ROLE OF HORMONES IN PERIODONTAL DISEASE.pptx

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J Midlife Health. 2021 Oct-Dec; 12(4): 263–266. Published online 2022 Jan 20. doi: 10.4103/jmh.jmh_142_21
PMCID: PMC8849144PMID: 35264831
Influence of Female Sex Hormones in Different Stages of Women on Periodontium
Ramanarayana Boyapati, Sai Abhishiktha Cherukuri,1 Ruparani Bodduru,2 and Ambati Kiranmaye2
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Abstract
The primary etiologic factor for periodontal diseases is “Dental plaque.” Although pathogenic bacteria in dental plaque are required for the incidence of periodontal disease, a susceptible host is also very important. The susceptibility of the host can be modified by many systemic factors with hormones level being one. The periodontium shows an exaggerated inflammatory response to plaque modified by female sex hormones during puberty, pregnancy, in women taking oral contraceptives, and at the postmenopausal stage. This review provides an in detail analysis of how periodontium is influenced by the fluctuation in sex steroid hormones of females during different phases of their lifetime and to discuss how much the same hormone at different ages and stages shows Back to TopSkip to main content
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As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health.
Learn more: PMC Disclaimer | PMC Copyright Notice
Logo of jmidhlth
J Midlife Health. 2021 Oct-Dec; 12(4): 263–266. Published online 2022 Jan 20. doi: 10.4103/jmh.jmh_142_21
PMCID: PMC8849144PMID: 35264831
Influence of Female Sex Hormones in Different Stages of Women on Periodontium
Ramanarayana Boyapati, Sai Abhishiktha Cherukuri,1 Ruparani Bodduru,2 and Ambati Kiranmaye2
Author information Article notes Copyright and License information PMC Disclaimer
Go to:
Abstract
The primary etiologic factor for periodontal diseases is “Dental plaque.” Although pathogenic bacteria in dental plaque are required for the incidence of periodontal disease, a susceptible host is also very important. The susceptibility of the host can be modified by many systemic factors with hormones level being one. The peri

1. ROLE OF HORMONES IN PERIODONTAL DISEASE Presented by: B.Sowjanya , I-MDS.

2. Contents Introduction Classification of hormones Central endocrine system Effect of central endocrine hormones on periodontium Peripheral endocrine system Effect of peripheral endocrine hormones on periodontium -Thyroid hormones -Parathyroid hormones -Adrenal gland hormones -Pancreatic hormones -Sex hormones Conclusion References

3. Introduction Chronic periodontitis “an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.” - Flemmig TF Endocrine system plays one of the key roles in the homeostasis of periodontium.

4. Hormones are chemical messengers, synthesized by endocrine (ductless) glands, secreted into the blood stream and act on tissues distant from their origin .

5. Central endocrine glands

6. Central endocrine system Hypothalamus i . Significant role in homeostatic regulation ii. Regulates the anterior pituitary gland , water balance, ANS, regulation of eating ⁄ drinking behavior and reproductive system, as well as the generation and regulation of circadian rhythms .

7. It fulfills this regulatory role through the release of several small peptide hormones, including a. TRH b. GHRH, c. Somatostatin, d. Gonadotropin-releasing hormone and e. Corticotropin-releasing hormone f. Catecholamine hormone,Dopamine .

8. Pituitary gland Pituitary gland hormones are essential for reproduction, growth, metabolic homeostasis , responses to stressors and blood volume regulation. The secretion of both anterior and posterior pituitary hormones is controlled by the hypothalamus.

9. Posterior pituitary hormone (e.g. Vasopressin and oxytocin ) are synthesized in neuronal cell bodies in hypothalamic nuclei, transported to nerve terminals in the posterior pituitary and then released in response to neural activity originating in the hypothalamus .

10. Hypothalamus controls anterior pituitary by secreting the releasing and inhibitory hormones (factors), which are called neurohormones . These hormones from hypothalamus are transported anterior pituitary through hypothalamic-hypophyseal portal vessels.

11. Effect of central endocrine gland on periodontium It has been difficult to ascertain the direct effects due to inability to discriminate between the direct effects of the hypothalamic or pituitary hormones vs. successive hormone effects and ⁄ or complementary, antagonistic or pleiotropic actions of additional hormones and ⁄ or secondary metabolic consequences occurring in periodontal tissues.

