ENDOCRINE HORMONES

AND

PERIODONTIUM
PRESENTED BY DR.TEJASHVI SETH
GUIDED BY DR. TRIVENI KALE
 INTRODUCTION

▪ Cell function is broadly controlled by two mechanism:

- Neural control
- Endocrinal control

▪ Endocrinal control is by release of physiologically active

substances directly into blood stream called as hormones

▪ Chemical messengers are the substances involved in cell

signaling,
▪ All these chemical messengers carry the message (signal)
from the signaling cells (controlling cells) to the target cells

Signaling cells message Target cells

▪ Chemical messengers are classified into four types

- Endocrine messenger
- Paracrine messenger
- Autocrine messenger
- Neurocrine messenger
▪ Endocrine messengers

- Are the classical hormones

- Synthesized by endocrine glands and transported by blood
to the target organs or tissue (site of action)
- Eg. Growth hormone and Insulin
▪ Paracrine messenger

-Eg. prostaglandins and histamine

▪ Autocrine messenger

- Chemical messengers that controls the source cells which

secretes them
- Eg. Leukotrienes
▪ Neurocrine messenger
- Neurotransmitter or neurohormones

- Neurotransmitter is an endogeneous signaling molecule that

carries information from one nerve cell to another nerve cell
or muscle or another tissue
- Eg. Acetylcholine and dopamine
- Neurohormone is a chemical substance that is released
by the nerve cell directly into the blood and transported
to the distant target cells

- Eg. Oxytocin, antidiuretic hormone and hypothalamic

releasing hormone
ENDOCRINE GLANDS
 CHEMICAL STRUCTURE AND SYNTHESIS OF HORMONES

▪ There are three general classes of hormones:

▪ Proteins and polypeptides

- including hormones secreted by the anterior and posterior
pituitary gland,
- the pancreas (insulin and glucagon),
- the parathyroid gland (parathyroid hormone)
▪ Steroids secreted by
- the adrenal cortex (cortisol and aldosterone),
- the ovaries (estrogen and progesterone),
- the testes (testosterone),
- the placenta (estrogen and progesterone).

▪ Derivatives of the amino acid tyrosine, secreted by

- the thyroid (thyroxine and triiodothyronine)
- the adrenal medullae (epinephrine and norepinephrine).
 PITUITARY GLAND
▪ The pituitary-hypothalamus forms a single functional unit
▪ gland is physiologically divided
into
- Adenohypophysis
- Neurohypophysis
- Pars intermedia
▪ Adenohypophysis
- Growth hormone
- Adrenocorticotropin
- Thyroid-stimulating hormone
- Prolactin
- Follicle-stimulating hormone
- luteinizing hormone
Source Hormone Target tissue Principal Effect on
function periodontium

Hypothalamus Thyrotropin Anterior Release of TSH Unknown

releasing pituitary gland
hormone

Prolactin- Anterior Inhibits Stimulates

inhibiting pituitary gland prolactin release periodontal
hormone ligament cell
proliferation

Growth Anterior Stimulates Unknown

hormone pituitary gland release of
releasing growth hormone
hormone
Source Hormone Target tissue Principal function Effect on
periodontium
Hypothalamus Somatostatin GIT and Inhibits digestion Unknown
(growth pancreatic and absorption of
inhibiting islets nutrients; inhibits
hormone) secretion of
pancreatic
hormones

Gonadotropin Anterior Stimulates release Unknown

releasing pituitary gland of LH and FSH
hormone
Corticotropin Anterior Stimulates release Unknown
releasing pituitary gland of
hormone adrenocorticotropin
hormone
Source Hormone Target tissue Principal function Effect on
periodontium
Anterior growth hormone Bone, soft Promotes growth, Protective
pituitary (somatotropin) tissue and liver affects lipid, and effect on
carbohydrate periodontium
metabolism

Thyroid stimulating Thyroid gland Stimulates growth Unknown

hormone of thyroid gland
and secretion of
thyroid hormones

Adrenocorticotropic Adrenal cortex Stimulates cortisol Unknown

hormone secretion

Prolactin Mammary Stimulates secretion Unknown

glands of milk
source Hormone Target tissue Principal function Effect on
periodontium
Anterior Luteinizing gonads Stimulates sex hormone Protective
pituitary hormone production effect on
periodontium

