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.
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.
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.
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.
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.
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.
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.
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.
Normal pregnancy does not necessarily contraindicate dental treatment if the stage of gestation and the extent of dental procedures are taken into account. The first trimester is the period of organogenesis. In addition, approximately 75–80% of spontaneous abortions occur before the 16th week of gestation. T he fetus is thus very sensitive to environmental influences at this time. In the last half of the third trimester, premature delivery becomes a hazard. Prolonged chair time should be avoided because supine hypotensive syndrome may occur. Whether a pregnant woman is in a semireclining or a supine position, the great vessels, particularly the inferior vena cava, are compressed by the uterus. By interfering with venous return, this compression causes hypotension, decreased cardiac output, and eventual loss of consciousness. Supine hypotensive syndrome can usually be reversed byturning the patient on her left side, thereby relieving the pressure on the vena cava and allowing blood to return to the lower extremities and pelvic areas. Because of these hazards, however, no elective procedures, such as definitive periodontal surgery, should be performed during the first and third trimesters.
The second trimester is the safest period during which routine dental care can be provided. Even so, it is advisable to limit care to minimal treatment. Based on numerous studies that emphasize the role of local irritants in the initiation of periodontal disease during pregnancy, it is prudent to educate pregnant women about effective plaque control techniques early in pregnancy. All local irritants should be removed as soon as possible, before the effects of pregnancy are manifested in the gingival tissues.
If emergency treatment is indicated, it should be performed anytime during gestation to eliminate any associated physical or emotional stress. The pain and anxiety precipitated by a dental emergency may be more detrimental to a fetus than the treatment itself. One controversial area in the treatment of pregnant patients involves taking dental radiographs. Only serious dental emergencies require radiographic evaluation, especially in the first trimester, when a developing fetus is particularly susceptible to the effects of radiation. Routine radiographs should be avoided and taken only when necessary. If radiographs are taken, patients should wear a protective lead apron to reduce the amount of radiation to which the abdominal area is exposed.
Another area of concern involves drug therapy, because any drug given to a pregnant patient can affect her fetus by diffusion across the placental barrier. In most cases, it is safe practice to use a local anesthetic with a vasoconstrictor (1:100,000). Analgesics, including acetaminophen and aspirin (except during the third trimester, when bleeding problems can occur during or after delivery) are also safe.
Certain drugs occasionally prescribed by dentists are known to cause complications during pregnancy and therefore should be avoided. These include diazepam (Valium), chlordiazepoxide (Librium), flurazepam (Dalmane), meprobamate (Miltown), streptomycin, and tetracycline. Nitrous oxide should not be administered during organogenesis (first trimester), and neither general anesthesia nor intravenous sedation should be used at all during pregnancy.
Current evidence suggests an association between periodontal disease and increased risk of systemic diseases such as atherosclerosis, myocardial infarction, stroke, diabetes mellitus, and adverse pregnancy outcomes. Since the first report on the association between periodontal disease and preterm low birth in 1996 there has been an established link between periodontal disease and adverse pregnancy outcomes including preterm birth, low birth weight, miscarriage, and preeclampsia. Additionally, in 2003 a randomized controlled trial indicated that periodontal treatment consisting of scaling root planning to pregnant women with periodontitis may reduce the risk of preterm birth before 37 weeks of gestation and very preterm birth before 35 weeks of gestation.
Chronic periodontal infections can produce both local and systemic inflammatory response. The activation of the maternal inflammatory cell response and cytokine release plays an important role in the pathophysiological process of preterm birth, low birth weight and preeclampsia.
However, the limited number of randomized controlled trials prevents us from drawing a solid and clear conclusion. There is definite need for additional well-designed epidemiological studies that will test the hypothesis that periodontal treatment can significantly reduce the rates of certain adverse pregnancy outcomes.
The effects of pregnancy on host response and oral flora
The effects of pregnancy on the host response and oral flora Although the damaging processes accompanying periodontal disease (such as bone and periodontal ligament destruction) are associated with plaque bacteria they are, in fact, mainly a result of the host response to this microbial assault.