12. The effects of Dopamine have been examined only on human periodontal ligament cells in cell culture. Specifically, at 1 g ⁄ , dopamine was able to stimulate cell growth without being toxic to the cells in culture , suggesting a possible role for dopamine in the growth and proliferation of the periodontal ligament.  

13. Growth hormone Protective influence of GH in the periodontium. In one case– control study examining attachment loss in patients with GH deficiency, subjects with untreated congenital GH deficiency had a statistically greater prevalence of periodontitis (odds ratio = 17.4) when compared with healthy controls . - BRITTO ET AL,2011

14. In regard to gingival diseases, weak evidence from two separate case reports ( Bhowmick et al,and Oikarinen K et al) has noted hereditary gingival fibromatosis in patients with GH deficiency.

15. Peripheral endocrine system Thyroid gland hormones Two families of hormones: 1.Single modified amino-acid thyroid hormones Thyroxine and triiodothyronine -Producing site-spherical Colloid filled thyroid follicles. 2.Polypeptide- Calcitonin -Producing site-Parafollicular thyroidal C cells

16. Thyroxine ( T 4 ) and triiodothyronine ( T 3 )are -amino acid derivatives of tyrosine . These thyroid hormones have three unique properties: ( i ) They contain iodine, (ii) They have no specific target tissue but exert effects in virtually every cell type, and (iii) Their concentrations in the blood are relatively constant.  

17. Like other lipophilic hormones, the classical mechanism of action involves binding to an intracellular receptor to form a hormone–receptor complex and subsequent binding of the complex to DNA to alter the rate of gene transcription. The thyroid hormone receptor has affinity ( T 3 ) > ( T 4 )

18. Functions of Calcitonin Principal function -regulation of calcium and phosphorus concentrations in the blood and it is the antipode of parathyroid hormone. More specifically, calcitonin calcium levels in the serum by inhibition of: ( i ) osteoclast activity , and (ii) renal tubular resorption of calcium .

19. Calcitonin Stimulating factors serum ca 2+ glucocorticoids, gastrin, glucagon and -adrenergic agents   Inhibiting factors Calcitriol (1,25[OH]2D3)

20. Effects of thyroid gland hormones on the 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. 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.

21. In regard to the actions of calcitonin on periodontal tissues, the physiological significance of this hormone for skeletal conservation in the human remains elusive.

22. Parathyroid gland hormone PTH is a peptide hormone secreted by the parathyroid glands, which is essential for calcium regulation. More specifically, PTH acts on bone, kidneys and intestine, and plasma Ca 2+ levels and plasma PO 4 concentration .

23. Effects of parathyroid gland hormone on the periodontium Primary hyperparathyroidism , resulting principally from adenomas , and Secondary hyperparathyroidism , resulting primarily from CRF , have been implicated in alveolar bone destruction as a consequence of elevated PTH levels. In general, increased tooth loss and poor oral hygiene have been associated with hyperparathyroidism.

24. Brown tumors (i.e. circumferential intrabony jaw tumors), typically diagnosed in primary hyperparathyroidism , can cause dislocation of teeth . Similarly, there are supporting data that secondary hyperparathyroidism in chronic renal failure has been associated with destructive periodontal disease .

25. Recent clinical studies showed cortical bone density , incidence of tori, as well as a + ve correlation between serum PTH levels and periodontal ligament space width in patients suffering from primary hyperparathyroidism when compared with the thyroid control group

26. There was a significant reduction in the number of inflammatory cells at the marginal gingival area in sections obtained from animals receiving PTH compared with control animals. - Barrows et al,2003

27. Adrenal gland hormones Location - retroperitoneum superior to the kidneys.

28. Aldosterone Primarily regulates extracellular volume Control of K + homeostasis and Enhanced cardiac muscle contraction, vascular resistance and fibrinolysis. Cortisol Affects numerous physiological processes (e.g. metabolism, inflammation, growth and levels of awareness). DHEA and androstenedione are weak androgens that can be converted to more potent androgenic or estrogenic hormones by peripheral tissues.

