Periodontal Therapy for Managing Hormonal Changes in Women

Periodontal therapy in female
patients

1 Dr. Nitika Jain 8/31/2012

Contents


Contents
 Hormone and types of hormones
 Female hormonal system
 Conditions – clinical features and
management.
 Puberty
 Menstrual cycle
 Pregnancy
 Local anesthetic and analgesic
administration during pregnancy
 Antibiotic administration during

 Periodontal disease and Preterm low
birth weight births
 Association of periodontal disease and
pre eclampsia
 Oral contraceptives
 Menopause
 Osteoporosis

 Hormone replacement therapy
 Conclusion
 References


 Hormones are specific regulatory molecules that
modulate reproduction, growth and development,
maintenance of the internal environment, as well
as energy production, utilization, and storage
(Mariotti 1994). Hormonal effects reflect
physiological/ pathological changes
Steroids
in almost all types of tissues of the body
Glycoprotein

Polypeptides

Amines
5 Dr. nitika jain 31 August 2012

FEMALE
HORMONAL SYSTEM


The female hormonal system, consists of
three hierarchies of hormones, as follows:

 1. A hypothalamic releasing hormone, Gonadotropin-
releasing hormone (GnRH)
 2. The anterior pituitary sex hormones, follicle-
stimulating hormone (FSH) and luteinizing hormone
(LH), both of which are secreted in response to the
release of GnRH from the hypothalamus
 3. The ovarian hormones, estrogen and
progesterone, which are secreted by the ovaries in
response to the two female sex hormones from the
anterior pituitary gland.

Ovarian hormones

Estrogen

Progesterone


Age

Puberty

Menstrual cycle

Pregnancy

Menopause


Puberty


Pubertal changes
 It is the transitional phase when a sexually
immature girl or boy becomes sexually
mature.
 It lasts for 36 months.

 Ovarian cycle – ovulation
 Accessory sex organs grow
 Bone and muscle growth takes place
 Hormones FSH, LH sex steroid secretion - all
increase

Effects on Periodontium
 Enhanced blood circulation in the end
terminal capillary loops and associated
increased prevalence of
gingivitis/bleeding tendency
(Muhlemann 1948, Massler et al. 1950,
Curilovic et al. 1958, Sutcliffe 1972,
Daniell 1983)
 Higher bacterial counts (especially
Prevotella intermedia (Pi) and
12
Capnocytophaga species)(Kornman &
Dr. Nitika Jain 8/31/2012
Loesche 1982, Mombelli et al. 1990,

Management
 Preventive care
 Milder gingivitis case  scaling
and root planing with frequent oral
hygiene instructions.
 Severe gingivitis case  microbial
culturing, antimicrobial mouth
washes and local site delivery, or
antibiotic therapy.
14  Supportive periodontal therapy

Menstrual cycle


Pre menstrual
syndrome

Menstrual
cycle


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


Management of PMS
 PMS is often treated by antidepressants. Selective
serotonin reuptake inhibitors are generally the first
line choice of drugs.
 Increase the extracellular level of the
neurotransmitter serotonin by inhibiting its reuptake
into the presynaptic cell, increasing the level of
serotonin in the synaptic cleft available to bind to
the postsynaptic receptor. E.g. Fluoxetine,
Sertraline, Fluvoxamine, paroxetine, and
citalopram.
 Other antidepressants are selective serotonin,
norepinephrine reuptake inhibitors( SNRI’s)
{increase the levels of two neurotransmitters in the brain
that are known to play an important part in mood,
serotonin, and norepinephrine.}, tricyclics, trazodone,
18
mirtazapine, nefazodone, maprotilline.

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


 Two different clinical findings have been observed
in the oral cavity:
 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).


 Tumor necrosis factor α fluctuates during the
menstrual cycle, PGE2 elevated, 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.