Follicle gonads Promotes growth of Unknown

stimulating reproductive organs
hormone

Posterior vasopressin Kidney tubules Resorption of water from Unknown

pituitary and arterioles collecting ducts of kidney

oxyctocin Uterus Increased uterine Unknown

contractibility
Effects Of Central Endocrine Gland Hormones On The Periodontium

▪ Britto et al. in 2011 investigated the association with isolated growth hormone
deficiency and periodontal attachment loss

- subjects with untreated congenital growth hormone deficiency had a

statistically greater prevalence of periodontitis

- Suggesting that the presence of growth hormone reduced the development of

destructive periodontal disease
 Peripheral Endocrine Glands
▪ Thyroid gland secretes three hormones
- Tetra-iodothyronine
- Tri-iodothyronine
- Calcitonin
▪ Weighs about 20 to 40g in adults.
▪ The structure & function changes in
different stages of sexual cycle in females
- Pregnancy and lactation
- menopause
SYNTHESIS OF THYROID HORMONE
 Source Hormone Target tissue Principal Effect on
function periodontium

Thyroid gland Tri- Most of the Regulation of Associated with

iodothyronine cells of the numerous tissue destructive
and body including periodontal
thyroxine cardiac and diseases
brain, involved
with growth and
metabolism
Calcitonin Bone and Lowers blood Unknown
kidney calcium
 Effects of Thyroid Gland Hormones on Periodontium

▪ Early investigators reported clinical observations of severe alveolar bone loss

in patients with myxedema, but contemporary clinical studies evaluating the
effects of thyroid hormone are lacking. (Hutton JH, 1936)

▪ Although thyroid hormones are critical factors for postnatal skeletal

development and regulation of the rate of bone remodeling , the influence of
thyroid hormones on alveolar bone and destructive periodontal diseases are
largely unknown.
▪ Scardina et al(2008) suggested the possible association of thyroid dysfunction
and periodontitis.

- Decrease in serum level of thyroid hormone can induce a low-grade

inflammation by impaired nitric oxide availability and increased serum
prostaglandins, cytokines, and matrix metalloproteinases (MMPs)

- ultimately leading to poor periodontal health status and alveolar bone resorption
 PARATHYROID GLANDS
▪ Humans have 4 parathyroid glands situated on the posterior surface of upper
and lower poles of thyroid gland

▪ Measuring 6mm long, 3mm wide and

2mm thick, dark brown in colour.

▪ Target tissue: bone, kidney and intestine

▪ Principal function in body is to increase

plasma calcium concentration
BIOSYNTHESIS OF PARATHORMONE
 Effects Of Parathyroid Gland Hormone On Periodontium
▪ Primary hyperparathyroidism (Carlson D, 2010) resulting principally from
adenomas and secondary hyperparathyroidism (Cunningham J, 2008) resulting
primarily from chronic renal failure have been implicated in alveolar bone
destruction as a consequence of elevated parathyroid hormone levels.

▪ In general, increased tooth loss and poor oral hygiene have been associated
with hyperparathyroidism (Klassen JT, Krasko BM. 2002)
▪ Patients suffering from primary hyperparathyroidism as compared to control
thyroid group (Padbury AD Jr et al. 2006)

- Decreased cortical bone density,

- increased incidence of tori,

- as well as a positive correlation between serum parathyroid hormone levels

and periodontal ligament space width
 ADRENAL GLAND HORMONES
▪ Adrenal glands also called as essential endocrine gland or suprarenal glands
▪ Adrenal glands made up of two distinct
parts:

- Adrenal cortex, outer portion constituting

80% of the gland

- Adrenal medulla, central portion

Constituting 20% of the gland
▪ Hormones secreted by adrenal cortex: corticosteroids
- Mineralocorticoids (aldosterone, deoxycorticosterone)
- Glucocorticoids (cortisol, corticosterone)
- Sex hormones (androgens, oestrogen, progesterone)

▪ Hormones secreted by adrenal medulla: catecholamines

- Adrenaline or epinephrine
- Noradrenaline or norepinephrine
- Dopamine
Source Hormone Target tissue Principal function Effect on
periodontium