29. The hormones produced by the adrenal medulla are primarily Catecholamines (e.g. epinephrine and norepinephrine). Catecholamine secretion is increased by ACTH and glucocorticoids but can also be affected by sympathetic nerve stimulation, hypoglycemia, hypoxia, hypercapnia, acidosis, hemorrhage, glucagon, histamine and angiotensin II . Catecholamines are generally associated with the flight or fight response .

30. Effects of adrenal gland hormones on the periodontium : Cortisol : more effects on periodontium A few, relatively small, descriptive clinical studies have attempted to demonstrate an association between elevated cortisol levels and periodontitis (Rai B, Rosania AE) The putative effects of cortisol have not come from evaluating changes in the periodontium during disease states, but from the effects that this hormone may produce as a result of stress

31. Pancreatic hormones: They play a major role in carbohydrate and lipid metabolism as well as in the control of energy stores.

32. Functions of insulin

33. Functions of glucagon

34. Somatostatin Somatostatin is also known as GHIH 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 GI hormones (e.g. gastrin, cholecystokinin, secretin and motilin). The inhibitory effect of somatostatin acts as negative feedback and prevents excessive plasma levels of nutrient by-products.

35. 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 -cells of the pancreas and ⁄ or the development of peripheral cellular resistance to insulin action.  

36. Diabetes Diabetes has been associated with increased prevalence and severity of gingivitis . Gusberti et al. studied children with type-1 DM. Before puberty, poorly controlled diabetes mellitus children had a higher incidence and severity of gingival inflammation than did well controlled children. During puberty, there was a general increase in gingivitis, independent of glycemia. Cianciola et al. confirmed an increase in gingivitis in type 1 diabetes mellitus children after the age of 11 when compared to non-diabetes mellitus controls.

37. Alterations in subgingival microbiota and GCF: In young type 1 DM subjects, Mashimo et al. (1983) reported an increase in proportions of Capnocytophaga species, while Fusobacterium and Bacteroides species remained at low levels. Sastrowijoto et al .(1989) 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.

38. Zambon et al .(1998) demonstrated a different serotype of P. gingivalis in type-2 diabetes mellitus subjects.

39. In addition to decreased synthesis, newly formed collagen is susceptible to degradation by collagenase, a MMP 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, advanced glycation end products, and wound healing:

40. DM is a prevalent metabolic disorder that impairs barrier function and healing responses throughout the human body. In the oral cavity, d iabetes is a known risk factor for exacerbated periodontal disease and delayed wound healing , which includes both soft and hard tissue components.

41. Due to their anti collagenolytic effect, tetracyclines and chemically modified tetracyclines have potential benefits in inhibiting the onset and progression of periodontitis, arthritis, and osteoporosis, among other conditions. Since collagenase production is increased in DM, these drugs may have beneficial effects by normalizing collagen metabolism and wound healing events.

42. Changes in host immuno inflammatory response:

43. Bidirectional relationship of diabetes and periodontitis

44. The impact of periodontal treatment on diabetes

45. Westfelt et al . performed a longitudinal assessment of periodontal therapy, including SRP, modified Widman flap surgery, and regular maintenance, in DM subjects and non-diabetes mellitus controls with moderate to advanced periodontitis. Results : At the 5-year re-evaluation, DM patients had a similar percentage of sites gaining or losing attachment, and a similar percentage of sites with stable attachment levels, compared to non-diabetes mellitus subjects. J Clin Periodontol 1996: 23: 92 –100

46. Management of diabetes

47. It is important to note that most of the complications during the treatment of a diabetic patient are due to hypoglycemia and not hyperglycemia. In general, morning appointments are suitable for a diabetic patient because the endogenous corticosteroid levels are generally high at this time which increases the blood glucose level.

48. If the patient is taking insulin , the visits should be arranged in such a way that the treatment time does not coincide with the peak activity of insulin .

49. Pineal gland hormones Melatonin A study by Gomez et al(2007) ,suggest that melatonin could act as a protective function in fighting periodontal infection. Another study by Almughrabi et al ,(2012) concluded that, the melatonin levels in GCF and saliva are decreased in diseased periodontal tissues, especially periodontitis . The melatonin level was lowest in the aggressive periodontitis group.