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.
 Careful retraction of the oral mucosa, cheeks, and lips
is necessary in patients prone to aphthous or herpetic
lesions.
 Because the hypoglycemic threshold is elevated, the
clinician should advise the patient to have a light
24 Dr. Nitika Jain before her appointment.
snack 8/31/2012

Pregnancy


 One Tooth Is Lost With Every pregnancy

Myth……..
But Women Do Experience
Some Changes in General and
Oral Health During Pregnancy,
Primarily Due to
Hormonal Level Changes
 So They Characterize a Special
Group for Whom Extra care and
Special Care Need to Be Provided


Pregnancy


Stages of Pregnancy

1st Trimester (1-12 weeks)
Fetal organ formation and
differentiation.
Most susceptible to adverse
effects of teratogens.
Avoid all elective care but
provide care as needed.

8/31/2012 Dr. Nitika Jain 28

Stages of Pregnancy

2nd Trimester (13-24 weeks)
Fetal growth and maturation.
Safest period to provide dental
care.


Stages of Pregnancy

3rd Trimester (25-40 weeks)
Fetal growth continues.


 Increased tendency for gingivitis and larger gingival
probing depths (Loe & Silness 1963,Silness & Loe
1964, Miyazaki et al. 1991, Robinson & Amar 1992,
Machuca et al. 1999, Soory 2000) and periodontitis
(Robinson & Amar 1992)
 Increased susceptibility to infection (Cohen et al.
1969, Brabin 1985)
 Decreased neutrophil chemotaxis and depressed
antibody production (Sooriyamoorthy & Gower 1989b,
Raber-Durlacher et al. 1991, Raber-Durlacher et al.
1993)
 Increased numbers of periodontopathogens
(especially Porphyromonas gingivalis and Pi)
(Kornman & Loesche 1980, Tsai & Chen 1995)
 Increased synthesis of PGE2 (ElAttar 1976)

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 be
ulcerated
32 Dr. nitika jain Color – purplish red to deep blue.
31 August 2012

Marginal gingival enlargement/
pregnancy gingivitis
Extremely common
Incidence: 30 – 75 %
 Clinical features: Erythema ,
edema, hyperplasia, increased
bleeding.
Mild inflammation, pain ,
bleeding
Alteration in
immunocompetency during
pregnancy may create an
exaggerated response on
Periodontium.
Mainly anterior region and inter
proximal surfaces
Dr. nitika jain 31 August 2012
34 Anterior site inflammation may
be exacerbated by increased

Other oral manifestations of
pregnancy
 Perimylolysis or acid production of teeth may
occur due to excessive morning sickness or
esophageal reflux
 Xerostomia – 44% reported dryness ( El- Ashiry
G. comparative study of the pregnancy and oral
contraceptives on the gingiva. Oral Surg 1970.)


Clinical management
 Plaque control  oral hygiene techniques must be taught,
reinforced, and monitored throughout the pregnancy.
 Scaling and root planing must be performed when ever
necessary.
 Avoid the use of high alcohol content antimicrobial rinses
in pregnant and prefer to use non – alcohol based oral
rinse.

 Prenatal fluoride  a controversial and inconclusive.
 Studies by Glenn FB(1977, 1982) claimed the benefits
whereas studies by reported by (Reference manual. Pediarr
dent 1994) showed no clinical efficacy of prenatal fluoride.
 ADA does not recommend the use of prenatal fluoride.
“prenatal F administration may reduce the incidence of
caries in the offspring”
Cox & Okerse.

Treatment for Acid Exposure
 Do NOT brush immediately after vomiting
 Rinse
 Water with baking soda
 Antacid
 Plain water

 Eat some cheese


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,
39
decreased cardiac output, and eventual
loss of consciousness.

