The Obstetrician & Gynaecologist 2007;9:1:21-26
doi: 10.1576/toag.9.1.021.27292
Copyright © 2007 by the Royal College of Obstetricians and Gynaecologists.
Dental manifestations of pregnancy
Martina Pirie, BMSc BDS MFDSRCS, Clinical Research Fellow1,
Inez Cooke, MA MRCOG, Senior Lecturer and Consultant2,
Gerard Linden, BSc, BDS, PhD, FDSRCS, FFDRCSI, Chair and Consultant3 and
Chris Irwin, BSc, BDS, PhD, FDSRCPS, Reader and Consultant4
1. Division of Restorative Dentistry, School of Dentistry, Queen's University Belfast, Grosvenor Road, Belfast BT12 6BP, UK Email: m.pirie{at}qub.ac.uk (corresponding author)
2. Department of Obstetrics and Gynaecology, Queen's University Belfast, UK
3. Division of Restorative Dentistry, School of Dentistry, Queen's University Belfast, UK
4. Division of Restorative Dentistry, School of Dentistry, Queen's University Belfast, UK
 |
Abstract
|
|---|
Key content:- Pregnancy has significant effects on the periodontal tissues and pregnancy gingivitis is a common manifestation of this.
- The host response and oral flora are affected and tooth surface loss and mobility may develop.
- Further research is required to establish the association between periodontal health and adverse pregnancy outcome.
Learning objectives:
- To identify the main dental manifestations of pregnancy.
- To be able to advise pregnant women on how to maintain good dental health.
- To be aware of the need for effective communication between the dental and medical disciplines to ensure that pregnant women receive the best care possible for oral, obstetric and general health.
Ethical issues:
- The treatment of gingivitis and periodontitis during pregnancy is safe and effective in treating gum disease.
Please cite this article as: Pirie M, Cooke I, Linden G, Irwin C. Dental manifestations of pregnancy. The Obstetrician & Gynaecologist 2007;9:21–26.
Keywords periodontal health / pregnancy epulis / pregnancy gingivitis / pregnancy outcome
|
Introduction
|
|---|
The numerous physical and physiological changes that occur during pregnancy1 affect every major body system and result in localised physical alterations in many parts of the body, including the oral cavity.2 The aim of this paper is to increase awareness of the main potential dental manifestations which can occur in pregnancy.
|
The effects of pregnancy on periodontal tissues
|
|---|
Pregnancy gingivitis
Gingivitis is a plaque induced inflammation of the gingiva, part of the oral mucosa which surrounds the tooth and covers the alveolar bone (a healthy gingiva is shown in Figure 1). During pregnancy the inflammatory response to dental plaque is increased, leading to swollen gingivae which tend to bleed on brushing. Gingivitis exacerbated by the hormonal changes of pregnancy is known as pregnancy gingivitis,3 although this does not essentially differ histologically from that which develops in the non pregnant state.4 Pregnancy gingivitis is considered the most common oral manifestation of pregnancy and has been reported as occurring in up to 100% of pregnant women.5 Characteristic features of healthy and inflamed gingivae are listed in Box 1.
Pregnancy gingivitis commonly becomes apparent later in the second month of gestation and worsens as the pregnancy progresses before reaching a peak in the eighth month. In the last month of gestation gingivitis usually decreases and immediately post partum the gingival tissues are found to be comparable to those seen during the second month of gestation.5 However, this does not automatically indicate a return to health. Although the clinical features of pregnancy gingivitis may be localised or generalised, the changes affecting the anterior teeth are the most obvious (Figure 2),5 despite increased amounts of plaque being associated with the posterior teeth.6 Bearing in mind that gingivitis is considered to be plaque induced, it is interesting that Raber-Durlacher et al.6 demonstrated that pregnancy gingivitis is not caused by an increase in dental plaque. It may be due to the effects of pregnancy on the gingival tissues where both estrogen and progesterone receptors are found, although exactly how these hormones increase gingival inflammation is unknown. It is possible that the pregnancy related gingival changes may be explained by increased vascularity and vascular flow alongside alterations in the immune system and/or changes in connective tissue metabolism.4
View larger version (55K):
[in this window]
[in a new window]
|
Figure 2
Pregnancy gingivitis affecting the gingival tissues, particularly associated with the lower anterior teeth despite minimal plaque stains on the tooth surfaces
|
|
Management of pregnancy gingivitis involves regular dental visits for professional cleaning and monitoring with education of the woman regarding both the aetiology and prevention of the condition. Elimination of factors which compromise removal of plaque, for example overhanging restoration margins, should be carried out so that plaque levels can be minimised.
