Hormonal fluctuations in females can impact periodontal disease. Puberty, menstruation, pregnancy, menopause, and oral contraceptive use can all influence the gingival tissues and affect susceptibility to periodontal disease. Pregnancy in particular increases sex hormone levels like estrogen and progesterone, which can directly impact the periodontium and immune response, resulting in conditions like pregnancy gingivitis. Periodontal disease has also been associated with adverse pregnancy outcomes like preterm birth and preeclampsia. Proper oral hygiene and treatment during stages of hormonal change in females can help reduce risks to oral and overall health.

1. HARMONAL CHANGES IN
FEMALE PATIENTS AND
PERIODONTAL DISEASE
1

3. INDEX
Hormonal fluctuations and gingival changes in female patient:
 Puberty
 Menstruation
 Pregnancy
 Menopause
 Oral Contraceptives
 Osteoporosis

4. Need for assessment
To identify high-risk stages of female
patients in prior so that preventive
and treatment procedures can be
tailored

5. These hormonal fluctuations affect
the periodontal tissues directly,
modify the tissue response to local
factors and produce anatomic
changes in the gingiva that may
favor plaque accumulation and
disease progression

6. Hormonal fluctuations in female patient:
 Puberty
 Menstruation
 Pregnancy
 Menopause
 Oral Contraceptives
 Osteoporosis

7. PUBERTY

8. PUBERTY
 Increased testosterone (in males) and increased estradiol (in
females) is seen.
 Increased no. of Prevotella Intermedia sp. seen, as they
substitute Progesterone & estrogen for menadione (Vitamin
K) as an essential nutrient.
 Increase in no. of Capnocytophaga species is seen,
responsible for the increased bleeding tendency observed
during puberty .
Oral manifestations: Gingivitis,
Gingival enlargement, Recurrent
apthous ulcers, Aggressive
periodontitis (0.1% to 0.4%)

9. Clinical Features Of Puberty Induced Gingivitis
i) Marginal & interdental gingival
enlargement found primarily on the facial
surfaces, with lingual surfaces remaining
relatively unaltered.
ii) Increased gingival bleeding tendency
iii) Increased inflammation with relative less
amounts of plaque
iv) When puberty is passed, the
inflammation tends to subside but
does not disappear until adequate
plaque control is achieved.

10. TREATMENT
i) Scaling and root planing is the
treatment of choice as symptoms
reduced when puberty ends.
ii) If enlargement is more,
Gingivectomy is done

11. MENSTRUATION

12. MENSTRUATION
During
menstruation,
changes seen
are
Gingivitis
Increase in
GCF flow
Enlarged hemorrhagic
gingiva in days
preceding menstrual
Minor
increase in
Tooth
mobility

13. In addition to gingival inflammation
 intraoral recurrent apthous ulceration
 herpes labialis lesions
 infections with Candida Albicans
are seen in some women and seem to be associated with increased
Progesterone levels during reproductive cycle.

14. PREGNANCY

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

16. PREGNANCYGINGIVITIS

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

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

19. 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

20. 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

21. 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.

22. PATHOGENESIS

23. 1. EFFECT ON
MICROBIOTA

24.  . 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

25.  .
Campylobacter level is directly
related to estradiol level
Bacteroides melaninogenicus also
increases in pregnancy (55 fold) and
in those taking contraceptives (16
fold)

26. 2. EFFECT OF
ESTROGEN AND
PROGESTERONE

27. 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

28. 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.

29. 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

30.  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

31. 3. EFFECT ON
IMMUNE SYSTEM

32.  .
↓ 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

33.  .
↓ 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

34. CLINICAL FEATURES

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

36. 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

37. 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.

38.  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.

39. 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.

40. 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

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

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

43. 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.

44.  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.

45. EFFECT OF PERIODONTITIS
ON PREGNANCY
 Preterm low birth weight (PLBW) infants
 Preeclampsia
45

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

47. Preterm low birth weight
(PLBW) infants

48. 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.

49.  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.

50.  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.

51.  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.

52. 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.

53.  MECHANISM:
53Periodontal Infection
Bacteria & their products in
amnion
Inflammatory response with
cytokine production in
amnion
Increased amniotic
prostaglandin production
Preterm labour with
LBW infants

54. 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.

55. Preeclampsia

56. 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

57. 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.

58.  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.

59. 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.

60.  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.

61. MENOPAUSE

62. Menopausal Gingivostomatitis
• There is overall ↓ in estrogen output with estrone as the predominant form
• ↓ salivary gland flow
• Oral discomfort, burning sensation(20-90%), xerostomia or bad taste
• Atrophic gingivitis develop in some cases, in which gingival tissues develop
abnormal paleness.

63. Menopausal Gingivostomatitis
 Some may develop menopausal gingivostomatits, in which gingival tissues are
shiny and dry, bleed readily, and appear pale to erythematous in color.
 Gingival lesions during this phase tend to be desquamative in nature
 Patients with periodontitis have more chances of osteoporosis.

64.  Osteoporosis is frequently seen in women during
menopause due to decreased production of
estrogen. It causes suppression of calcium
absorption, increase in calcium excretion and
osteocyte apoptosis.
 Periodontitis in such patients release TNF-α that
induce collagenase activity, resulting in more bone
loss

65. TREATMENT
 During menopause, women with both
periodontitis and osteoporosis should be treated
for both.

66. ORAL CONTRACEPTIVES

67. HORMONAL CONTRACEPTIVES
 Contraceptives utilize synthetic gestational hormones (estrogen and
progesterone), to reduce the likelihood of ovulation/implantation
 Less dramatic but similar effects to pregnancy are sometimes observed
in the gingiva of hormonal contraceptive users.
 The most common oral manifestation of elevated levels of ovarian
hormones is an increase in gingival inflammation with an
accompanying increase in gingival exudate.

68. Effect on tissue response
Gingivitis can be minimized by establishing low plaque levels at the beginning of oral contraceptive
therapy
Human gingiva has receptors for progesterone and estrogen providing evidence that
gingiva is a target tissue for both gestational hormones.
Both estrogen and progesterone increase gingival exudate, associated with
inflammatory edema

69. OSTEOPOROSIS

70. OSTEOPOROSIS
Osteoporosis means
literally _porous bone, a
condition where there is
too little bone to
provide mechanical
support.
Osteopenia- reduction
in bone mineral density
below than what is
required for mechanical
support.

71. Relationship between Periodontal disease and Osteoporosis
 Many studies have shown positive association between
osteoporosis and alveolar crest resorption.
 Fractures are very common in these patients
 Calcium and Vitamin D supplements have shown positive impact
on osteoporosis and periodontal disease.

72.  Osteoporosis is frequently seen in women during
menopause due to decreased production of
estrogen. It causes suppression of calcium
absorption, increase in calcium excretion and
osteocyte apoptosis.
 Periodontitis in such patients release TNF-α that
induce collagenase activity, resulting in more bone
loss

73.  Hormone relacement therapy (HRT) is estrogen therapy that decrease osteoclast
formation and increase lifespan of osteoblasts and osteocytes. Dentist should refer
to medical practitioner for this.
 Nasal and subcutaneous calcitonin are available for postmenopausal osteoporosis.
Calcitonin is inhibitor of osteoclastic activity.
 HRT, Parathyroid harmone (PTH), Teriparatide improve osteoporosis and
periodontal regeneration
TREATMENT