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


SUPINE HYPOTENSION
SYNDROME (Vena Cava Compression)

 SUPINE POSITION AFTER 5TH MONTH
 UTERUS COMPRESSES THE INFERIOR
VENA CAVA
 ↑VOL. BLOOD
 ↓RETURN TO THE HEART
 REDUCED PERFUSION OF UTERUS
 FETAL HYPOXIA


Supine Hypotension Syndrome

 Obstruction of inferior vena cava and aorta from
pressure of the large fetus.
Symptoms:
Sweating
Nausea
Weakness
Sense of lack of air


Supine Hypotension Syndrome

Other symptoms:
 Drop in blood pressure
 Bradycardia
 Possible loss of consciousness


Prevention of Supine Hypotensive
Syndrome

Elevate right hip 10-12 cm.
Weight is taken off the major
vessels


Treatment of Supine Hypotensive
Syndrome

Roll patient onto her
left side.


Use of Radiation on Pregnant Patient
 Dose given and time of gestation are important
 doses < 5-10 rads (Gy) not teratogenic
 fetus is most susceptible to radiation between the 2nd
and 6th week of gestation
 single dental x-ray exposes patient to 0.01 millirads of
radiation. In relative terms, this amount is 40 times less
than daily dose acquired from cosmic radiation.
Therefore, diagnostic radiation should not be withheld
during pregnancy


Radiographs during Pregnancy

 Take as needed with optimal methods for reducing
secondary radiation and exposure time.
 Always use a lead apron.
 Exposure to fetus (with apron use) is .00001
centiGray.(rad)
 Daily cosmic radiation - .0004 centiGray (rad)


Risks of Dental X-Rays
 X-ray only if necessary (i.e. root canal therapy,
trauma)
 When x-rays are indicated, radiation exposure is
extremely low
 Exposure can be limited by:
 Lead apron shielding
 Modern fast film
 Avoiding retakes


Drugs in pregnancy


FDA drug classification for pregnancy

 Combines risk statements including congenital
anomalies, fetal effects, perinatal risks, and
therapeutic risk-benefit ratio
 Untreated disease or condition may pose more
serious risks to both mother and fetus than any
theoretical risks from the medication
 Category A thru D and X


Local anesthetic and analgesic
administration during pregnancy


Antibiotic administration during
pregnancy


Periodontal
disease and Preterm
low birth weight
births
56

WHO defination
 Preterm birth as any live birth at less than 37
weeks of gestation.
 Delivery at less than 32 weeks is termed as very
preterm
 Delivery at less than 28 weeks is termed as
extremely preterm
 Birth weight to be considered low if < 2500g, very
low if < 1500g and extremely low if <1000g.


Health consequences of preterm
birth
 Short term  Long term
consequences consequences
 Respiratory distress  Cerebral palsy
syndrome  Retinopathy of
 Intraventricular prematurity
hemorrhage  Mental retardation
 Sepsis  Cardiovascular
 Patent ductus malformations
arteriosus


 Risk factor  An exposure that
increases the probability that disease will
occur

 Risk indicator  A suspected risk factor
that is correctly identified through cross-
sectional study designs but there are not
yet longitudinal study data

Primary and secondary predictors of
pre term delivery
 Primary predictors:
 Black race
 Young mother
 Domestic violence
 Low socio economic status
 Stress or depression
 Cigarette smoking
 Cocaine or heroin use
 Low body mass index
 Low maternal weight gain before pregnancy
 Previous induced abortion
 Chronic lung disease
 Chronic hypertension
 Diabetes
 Renal diseases


 Secondary predictors
 No or adequate prenatal care
 In vitro fertilization
 Iron deficiency anaemia
 Pre eclampsia
 Early contractions
 Placental abruptions
 Multiple fetuses


 Offenbacher et al were the first to report a link
between poor maternal periodontal health and
adverse pregnancy outcomes.
 The biological mechanism linking periodontal
infection and preterm birth can begin with
endotoxins resulting from gram-negative bacterial
infections, which stimulate the production of
cytokines and prostaglandins. It is known that
prostaglandins and certain cytokines (interleukin-
1b, interleukin-6 and tumor neucrosis factor-alfa),
in sufficient quantities, may stimulate labour
(Jeffcoat et al., 2001).

