During pregnancy, women undergo certain hormonal and physiological changes that can affect their mouths. EFFECT OF PREGNANCY ON PERIODONTAL TISSUES PREGNANCY GINGIVITIS EFFECT OF PERIODONTITIS ON PREGNANCY PRETERM LOW BIRTH WEIGHT (PLBW) INFANTS PREECLAMPSIA

1. PREGNANCY AND
PERIODONTAL
DISEASE
1

3. INDEX
 EFFECT OF PREGNANCY ON PERIODONTAL
TISSUES
 PREGNANCY GINGIVITIS
 EFFECT OF PERIODONTITIS ON PREGNANCY
 PRETERM LOW BIRTH WEIGHT (PLBW) INFANTS
 PREECLAMPSIA

4. PREGNANCYGINGIVITIS

5. PREGNANCY GINGIVITIS (INDEX)
 Pathogenesis
 Effect on Microbiota
 Effect of Estrogen and Progesterone
 Effect on Immune system
 Clinical Features
 Treatment

6. During pregnancy there is increased
levels of sex steroid hormones
Main estrogen in plasma in
is estradiol; and main progesterone is
progestin

7. By the end of 3rd trimester, plasma
peak levels of these hormones are 100
ng/ml and 6ng/ml which is 10-30
times more than menstrual levels

8. PREGNANCY GINGIVITIS
Gingival inflammation, initiated by plaque, and
exacerbated by these hormonal changes in 2nd
and 3rd trimester of pregnancy, is referred as
Pregnancy Gingivitis. (seen in 30-100% cases)
First described in 1877

9. Gingival inflammatory changes
usually begin in 2nd month of
pregnancy, and  in severity to 8th
month, after which there is abrupt
decrease related to reduction of sex
steroid hormone secretion.

10. PATHOGENESIS

11. 1. EFFECT ON
MICROBIOTA

12.  . There is 55 fold increase in P.
Intermedia in subgingival
plaque
Gestational hormones act as
growth factors for P. Intermedia
by satisfying the
napthoquinone requirement
bacteria

13.  .
Campylobacter level is directly
related to estradiol level
Bacteroides melaninogenicus also
increases in pregnancy (55 fold) and
in those taking contraceptives (16
fold)

14. 2. EFFECT OF
ESTROGEN AND
PROGESTERONE

15. Effect of Estrogen
Estrogen stimulates proliferation of gingival fibroblasts, synthesis
and maturation of the gingival CT.
Cause increase in leakage of leukocytes and plasma proteins from
post capillary venules by affecting the endothelial lining,
contributing to enhanced gingival inflammation↓ Keratinization along with increase in epithelial glycogen results in
decreased effectiveness of the epithelial barrier

16. Effect of Progesterone
Increased Circulatory levels of Progesterone enhances capillary
permeability and dilatation by forming gaps in endothelial
lining of vessels, resulting in increased gingival exudate
This increased gingival exudate effect caused by
progesterone is of long duration as compared
same effect produced by histamine that is of
short duration.

17. Effect of Progesterone
It inhibits collagenase activity thus resulting in
accumulation of excess collagen in connective
tissue, causing enlargement.
Increased Progesterone levels ↓ the degree of
keratinization of gingival epithelium

18.  These hormones also  rate of folate metabolism in oral
mucosa.
 Since folate is required for tissue maintenance (DNA
formation), increased metabolism could deplete folate
stores and inhibit tissue repair.
 Thus folic acid tablet is always recommended in
pregnancy

19. 3. EFFECT ON
IMMUNE SYSTEM

20.  .
↓ Neutrophil chemotaxis and phagocytosis, along with ↓ T-cell responses causes
the suppression of immune system to plaque
Progesterone in particular stimulates the production of inflammatory mediator
PGE2
Peripheral blood lymphocytes showed a decreased response to bacterial
antigens

21.  .
↓ IL-6 production by human gingival fibroblasts (upto 50%)
↓ CD4 T and B lymphocytes during pregnancy, thus CD4/CD8 ratio also
decreases, leading to an immunodeficient state.
↓ levels of Plasminogen activator inhibitor type 2 (PAI-2), an important inhibitor
of tissue proteolysis

22. CLINICAL FEATURES

23. Pregnancy Gingivitis
 Gingival enlargement occur in 2 forms:
1. marginal and generalized
2. single or multiple tumor like masses

24. 1. Marginal enlargement
 Generalized enlargement, more prominent interproximally than on
facial/lingual surface.
 Enlarged gingiva is bright red or magenta, soft, friable and has a smooth
shiny surface
 Spontaneous bleeding or on slightest provocation

25. 2. Tumor like enlargement
 discrete, mushroom shaped, flattened spherical mass that protrudes
from gingival margin / interproximal space
 Tends to expand laterally, and pressure from tongue and cheek
perpetuate its flattened appearance
 Dusky red or magenta, with smooth, glistening surface that often
exhibits numerous deep red, pinpoint markings.

26.  Superficial lesion, that do not invade underlying bone.
 Usually painless, unless complicated by plaque accumulation.
 Site – anterior papilla of maxillary teeth (most common)
 Gingiva is involved in 70% of cases, followed by tongue, lips and
buccal mucosa.

27. Histopathology
 Angiogranuloma
 Both marginal and tumor like enlargements consisting of central
mass of CT with numerous diffusely arranged, newly formed
engorged capillaries
 Chronic inflammatory infiltrate
 Thickened stratified squamous epithelium, with prominent rete
pegs, intercellular bridges, and leukocytic infiltration.

