Periodontal therapy in the female patient

1. Periodontal Therapy in the
Female Patient
DR. NEELAM MISHRA
1

2. Contents
• Introduction
• Hormones and types of Hormones
• Female hormonal system
• Puberty
• Menses
• Pregnancy
• Oral contraceptives
• Menopause
• Conclusion
2

3. Introduction 3

4. • Throughout a woman's life cycle, the
hormonal influences that take place can
affect the therapeutic decision making in
Periodontics.
• However at times there are various
contributing factors that exaggerate the
existing periodontal disease.
• One such is observed in female patients
where, as a result of hormonal influences
seen during their life cycle.
4

5. The already existing
periodontal disease worsens
resulting in loss of
periodontium.
Puberty
Menses
Pregnancy
Oral contraceptives
Menopause
5

6. Hormones 6

7. • Hormones are specific regulatory
molecules that modulate
reproduction, growth and
development, maintenance of the
internal environment, as well as
energy production, utilization, and
storage.
• Hormonal effects reflect
physiological/ pathological changes in
almost all types of tissues of the
body.
7

8. Female hormonal system 8

9. • Consists of three hierarchies of hormones;
1. Hypothalamic releasing hormone
• Gonadotropin releasing hormone (GnRH).
2.The anterior pituitary sex hormones
• Follicle stimulating hormone (FSH) and
luteinizing hormone(LH).
3. The ovarian hormones
• Estrogen and Progesterone.
9

10. 10

11. Puberty 11

12. • 11 to 14 years in most women.
• Prevalence of gingivitis increases, without an increase in the amount of plaque.
• Gram negative anaerobes, implicated in association with puberty gingivitis.
• Kornman and Loesche (1979) postulated that these anaerobic organisms may use
ovarian hormones as a substitute for vitamin K growth factor.1
• Prevotella intermedia and Capnocytophaga species have been implicated in the
increased bleeding tendency observed during puberty.2
12
1. Kornman K, Loseche JF: Direct interaction of estradiol and progesterone with Bacteroides melaninogenicus, J Dent Res 58A:10, 1979.
2. Gusberti FA, Mombelli A, Lang NP, et al: Changes in subgingival microbiota during
puberty, J Clin Periodontol 17:685, 1990.

13. Clinical Features
• Exaggerated response to local factors.
• Hyperplasic reaction of the gingiva may
occur.
• Inflamed tissues become
erythematous, lobulated, and
retractable.
• Easily Bleeds.
• Inflammatory hyperplasia seen.
13

14. • Chronic regurgitation of gastric
contents on intraoral tissues which is
a common complaint in the puberty
phase.
• Bulimia and anorexia nervosa.3
• Perimylosis typically on the palatal
surfaces of maxillary anterior teeth
varies with duration and frequency
of eating disorder.
14
3. Brown S, Bonifaz DZ: An overview of anorexia and bulimia nervosa and the impact of
eating disorders on the oral cavity, Compend Contin Educ Dent 14:1594, 1993.

15. Management
• Education of patient and caregiver.
• Preventive care, such as teeth brushing and flossing.
• Mild Gingivitis- Respond well to scaling and root planning.4
• Severe cases of gingivitis-
a. Scaling and root planning
b. Microbial culturing
c. Antimicrobial mouthwashes
d. Antibiotic therapy
15
4. American Dental Association (ADA), Council on Access, Prevention, and Interpersonal Relations: Women's oral health issues, Chicago,
1995, ADA.

16. • Also, enlargement of the parotid glands
(occasionally sublingual glands) has been estimated
to occur in 10% to 50% of patients who “binge and
purge.”5
• Therefore a diminished salivary flow rate may also
be present, which will increase oral mucous
membrane sensitivity, gingival erythema, and caries
susceptibility.
165. Mandel L, Kaynar A: Bulimia and parotid swelling: a review and case report, J Oral Maxillofac Surg 50:1122, 1992.

17. MENSES
17

18. • During the reproductive years, the ovarian cycle is controlled by the
anterior pituitary gland which secretes follicle stimulating hormone
(FSH) and Luteinizing hormone (LH) are produced from anterior
pituitary gland.
• Under the influence of FSH and LH, estrogen and progesterone are
steroid hormones produced by the ovaries during the menstrual cycle.
• Average ovarian cycle lasts for 28 days, which is interrupted only by
pregnancy.
• During the reproductive cycle, the purpose of estrogen and
progesterone is to prepare the uterus for implantation of the egg.
18

19. 19
Pre menstrual
syndrome
Menstrual
cycle

20. Pre menstrual syndrome ( PMS)
• During the peak level of progesterone (about 7 – 10 days prior to menstruation) PMS also
occur.
• No significant differences in estrogen and progesterone levels between women who suffer
PMS and women who do not.
• Depression, irritability, mood swings, and difficulty with memory and concentration due to
reduced neuro transmitters.
• PMS women have lower of certain neuro transmitters such as:
• Enkaphalins
• Endorphins
• Amino butyric acid (GABA)
• Serotonin
20