 According to Collins et al 1994, periodontitis serve as
a reservoir of gram negative organisms, LPS,
endotoxins and inflammation mediators TNF α which
are potential threat to fetal placental unit.
 Local increase of PGE2 and TNF α in chamber fluid
with P.Gingivalis and 15 – 18 % of fetal weight.
levels of PGE 2 and TNF α is inversely proportional to
fetal birth weight.
 Previous sensitization or exposure to these
pathogens prior to pregnancy enhanced the severity
of the fetal growth restriction when a secondary
exposure occurred.

 GCF levels of fluid levels of PGE2 were positively
associated with intra amniotic PGE2 levels,
suggesting that gram negative periodontal
infection may present systemic challenge
sufficient to initiate the onset of premature labor
as a source of LPS or through stimulation of
secondary inflammatory mediators such as PGE2
and interleukin 1.
 Four organism associated with PLBW:
 Bacteroides forsythus
 Porphymonas gingivalis
 Actinobacillus actinmycetemcomitans
 Treponema denticola

Various studies
 Jeffcoat et al. (2001) studied 1,313 pregnant
women and the relationship between periodontal
disease and preterm birth, adjusting for a range
of risk factors including smoking, parity, race and
maternal age. The study found that pre-existing
periodontal disease in the second trimester of
pregnancy increased the risk of preterm birth.
 Mitchell-Lewis et al (2001) cohort study
examined 21women for periodontal status. The
findings suggest that women who received basic
periodontal therapy during pregnancy were at a
substantially reduced risk of preterm, low
birthweight babies

 (Lopez et al., 2002) investigated whether the
women who had gingivitis and received treatment
before birth (n=406) reduced the risk of preterm
lowweight children comparing to women who had
periodontal (n=233) disease and were treated
after delivery. The study concluded that
periodontal disease is an independent risk factor
for preterm birth and low birth weight.


Association of periodontal disease
and pre eclampsia
 Pre – eclampsia is a common hypertensive
disorder of pregnancy that independently
contributes to maternal and infant morbidity and
mortality.
 multi system disorder.
 5-10% of all pregnancies.
 Atherosclerotic changes in placental tissues
involving oxidative and inflammatory events
initiate the development of pre – eclampsia(
Ramos et al 1995)


 1st stage: Signs and symptoms:
 peripheral edema,
 pulmonary oedema
 blood pressure 140/90mmHg.
 proteinuria 300mg/day urine sample.
 2nd stage - HELLP -
 hemolysis,
 elevated liver enzymes,
 low platelet count.


Triad of physiological derangement in
pre eclampsia:

Intense vasospasm
All these
factors leads to
intrauterine
fetal growth Disseminated
intravascular
retardation
coagulation
and fetal death
in uterus only.
Plasma volume
contraction


Oral
Contraceptives


 Combined oral contraceptive pills were developed
to prevent ovulation by suppressing the release of
gonadotropins. Combined hormonal
contraceptives, including COCPs, inhibit follicular
development and prevent ovulation as their
primary mechanism of action


Different formulations of hormonal
contraceptives
 Combined oral contraceptive containing artificial
analogues of estrogen and progesterone
 Low doses of estrogen and progesterone
(50µg/day) and /or progestins (1.5mg/day)
 Progesterone based mini pill.
 Slow release progesterone implants placed sub
dermally (NORPLANT)
 DEPO PROVERA , a very effective progestin
injection


Oral manifestations:
 Inflammation ranges from mild edema and
erythema to severe inflammation with
hyperplastic gingival tissues.
 Increased exudate in inflammed gingival tissues
of OC users.
 Kalkwarf reported the response may be due to
alterations of the microvasculature, increased
gingival permeability, and increasing synthesis of
Prostaglandin.
 PGE2 increases with increasing sex hormones
 16 fold increase in bacteroides species ( because
74 increased sex hormones substituting for the 8/31/2012
Dr. Nitika Jain

Oral contraceptives
 Treatment for gingival inflammation exaggerated
by oral contraceptives should include establishing
an oral hygiene program and eliminating local
predisposing factors.
 Periodontal surgery may be indicated if there is
inadequate resolution after initial therapy.
 Antimicrobial mouthwashes may be indicated as
part of the home care regimen.
 Extraction of teeth to be performed on non –
estrogenic days( days 23 to 28) of the pill cycle,
to reduce the risk of postoperative localized
75
osteitis.