Pregnancy epulis (pyogenic granuloma of pregnancy)
The pregnancy epulis (Figure 3) is a localised, soft hyperplastic lesion which develops on the gingiva in up to 5% of pregnancies.4,7 This bright red, highly vascularised lesion, which may have small white flecks superficially, is usually pedunculated and can measure up to 2 cm in diameter. Although it can arise from any gingival site it mostly occurs on the interdental papillary gingiva, particularly on the labial aspect and more commonly on the upper jaw than the lower.8 Teeth adjacent to the pregnancy epulis may be seen to drift and become increasingly mobile,7 although bony destruction rarely develops around the teeth directly involved.4 It may develop at any time but appears to be most common in early pregnancy. It has been suggested that this lesion arises from an already inflamed gingival papilla, therefore plaque is considered an important initiating factor.
In addition to dental plaque, the pregnancy related hormonal changes that produce an exaggerated gingival response to plaque are thought to underlie the formation of the pregnancy epulis.4, 7 It is clinically and histologically indistinguishable from the pyogenic granuloma in men and nonpregnant women.4 During pregnancy, non-surgical management involves elimination, or at least the significant reduction, of dental plaque, particularly around the epulis. This is best achieved by the woman regularly attending the dentist or dental hygienist for thorough cleaning in addition to plaque control instruction to ensure that the oral home care regimen is of a suitably high standard.7, 9
Given the unsightly appearance of the pregnancy epulis, which is often at the front of the mouth, and its propensity to bleed, it is, understandably, concerning for the woman. However, surgical removal should only be performed during pregnancy if the epulis is traumatised by opposing teeth or restorations resulting in pain and bleeding,8 if it is interfering with normal speech and/or mastication, or if it bleeds severely and/or becomes painful.9 Correction of any associated local contributing factors must also be carried out. Given the high recurrence rate of this lesion, surgery should ideally be delayed until after delivery, when the epulis often regresses completely or, at the very least, is smaller, more fibrous and easier to remove.8 However, if surgery cannot be delayed, removal should be done during the second trimester and the woman informed of the risk of recurrence.
|
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.4, 10 The key developments are a decrease in the number of neutrophils, decreased chemotaxis and phagocytosis, and depressed antibody responses and cell-mediated immunity.11
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 E2(PGE2), 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.4, 9
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. 12 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 Gram-negative rods present. 4 However, an increase in the selective growth of P.intermedia, 6, 13 P. gingivalis 10 and Tannerella species (formerly Bacteroides) 14 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.4, 10 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 pocket depths creating a more favourable environment for anaerobes.4
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.15 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.4 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.1 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.16
|
Tooth surface loss
|
|---|
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 (Figure 4). 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.7 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.
View larger version (56K):
[in this window]
[in a new window]
|
Figure 4
Tooth surface loss on the palatal aspects of the upper anterior teeth due to acid erosion following repeated vomiting
|
|
|
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.17 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.7
|
The impact of periodontal health on pregnancy
|
|---|
Given the considerable effect of pregnancy on oral health it is interesting that the impact of periodontal disease on pregnancy outcome is now under scrutiny. The idea that it may contribute to pregnancy outcome was presented in 1931 when Galloway18 stated that periodontal disease may provide ‘sufficient infectious microbial challenge’ to have ‘potentially harmful effects on the pregnant mother and developing fetus’. Infection, especially symptomatic infection of the genitourinary tract, is considered an important risk factor for preterm birth and/or low birthweight. Essentially, bacterial infection results in the activation of cell-mediated immunity and the subsequent production of cytokines such as interleukins (IL-1, IL-6), tumour necrosis factor alpha (TNF-
) and prostaglandins, especially PGE2.
Currently, one proposed mechanism of labour suggests that the intra-amniotic levels of these mediators rise steadily throughout pregnancy until a threshold is reached at which labour is induced. Thus, it is possible that the presence of infection which results in an abnormally elevated production of these normal physiological mediators of parturition may trigger preterm birth, also resulting in low birthweight.19 More recently, it has been suggested that subclinical infections such as periodontitis may also pose a challenge to the developing fetus.