21. • The monthly reproductive cycle has two phases:
• Levels of FSH are elevated, the major form of estrogen, is
synthesized by the developing follicle and peaks
approximately 2 days before ovulation.
• The effect of estrogen stimulates the egg to move down
the fallopian tubules (ovulation).
Follicular
phase.
•Synthesizes both estrogen and progesterone.
•Estrogen and progesterone peaks to complete the rebuilding of the
endometrium for implantation of the fertilized egg.
•The corpus luteum involutes, ovarian hormone levels drops, and
menstruation ensues.
Luteal
phase.
21
14 days
14 days

22. Menstrual cycle
• Recurs at the interval of 28 days.
• 4 phases :
• Menstruation – bleeding phase ; 1 – 4
days
• Proliferative phase – follicular phase ;
5 – 13 days
• Phase of ovulation – 14th day
• Secretive phase – luteal phase ; 14 –
28 days
22
1-4 days
5-13 days
14th day
14-28 days

23. 23
Follicle growth and
development

24. Clinical Features-
• Progesterone plays a role in stimulating the production of prostaglandins that
mediate the body’s response to inflammation.
• PGE2 is one of the major secretory products of monocytes and is increased in
inflamed gingiva.
• Gingival tissues have been reported to be more edematous during menses and
erythematous before the onset of menses in some women.6
• In addition, an increase of gingival exudate has been observed during the
menstrual period and is sometimes associated with a minor increase in tooth
mobility.7
24
6. Grant D, Stern J, Listgarten M: The epidemiology, etiology, and public health aspects of periodontal disease. In Grant D, Stern
J, Listegarten M, editors: Periodontics, St Louis,1988, Mosby.
7. Machtei EE, Mahler D, Sanduri H, Peled M: The effect of the menstrual cycle on
periodontal health, J Periodontol 75:408, 2004.

25. • Possible mechanisms have been suggested for the increase in
hormonal gingival interaction in the menstrual cycle.
• Tumor necrosis factor alpha (TNF-α), which fluctuates during the
menstrual cycle; elevated prostaglandin E2 (PGE2) synthesis; and
angiogenetic factors, endothelial growth factors, and receptors may
be modulated by progesterone and estrogen, contributing to
increases in gingival inflammation during certain stages of the
menstrual cycle.
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26. The main potential effects of these hormones on the periodontal tissues
can be summarized as:
• Gingival bleeding and increased
production of gingival exudate
(Kribbs & Chesnut1984, Kribbs et al. 1989, Kribbs
1990,1992, Grodstein et al. 1996a, b).
• Ulcerations of the oral mucosa and
vesicular lesions have also been noted
in the luteal phase of the menstrual
cycle, although the incidence is low.
(Segal et al. 1974, Ferguson et al. 1978, 1984).
• Gingival tissues are more edematous
during menses and erythematous
before the onset in some women.
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27. Management
• Women who have increased gingival bleeding associated with the menstrual
cycle, SPT for continuous 3 – 4 months is must.
• Antimicrobial mouth rinses prior to cyclic inflammation is indicated.
• The dentist should treat the gingival and oral mucosal tissues gently. Gauze pads
or cotton rolls should be moistened with a lubricant, chlorhexidine rinse, or water
before placing them in the aphtha-prone patient.
• The clinician should be aware that NSAIDs, infection and acidic food exacerbate
Gastroesophageal Reflux Disease (GERD).
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28. PREGNANCY
• The link between pregnancy and periodontal inflammation has been known for
many years.
• In 1778, Vermeeren discussed tooth pains in pregnancy.
• In 1818, Pitcairn described gingival hyperplasia in pregnancy.
• In 1877, Pinard recorded the first case of pregnancy gingivitis.
• During pregnancy, the increased levels of sex steroid hormones are maintained
from the luteal phase implantation of the embryo, until parturition.
• Pregnant women, near or at term produce large quantities of estradiol (20
mg/day), estriol (80mg/day) and progesterone (300 mg/day).
28

29. 29

30. Clinical Features-
• Gingival inflammation initiated by plaque, and
exacerbated by these hormonal changes in the second
and third trimester of pregnancy pregnancy
gingivitis.
• Increased tendency for gingivitis and larger gingival
probing depths.
• Increased susceptibility to infection.
• Decreased neutrophil chemotaxis and depressed
antibody production.
• Increased numbers of periodontopathogens.
• Increased synthesis of PGE2.
30

31. 1) Tumor like enlargement/Pyogenic granuloma-
• Incidence : 0.2 – 9.6 %
• Pregnancy tumor or pregnancy epulis is
different from pyogenic granuloma which occur
in non pregnant females.
• 2nd or 3rd trimester.
• Clinical features : Tumor like growth,
• appear on inter dental papilla of maxillary
anterior teeth
• Grow rapidly, bleed easily, and become
hyperplastic, and nodular
• Sessile or pedunculated or may beulcerated
• Color – purplish red to deep blue.
31