Adrenal aldosterone Kidney Influences Na⁺ and K⁺ unknown

gland balance

cortisol Most tissues of Glucose, protein lipid Destructive

the body metabolism periodontal
disease
Source Hormone Target tissue Principal function Effect on
periodontium

Adrenal Weak androgens Sex accessory Minor effects on Influences

glands and oestrogens tissues reproductive functions disease
progression of
periodontal
disease

catecholamines Cells with Increases the rate and unknown

adrenergic strength of cardiac
receptors contraction, cardiac
output and peripheral
vascular resistance
Effects of Adrenal Gland Hormone on Periodontium
 PANCREAS
▪ The pancreas secretes hormones, from

- Alpha -cells (a source of glucagon synthesis)

- Beta-cells (a source of insulin synthesis),

- Delta-cells (a source of somatostatin synthesis)

- F cells (secretes pancreatic polypeptide).

▪ major role in carbohydrate and lipid metabolism as well as in the control of

energy stores.
 FUNCTIONS OF INSULIN

▪ Insulin lowers the blood levels of glucose, fatty acids and amino acids, and
promotes their storage.

▪ Affect the transport of specific blood-borne nutrients into cells or it can affect
enzymatic activity .

▪ It facilitates glucose transport into most cells, stimulates glycogenesis and inhibits
glycogenolysis,

▪ decreases hepatic glucose output by inhibiting glyconeogenesis.

▪ Hypersecretion leads to hypoglycemia

 FUNCTIONS OF GLUCAGON

▪ In contrast, glucagon opposes the actions of insulin.

▪ Glucagon causes an increase in hepatic glucose production and release and thus
an increase in blood glucose levels.

▪ It induces glycogenolysis and stimulates glyconeogenesis.

▪ Glucagon also promotes fat breakdown and inhibits triglyceride synthesis .

▪ Promotes ketogenesis

▪ Hypersecretion leads to hyperglycemia, hyposecretion leads to DM.

 FUNCTION OF SOMATOSTATIN

▪ Somatostatin is also known as a growth hormone inhibiting hormone and

somatotropin release-inhibiting factor.

▪ Somatostatin is a peptide hormone that affects the digestive system primarily by

inhibiting the digestion and absorption of nutrients through suppressing the
release of gastrointestinal hormones (e.g. gastrin, cholecystokinin, secretin and
motilin).

▪ Inhibits secretion of both insulin and glucagon

 EFFECTS OF PANCREATIC GLAND HORMONES ON THE PERIODONTIUM

▪ The metabolic disturbances and the resulting disease sequelae of diabetes

mellitus are ultimately the result of a complete or partial reduction in insulin
secretion from the b-cells of the pancreas and ⁄ or the development of
peripheral cellular resistance to insulin action.

▪ Diabetes has been associated with increased prevalence and severity of

gingivitis.
MECHANISM OF ACTION OF INTERACTION
 ALTERATIONS IN SUBGINGIVAL MICROBIOTA AND
GINGIVAL CREVICULAR FLUID:
▪ In young type 1 diabetes mellitus subjects, Mashimo et al. reported an increase in
proportions of Capnocytophaga species, while Fusobacterium and Bacteroides
species remained at low levels.

▪ Sastrowijoto et al. found a high prevalence of Capnocytophaga in type 1 diabetes

mellitus subjects, but the proportion of organisms was low in both diseased and
healthy sites.

▪ Nishimura et al. showed decreased chemotaxis of periodontal ligament fibroblasts

in response to platelet-derived growth factor when cultured in a hyperglycemic
environment, compared to normoglycemic conditions.
 COLLAGEN METABOLISM, ADVANCED
GLYCATION END PRODUCTS, AND WOUND
HEALING

▪ Decreased collagen synthesis and glycosoaminoglycans.

▪ newly formed collagen is susceptible to degradation by collagenase, a matrix

metalloproteinase which is elevated in diabetic tissues, including the
periodontium.

▪ The primary source of collagenase in the gingival crevicular fluid of diabetes

mellitus patients appears to be the neutrophil.