A frequent observation potentially linking subclinical infection and preterm birth is that there is an increased incidence of histologic chorioamnionitis in preterm delivery, which is usually the result of infection. However, given that it may not be associated with symptomatic infections of the genitourinary tract and that culture may produce a negative result, it is proposed that infection remote from the fetoplacental complex and genitourinary tract may play a role. Essentially, it is hypothesised that subclinical infections such as periodontal disease contribute to premature delivery and low birthweight as a result of pathogenic micro-organisms, or indeed their microbial products, such as lipopolysaccharide (LPS), reaching the uterus via the bloodstream, inducing cytokine release in the decidua or the membranes, resulting in increased prostaglandin production or, indeed, uterine muscle contraction.20 Inflammatory mediators such as cytokines and prostaglandins, for example when produced in the periodontal tissues or in other systemic organs in response to LPS stimulation, may also pose a real threat to the fetoplacental unit and increase the risk of preterm delivery and low birthweight (Figure 5).19
View larger version (19K):
[in this window]
[in a new window]
|
Figure 5
Proposed biological mechanisms linking periodontal disease to preterm low birthweight delivery
|
|
In 1996, Offenbacher et al.19 published the results of a case control study which suggested that periodontitis was a statistically significant risk factor for premature delivery and low birthweight and, indeed, that mothers with periodontal disease were potentially seven times more likely to have a preterm or low birthweight baby. Subsequent research by Jeffcoat et al.21 supported this suggestion. They found a four-fold increase in the odds of preterm birth before 37 weeks of gestation, rising to a seven-fold increase before 32 weeks of gestation in women with generalised or severe periodontal disease in weeks 21–24 of pregnancy. The work of Madianos et al.22 added weight to this argument, reporting that preterm delivery and low birthweight were 11 times more likely to occur in women whose periodontal disease worsened during pregnancy compared with those who had good periodontal health. Recently, Offenbacher et al.23 reported that periodontal disease progression in pregnancy may be predictive of birth occurring at less than 32 weeks of gestation.
Not all studies have found an association between periodontal disease and preterm delivery and low birthweight. Davenport et al.24 found that the risk actually decreased with increasing pocket depth. Moore et al.25 found no association between periodontal disease and preterm delivery and low birthweight, although, interestingly, this work did suggest a link between indicators of poor periodontal health and late miscarriage. A recent systematic review by Xiong et al.26 concluded that, although periodontal disease may be adversely associated with pregnancy outcome, further ‘methodologically rigorous’ research is required. Bearing all of this in mind, it is hoped that current research, in particular intervention studies on pregnant women with periodontal disease, may help to establish whether a significant cause and effect relationship does exist and the impact periodontal treatment may have during pregnancy.
|
Conclusion
|
|---|
The aim of this paper is to increase awareness of the potential oral manifestations of pregnancy. Those involved in obstetric and prenatal care may well be the first health professionals to become aware of developing oral conditions and it is important that they can provide appropriate information, advice and reassurance followed by referral for a dental examination, treatment and monitoring as necessary. Given that periodontal health may also affect pregnancy, it is vital that effective communication occurs between the dental and medical disciplines to ensure that pregnant women receive the best care possible for oral, obstetric and, indeed, general health.
|
References
|
|---|
- Gajendra S, Kumar JV. Oral health and pregnancy: a review. NY State Dent J 2004;70:40–4.
- Suresh L, Radfar L. Pregnancy and lactation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;97:672–82.[Medline]
- Palmer R, Soory M. Modifying factors: diabetes, puberty, pregnancy and the menopause and tobacco smoking. In: Linde J, Karring T, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 4th ed. Oxford: Blackwell Munksgaard; 2003. p. 184–86.
- Laine MA. Effect of pregnancy on periodontal and dental health. Acta Odontol Scand 2002;60:257–64. doi:10.1080/00016350260248210[Medline]
- Löe H, Silness J. Periodontal disease in pregnancy: Prevalence and severity. Acta Odontol Scand 1963;21:533–51.[Medline]
- Raber-Durlacher JE, van Steenbergen TJ, van der Velden U, de Graaff J, Abraham-Inpijn L. Experimental gingivitis during pregnancy and post-partum: clinical, endocrinological, and microbiological aspects. J Clin Periodontol 1994;21:549–58. doi:10.1111/j.1600-051X.1994.tb01172.x[Medline]
- Hunter L, Hunter B. Oral and dental problems associated with pregnancy. In: Oral Healthcare in Pregnancy and Infancy. London: Macmillan Press Ltd; 1997. p. 27–34.