MENOPAUSE


Menopause
 As women approach menopause, the levels of
estrogen begin to drop mainly during the late
follicular and lacteal phase of the menstrual cycle
(Sherman & Korenman 1975).
 The time frame between regular cycles and the
cessation of menstrual periods, called
perimenopausal transition, is 2–7 years (Treloar
et al. 1970). During this period, the concentration
of circulating estrogen decreases while follicle-
stimulating hormone (FSH) and luteinizing
hormone (LH) concentrations increase (Monroe &
Menon 1977).

Menopause
 No ovulation
 No menstrual cycle
 No estrogen and progesterone is formed by the ovary

 Changes due to menopause occur in
 Sex organs – no ovulation
 Bone- osteoporosis
 Endocrinal – FSH and LH levels become high
 Metabolic – lipid profile alters and more susceptible to
atherosclerosis
 Cardiovascular – hot flushes can appear and
hypertension is common
 Psychological states - depression

Clinical changes in the periodontal
tissues during menopause and post
menopause
 Reduction in epithelial keratinisation so thinning
of the oral mucosa.
 A reduction in salivary gland flow
 Drying of the oral tissues ( burning mouth)
 Redness and abnormal paleness of the gingival
tissues
 Bleeding on probing and brushing
 Gingival recession
 Altered taste sensation
 Alveolar bone loss
 Alveolar ridge resorption

Menopause
 As gingival and mucosal tissue thinning occurs,
so brushing with extra soft tooth brush.
 Dentifrices with minimal abrasive particles should
be used.
 Rinses should have low alcohol concentration.


Osteoporosis
 Osteoporosis is a disease of bones that leads to
an increased risk of fracture.In osteoporosis the
bone mineral density (BMD) is reduced, bone
microarchitecture deteriorates, and the amount
and variety of proteins in bone is altered.
 Osteoporosis is defined by the World Health
Organization (WHO) as a bone mineral density
that is 2.5 standard deviations or more below the
mean peak bone mass (average of young,
healthy adults) as measured; the term
"established osteoporosis" includes the presence
of a fragility fracture

 The disease may be classified as
 primary type 1,
 primary type 2, or secondary.
 The form of osteoporosis most common in
women after menopause is referred to as primary
type 1 or postmenopausal osteoporosis.
Primary type 2 osteoporosis or senile
osteoporosis occurs after age 75 and is seen in
both females and males at a ratio of 2:1


Effect of osteoporosis upon
Periodontium
 Poor wound healing: less attachment formation
(von Wowern et al. 1994)
 Reduced bone mineral content in the jaws (von
Wowern et al. 1994, Payne et al. 1999)
 Increase of periodontosis and tooth loss
(Mittermayer et al. 1998)


Bone metabolism
 The estrogen deficiency leads to
 (1) increased osteoclastic activity in the bones,
 (2) decreased bone matrix, and
 (3)decreased deposition of bone calcium and
phosphate


Normal bone Osteoporotic bone


Prevention of osteoporosis
 􀂄 Education
 􀂄 Calcium and milk
 􀂄 Avoid smoking
 􀂄 Exercise
 􀂄 Appropriate drug treatment


Treatment
 Bisphosphonate drugs are the first-line treatment in
women
 sodium alendronate (Fosamax) 10 mg a day or 70 mg
once a week,
 risedronate (Actonel) 5 mg a day or 35 mg once a week
and/or
 ibandronate (Boniva) once a month.
 Estrogen replacement therapy remains a good
treatment for prevention of osteoporosis.
 Calcitonin works by directly inhibiting osteoclast
activity via the calcitonin receptor. Calcitonin
receptors have been identified on the surface of
osteoclasts. Calcitonin directly induces inhibition of
Dr. Nitika Jain
87 8/31/2012
osteoclastic bone resorption by affecting actin