▪ Collagen metabolism is altered by accumulation of AGEs in the periodontium.

▪ AGE accumulation results in increased cross-linking of collagen, reducing
collagen solubility and decreasing turnover rate

▪ Increased thickness of gingival capillary endothelial cell basement membranes

and the walls of small blood vessels may be seen in diabetic individuals

▪ This thickening may impair exchange of oxygen and metabolic waste products
across the basement membrane.

▪ AGE formation also stimulates proliferation of arterial smooth muscle cells,

increasing thickness of vessel walls and decreasing the vessel lumen
 CHANGES IN HOST IMMUNO-INFLAMMATORY RESPONSE

▪ Reduction in PMNs function, including chemotaxis, adherence and

phagocytosis.

▪ Hyper-responsive monocyte/macrophage phenotype in which stimulation by

bacterial antigens such as lipopolysaccharide results in dramatically increased
pro-inflammatory cytokine production.
 PINEAL GLAND
▪ The pineal gland, also known as

the pineal body, conarium or

epiphysis cerebri, is a small

endocrine gland in the vertebrate brain.

▪ It produces melatonin,

a serotonin derived hormone,

which affects the modulation of sleep patterns in both seasonal and circadian rhythms.
 FUNCTION OF MELATONIN

▪ Antioxidant property.

▪ Protection of the mucosa against various irritants.

▪ Melatonin appears to be an important modulator of the immune system as it

enhances the natural and acquired immunity in vivo, and activates monocytes
and neutrophils.

▪ Melatonin has an anti-inflammatory effect.

▪ It also stimulates type I collagen synthesis and promotes bone formation.

 Melatonin Association With Periodontitis
▪ Moreno et al in 2013 conducted a study to assess the levels of
melatonin in periodontal health and disease and found that

- Melatonin levels were decreased in diseased periodontal tissues

especially periodontitis

- Melatonin levels were lowest in aggressive periodontitis group

- Concluded that melatonin has a protective function against

periodontal infection.
 SEX STEROID HORMONES

▪ Sex steroid hormones have been shown to directly and indirectly exert
influence on cellular proliferation, differentiation and growth in target tissues,
including keratinocytes and fibroblasts in the gingiva (Mariotti A, 1994)

▪ There are two theories for the actions of the hormones on these cells:

▪ a) change of the effectiveness of the epithelial barrier to bacterial insult

▪ b) effect on collagen maintenance and repair.

 ESTROGEN
▪ 3 naturally occuring estrogens:

▪ Estrone : most abundant in postmenopausal women

▪ Estradiol : the ovary, testis, placenta, as well as by peripheral tissues.. Most

abundant in premenopausal women

▪ Estriol : the ovary

▪ Estradiol -17β : most potent

 BIOLOGICAL ACTIONS OF ESTROGEN
▪ Development, growth, and maintenance of secondary sex characteristics;

▪ uterine growth;

▪ feed-back control of pituitary gonadotropins

▪ Thickening of the vaginal mucosa; and Cytodifferentiation of stratified

squamous epithelium

▪ In males : pituitary gonadotropin release, sexual behavior and the reabsorption

of fluid in the efferent ducts of the
 EFFECTS OF ESTROGEN ON PERIODONTAL TISSUES

▪ Vascular effect: Increased cellular proliferation in blood vessels.

▪ Cellular effect: Decreases keratinization while increasing epithelial glycogen.

Stimulates the proliferation of the gingival fibroblasts.

▪ Immunological effect: Inhibit PMN chemotaxis and phagocytosis.

Suppress leukocyte production from the bone marrow

▪ Affects salivary peroxidases, which are active against a variety of
microorganisms by changing the redox potential

▪ Reduces T-cell mediated inflammation

▪ Inhibits proinflammatory cytokines released by human marrow cells

▪ Stimulates the synthesis and maturation of gingival connective tissues

▪ Increases the amount of gingival inflammation with no increase of plaque

 PROGESTERONE

▪ naturally occurring progestin,

▪ Secretion: corpus luteum,

placenta,

adrenal cortex.