50. Effect of sex -steroid hormones Synthesized from cholesterol Like cholesterol, poorly soluble in water.

51. 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 -17 β : most potent

52. Biological actions of estrogen Development, growth, and maintenance of secondary sex characteristics ; Uterine growth; Pulsatile release of luteinizing hormone (LH) from the central nervous system; Thickening of the vaginal mucosa; and Ductal development in the breast, Cytodifferentiation of stratified squamous epithelium, Synthesis and maintenance of fibrous collagen.

53. Effects of estrogen on periodontal tissues: keratinization while increasing epithelial glycogen. cellular proliferation in blood vessels. Inhibit PMNL chemotaxis and stimulates PMNL phagocytosis . Suppress leukocyte production from the bone marrow. Inhibits proinflammatory cytokines released by human marrow cells.

54. Affects salivary peroxidases , which are active against a variety of microorganisms by changing the redox potential, T-cell mediated inflammation, Stimulates the proliferation of the gingival fibroblasts , Stimulates the synthesis and maturation of gingival connective tissues, Increases the amount of gingival inflammation with no increase of plaque.

55. Progesterone: Naturally occurring progestin, secreted by the ovary (mainly the corpus luteum during the second half of the menstrual cycle), Synthesis and secretion : stimulated by LH produced in the pituitary gland Progestrone receptor occurs in two isoforms : A and B Not localised in gingival epithelial cells Seen in gingival fibroblasts.

56. Effect of progesterone on periodontium : Increases vascular dilatation, thus increases permeability Increases PMNL and Prostaglandin E2 in the GCF. Reduces glucocorticoid anti-inflammatory effect. Inhibits collagen and non-collagen synthesis in PDL fibroblast. Inhibits proliferation of human gingival fibroblast .

57. 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

58. Vasculature : Oestrogen  edema , bleeding, erythema and exudation. Progesterone is known to have little or no effect on the vasculature, but seen in gingiva due to unknown reasons. Fibroblasts: Androgens and progesterone have an inhibitory effect on fibroblast proliferation in cell cultures.

59. Effects of androgens on the periodontal tissue Enhance matrix synthesis by pdl fibroblasts and osteoblasts . ( Kasperk et al) Enhance osteoblast proliferation and differentiation .(Morley et al) (-) prostaglandin secretion.( ElAttar et al). IL-6 production during inflammation. ( Parkar et al,Gorstein et al).

60. Puberty: Puberty is the complex process of sexual maturation resulting in an individual capable of reproduction, induces changes in physical appearance and behavior that is the direct result of increase in sex steroid hormones , Primarily testosterone in males and Estradiol in females. 11 – 14 years in girls and 13- 16 years in boys.

61. Hormonal changes during puberty: Puberty gingivitis : Mean age of maximum : 12 years, 10 months for girls and 13 years, 7 months for boys. Mainly involving facial surfaces with lingual surfaces relatively uninvolved Enlargement of the gingiva may occur in areas where food debris, materia alba, plaque and calculus are deposited Inflamed tissues can become erythematous, lobulated and retractable. Bleeding may occur easily.

62. ↑ incidence of mouth breathing and asthma : gingival enlargement, especially in the anterior area of the dentition, possibly as a result of surface dehydration. ↑ 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 Enlarge parotids : ↓ salivary flow  erythema

63. Effect on microbiota : The prevalence : Prevotella intermedia is able to substitute progesterone and estrogen for menadione (vitamin K) as an essential nutrient. Capnocytophaga species ( Kornman & Loesche 1982, Mombelli et al. 1990, Mariotti 1994) An association between pubertal gingivitis, Prevotella intermedia and serum levels of testosterone, estrogen and progesterone has been reported in a longitudinal study (Nakagawa et al. 1994).

64. Management during puberty: Education of the parent or caregiver Vigorous implementation of oral hygiene, is vital for maintaining Severe cases  microbial culture, antimicrobial mouthwashes and local site delivery of an antiseptic. Periodontal maintenance appointments : more frequent when greater risk.

65. Asthmatic / mouthbreathers : meticulous home care and increase the frequency of periodontal maintenance appointments and dental caries evaluation. Topical application of an occlusive barrier (lubricant) over the inflamed gingiva after home-care procedures and immediately before bedtime  reduction of soft-tissue edema.

