Pregnancy Gingivitis PDF

2- Pregnancy Pregnancy itself does not cause gingivitis. Gingivitis in pregnancy is caused by bacterial plaque, just as it is in non-pregnant individuals. Pregnancy gingivitis is extremely common and affects 30-100% of all pregnant women.  Hormonal changes during pregnancy can aggravat...

2- Pregnancy Pregnancy itself does not cause gingivitis. Gingivitis in pregnancy is caused by bacterial plaque, just as it is in non-pregnant individuals. Pregnancy gingivitis is extremely common and affects 30-100% of all pregnant women.  Hormonal changes during pregnancy can aggravate existing gingivitis. The severity of gingivitis is increased in the second or third month and reaches a peak in the eighth month. Gingivitis becomes more severe by the eighth month and decreases during the ninth where plaque accumulation follows a similar pattern.  Partial reduction in severity of gingivitis is observed 2 month postpartum. After 1 year the gingival condition is comparable to that of non-pregnant individuals. The gingiva will not turn to normal as long as local factors are present. Also after pregnancy tooth mobility, pocket depth and gingival fluid are all reduced. The most striking gingival clinical features are: 1. Pronounced increase in bleeding tendency. 2. Increase in probing depth. 3. Increased gingival crevicular fluid flow. 4. Increased tooth mobility 5. Gingival changes are usually painless unless complicated by acute infection. 6. Clinical features of Inflamed gingiva: Site: Marginal and interdental gingiva Color: Bright red to bluish due to pronounced vascularity Size: Gingiva become edematous, pit on pressure Surface: Smooth, shiny and pliable. Consistency: Soft and edematous. Bleeding: Bleeds spontaneously or slight provocation. Pain: Painless until infected. Pregnancy Gingivitis 7. Sometimes, the inflamed gingiva forms discrete “tumor-like” masses, referred to as pregnancy tumors. 8. Pregnancy tumors are: Pedunculated Bright red mass on the gingiva. It is characterized by a rich profusion of anastomosing vascular channels. Other sites include the tongue, lip, vermilion border or buccal mucosa. Pregnancy Tumor  Treatment: Pregnancy tumor requires surgical excision which should be done post-gestation, surgical wound should be curetted. Plaque control, scaling and root planing should be performed regularly  Factors introduced by pregnancy which modified gingival inflammation: 1- Effect of sex hormones on vusculature. 2- Effect of sex hormones on Bacterial pathogens. 3- Effect of sex hormones on immune cell function. 4- Effect of sex hormones on inflammatory mediators (cytokines). 1- Effect of sex hormones on vusculature. Elevated estrogen levels increases cellular proliferation in blood vessels. Elevated progesterone levels enhance capillary permeability and dilatation. This will favor leakage of fluid into the perivascular tissue leading to edema. In respect to the periodontal membrane, slight edema has a tooth extruding effect, with this mechanism leading to increased horizontal mobility 2- Effect of sex hormones on bacterial pathogens Higher levels of P. gingivalis and Prevotella intermedia were found in pregnant females. This increase is attributed to the marked increase in levels of steroid hormones (as estrogen & progesterone in the cell plasma and in saliva. Apparently, these hormones serve as growth factors for the microbes. P. intermedia, can substitute estrogen & progesterone for vitamin K, an essential bacterial growth factor 3- Effect of sex hormones on immune cells Susceptibility to periodontal infection increases during early gestation due to hormonal changes. These hormones may alter immunologic factors and responses including: Decreased neutrophil chemotaxis and phagocytosis 3- Effect of sex hormones on immune cells (Cont.) Suppression of T-cell activity Altered lymphocyte response (depression of cell mediated immune response) Depressed antibody production. Expression of apoptotic factors and cell death.  4- Effect of sex hormones on inflammatory mediators Estrogen along with progesterone it also enhances the localized production of inflammatory mediators, especially prostaglandin E2 (PGE2), a potent inducer of osteoclastic activity. Destruction of gingival mast cells by the increased sex hormones and the resultant release of histamine and photolytic enzymes may also contribute to the exaggerated inflammatory response to local factors.