- Manson JD, Eley BM. The effect of systemic factors on the periodontal tissues. In: Outline of Periodontics. 3rd ed. Oxford: Butterworth-Heinemann Ltd; 1995. p. 71–89.
- Barak S, Oettinger-Barak O, Oettinger M, Machtei EE, Peled M, Ohel G. Common oral manifestations during pregnancy: a review. Obstet Gynecol Surv 2003;58:624–28. doi:10.1097/01.OGX.0000083542.14439.CF[Medline]
- Mascarenhas P, Gapski R, Al-Shammari K, Wang H-L. Influence of sex hormones on the periodontium. J Clin Periodontol 2003;30:671–81. doi:10.1034/j.1600-051X.2003.00055.x[Medline]
- Raber-Durlacher JE, Leene W, Palmer-Bouva CC, Raber J, Abraham-Inpijn L. Experimental gingivitis during pregnancy and post-partum: immunohistochemical aspects. J Periodontol 1993;64:211–18.[Medline]
- Kinane D. Causation and pathogenesis of periodontal disease. Periodontol 2000 2001;25:8–20. doi:10.1034/j.1600-0757.2001.22250102.x
- Muramatsu Y, Takaesu Y. Oral health status related to subgingival bacterial flora and sex hormones in saliva during pregnancy. Bull Tokyo Dent Coll 1994;35:139–51.[Medline]
- Darby ML, Walsh MM. Women's health. In: Dental Hygiene: Theory and Practice. 2nd ed. St Louis: WB Saunders; 2003. p. 932–44.
- Samaranayake L. Microbiology of dental caries. In: Essential Microbiology for Dentistry. 2nd ed. Edinburgh: Churchill Livingstone; 2001. p. 217–23.
- Laine M, Tenovuo J, Lehtonen OP, Ojanotko-Harri A, Vilja P, Tuohimaa P. Pregnancy-related changes in human whole saliva. Arch Oral Biol 1988;33:913–17. doi:10.1016/0003-9969(88)90022-2[Medline]
- Rateitschak KH. Tooth mobility changes in pregnancy. J Periodontal Res 1967;2:199–206. doi:10.1111/j.1600-0765.1967.tb01890.x[Medline]
- Galloway CE. Focal infection. Am J Surg 1931;14:643–45. doi:10.1016/S0002-9610(31)91140-9
- Offenbacher S, Katz V, Fertik G, Collins J, Boyd D, Maynor G, et al. Periodontal infection as a possible risk factor for preterm low birth weight. J Periodontol 1996;67:1103–13.[Medline]
- Gibbs RS. The relationship between infections and adverse pregnancy outcomes: an overview. Ann Periodontol 2001;6:153–63. doi:10.1902/annals.2001.6.1.153[Medline]
- Jeffcoat MK, Geurs NC, Reddy MS, Cliver SP, Goldenberg RL, Hauth JC. Periodontal infection and preterm birth: results of a prospective study. J Am Dent Assoc 2001;132:875–80.[Abstract/Free Full Text]
- Madianos PN, Lieff S, Murtha AP, Boggess KA, Auten RL Jr, Beck JD, et al. Maternal periodontitis and prematurity. Part II: Maternal infection and fetal exposure. Ann Periodontol 2001;6:175–82. doi:10.1902/annals.2001.6.1.175[Medline]
- Offenbacher S, Boggess KA, Murtha AP, Jared HL, Lieff S, McKaig RG, et al. Progressive periodontal disease and risk of very preterm delivery. Obstet Gynecol 2006;107:29–36.[Medline]
- Davenport ES, Williams CE, Sterne JA, Murad S, Sivapathasundram V, Curtis MA. Maternal periodontal disease and preterm low birthweight: case-control study. J Dent Res 2002;81:313–8.[Abstract/Free Full Text]
- Moore S, Ide M, Coward PY, Randhawa M, Borkowska E, Baylis R, et al. A prospective study to investigate the relationship between periodontal disease and adverse pregnancy outcome. Br Dent J 2004;197:251–8. doi:10.1038/sj.bdj.4811620[Medline]
- Xiong X, Buekens P, Fraser WD, Beck J, Offenbacher S. Periodontal disease and adverse pregnancy outcomes: a systematic review. BJOG 2006;113:135–43. doi:10.1111/j.1471-0528.2006.00968.x[Medline]
TOP
Abstract
Introduction