▪ stimulated by luteinizing hormone produced in the pituitary gland

▪ Not localised in gingival epithelial cells

▪ Seen in gingival fibroblasts

 BIOLOGICAL ACTIONS

▪ During the luteal phase of the menstrual cycle and pregnancy

- Maintenance of pregnancy (i.e., endometrial gland function, decreased

excitability of myometrium and possible effects on the immune system to
decrease rejection of the developing fetus).

- Decreases hepatic secretion of VLDL and HDL

- Diminishes insulin action.

- Elevates basal core body temperature at ovulation

 EFFECT OF PROGESTERONE ON PERIODONTIUM

▪ Increases vascular dilatation, thus increases permeability

▪ Increases the production of prostaglandins( self limiting process)

▪ Increases PMNs and Prostaglandin E2 in the Gingival crevicular fluid

▪ Reduces glucocorticoid anti-inflammatory effect

▪ Inhibits collagen and non-collagen synthesis in PDL fibroblast

▪ Inhibits proliferation of human gingival fibroblast.

▪ Alters rate and pattern of collagen production in gingiva
resulting in reduced repair and maintenance potential

▪ Increases the metabolic breakdown of folate which is

necessary for tissue maintenance and repair
 PUBERTY

▪ Puberty is the complex process of sexual maturation resulting in an individual

capable of reproduction, induces changes in physical appearance and behaviour
that is the direct result of increases in sex steroid hormones,

▪ primarily testosterone in males

▪ Estradiol in females.

▪ The production of sex hormones (estrogen and progesterone) increases, then

remains relatively constant during the remainder of the reproductive phase.

▪ 11 – 14 years in girls and 13- 16 years in boys

 PERIODONTAL MANIFESTATION

▪ Increase in the prevalence of gingivitis without an increase in the amount of

plaque

▪ This gingivitis manifests as marginal and interdental gingival enlargement found

primarily on the facial surfaces, with the lingual surfaces remaining relatively
unaltered

▪ An increased gingival bleeding tendency has also been reported

▪ other factors such as caries, mouth breathing, tooth eruption status, and
crowding of teeth may influence the increase in gingival inflammation

▪ ↑ incidence of anorexia nervosa and bulimia nervosa perimylosis (i.e.

smooth erosion of enamel and dentin), typically on the lingual surfaces of
maxillary anterior teeth
 EFFECT ON MICROBIOTA

▪ An association between pubertal gingivitis, Gram-negative anaerobe Prevotella

intermedia and serum levels of testosterone, estrogen and progesterone has
been reported in a longitudinal study (Nakagawa et al. 1994)

▪ Capnocytophaga species also increase in incidence as well as in proportion

(Kornman & Loesche 1982, Mombelli et al. 1990, Mariotti 1994)

▪ Bacteroides intermedius level increases with increased levels of gonadotrophic

hormones in puberty.
 Management During Puberty:

▪ education of the parent or caregiver

▪ vigorous implementation of oral hygiene, is vital for maintaining

▪ Milder gingivitis cases respond well to scaling and root planing, with frequent
oral hygiene reinforcement

▪ Severe cases: microbial culture, antimicrobial mouthwashes and local site

delivery or antibiotic therapy.

▪ Periodontal maintenance appointments : more frequent when greater risk

 MENSTRUATION
▪ The monthly reproductive cycle has two phases.
- The first phase is referred to as the follicular phase
- The second phase is called the luteal phase
 PERIODONTAL MANIFESTATION

▪ Muhlemann (1948) over 50 years ago described a case of ‘‘gingivitis

intermenstrualis’’, which he observed as consisting of bright red hemorrhagic
lesions of the interproximal papillae identified prior to menstruation.

▪ Gingival manifestations of bleeding and swollen gingiva

▪ an increase in gingival exudate most pronounced in the presence of pre-existing

gingivitis

▪ a minor increase in tooth mobility

▪ Management:

- For the women who have increased gingival bleeding and tenderness
associated with the menstrual cycle, adherence to 3 to 4-month supportive
periodontal therapy appointments is recommended.

- Antimicrobial mouthrinses prior to cyclic inflammation may be indicated.

- Particular emphasis should be placed on oral hygiene.