66. Role of hormones in periodontal disease Contents: Menstrual cycle Oral contraceptive pills Pregnancy Menopause Vitamine -D Conclusion References

67. MENSTRUAL CYCLE: Phases of menstrual cycle:

68. General and oral manifestations: Aphthous ulcers Anemia : 20% : angular cheilitis , atrophic glossitis and ⁄ or oral mucosal atrophy Luteal phase  the lower esophageal sphincter may relax  the gag reflex heightened  oral procedures difficult. GERD, with heartburn, regurgitation and chest pain,  unexplained coughing, hoarseness, sore throat, gingivitis and asthma.

69. Premenstrual syndrome: Physical and emotional symptoms that are associated with the menstrual cycle 70% of menstruating women have PMS but only 5% fall into strict diagnostic criteria Antidepressants  xerostomia , more sensitive to and less tolerant of therapeutic procedures while using SSRI and may have an exaggerated response to pain.

70. Menstrual cycle and periodontium: Klein (1934) :“gingival menstrualis ” and Muhlemann (1948) : “ gingivalis intermenstrualis ” : bright, red hemorrhagic lesions of interdental papilla prior to menstruation. Bleeding gums or a bloated, tense feeling in the gums in the days preceding menstrual flow. production of gingival exudate : luteal phase

71. Follicular phase  ↑ Estrogen Increased epithelial proliferation, hyperemia and bright appearance of gingival. Increased exudation, so that there are elevated signs of inflammation with no significant change in microbial load. Luteal phase  ↑ progesterone Anti-inflammatory changes due to anti- inflammatory and immune suppressive effects of progesterone.

72. Oral contraceptives: “Contraception”  ‘contra’ =against and ‘conception’ =fertilization. Oral contraceptives are medications taken by mouth for the purpose of birth control. “birth control pills”. First oral contraceptives(1960s ): high doses of estrogens (150 µg) and progestins (9.85 mg)  high risk of cardiovascular events Progressively lower doses Modern day formulations : 20-30µg /day estrogen , 0.5-1 mg/day progestin

73. Mechanism of action: Preventing ovulation by suppression of hypothalamic gonadotrophin releasing factors . Changing the lining of uterus to prevent pregnancy from developing. Changing the mucus at uterine cervix (opening of the uterus) to prevent sperm from entering.

74. General and oral manifestations: Elevated plasma levels of several clotting factors, related to the dose of estrogen, Changes in salivary composition , Two- to threefold increase in the incidence of localized osteitis after extraction of mandibular third molars , due to effect on clotting factors, Spotty melanotic pigmentation of the skin around lips,

75. Gingival melanosis. Aggravate the gingival response to local factors in a manner similar to that seen in pregnancy gingival inflammation + gingival exudate ( Mariotti 1994 )

76. Knight & Wade 1974 : women on hormonal contraceptives ≥ 1.5 years  greater periodontal destruction compared to the control group of comparable age and oral hygiene: higher dose of gestagens used in older contraceptive preparations. Preshaw et al in 2001 :no statistically significant difference between any of the clinical parameters measured whether or not women were using oral contraceptives. Current low dose contraceptives no longer pose a threat to gingivae .

77. Pregnancy :

78. PREGNANCY If fertilization and pregnancy do occur, the corpus luteum will continue to synthesize estrogen and progesterone in ever increasing amounts. Plasma progesterone levels may reach 100 ng/mL, approximately 10 times that seen during the luteal phase of the reproductive cycle. Estradiol levels in plasma may similarly be increased up to 30 times.

79. Effects of pregnancy on plaque induced gingival lesions: Gingiva : target organ for sex hormones A ccentuates the gingival response to plaque I ncidence of gingivitis : 5O%, to lO0% A ffects the severity of previously inflamed areas ; T ooth mobility, pocket depth, and gingival fluid are also increased. S everity of gingivitis : second or third month.

80. Effects on microbiota : P. intermedia is seen to increase during the second trimester of pregnancy followed by a decline to postpartum values during the third trimester, despite highly elevated hormone levels still present during the third trimester ( Mariotti et al ).