For bacteria to colonise subgingival sites and ultimately infiltrate the underlying connective tissue,many aspects of the host response must be evaded. It would appear that many facets of the immune response with regard to the periodontium are affected by pregnancy,with the overall effect being one of decreased activity and efficiency. The key developments are a decrease in the number of neutrophils, decreased chemotaxis and phagocytosis, and depressed antibody responses and cell-mediated immunity. Given that estrogen and progesterone receptors are found in the periodontal tissues, the progressive increase in levels of these hormones in pregnancy also affects the response of the tissues. The extracellular matrix, gingival vessels and fibroblasts are all affected.4 Although estrogen,which may be involved in the regulation of cellular proliferation, differentiation and keratinisation, seems to stimulate matrix synthesis, along with progesterone it also enhances the localised production of inflammatory mediators, especially prostaglandin E 2 (PGE 2), a potent inducer of osteoclastic activity.
Progesterone also compromises tissue homeostasis by reducing fibroblast proliferation, altering the pattern of collagen production and reducing the level of plasminogen activator inhibitor type 2 (PAI-2) which is an important inhibitor of tissue proteolysis. With regards to periodontal disease,Gram-negative anaerobic bacteria are the main culprits. They include: Prevotella intermedia (P. intermedia), Tannerella forsythensis, Porphyromonas gingivalis (P. gingivalis),Treponema denticola and Actinobacillus actinomycetemcomitans. Although the causal role of specific bacteria in pregnancy associated gingivitis has been difficult to establish, gingival bleeding and inflammation appears to be associated with a rise in the numbers of Gramnegative rods present. However, an increase in the selective growth of P. intermedia, P. gingivalis and Tannerella species (formerly Bacteroides) has been demonstrated in subgingival plaque during the onset of pregnancy gingivitis. This is likely to be a result of these species being able to use the pregnancy hormones, particularly progesterone, as a source of nutrition. This increase in selective growth may also be favoured by the changes that occur in the immune system during pregnancy alongside those that develop locally in the gingival crevice, such as blood from bleeding gingiva providing further nutrients and increased pocketdepths creating a more favourable environment for anaerobes.
Dental caries is a chronic endogenous infection which is multifactorial in nature and caused by the bacterial fermentation of dietary carbohydrates resulting in the localised destruction of the tooth. It appears that the important organisms in the initiation and subsequent progression of dental caries are the Mutans streptococci (a group name for seven different Streptococcus species), Lactobacilli and Actinomyces species. It is not thought that these are in any way affected by pregnancy directly in terms of their cariogenicity or that the structure of the tooth is changed resulting in the teeth becoming more susceptible to caries. Interestingly, increased levels of Mutans streptococci and
Lactobacilli are found in late pregnancy and during lactation. The dietary changes that may occur, especially in early pregnancy, such as regular consumption of sugary snacks and drinks to satisfy cravings or to prevent nausea and sickness will result in an increased risk of dental caries unless extra attention is paid to oral hygiene. This can be further complicated if the pregnant woman is unable to tolerate tooth brushing because of nausea and sickness to the extent that tooth brushing is significantly compromised.
In addition, the risk of caries may be further increased in pregnancy as a result of the estrogen enhanced proliferation and desquamation of the oral mucosa. It is suggested that the desquamating cells enhance the microenvironment by providing nutrition and a suitable environment for bacterial growth, therefore potentially predisposing to caries. Alterations in saliva flow, composition, pH and buffering capacity further compound this.
Tooth surface loss, primarily through acid-induced erosion, may be seen if there has been nausea and associated repeated vomiting during pregnancy. The palatal surfaces of the upper incisors and canines are often the most affected. The woman commonly presents complaining of sensitivity, which is a consequence of the resulting dentine exposure. Management is essentially preventative and includes the regular use of a fluoride mouth rinse, especially in those women who vomit frequently. In addition, these women should be advised to avoid tooth brushing directly after vomiting as the effect of erosion can be exacerbated by brushing an already demineralised tooth surface. Consumption of acidic fruits and juices as well as carbonated drinks should be restricted to avoid the potential for contact between additional acids and the tooth tissues. The use of drinking straws is recommended for the same reason, as is breaking the habit of holding such acidic drinks in the mouth for a longer time than is necessary.