- Careful retraction of the oral mucosa, cheeks and lips is necessary, especially
 PREGNANCY

▪ ↑ gonadotropin releasing hormones

▪ GH cell growth and proliferation

▪ Thyrotropin releasing hormones → stimulates fetal pituitary→ fetal

development

▪ ↓ FSH , LH

▪ ↑ Progestrone , estrogen

▪ ↑ prolactin
 Effects Of Pregnancy On Plaque Induced Gingival Lesions:

▪ Pregnancy accentuates the gingival response to plaque

▪ Incidence of gingivitis : 50%, to l00%

▪ Affects the severity of previously inflamed areas;

▪ Does not alter healthy gingiva.

▪ Impressions of increased incidence may be created by the aggravation of previously

inflamed but unnoticed areas

▪ Tooth mobility, pocket depth, and gingival fluid are also increased

▪ Severity of gingivitis : second or third month.

 EFFECTS ON MICROBIOTA
▪ Kornman and Loesche reported that

- the subgingival flora changes to a more anaerobic flora as pregnancy progresses

- The only microorganism that increases significantly during pregnancy is P.

intermedia

- This increase appears to be associated with elevations in systemic levels of estradiol

and progesterone and to coincide with the peak in gingival bleeding

- estradiol or progesterone can substitute for menadione (vitamin K) as an essential

growth factor for P. intermedia but not Porphyromonas gingivalis or Eikenella
corrodens.
 MATERNAL IMMUNORESPONSE
▪ Depression of cell-mediated immunity
▪ Decreased neutrophil chemotaxis
▪ Depression of antibody and T-cell responses
▪ Decrease in ratio of peripheral T helper cells to T suppressor-cytotoxic cells
(CD4/CD8 ratio)
▪ Cytotoxicity directed against macrophages and B cells may result in diminished
immunoresponsiveness.
▪ Decrease in absolute numbers of CD3+, CD4+, and CD19+ cells in peripheral
blood during pregnancy versus postpartum
▪ Stimulation of prostaglandin production
 Periodontal Manifestation In Pregnancy
▪ In 1877, Pinard recorded the first case of “pregnancy gingivitis

▪ Colour: bright red to bluish.

▪ Pronounced ease of bleeding is the most striking feature

▪ Usually painless unless complicated by acute infection

▪ Marginal and interdental gingiva: enlarged and edematous, pit on pressure,

appear smooth and shiny, are soft and pliable, and sometimes present a
raspberry-like appearance
▪ Gingivitis : more severe by the eighth month and ↓ during the ninth month of
pregnancy;

▪ Partial ↓ in the severity of gingivitis : by 2 months postpartum, and after 1 year the
condition of the gingiva is comparable to that of patients who have not been
pregnant.

▪ Gingiva does not return to normal as long as local factors are present.
 PREGNANCY TUMOR OR EPULIS

▪ occur in 0.2% to 9.6% of pregnancies

▪ A pedunculated, fibro-granulomatous lesion

▪ Size : less than 2 cm in diameter

▪ A bright red, hyperemic and edematous presentation.

▪ Vascular response by progesterone + matrix stimulatory effects of estradiol

leads to development of pregnancy granulomas

▪ Location : the anterior papillae of the maxillary teeth

▪ Bleeds when traumatized.

▪ Removal is best deferred until after parturition, when there is often

considerable regression in their size (Wang et al. 1997)

▪ TREATMENT : surgical removal of the granuloma

▪ recurrence due to a combination of poor plaque control and hormone

mediated growth of the lesion.

▪ Careful oral hygiene and debridement during pregnancy

 PERIODONTAL DISEASE AND PRETERM, LOW-BIRTH-
WEIGHT INFANT
▪ Initially, Offenbacher et al provided evidence that untreated periodontal

disease in pregnant women may be a significant risk factor for preterm (<37
weeks’ gestation), low-birth-weight (<2500 g) infants.

▪ The current opinion is that the correlation of periodontal disease to PLBW

births may occur as a result of infection and is mediated indirectly, principally
by the translocation of bacterial products such as endotoxin
(lipopolysaccharide) and the action of maternally produced inflammatory
mediators. [Gibbs RS, Romero R, Hillier SL,]
 ORAL CONTRACEPTIVES:

▪ Oral contraceptives are medications taken orally for the purpose of birth
control.

