Nutrition and Oral Medicine (Nutrition and Health)

Chapter 5 / Bidirectional Impact 65of a fine balance between two main factors, bacterial plaque and the host response to thisbacterial challenge. Host response mechanisms encompass both the inflammatory andthe immune responses. Although these mechanisms appear independently, they act inconcert to resolve the bacterial challenge, inducing changes in vasculature and variousinflammatory and immune cells (2a,2b). These responses are coordinated by a multitudeof mediators including interleukin (IL)-1 IL-6, and tumor necrosis factor (TNF)- thateventually activate the effectors of periodontal inflammation and destruction such asproteinases and osteoclasts.Under normal conditions, the balance between bacteria and host response is maintained,and a clinical healthy periodontal state is achieved. When this balance is disturbedby any factor affecting either arm of the balance, periodontal disease may occur. Severalsystemic conditions can modulate the expression of periodontal disease by affecting thehost response, and these modulating factors can intervene at any level in the chain ofpathogenesis of periodontal diseases.2.1.1. PLAQUE-INDUCED GINGIVAL DISEASEPlaque-induced gingival diseases are inflammatory conditions of the gingiva, calledgingivitis, and they are characterized by the absence of clinical attachment loss. Clinicalsigns of gingivitis include erythema; edema of the gingiva; changes in contour, consistency,and texture; and bleeding on provocation. Plaque-induced gingivitis is a commonoccurrence in both children and adults (3). However, several systemic conditions such ashormonal-associated physiological (pregnancy, menstrual cycle, puberty) or pathologicalconditions (e.g., diabetes mellitus), nutrition, blood disorders, and various medicationshave been found to significantly increase the risk of gingivitis.2.1.2. PREGNANCY-ASSOCIATED GINGIVITISPregnancy is associated with an increase in prevalence, severity, and extent of gingivitis.The prevalence of gingivitis in pregnant women can vary between 30 and 100%(4,5) and may be higher in woman with previous pregnancies (4,5). During pregnancy,gingivitis increases in severity as early as the second month of pregnancy, increasesfurther as the pregnancy advances, reaches a maximum around months 7 and 8 , decreasesin month 9 (6,7), and returns to prepregnancy values in the postpartum period (8,9). Thesechanges are independent of plaque accumulation (9), suggesting that the host factors areinvolved in its pathogenesis. The clinical signs of pregnancy gingivitis are similar to thesigns of plaque-induced gingivitis. For example, there is a significant increase in inflammatoryindexes such as gingival bleeding, pocket depth, and gingival crevicular fluid(10). The percentage of bleeding sites may almost double in pregnant women comparedto nonpregnant women (9). The percentage of pregnant woman with pockets deeper than4 mm may be twice that of nonpregnant women (11). In a significant percentage ofwomen, there may also be significant enlargement of the gingiva, particularly affectingareas of previous gingival inflammation.2.1.3. MENSTRUAL CYCLE-ASSOCIATED GINGIVITISChanges in gingival appearance may also occur in relation to the menstrual cycle.These changes may be less obvious and may manifest themselves as increases in gingivalcrevicular fluid. It appears that this increase occurs particularly during the ovulationperiod and depends on the presence of bacterial plaque (12,13).