Association of oral health with various work problems: a cross-sectional study of Japanese workers.

BACKGROUND: Oral diseases affect quality of life and known to decrease productivity. We examined the impact of oral health status on various types of work problems. METHODS: This cross-sectional study used data from an internet-based self-report questionnaire survey administered to workers in Japan. Responses to the questionnaire regarding seven types of oral health-related work problems (1. Stress; 2. Lack of focus; 3. Lack of sleep; 4. Lack of energy; 5. Lack of communication due to halitosis; 6. Lack of communication due to appearance; 7. Lack of ability due to dental-related pain) were investigated and statistically analyzed. Explanatory variables were self-reported oral health status, number of teeth, and gum bleeding. To examine the association of oral health with the presence of work problems, logistic regression analysis was used to estimate the odds ratio (OR) and 95% confidence interval (CI). Age, sex, educational attainment, income, the presence of diabetes, and industrial classifications were used as the covariates. RESULTS: A total of 3,930 workers (mean age: 43.3 (SD = 11.7), 2,057 males and 1,873 females) were included. Overall, a total of 6.2% of workers reported having at least one oral health-related work problem in the past year, whereas 21.8% of those with poor self-reported oral health reported work problems. Workers with poor self-reported oral health were 3.58 (95% CI (1.70-7.56) times higher odds of reporting work problems than those with excellent self-reported oral health. CONCLUSIONS: Oral health was found to be associated with various work problems. Oral health promotion policies are needed in the workplace.

Proteoglycans released from cultured bovine aortic endothelial cell layers by sodium spirulan are both perlecan and biglycan.

Sodium spirulan (Na-SP) is a sulfated polysaccharide isolated from the blue-green alga Spirulina platensis. Na-SP has anticoagulant and fibrinolytic properties in vitro, including activation of heparin cofactor II, enhancement of vascular endothelial cell fibrinolytic activity and stimulation of endothelial proteoglycan (PG) release. In the present study, we investigated the types of endothelial PGs whose release is stimulated by Na-SP. Na-SP stimulated the PG release in a dose- and time-dependent manner. However, heparin, dextran sulfate and hyaluronan stimulated the release of heparan sulfate PGs rather than chondroitin/dermatan sulfate PGs, whereas the release of both types of PGs was strongly stimulated by Na-SP. Sepharose CL-6B chromatography of [35S]sulfate-labeled PGs showed that PGs were partially released after partial degradation of the core proteins without a change in chain length of the glycosaminoglycan chains after Na-SP treatment. On the other hand, SDS-polyacrylamide gel electrophoresis and Western blot analysis of the PG core proteins indicated that the Na-SP-releasable PGs are both a large heparan sulfate PG, perlecan, and a small chondroitin/dermatan sulfate PG, biglycan, without change in the size of the core proteins. Taken together, these results suggest that Na-SP stimulates the endothelial release of both perlecan and biglycan with the intact structures, possibly by mechanisms different from those of heparin, dextran sulfate and hyaluronan; a part of the PG core proteins may be degraded after Na-SP treatment. Since perlecan and biglycan have antithrombin activities, the present data support the hypothesis that Na-SP may enhance local anticoagulant activity in the liquid phase on the endothelium via stimulation of endothelial PG release.

Sodium spirulan as a potent inhibitor of arterial smooth muscle cell proliferation in vitro.

Sodium spirulan (Na-SP) is a sulfated polysaccharide with M(r) approximately 220,000 isolated from the blue-green alga Spirulina platensis. The polysaccharide consists of two types of disaccharide repeating units, O-hexuronosyl-rhamnose (aldobiuronic acid) and O-rhamnosyl-3-O-methylrhamnose (acofriose) with sulfate groups, other minor saccharides and sodium ion. Since vascular smooth muscle cell proliferation is a crucial event in the progression of atherosclerosis, we investigated the effect of Na-SP on the proliferation of bovine arterial smooth muscle cells in culture. It was found that Na-SP markedly inhibits the proliferation without nonspecific cell damage. Either replacement of sodium ion with calcium ion or depolymerization of the Na-SP molecule to M(r) approximately 14,700 maintained the inhibitory activity, however, removal of sodium ion or desulfation markedly reduced the activity. Heparin and heparan sulfate also inhibited vascular smooth muscle cell growth but their effect was weaker than that of Na-SP; dextran sulfate, chondroitin sulfate, dermatan sulfate and hyaluronan failed to inhibit the cell growth. The present data suggest that Na-SP is a potent inhibitor of arterial smooth muscle cell proliferation, and the inhibitory effect requires a certain minimum sequence of polysaccharide structure whose molecular conformation is maintained by sodium ion bound to sulfate group.

Inhibition of cultured bovine aortic endothelial cell proliferation by sodium spirulan, a new sulfated polysaccharide isolated from Spirulina platensis.

Sodium spirulan (Na-SP) is a sulfated polysaccharide isolated from the blue-green alga Spirulina platensis, which consists of two types of disaccharide repeating units, O-hexuronosyl-rhamnose (aldobiuronic acid) and O-rhamnosyl-3-O-methylrhamnose (acofriose) with sulfate groups, other minor saccharides and sodium ion. Vascular endothelial cells are present on the inner surface of blood vessels in a monolayer and have anticoagulant properties. To address the question whether Na-SP influences the maintenance of endothelial cell monolayers, we investigated the proliferation of cultured bovine aortic endothelial cells treated with Na-SP. It was found that Na-SP has an inhibitory activity on endothelial cell proliferation accompanied with suppression of whole protein synthesis but without non-specific cell damage. The inhibitory activity of Na-SP was the strongest when compared to that of heparan sulfate, heparin, dextran sulfate, dermatan sulfate, chondroitin sulfate A/C and hyaluronan. Furthermore, it was shown that the inhibitory activity of Na-SP disappeared by either desulfation or depolymerization. The present data suggest that Na-SP is a unique sulfated polysaccharide that strongly inhibits vascular endothelial cell proliferation, and the inhibitory activity requires polymerization of sulfated O-rhamnosyl-acofriose repeating units.

Repair of wounded monolayers of cultured bovine aortic endothelial cells is inhibited by calcium spirulan, a novel sulfated polysaccharide isolated from Spirulina platensis.

Calcium spirulan (Ca-SP) is a novel sulfated polysaccharide isolated from a blue-green alga Spirulina platensis. Ca-SP inhibits thrombin by activation of heparin cofactor II. Therefore, it could serve as an origin of anti-atherogenic medicines. Since maintenance of vascular endothelial cell monolayers is important for prevention of vascular lesions such as atherosclerosis, the effect of Ca-SP at 20 microg/ml or less on the repair of wounded bovine aortic endothelial cell monolayers in culture was investigated in the present study. When the monolayers were wounded and cultured in the presence of Ca-SP, the polysaccharide inhibited the appearance of the cells in the wounded area. The inhibition was also observed even when the repair was promoted by excess basic fibroblast growth factor, which is one of the autocrine growth factors that are involved in the endothelial cell monolayer maintenance. On the other hand, Ca-SP inhibited the cell growth and the incorporation of [3H]thymidine into the acid-insoluble fraction of proliferating endothelial cells, suggesting that Ca-SP inhibits endothelial cell proliferation. From these results, it is concluded that Ca-SP may retard the repair process of damaged vascular endothelium through inhibition of vascular endothelial cell proliferation by induction of a lower ability to respond to stimulation by endogenous basic fibroblast growth factor.