Effect of the menstrual cycle on inflammatory cytokines in the periodontium.

BACKGROUND AND OBJECTIVE: The effects of different levels of steroid hormones, as experienced during puberty, pregnancy and menopause, on the periodontium have been demonstrated, but changes in sex hormone levels during the menstrual cycle, and the influence of these changes on the periodontium, remain unresolved. The aim of this study was to investigate the effect of the menstrual cycle on the levels of interleukin-1beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α) in gingival crevicular fluid and on periodontal clinical parameters, including the gingival bleeding index (GBI) and the modified gingival index (MGI), in periodontally healthy women. MATERIAL AND METHODS: Twenty-seven periodontally healthy women with a regular menstrual cycle were included in the study. Clinical parameters, including the GBI, the MGI and the simplified oral health index, were recorded during menstruation, ovulation and premenstruation phases (e.g. on days 1-2, 12-14 and 22-24, respectively) of the menstrual cycle. Gingival crevicular fluid and unstimulated saliva were collected, at each study phase, for assessment of IL-1ß, TNF-α, estrogen and progesterone. RESULTS: Both the GBI and the MGI increased significantly during the menstrual cycle, and were significantly higher during ovulation than during menstruation or premenstruation (p < 0.001). No significant change in the simplified oral health index was observed during the menstrual cycle ( p = 0.18). The levels of IL-1ß and TNF-α increased during the different phases of the menstrual cycle, but only the change in the TNF-α concentration was significant ( p < 0.05). CONCLUSION: This study indicated that changes occurring during the menstrual cycle influence the periodontium and induce inflammatory conditions.

Immunotoxic effects of exposure of rats to xenobiotics via maternal lactation. Part I 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Exposure of lactating female Leeds rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in a reduction in the body, spleen and liver weights of their male offspring at 130 days of age. None of the total administered doses (0.2, 1.0 or 5.0 micrograms/kg b.wt over 18 days) induced thymic atrophy in the offspring of either sex as adults. Most of the growth inhibition occurred during the suckling period and the effect was near maximal following maternal exposure to the lowest dose of TCDD. After this dose, at post-natal day 130 the body weights of the female offspring remained depressed, while those of the males had recovered to untreated control values. Maternal exposure to TCDD affected the immunocompetence of the adult offspring: in vitro T cell dependent and T cell independent responses and mitogen induced in vitro production of interleukin 1 (IL-1) and interleukin 2 (IL-2) were suppressed at post-natal day 130. The total dose of TCDD that has to be administered to dams over an 18-day nursing period in order to reduce the humoral responses of their offspring as adults by 50% of the maximum was estimated to be in the range 0.3-1.0 micrograms/kg b.wt to the antigens SRBC, DNP-Ficoll or TNP-LPS and 3.5-3.9 micrograms/kg b.wt. to the antigen LPS.

Immunotoxic effects of prolonged dietary exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The effects of low level exposure of rats to 2,3,7,8-tetrachlorodibenzo-p- dioxin (TCDD) on their immune system was investigated Dietary administration to young adult male Leeds strain rats of a total dose of 3 micrograms/kg body weight of TCDD resulted in an exposure duration-dependent reduction of in vitro lipopolysaccharide-induced production of interleukin (IL)-1 in cultures of their splenic macrophages. A 30-day exposure produced approximately 30% suppression and 180-day exposure produced approximately 52% suppression. This reduction did not negatively influence lipopolysaccharide- induced proliferation of B cells, instead an enhancement of B cell proliferation was observed after 30 days exposure. A 180 day exposure significantly suppressed the generation of IL-2 by either concanavalin A or phorbol myristate acetate/calcium ionophore stimulation, and reduced the lectin-induced proliferation of splenic T cells. The 30-day TCDD exposure showed no such immunotoxicity. TCDD at both exposure durations suppressed the expression of the alpha chain of the IL-2 receptor in concanavalin A-activated T cells, without affecting the CD4+/CD8+ ratio. The results suggest that exposure to a low dietary dose of TCDD suppresses the functions of several T cell subsets, some of the immunotoxic effects being produced early, while others require a longer exposure also down-regulates the IL-1 production function of macrophages. A common mechanism of TCDD immunotoxicity may be on the multifunctional signal transduction pathways downstream to the activation of protein kinase C and Ca2+ flux.