28. TREATMENT
 Pregnant women need to be educated on the consequences of pregnancy on
gingival tissues and thoroughly motivated in plaque control measures, with
professional treatment as required.
 They are likely to be more comfortable to receive dental treatment during
the second trimester than in the first or third trimester of pregnancy,
although emergency treatment is permissible at any stage during pregnancy

29.  Scaling and root planing
 Treatment of tumor like gingival enlargements consist of surgical excision
The enlargement recurs unless all irritants are removed.

30.  Penicillin and cephalosporin are relatively safer but
patient obstetrician consultation is warranted.
 Paracetamol is the safest anti inflammatory drug

31. When to Treat
 Gingival lesions in pregnancy should be treated as soon as they are
detected, although not necessarily by surgical means. 2nd trimester is the
safest period of surgical excision.
 SRP and adequate oral hygiene measures may reduce the size of the
enlargement. Gingival enlargements do shrink after pregnancy, but they
usually do not disappear.

32.  Lesions should be removed surgically during pregnancy only if they interfere
with mastication or produce an esthetic disfigurement that the patient
wishes to remove.
 After pregnancy, the entire mouth should be reevaluated, radiographs
should be taken, and the necessary treatment undertaken.
 Emphasis should be on 1) preventing gingival disease before it occurs (by
doing scaling in each trimester) and 2) treating existing gingival disease
before it worsens.

33. EFFECT OF PERIODONTITIS
ON PREGNANCY
 Preterm low birth weight (PLBW) infants
 Preeclampsia
33

34.  Periodontal disease during pregnancy has been linked to
preterm low birth weight (PLBW) infants, early pregnancy loss,
and preeclampsia.

35. Preterm low birth weight
(PLBW) infants

36. Preterm low birth weight (PLBW)
infants
 Periodontitis is a remote gram negative infection that may play role in PLBW
infants (PLBW < 2500gm)
 Premature and low-birth-weight (PLBW) infants are 40 times more likely to
die during the neonatal period. Such infants who survive the neonatal
period, face a higher risk of several neurodevelopment disturbances, health
problems (such as asthma, upper and lower respiratory infections and ear
infections) and congenital anomalies.

37.  Offenbacher and co-authors in 1996 from a case controlled study
suggested that women who delivered preterm low birth weight (PLBW)
infants had poorer periodontal health than mothers with normal birth
weight infants. They found the presence of higher levels
of Porphyromonas gingivalis, Bacteroides forsythus, Actinobacillus
actinomycetemcomitans and Treponema denticola organisms normally
associated with periodontal disease in mothers of PLBW babies as
compared to normal controls.

38.  In periodontal disease, transient bacteremia can occur leading to selective
colonization of undesired sites. Study by Han et al (2004) have shown that
hematogenous injection of orally related F. nucleatum in mice resulted in
preferential localization to placental blood vessels from which it crossed
the endothelium to the amniotic fluid and induced premature delivery and
stillbirths in a pattern similar to that seen in humans. This supports the
hypothesis that after transient bacteremia, oral bacteria like
F.nucleatum translocates to pregnant uterus and possibly to the fetus
hematogenously.

39.  Bacterial migration from periodontal tissues into blood circulation, also
stimulate the production of inflammatory mediators and increased
prostaglandin PGE2 production responsible for uterine contraction and the
onset of preterm delivery.
 F. nucleatum and P. gingivalis had been isolated from amniotic fluid and
cord blood in cases of preterm birth and neonatal sepsis by Gauthier S et
al (2011) and Katz J et al (2009) respectively.

40. Proposed mechanisms are-
 Translocation of the periodontal bacteria to fetoplacental unit
 Systemic dissemination of endotoxins on fetoplacental unit
 Systemic dissemination of inflammatory mediators (IL-1, IL-6, TNF-α,
PGE2) on fetoplacental unit.

41.  MECHANISM:
41Periodontal Infection
Bacteria & their products in
amnion
Inflammatory response with
cytokine production in
amnion
Increased amniotic
prostaglandin production
Preterm labour with
LBW infants

42. PREVENTION
 Hence periodontal disease appears to be an independent risk
factor for PLBW (preterm low birth weight infants) and there is
need to expand preventive measures by introducing oral health
programs as an integral component of prenatal care for
pregnant mothers.

43. Preeclampsia

44. Preeclampsia
 Preeclampsia is a pregnancy-specific disorder characterized by
increase in systolic arterial pressure (≥140 mmHg) and/or
diastolic pressure (≥90 mmHg) and proteinuria (≥300 mg/24 h),
after 20 weeks of gestation. It is dangerous for both mother and
fetus. Periodontitis is considered as a risk factor for it.
 Etiology: An increased systemic inflammatory response to pregnancy

45. Preeclampsia
 It is characterized by an abnormal vascular response to
placentation, manifesting as generalized vasospasm, activation
coagulation system and reduced organ perfusion affecting the
kidney, liver and brain.
 Periodontal disease burden pregnant women systemically with
endotoxins, inflammatory cytokines and oxidative stressors at
the maternal-fetal interface, thus acting as vascular stressor
that plays a role in development of Preeclampsia in pregnancy.

46.  Normal pregnancy is considered as mild pro-inflammatory state whereas
preeclampsia indicate more severe level of inflammation. The subgingival bacteria,
their products and pro-inflammatory cytokines may enter the bloodstream, reach
maternal–fetal interface, trigger/worsen maternal inflammatory response, increases
prostaglandin and cytokines levels in the plasma, causing complications in
pregnancy.

47. Prevention
 Maternal periodontal disease is a preventable disease in
contrast to preeclampsia, which can be treated but is difficult to
prevent. Hence, maternal periodontal disease must be taken as
an independent risk factor for adverse pregnancy outcomes
during evaluation of the pregnant women.

48.  The study by Jaiman G et al (2018) showed that birth weight of
newborn was significantly less in the preeclamptic group
suggesting that maternal preeclampsia could increase risk for
low birth weight infants.