32. 2) Marginal gingival enlargement/ pregnancy gingivitis-
• Extremely common
• Incidence: 30 – 75 %
• Clinical features: Erythema ,edema, hyperplasia,
increased bleeding.
• Mild inflammation, pain ,bleeding, Mainly
anterior region and inter proximal surfaces.
• Alteration in immunocompetency during
pregnancy may create an exaggerated response
on Periodontium.
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33. Other oral manifestations-
• Xerostomia – 44% reported dryness ( El- Ashiry 1970.).
•Management-
• Plaque control : oral hygiene techniques must be taught, reinforced, and
monitored throughout the pregnancy.
• Scaling and root planing must be performed when evernnecessary.
• Avoid the use of high alcohol content antimicrobial rinses in pregnant and prefer
to use non – alcohol based oral rinse.
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34. • Treatment for Acid Exposure-
• Do NOT brush immediately after vomiting
• Rinse
• Water with baking soda
• Antacid
• Plain water
• Eat some cheese
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35. Periodontal Disease and Preterm, Low Birth Weight
Infants-
• “Adverse pregnancy outcome” is a broad term which encompasses several disparate
outcomes like:
• low birth weight (LBW <2500 g)/VERY LBW (<1500 g)
• preterm birth (<37 weeks or very preterm <32 weeks)
• pre-eclampsia
• miscarriage
• still birth.
35

36. 36

37. 37

38. Elective dental treatment-
• Prolonged chair time should be avoided
because the woman is most uncomfortable
at this time.
• Supine hypotensive syndrome may occur.
• In a semi reclined or supine position , the
great vessels particularly inferior vena cava
are compressed by the gravid uterus. and
this compression will cause maternal
hypotension, decreased cardiac output, and
eventual loss of consciousness.
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39. How should the pregnant woman be positioned?
• Flat position may
cause hypotension and
Hypoxia.
• Place a small pillow
under right hip - left
lateral displacement.
• Head above feet.
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40. Breastfeeding
40

41. ORAL CONTRACEPTIVE USAGE
• Contraceptives utilize synthetic gestational hormones (estrogen and
progesterone), to reduce the likelihood of ovulation/implantation.
(Guyton 1987)
• Women using oral contraceptives show elevated plasma levels of several clotting
factors, related to the dose of estrogen.
• Less dramatic but similar effects to pregnancy are sometimes observed in the
gingiva of hormonal contraceptive users.
• It has been reported that more exudate is present in inflamed gingival tissues of
OC users than in pregnant women.
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42. Special Features-
• Exaggerated response to local irritants.
• Inflammation may be chronic (Lindhe&
Bjorn 1967).
• Exaggerated responses due to - increased
vascular permeability, altered
microvasculature, synthesis of
prostaglandin.
• Hyperplasic gingival tissue.
42

43. Management
1. Medical history.
2. Patient should be informed about the oral and periodontal side effects of OCs.
3. Good meticulous home care and compliance with regular periodontal
maintenance.
4. Scaling and root planning at regular 6 monthly intervals.
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44. Menopause
• Througout women’s lifetime, the number of oocytes steadily diminishes.
• Menopause is associated with symptoms of estrogen deficiency.
• Levels of FSH and LH begin to rise, and levels of sex hormones begins to fluctuate.
• This stage of ‘perimenopause’ is characterised by increasing ovarian
unresponsiveness, and thus sporadic ovulation.
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45. • No ovulation.
• No menstrual cycle.
• No estrogen and progestron formed by the ovary.
Menopause
• Sex organ
• Endocrine.
• Bone-Osteoporosis
• Metabolic
• CVS
• Lipid profile
• Hypertension, etc
Changes due to menopause occur in:
45

46. • Reduction in epithelial keratinization so thinning of oral
mucosa.
• Reduction in salivary gland flow.
• Drying of oral tissue (burning mouth)
• Redness and abnormal palness of gingival tissues.
• Bleeding on probing and brushing.
• Gingival recession.
• Altered taste sensation.
• Alveolar bone loss.
• Alveolar ridge resorption.
Clinical findings in periodontal tissues-
• Poor wound Healing.
• Reduced bone mineral content in jaws.
• Increased periodontitis and tooth loss.
Effects of osteoporosis in periodontal tissues-
• Estrogen deficiency-
• Inc. osteoclastic activity.
• Dec. bone matrix.
• Decreases deposition od bone calcium and
phosphate.
Bone metabolism-
46

47. Management
• Drugs are first line of treatment.
• Sodium alendronate- 10mg a day or 70 mg once a week.
• Risedronate 5 mg a day or 35 mg once in a week.
• Estrogen replacement therapy remains a good
treatment for prevention.
• Calcitonin works by directly inhibiting osteoclastic
activity via calcitonin receptor .
47