral health problems and malnutrition are commonly seen in hospitalised adult patients. The association between the two calls for raised awareness of oral health issues in assessing patients' nutritional status. Further study is required to clarify whether oral health problems constitute a causal factor in malnutrition.

Vitamin D, oral health, and disease characteristics in juvenile idiopathic arthritis: a multicenter cross-sectional study.

BACKGROUND: Vitamin D deficiency has been associated with autoimmune diseases and oral health. Knowledge about the association between vitamin D status and oral conditions in JIA is limited. We aimed to investigate vitamin D status in a cohort of Norwegian children and adolescents with JIA and possible associations between serum vitamin D levels, clinical indicators of oral health, and JIA disease characteristics. METHODS: This multi-center, cross-sectional study, included individuals with JIA aged 4-16 years from three geographically spread regions in Norway. Demographic data, age at disease onset, disease duration, JIA category, disease status, medication, and vitamin D intake were registered. One blood sample per individual was analyzed for 25(OH) vitamin D, and the level of insufficiency was defined as < 50 nmol/L. A clinical oral examination was performed applying commonly used indices in epidemiological studies of dental caries, dental erosion, enamel defects, gingival bleeding, and oral hygiene. Serum vitamin D was used as exposure variable in multivariable regression analyses to estimate the associations between insufficient vitamin D level, JIA disease status, and oral conditions, with adjustments for age, sex, geographical region, BMI, seasonal blood sampling, and parental education. RESULTS: Among the 223 participants with JIA, 97.3% were Caucasians, 59.2% were girls, and median age was 12.6 years. Median disease duration was 4.6 years, and 44.4% had oligoarticular JIA. Mean serum vitamin D level was 61.4 nmol/L and 29.6% had insufficient levels. Vitamin D levels did not differ between sexes, but between regions, iso-BMI categories, age groups, and seasons for blood sampling. Insufficient vitamin D levels were associated with dentin caries (adjusted OR 2.89, 95% CI 1.43-5.86) and gingival bleeding (adjusted OR 2.36, 95% CI 1.10-5.01). No associations were found with active JIA disease or more severe disease characteristics. CONCLUSION: In our study, nearly 30% had vitamin D insufficiency, with a particularly high prevalence among adolescents. Vitamin D insufficiency was associated with dentin caries and gingival bleeding, but not with JIA disease activity. These results point to the need for a multidisciplinary approach in the follow-up of children with JIA, including an increased focus on vitamin D status and oral health.

Systematic assessment of salivary inflammatory markers and dental caries in children: an exploratory study.

OBJECTIVE: To investigate associations between a wide panel of salivary inflammatory markers and the presence of dental caries among children. MATERIAL AND METHODS: In this exploratory, cross-sectional study, 176 children, aged 7-9, underwent a dental examination. Information on the children's oral health habits and lifestyles was collected from their mothers. In addition, saliva samples were collected and analyzed using a multiplex immunoassay. Of 92 inflammatory markers measured, 56 were included in the statistical analyses. To identify potential inflammatory markers associated with caries, we applied low to advanced statistical analyses. First, we performed traditional logistic regression analysis followed by Bonferroni corrections. Thereafter, a more robust and less conservative statistical approach, i.e. Least Absolute Shrinkage and Selection Operator (LASSO), was applied. The models were adjusted for potential confounders. RESULTS: Of the 176 children in the study, 22.2% were affected by caries. Among the 56 salivary inflammatory markers, only macrophage colony-stimulating factor 1 (CSF1) was selected by the LASSO and found to be positively associated with the presence of caries. CONCLUSIONS: The observed association between CSF1 and the presence of caries may be of clinical value in caries risk management and early diagnosis. Larger studies are warranted to assess the replicability of our findings.

Cytosolic Phospholipase A2 Alpha Regulates TLR Signaling and Migration in Metastatic 4T1 Cells.

