Oral health in pregnancy

The numerous physical and physiological changes that occur during pregnancy affect every major body
system and result in localised physical alterations in many parts of the body, including the oral cavity.
There is a need to increase awareness of the main potential dental manifestations which can occur in
pregnancy.
Following are a few commonly seen oral conditions during pregnancy:
Intra oral
1. Pregnancy gingivitis
2. Pyogenic granuloma
3. Tooth surface loss due to excessive vomiting
4. Increased dental caries
5. Tooth mobility
6. Periodontitis
Extra oral
1. Hyperpigmentation
2. TMJ and myofacial pain

Effect of female sex hormones on periodontal tissues
Estrogen and progesterone receptors have been found in gingiva, and these hormones have been shown
to increase vascular permeability and the amount of gingival crevicular fluid flow. In addition, estrogen
and progesterone may alter the immune system, and progesterone can stimulate the production of an
inflammatory mediator PGE2. Estrogen receptors have also been found in periosteal fibroblasts as well
as in periodontal ligament fibroblasts; and thus, the sex hormones may directly affect these periodontal
tissues. In addition, both estrogen and progesterone have been demonstrated to have an impact on bone
metabolism.
Pregnancy does not cause gingivitis, but may worsen pre-existing disease. The prevalence and severity
of gingival inflammation have been shown to increase during pregnancy, with these changes
disappearing postpartum. Estrogen and progesterone affect cellular proliferation, differentiation, and
growth of gingival fibroblasts. Studies have also revealed that both estrogen and progesterone have a
role in bone resorption and formation. Susceptibility to infections, including periodontal disease,
increases during pregnancy, and the underlying mechanisms consist of alterations in the immune system,
hormonal changes, limited T-cell activity, decreased neutrophil chomotaxis and phagocytosis, and
depressed antibody production. Periodontal bacteria P.i. and P.g. can use female sex hormones as a
source of nutrients, and the amount of these bacteria is increased in the gingival crevicular fluid of
pregnant women; this correlates positively with the severity of pregnancy gingivitis.
Studies have established that pregnant women have more gingival bleeding and inflammation than
women postpartum; these changes are not associated with the amount of plaque. The gingival
inflammatory changes begin during the second month of pregnancy and increase in severity until the
eighth month of pregnancy showed that changes in bleeding on probing and periodontal pocket depth
increased simultaneously without a relation to plaque between the first and second trimesters and then
decreased during subsequent visits. Thus, these changes were reversible, indicating that pregnancy
gingivitis does not predispose or proceed to periodontal disease.

Pregnancy gingivitis
The frequently observed gingival changes that occur during pregnancy were reported as early as 1877.
For many years, however, there have been questions about the reported prevalence of periodontal disease
in pregnancy, the role that local and hormonal factors may have in the pathogenesis, and the implication
of certain microorganisms in the etiology of this disease. Based on clinical observation, the reported
frequency of so-called pregnancy gingivitis ranges from 35%2 to 100%. This variation may be a reflection
of both the populations studied and the clinical parameters used. Moderately severe pregnancy gingivitis
in a 30-year-old patient during the eighth month of pregnancy.
According to studies using well-defined indices, gingival inflammation is a heightened or exacerbated
response to dental plaque during a period of progesterone and estrogen imbalance.4 In addition, the
effect of pregnancy on pre-existing gingival inflammation is first noticeable in the second month of
gestation and peaks in the eighth month. During the last month of gestation, a definite decrease in
gingivitis generally occurs, and the gingival status immediately postpartum is found to be similar to that
at the second month of pregnancy. The greatest relative increase in gingivitis during pregnancy is
observed around the anterior teeth, although the molars demonstrate the highest gingivitis scores
throughout pregnancy. The papillae (interproximal areas) are the most frequent sites of gingival
inflammation both during pregnancy and after parturition.
CLINICAL MANIFESTATIONS
The marginal gingiva and interdental papillae are fiery red and the gingiva is enlarged, mostly affecting
the interdental papillae. The gingiva shows an increased tendency to bleed, and in advanced cases,
patients sometimes even experience slight pain. During the second and third trimester, the inflammation
often becomes more severe. It should be noted that not all women respond in this fashion: in fact, many
do not have a clinically altered gingival condition. When there is no dental plaque-associated gingivitis
before pregnancy and attentive oral hygiene is monitored, gingivitis usually does not develop. Preventive
measures, such as more frequent dental visits for prophylaxis and meticulous plaque control, are
therefore indicated for pregnant women.

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.
HISTOPATHOLOGY
A pregnancy granuloma is composed of capillaries, fibrous tissue, and inflammatory cells, with marked
vascularity being the most characteristic histologic feature. As such, distinguishing it from a pyogenic
granuloma without other clinical data is difficult. The epithelium is generally thin and atrophic, but may
be hyperplastic. If the lesion is ulcerated, it shows a fibrous exudate of varying thickness over the surface
and a moderately intense infiltration of polymorphonuclear leukocytes, lymphocytes, and plasma cells.
The excessive vascularity accounts for the bright red color, and the hyperemia and edema account for the
enlargement.
Differential diagnosis
The differential diagnosis of a small, pedunculated hemorrhagic lesion of the marginal gingival tissue
must include the following:
1. Peripheral fibroma
2. Pyogenic granuloma
3. Peripheral giant granuloma
4. Eosinophilia granuloma
5. Lymphomas or leukemic infiltrates
6. Hemangiomas
TREATMENT
It is prudent, if possible, to wait until parturition for surgical excision of a pregnancy granuloma, unless
the lesion is creating a functional problem or appears to be having a deleterious effect on the adjacent
periodontium. These lesions may regress after birth; however, surgical excision is usually warranted. The
surgery can be accomplished safely throughout pregnancy with the use of local anesthesia and most
effectively with the aid of lasers in place of scalpel blades. Lasers have the tendency to reduce the
postsurgical  bleeding typically experienced after excision of a pyogenic granuloma. Incomplete excision
results in recurrence. A residual fibrous mass may remain if the lesion is large and is allowed to regress
postpartum without surgical intervention.

