Diabetes-related parameters and periodontal conditions in children.

BACKGROUND AND OBJECTIVE: The relationship between diabetes and periodontal diseases is well established. Our aim in this study was to explore the diabetes-related parameters that are associated with accelerated periodontal destruction in diabetic youth. MATERIAL AND METHODS: Three-hundred and fifty 6-18-year-old children with diabetes received a periodontal examination. Data on important diabetes-related variables were collected. Analyses were performed using logistic regression, with gingival/periodontal disease as the dependent variable, for the whole cohort and separately for two subgroups (6-11 and 12-18 years of age). RESULTS: Regression analyses, adjusting for age, gender, ethnicity, frequency of prior dental visits, dental plaque, and dental examiner, revealed a strong positive association between mean hemoglobin A1c over the 2 years prior to inclusion in the study and periodontitis (odds ratio = 1.31, p = 0.030). This association approached significance in the younger subgroup (odds ratio = 1.56, p = 0.052, n = 183). There was no significant relationship between diabetes duration or body mass index-for-age and measures of gingival/periodontal disease in this cohort. CONCLUSION: These findings suggest that accelerated periodontal destruction in young people with diabetes is related to the level of metabolic control. Good metabolic control may be important in addressing periodontal complications in young patients with diabetes, similarly to what is well established for other systemic complications of this disease.

Hirsutism, polycystic ovarian disease, and ovarian 17-ketosteroid reductase deficiency.

We studied an 18-year-old woman with progressive hirsutism, secondary amenorrhea, and polycystic ovarian disease. Excess androstenedione was secreted by the ovaries, most likely because of a genetic deficiency of ovarian 17-ketosteroid reductase, the enzyme that converts androstenedione to testosterone. Markedly elevated basal plasma levels of androstenedione, estrone, and testosterone were regulated by gonadotropin but not by ACTH. The rate of androstenedione production in the patient's blood at base line and after administration of dexamethasone was very high (10.0 to 11.6 mg per day; value in control women with hirsutism, less than 4.1 mg per day), whereas her blood production of testosterone was 0.64 to 0.7 mg per day, similar to or higher than that in control women with hirsutism. The fractional blood conversion ratio of androstenedione to testosterone was normal (5.6 percent). Thus, 88 to 93 percent of the testosterone in the blood was derived from the peripheral conversion of androstenedione, and very little testosterone was secreted by the ovaries. These in vivo biochemical data suggest that the patient had a deficiency of ovarian 17-ketosteroid reductase activity but normal pubertal activity. The patient's two younger sisters with peripubertal symptoms of androgen excess also had elevated serum levels of androstenedione. We propose that the increased secretion of androstenedione in the three siblings in this family was probably due to a genetic deficiency of ovarian 17-ketosteroid reductase.