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Nutrition and Oral Medicine (Nutrition and Health)

Nutrition and Oral Medicine (Nutrition and Health)

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66 Part II / <strong>Oral</strong> <strong>and</strong> General <strong>Health</strong>2.1.4. PUBERTY-ASSOCIATED GINGIVITISPuberty is a stage in the development of human beings characterized by sexual maturation.Studies suggest that the prevalence, severity, <strong>and</strong> extent of gingivitis increase inchildren reaches a peak around the age of 12–14 <strong>and</strong> decreasing thereafter, with significantlylower values by the age of 16–17 (14). The increase in the severity <strong>and</strong> extent ofgingivitis appear to parallel sexual maturation rather than plaque index, suggesting anenhanced response of gingival tissues to the presence of dental plaque <strong>and</strong> supporting therole of puberty in the pathogenesis of gingivitis (15).One of the most significant changes occurring during pregnancy, menstrual cycle, <strong>and</strong>puberty are major hormonal shifts, <strong>and</strong> these hormonal changes have been proposed asone of the mechanisms responsible for the increase in the expression of gingivitis duringthese physiological states (10,16). During pregnancy, there is a significant increase ingonadotropins in the first trimester <strong>and</strong> progesterone <strong>and</strong> estrogens in the second <strong>and</strong> thirdtrimesters. The menstrual cycle is also associated with significant surges in progesterone<strong>and</strong> estrogen, although these changes are less dramatic than those seen in pregnancy.During puberty, the changes in the hormonal makeup vary between girls <strong>and</strong> boys. Ingirls, there is a significant increase in estrogen <strong>and</strong> progesterone; in boys, testosteronereaches significantly high values. The main mechanisms by which sex hormones affectperiodontal tissues are the effects on the elements of the host response such as increasedblood vessel permeability, vasodilation, decreased epithelial keratinization, reduction inneutrophil chemotaxis, <strong>and</strong> changes in T cells <strong>and</strong> signal transduction molecules (4,17).Studies have shown that the bacterial makeup changes during pregnancy <strong>and</strong> puberty,with a significant increase in the proportion of anaerobic to aerobic bacteria, particularlythe periodontopathogen Provotella intermidia, probably because of the ability of thesebacteria to use progesterone <strong>and</strong> estrogen as growth factors (9).2.1.5. DIABETES-ASSOCIATED GINGIVITISThe relationship between diabetes <strong>and</strong> periodontal disease is also discussed in Chapter11; the topic is reviewed here in the context of diabetes risk factors for periodontaldisease. Diabetes mellitus (DM) is an endocrine disorder with significant metabolicdisturbances. Type 1 diabetes (T1DM) is characterized by destruction of the pancreatic-cells through autoimmune mechanisms with consequent decrement or complete depletionof the insulin. Type 2 DM (T2DM) is characterized by the inability of insulin toexert its functions on target tissues because of deficiencies in its transduction system.T1DM constitutes 5–10% of all diagnosed diabetes, generally has its onset before theage of 21, <strong>and</strong> affects approx 1 in 400–500 children <strong>and</strong> adolescents. T2DM constitutes90–95% of all diagnosed cases of diabetes <strong>and</strong> has its onset in adulthood, although it hasbecome increasingly diagnosed in children <strong>and</strong> adolescents (18).Although gingivitis is prevalent in children, adolescents, <strong>and</strong> adults, DM adds anadditional risk to its development (3,19). In adults, the prevalence of people with diabeteshaving gingival inflammation is higher than in people without diabetes, whereas inchildren <strong>and</strong> adolescents with diabetes, the prevalence of gingivitis may almost doublecompared to healthy children <strong>and</strong> adolescents (20,21). When evaluated in children, theseverity <strong>and</strong> extent of gingivitis may also be significantly increased (22–27) <strong>and</strong> maydepend on glycemic control (25,28). Moderate to severe gingivitis is twice as extensivein subjects with diabetes compared to subjects without diabetes (24).

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