Periodontitis
Gingivitis, or inflammation of the gingiva, is considered to be a reversible process. In contrast,
periodontitis results in the loss of tooth attachment (periodontal ligament and alveolar bone) and pocket
formation. Though gingivitis is often associated with periodontitis, gingivitis does not usually develop into
periodontitis because the putative pathogenic bacteria in periodontitis differ from those associated with
gingivitis and because periodontitis is believed to be dependent on different immune mechanisms. A
number of investigators have noted sex hormone-mediated alteration of the subgingival flora and the
subsequent increase in gingival inflammation. When pregnant and nonpregnant women with periodontitis
are compared, however, the differences become less obvious. It has been shown that in contrast to
subjects with gingivitis, no significant differences are noted in the total bacterial counts and the
proportion of P. intermedia in periodontal pockets of pregnant versus nonpregnant women. Although
differences exist in the degree of periodontitis between pregnant and nonpregnant female populations,
these reported differences are not impressive. Therefore, conventional approaches for the prevention and
treatment of periodontitis are indicated for pregnant patients.

Dental caries
Many lay-persons appear to believe that pregnancy is a direct cause of dental caries. The old wives' tale
“with each child, a tooth” has been quoted even in dental and medical literature. In 1875 Coles wrote, “We
have during pregnancy, an increasing liability to caries, with each generation.” He noted that during the
first months of pregnancy, patients may have “severe toothache” secondary to caries. He explained this
as “a diminution of earthy salts” during pregnancy. This belief has been fostered and has been one of the
most stubborn misconceptions to appear in dental and medical literature. There is no scientifically proven
evidence to support this belief.
The hydroxyapatite crystal, of which enamel is made, does not respond to the biochemical and metabolic
changes of pregnancy, nor does it respond to changes in calcium metabolism. The belief that morning
sickness and vomiting can create an acid pH and therefore increase the decay rate is highly suspect as
well. The few seconds that the pH of the oral environment may be lowered is a very brief period of time
compared to the months needed for the production of decay.

Use of fluoride during pregnancy
Administration of fluoride supplements to pregnant patients in an effort to benefit the teeth of the offspring
has been evaluated in several clinical studies. Although the collective findings of these studies indicate a
possible benefit to the primary teeth of the offspring, the evidence is not sufficiently conclusive to warrant
recommending prescribing fluoride. The question of whether the fluoride ingested by expectant mothers
living in an area with fluoridated water will lead to increased caries resistance in the primary teeth of the
offspring cannot be definitely answered because the evidence is conflicting. The data have failed to show
any difference in the caries resistance of the primary teeth of children born just before the fluoridation of a
water supply and children born afterward who were exposed to fluoride both prenatally and postnatally.
A recent study provides strong evidence that the children of mothers with poor self-rated oral health are
more likely to grow up to have poorer oral health than those of mothers with good self-rated oral health.
Maternal self-rated oral health when children are young appears to be a valid representation of the
intricacies of the shared genetic and environmental factors that contribute to oral health throughout the
life-course. Unfavorable maternal self-rated oral health should be regarded as a risk indicator for poor
oral health among offspring later in life. Simple questions about maternal oral health should form part of
a preliminary and inexpensive assessment of a child’s future oral diseases risk (on both clinical and
public health grounds). In addition, it is important that mothers are told that their oral health can have an
impact on their child’s oral health, and dentists should encourage mothers of young children to receive
dental care.

Interceptive care
Ideally a patient's oral health status should be evaluated and treated by a dentist when pregnancy is
anticipated. The evaluation should be comprehensive and identify any potential problem areas (e.g.,
dental caries, broken teeth and/or restorations, periodontal disease, endodontic involvement). This
interceptive approach to treatment is recommended for three reasons: (1) to avoid a dental emergency
during pregnancy, which could potentially alter or compromise ideal dental treatment; (2) to reduce the
possibility or severity of periodontal disease (e.g., pregnancy granulomas) during pregnancy through
instruction and improvement in the patient's oral hygiene before pregnancy; and (3) to prevent the
possibility of a directly negative effect of oral disease on the fetus. The third reason is supported by recent
evidence showing that periodontal disease represents a significant risk factor for preterm, low-birth-
weight neonates (less than 2500 g). In Offenbacher et al.'s study, pregnant or postpartum mothers were
evaluated to determine whether the prevalence of material periodontal infection was associated with the
birth of preterm, low-birth-weight infants. It was found that low-birth-weight infants had mothers with
significantly worse periodontal disease as compared to mothers of normal birth- weight infants.
Additionally, the study showed that expectant mothers with periodontal disease were seven times more
likely than others to deliver a preterm, low birth-weight infant.