ETIOLOGY
The causes of gingivitis in pregnancy can be separated into two general headings: host factors and microbial changes. Relative to host factors, the onset of increased gingival inflammation observed in the second month of gestation coincides with an increase in the circulating levels of estrogen and progesterone. The continuous rise in these two hormone levels up to the eighth month is reflected in the greatest amount of gingival inflammation noted during pregnancy. In addition, a marked reduction in gingivitis after the eighth month correlates with an abrupt decrease of the circulating levels of these hormones. Estrogen and progesterone receptors have been demonstrated in human gingiva, indicating that it is a target tissue for hormones. Additionally, it has been demonstrated that progesterone is metabolized faster by inflamed human gingiva than by normal gingiva. The kinetics of progesterone in the gingiva, coupled with the clinical observations that the abnormal changes in gingiva during pregnancy parallel the circulatory levels of progesterone and estrogen, provide convincing evidence that these two hormones play a role in exacerbating gingivitis.
The mechanisms of action of progesterone-induced and estrogen-induced gingival changes during pregnancy have become much better understood. Increased circulating levels of progesterone in pregnancy cause dilatation of gingival capillaries, increased capillary permeability, and gingival exudate. Vittek and colleagues8 described the effect of progesterone on the gingival vasculature and the resultant increased exudation. The effects included a direct action of progesterone on the endothelial cells, possible effects on the synthesis of prostaglandins, and suppression of the cellular immune response.
Progesterone causes dramatic morphologic changes in the gingival microvasculature. The morphologic basis of the induced vascular permeability is the formation of gaps in the normally intact endothelial lining, together with channels resulting from coalescence of adjacent vesicles. The changes in both capillaries and venules, as well as the long duration of leakage from these vessels, are unlike the short action of histamine.
The keratinization of the gingiva is known to be decreased during pregnancy, and this, together with an increase in epithelial glycogen, results in a diminution in the effectiveness of the epithelial barrier. Estrogen also causes changes in the keratinization of the gingival epithelium and alters the degree of polymerization of ground substance. Because of the vascular changes caused by these hormones, there is a more florid response to the irritant effects of dental plaque. Increased serum levels of progesterone have been correlated with increased gingival crevicular fluid flow rate, which in periodontal diagnosis has been shown to reflect gingival inflammatory conditions.
Physiologic levels of estrogen and progesterone in pregnancy have been shown to be stimulatory to prostaglandin synthesis. Prostaglandins, especially PGE1 and PGE2, act as long-term mediators of inflammation. Prostaglandins are synthesized by activated macrophages and, to a lesser degree, by polymorphonuclear neutrophils in response to inflammatory stimuli, both of which increase in number as the gingiva becomes inflamed. Prostaglandin concentration within the gingiva and gingival fluid also increases dramatically, with the occurrence of gingival inflammation. Along with initiation of vascular changes, stimulation of prostaglandin synthesis illustrates another mechanism that raises progesterone levels in pregnancy, magnifying the clinical features of dental plaque-induced gingivitis.
Immune mechanisms have also been suggested to have an important role in the initiation and development of gingivitis and periodontitis. Little is known about the effects of pregnancy on immune response in the oral cavity. Nevertheless, it has been demonstrated that the cell-mediated response is depressed during pregnancy, possibly contributing to the altered responsiveness of the gingival tissue to dental plaque.
Dental plaque is the principal etiologic factor in gingivitis. In periodontal disease, it is well established that the subgingival plaque is characterized by a shift toward a more anaerobic flora. Strong evidence supports the observation that gingival inflammation during pregnancy results from an alteration of the subgingival flora to a more anaerobic state. The anaerobe to aerobe ratio increases significantly during the 13th through 60th week of pregnancy and remains high during the third trimester. It has been shown that increased proportions of Prevotella intermedia are concomitant with an increase in gingivitis and elevated serum levels of estrogen and progesterone in pregnancy. When the proportion of Bacteroides species was monitored in the dental plaque of pregnant women, nonpregnant women, and nonpregnant women taking contraceptives, a 55-fold increase over the control group was noted in the populations of the Bacteroides species in pregnant women and a 16-fold increase in women taking oral contraceptives. This concomitant increase in P. intermedia is most pronounced in the second trimester and correlates with increased gingivitis scores. Subsequent pure culture studies have shown that the marked increase in the proportion of Bacteroides species during pregnancy seems to be associated with increased serum levels of circulating progesterone and estrogens. Both hormones can substitute for naphthoquinone, which is an essential growth factor for P. intermedia. The studies reported to date indicate that female sex hormones may be capable of altering the gingival vascular system, the immune response, and the normal subgingival flora.
drsnehamaheshwari