Tooth mobility
Increased tooth mobility has been detected in pregnancy even in periodontally healthy women. The upper incisors are most mobile during the last month of pregnancy. Development of such mobility is possibly due to mineral shifts in the lamina dura and not to modification of the alveolar bone. The degree of periodontal disease present and disturbance of the supporting attachment tissues are also thought to contribute to this mobility, which usually resolves post delivery.
The following are guidelines suggested by the American Academy of Pediatrics (AAP), in response to the increased concern about oral health during pregnancy:
1) Oral Health Education– DO have consultations with your dentist before, during and after your pregnancy. Early intervention is key, but ongoing care is just as important!
2) Oral Hygiene– DO brush and floss regularly – and properly. It is especially important to try and always brush after meals and snacks, especially sugary ones. Also, have more frequent dental cleanings than you normally would (2-3 during your pregnancy is about right). This will greatly increase the amount of plaque that is removed from the teeth and gums, thereby lowering your risk.
3) Nutrition– DON’T eat junk. This is good advice in general during your pregnancy, but just know that proper diet and nutrition during pregnancy will limit sugar intake which, in turn, will minimize plaque build up.
4) Treat Tooth Decay– DO try and have all urgent dental work completed prior to becoming pregnant. Although, it is safe to perform certain emergency dental procedures during your pregnancy, it is best to have it done prior to becoming pregnant, and especially prior to it becoming an emergency dental treatment!
5) Transmission of Bacteria– DON’T share food and utensils, so as not to potentially transmit bacteria known to cause tooth decay.
6) Use of Xylitol Gum– DO chew gum. Expectant mothers, and everyone, are encouraged to chew xylitol gum (around 4x/day), since research suggests that it may decrease the rate of tooth decay. Chewing sugarless gum increases saliva and thus increases the production of salivary enzymes that help equalize the Ph in the mouth and thus reduce cavity growth.
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Oral health in pregnancy
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.
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Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
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.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
Certain drugs occasionally prescribed by dentists are known to cause complications during pregnancy and therefore should be avoided. These include diazepam (Valium), chlordiazepoxide (Librium), flurazepam (Dalmane), meprobamate (Miltown), streptomycin, and tetracycline. Nitrous oxide should not be administered during organogenesis (first trimester), and neither general anesthesia nor intravenous sedation should be used at all during pregnancy.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
However, the limited number of randomized controlled trials prevents us from drawing a solid and clear conclusion. There is definite need for additional well-designed epidemiological studies that will test the hypothesis that periodontal treatment can significantly reduce the rates of certain adverse pregnancy outcomes.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
In addition, the risk of caries may be further increased in pregnancy as a result of the estrogen enhanced proliferation and desquamation of the oral mucosa. It is suggested that the desquamating cells enhance the microenvironment by providing nutrition and a suitable environment for bacterial growth, therefore potentially predisposing to caries. Alterations in saliva flow, composition, pH and buffering capacity further compound this.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
Increased tooth mobility has been detected in pregnancy even in periodontally healthy women. The upper incisors are most mobile during the last month of pregnancy. Development of such mobility is possibly due to mineral shifts in the lamina dura and not to modification of the alveolar bone. The degree of periodontal disease present and disturbance of the supporting attachment tissues are also thought to contribute to this mobility, which usually resolves post delivery.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
6) Use of Xylitol Gum – DO chew gum. Expectant mothers, and everyone, are encouraged to chew xylitol gum (around 4x/day), since research suggests that it may decrease the rate of tooth decay. Chewing sugarless gum increases saliva and thus increases the production of salivary enzymes that help equalize the Ph in the mouth and thus reduce cavity growth.
For any help on posting on the site, email at [email protected]
Oral health in pregnancy
Thanks.
At Smiles at San Tan Ranch, we offer the best cosmetic dentistry treatment for your healthy smile. We have many different financing options available to help make payments for orthodontic treatment very comfortable. Get in touch with us for more details.
Oral health in pregnancy
Informative Post!!
We are a passionate dentist team famous for providing a choice of quality dental treatments in Mesa, Arizona. We specialize in sedation dentistry, family dentistry, periodontal disease and emergency dental care. Schedule an appointment today!
Oral health in pregnancy
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Here at Texas Dental Surgery, we are passionate to offer oral surgery including dental implants, wisdom tooth formation, gum grafts, periodontal disease treatment and more in and nearby Plano. Contact us anytime!