Metastatic disease is the leading cause of death in breast cancer patients. Disrupting the cancer cell's ability to migrate may be a strategy for hindering metastasis. Cytosolic phospholipase A2 α (cPLA2α), along with downstream proinflammatory and promigratory metabolites, has been implicated in several aspects of tumorigenesis, as well as metastasis, in various types of cancer. In this study, we aim to characterize the response to reduced cPLA2α activity in metastatic versus non-metastatic cells. We employ an isogenic murine cell line pair displaying metastatic (4T1) and non-metastatic (67NR) phenotype to investigate the role of cPLA2α on migration. Furthermore, we elucidate the effect of reduced cPLA2α activity on global gene expression in the metastatic cell line. Enzyme inhibition is achieved by using a competitive pharmacological inhibitor, cPLA2α inhibitor X (CIX). Our data show that 4T1 expresses significantly higher cPLA2α levels as compared to 67NR, and the two cell lines show different sensitivity to the CIX treatment with regards to metabolism and proliferation. Inhibition of cPLA2α at nontoxic concentrations attenuates migration of highly metastatic 4T1 cells, but not non-metastatic 67NR cells. Gene expression analysis indicates that processes such as interferon type I (IFN-I) signaling and cell cycle regulation are key processes regulated by cPLA2a in metastatic 4T1 cells, supporting the findings from the biological assays. This study demonstrates that two isogenic cancer cell lines with different metastatic potential respond differently to reduced cPLA2α activity. In conclusion, we argue that cPLA2α is a potential therapeutic target in cancer and that enzyme inhibition may inhibit metastasis through an anti-migratory mechanism, possibly involving Toll-like receptor signaling and type I interferons.

Anti-vascular effects of the cytosolic phospholipase A2 inhibitor AVX235 in a patient-derived basal-like breast cancer model.

BACKGROUND: Group IVA cytosolic phospholipase A2 (cPLA2α) plays an important role in tumorigenesis and angiogenesis. It is overexpressed in basal-like breast cancer (BLBC), which is aggressive and usually triple-negative, making it unresponsive to current targeted therapies. Here, we evaluated the anti-angiogenic effects of a specific cPLA2α inhibitor, AVX235, in a patient-derived triple-negative BLBC model. METHODS: Mice bearing orthotopic xenografts received i.p. injections of AVX235 or DMSO vehicle daily for 1 week and then every other day for up to 19 days. Six treated and six control mice were terminated after 2 days of treatment, and the tumors excised for high resolution magic angle spinning magnetic resonance spectroscopy (HR MAS MRS) and prostaglandin E2 (PGE2) enzyme immunoassay (EIA) analysis. A 1-week imaging study was performed on a separate cohort of mice. Longitudinal dynamic contrast enhanced (DCE)-MRI was performed before, after 4 days, and after 1 week of treatment. The mice were then perfused with a radiopaque vascular casting agent, and the tumors excised for micro-CT angiography. Subsequently, tumors were sectioned and stained with lectin and for Ki67 or α-smooth muscle actin to quantify endothelial cell proliferation and vessel maturity, respectively. Partial least squares discriminant analysis was performed on the multivariate HR MAS MRS data, and non-parametric univariate analyses using Mann-Whitney U tests (α = 0.05) were performed on all other data. RESULTS: Glycerophosphocholine and PGE2 levels, measured by HR MAS MRS and EIA, respectively, were lower in treated tumors after 2 days of treatment. These molecular changes are expected downstream effects of cPLA2α inhibition and were followed by significant tumor growth inhibition after 8 days of treatment. DCE-MRI revealed that AVX235 treatment caused a decrease in tumor perfusion. Concordantly, micro-CT angiography showed that vessel volume fraction, density, and caliber were reduced in treated tumors. Moreover, histology showed decreased endothelial cell proliferation and fewer immature vessels in treated tumors. CONCLUSIONS: These results demonstrate that cPLA2α inhibition with AVX235 resulted in decreased vascularization and perfusion and subsequent inhibition of tumor growth. Thus, cPLA2α inhibition may be a potential new therapeutic option for triple-negative basal-like breast cancer.