▪ oral contraceptive (OC) use mimics hormonal levels of pregnancy, clinical

manifestations are similar.

▪ Modern day formulations : 20-30µg /day estrogen , 0.5-1 mg/day progestin

 PERIODONTAL MANIFESTATIONS

▪ increased gingival exudate (Lindhe & Bjorn 1967).

▪ exaggerated response to local irritants occurs in gingival tissues.

▪ Inflammation ranges from mild edema and erythema to severe inflammation

with hemorrhagic or hyperplasic gingival tissues.

▪ Spotty melanotic pigmentation of the skin around lips and Gingival melanosis

▪ decreased concentration of protein, sialic acid, hexosamine fucose, hydrogen

ions and total electrolytes in saliva.
▪ Two- to threefold increase in the incidence of localized osteitis after extraction of
mandibular third molars due to effect on clotting factors (Cohen ME, Simecek JW,
1995)

▪ The oral contraceptive-associated gingival inflammation may become chronic (as

opposed to the acute inflammation of pregnancy) due to the extended periods of time
women are exposed to elevated levels of estrogen and progesterone. (Knight & Wade
1974)

▪ Kalkwarf reported that the response may be due to alteration of the microvasculature,
increased gingival permeability, and increasing synthesis of prostaglandgin.
▪ Management :

- establishing an oral hygiene program and eliminating local predisposing factors.

- patient be informed of their heightened risks and the need for meticulous home care and
compliance with supportive periodontal therapy visits.

- Periodontal surgery may be indicated if there is inadequate resolution after initial therapy
(scaling and root planing).

- Antimicrobial mouthwashes may be indicated as part of the home care regimen.

- advisable to perform extraction of teeth (especially of third molars) on non-estrogenic

days (days 23 to 28) of the pill cycle,
 MENOPAUSE
▪ WHO : menopause as the permanent cessation of menstruation from loss of ovarian
follicular activity

▪ Perimenopause : ↑ FSH
▪ Early Post Menopause: ↑ FSH , ↑ LH
▪ Late Post menopause : small amounts of androstenedione and testosterone

▪ Health conditions related to estrogen deficiency:

- bone loss, osteoporosis and
- possibly an increase in cardiac morbidity.
- Xerostomia
 Menopausal Gingivostomatitis (Senile Atrophic Gingivitis)

▪ Occurs during menopause or postmenopausal period.

▪ Not a common condition

▪ Mild signs and symptoms sometimes appear,

▪ associated with the earliest menopausal changes.

▪ The gingiva and remaining oral mucosa :

- dry and shiny, vary in colour from abnormal paleness to redness, and bleed easily.
▪ Fissuring occurs in the mucobuccal fold in some women,

▪ Dry, burning sensation throughout the oral cavity,

▪ associated with extreme sensitivity to thermal changes;

▪ abnormal taste sensations described as “salty," "peppery," or "sour";

▪ difficulty with removable partial prostheses

▪ Microscopically:
- Atrophy of the germinal and prickle cell layers of the epithelium
▪ Management:

- Estrogen, often in combination with progestin.

- Low-dose estrogen (i.e. ≤0.3 mg of conjugated equine estrogen, ≤ 0.5 mg of oral

micronized estradiol, ≤ 25 µg of transdermal estradiol or ≤ 2.5 µg of ethinyl estradiol) has
been shown to be effective for many women.

- Dentrifices with less abrasives and mouthrinses with low alcohol content.

- Gentle root surface debridement.

- Osteoporosis : Biphosphonates (e.g. alendronate, risendronte, ibandronate and zoledronic

acid)
 CONCLUSION

▪ The influence of hormones from the endocrine system on periodontal health or

disease is colossal.

▪ Even as our understanding expands regarding how the disruption of hormone

production and ⁄ or function affects different organs, the current understanding
of the effects of these powerful chemical messengers remain largely unknown
in the periodontium.
▪ Hormonal fluctuations differ from patient to patient. The dental
professional should explore hormonal stability and medications
associated with hormone regulation.

▪ Patients should be educated regarding the profound effects that sex

hormones may play on periodontal and oral tissues as well as the
need for proper oral self-care and a frequent professional
intervention.
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