Effects of academic stress on oral hygiene--a potential link between stress and plaque-associated disease?

BACKGROUND: While there seems to be a common belief that psychosocial stress affects oral hygiene behavior, this assumption has rarely been proved. The present study thus aims to analyse stress effects on oral hygiene. MATERIAL AND METHODS: 16 matched pairs of medical students each consisting of 1 student participating in a major academic exam and 1 control without current academic stress, were formed on the basis of baseline plaque levels. At baseline, a professional tooth cleaning was performed. On the last day of exams, students answered questionnaires about oral hygiene during the exams and were afterwards asked to attend for a 2nd dental examination, of which they had no prior knowledge. RESULTS: On the last day of exams, approximately 6 weeks after professional tooth cleaning, 20.9+/-18.3% of control students' sites but only 10.5+/-9.3% of exam students' sites were found to be free of any plaque (p=0.022). Differences were most obvious at oral, as compared to vestibular, sites. Exam students reported a reduction in thoroughness (p=0.019) but not of frequency of oral hygiene behavior. CONCLUSION: The study strongly supports the assumption that psychosocial stress may induce neglect of oral hygiene and increase of plaque accumulation.

Accumulation and elimination of macromolecular lesions in susceptible and non-susceptible rat tissues after repeated administration of trans-4-acetylaminostilbene.

Trans-4-acetylaminostilbene (trans-AAS) is a potent carcinogen and quite specifically produces sebaceous gland tumors, predominantly in the Zymbal's gland of rats. It is also acutely toxic to the rat glandular stomach. Recent results have shown that these target tissues are not notably exposed to reactive metabolites after single administration of the compound. Therefore, experiments were designed to test whether multiple exposures cause changes in metabolic activation or repair of DNA-bound metabolites to the effect that target and non-target tissues accumulate macromolecular damage differently. Trans-[3H]AAS was orally administered to female Wistar rats in 12 doses over 6 weeks and binding of metabolites to proteins, RNA and DNA in several tissues as well as the pattern of adducts in liver nucleic acids were measured. In addition, the elimination of macromolecular-bound metabolites was determined at various intervals during the treatment. Metabolism and clearance of bound metabolites remained unaltered. As a consequence, DNA-bound metabolites accumulated in all tissues measured; to the greatest extent in the non-target tissues liver and kidney. Tissue exposure, as estimated by protein-binding, differed by a factor of 10 and decreased in the following order: liver, kidney, lung, Zymbal's gland, glandular stomach, mammary tissue. The results support the notion that neither the extent nor the persistence of DNA-binding correlate with the biological effects of trans-AAS.

The role of partial hepatectomy and of promoters in the formation of tumors in non-target tissues of trans-4-acetylaminostilbene in rats.

After repeated administration of trans-4-acetylaminostilbene to rats, DNA-bound metabolites accumulate to the greatest extent in liver and kidney, which are considered to be nontarget tissues for this carcinogen. To test whether the persistent DNA adducts represent procarcinogenic lesions, an initiation-promotion experiment was carried out using trans-4-acetylaminostilbene as an initiator and phenobarbital, DDT and diethylstilbestrol as promoters. In addition, partial hepatectomy was performed in some groups. Partial hepatectomy alone or in combination with promoters led to the formation of preneoplastic enzyme deficient foci, hyperplastic nodules and hepatoma in great yields. In addition, mammary tumors were observed with diethylstilbestrol promotion. The results support our proposal that aminostilbene derivatives produce procarcinogenic DNA-lesions in many, if not all, tissues and that secondary factors determine when and where tumors arise.

The effects of partial hepatectomy and of promoters on macromolecular binding of trans-4-acetylaminostilbene metabolites in liver and some extrahepatic tissues of rats.

Trans-4-acetylaminostilbene (trans-AAS) is a complete carcinogen for sebaceous glands and an initiator for liver in rats. Partial hepatectomy alone or in combination with phenobarbital, 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane or diethylstilbestrol produce liver tumors in trans-AAS pretreated rats. The effects of such secondary treatments on the macromolecular binding of [3H]trans-AAS metabolites was studied in several tissues. Partial hepatectomy was performed either 24 h before or after a single trans-AAS dose, and binding to proteins, RNA and DNA was measured 1, 3, and 17 d after the last treatment. Initial DNA-binding in liver was, if at all, somewhat lower than in controls, and then decreased more rapidly independent of the time of partial hepatectomy. In extrahepatic tissues, exposure and initial macromolecular binding was considerably higher, and elimination differentially delayed, if partial hepatectomy preceded dosing. With subsequent partial hepatectomy, initial binding was similar to controls, but elimination of DNA-binding was retarded in lung and glandular stomach. In a similar experiment, promoters were added to the feed 1 d after a single trans-AAS dose and macromolecular binding was determined 2 and 16 d thereafter. DNA-binding was little affected in liver, and in extrahepatic tissues at the first time point. In lung and glandular stomach its elimination was retarded, while in kidney DNA-binding even increased during promoter feeding. It is concluded that the secondary treatments have little impact on the primary lesion in the target tissue liver, but profoundly alter the disposal of trans-AAS metabolites which leads to increased tissue doses in extra-hepatic tissues.