National institutes of health consensus
conference recommendations for optimal
calcium intake

 Pre menopausal women(25 – 50 yrs)
1000mg/day
 Post menopausal women(estrogen therapy)
1000mg/day
 Post menopausal women(no estrogen therapy)
1500mg/day
 Men
1000mg/day
 Women and men > 65 years old
88 1500mg/day

Hormone replacement therapy
 It is based on the idea that the treatment may
prevent discomfort caused by diminished
circulating oestrogen and progesterone
hormones, or in the case of the surgically or
prematurely menopausal, that it may prolong life
and may reduce incidence of dementia. It
involves the use of one or more of a group of
medications designed to artificially boost
hormone levels. The main types of hormones
involved are oestrogens, progesterone or
progestins, and sometimes testosterone.


 CONVENTIONAL HORMONE REPLACEMENT
DRUGS
 The most frequently prescribed estrogen product for
HRT is conjugated equine estrogens (brand name
Premarin). The most frequently prescribed progestin for
HRT is medroxyprogesterone acetate (MPA).
 BIO-IDENTICAL HORMONES COMPOUNDED
 There are many alternatives to conventional drug
products, including natural or bio-identical hormones,
which are identical in chemical structure to the
hormones naturally produced by our bodies. This type of
HRT is referred to as natural hormone replacement
therapy, or NHRT.
 NHRT is available both in brand-name products and
from compounding pharmacies, which can supply any of
the bio-identical hormones alone or combine them into
one dose in the form desired (e.g, sublingual tablets, oil
Dr. Nitika Jain
90 caps, or cream). 8/31/2012

 Dosages prescribed for ERT, HRT and NHRT
vary and can be adjusted to meet a woman’s
specific needs.
 Relatively low doses of estrogen and
estrogen/progestin is effective for treating
symptoms of menopause and can also maintain
bone density.
 Low doses of estrogen, doses of conjugated
equine estrogen (Premarin) as low as .3 mg
(compared to the "standard" dose of .625 mg)
alone or combined with a reduced dose of
progestin; doses of oral estradiol as low as .25
mg; and a transdermal patch dose of .025
91 micrograms. Using lower doses of estrogens8/31/2012
Dr. Nitika Jain
and

Conclusion
 Female patients may present with periodontal
and systemic considerations that alter
conventional therapy.
 Patients should be educated regarding the
profound effects of the sex hormone on
periodontal and oral tissues as well as the
consistent need for home and office removal of
local irritants.
 Thorough medical history in the female patient
should include questions regarding menstrual
regularity, oral contraceptive use , hormone
replacement therapy, fertility medications,
Dr. Nitika Jain
92 8/31/2012
pregnancy, breast feeding.

REFERENCES


 Clinical periodontology, Carranza 10th edition.
 Periodontal medicine. Rose, Genco, Mealey ,
Cohen.
 Mascarenhas P, Gapski R, Al-Shammari K, Wang
H-L: Influence of sex hormones on the
Periodontium. J Clin Periodontol 2003; 30: 671–
681. rBlackwell Munksgaard, 2003.
 GN güncü, TF tözüm, F ça˘glayan: effects of
endogenous sex hormones on the periodontium –
review of literature. Australian dental journal
2005;50:(3):138-145.

 Concise medical physiology 5th edition, chaudhari
 Despopoulos, color atlas of physiology 5th
edition.
 Text book of medical physiology, 11th edition.
Guyton and hall.
 MARJORIE K et al. Post-menopausal bone loss
and its relationship to oral bone loss.
Periodontology 2000, Vol. 23, 2000, 94–102.


Periodontal Therapy for Managing Hormonal Changes in Women

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