Oral health in pregnancy

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.