81. Clinical changes Pregnancy gingivitis is extremely common and affects 30-100% of all pregnant women. Gingival inflammatory changes in pregnancy usually begin during the 2nd month and increase in severity through the 8th month, after which there is an abrupt decrease related to a concomitant reduction in sex steroid hormone secretion. The greatest involvement appears to be in anterior areas of the oral cavity, with interproximal sites most commonly affected.

82. Increased gingival probing depths Increased BOP on mechanical stimulation Increased GCF flow Increased tooth mobility

83. Pregnancy granuloma (or) epulis (or) granuloma gravidarum: 0.5-2% CAUSE : local irritants , trauma, P apilloma viruses , B artonella sps . A pedunculated , fibro- granulomatous lesion V ascular response by progesterone + matrix stimulatory effects of estradiol  development of pregnancy granulomas A bright red, hyperemic and edematous presentation. Location : the anterior papillae of the maxillary teeth Size : < 2 cm in diameter

84. Bleeds when traumatized. Removal is best deferred until after parturition, when there is often considerable regression in their size ( Wang et al. 1997 )

85. Study Result Hugoson (1970) Miyazaki et al. (1991) gingival probing depth bleeding on probing and crevicular fluid flow were found to be increased. Cohen et al. (1969) and Tilakaratne et al. (2000) the values for loss of attachment remained unchanged during pregnancy and three months postpartum Tilakaratne et al. 2000 Srilankan women : progressive increase in inflammation with advancing pregnancy which was more significant in the second and third trimester of pregnancy, despite the plaque levels remaining unchanged. At the third month after parturition, the level of gingival inflammation was similar to that observed in the first trimester of pregnancy

86. Menopause: WHO : menopause as the permanent cessation of menstruation from loss of ovarian follicular activity Greek word: ‘ pausis ’ means cessation and ‘men’ means monthly Concomitant endocrinologic, somatic and psychological changes occur. Aging and the decrease in estrogen levels

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

88. Fat  estrogen .. thinner women experience a slightly earlier menopause. (Mac Mohan et al) Consumption of alcohol is associated with later menopause, consistent with the finding that these women have higher levels of estrogen and greater bone density ( Torgerson et al).

89. Clinical features: Disturbances in menstrual patterns, including anovulation , and reduced fertility, progressing to amenorrhea. Vasomotor instability (i.e. hot flashes and sweats). Atrophy of genitourinary tissues. Cognitive decline. Mood symptoms. Health conditions related to estrogen deficiency : bone loss, osteoporosis and possibly an increase in cardiac morbidity. Xerostomia

90. Osteoporosis and menopause: Bone formation and resorption are in balance with each other during the young to mid-adult years. After 40–50 years of age, bone loss may progress slowly in both sexes, with a period of more rapid loss in women during the menopause accounting for bone loss of 12–20% over a period of 5 years. Thereafter, age-related bone loss is modest (0.6% per year), but because of long life expectancy, both sexes may lose a total of 40% of bone over their lifetime.

91. Estrogen ameliorates menopausal bone loss, increases bone mass and reduces the risk of vertebral and hip fractures. The discontinuation of estrogen replacement results in Accelerated bone loss and an increased risk of fractures, Alteration in the calcium phosphate equilibrium due to deficient absorption of dietary calcium and Increased excretion due to diminished estrogen levels usually involving the mandible >the maxilla.

92. Menopausal Gingivostomatitis (Senile Atrophic Gingivitis) SIGNS AND SYMPTOMS : Mild signs and symptoms sometimes appear, Not a common condition. The gingiva and remaining oral mucosa : dry and shiny, vary in color from abnormal paleness to redness, and bleed easily. Fissuring occurs in the mucobuccal fold in some women, and comparable changes may occur in the vaginal mucosa.

93. Dry, burning sensation throughout the oral cavity, associated with extreme sensitivity to thermal changes; abnormal taste sensations described as “ salty," "peppery," or "sour"; and difficulty with removable partial prostheses. Comparable to those of chronic desquamative gingivitis Similar signs and symptoms after ovariectomy

94. 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.

95. Vitamin D: It resembles sterol in structure and functions like a hormone. Important forms : D3 and D2 Vit D and calcium deficiency is found to result in generalized jaw bone resorption and loss of PDL ( Dorsky 2001)

96. The effect of Vit. D deficiency or imbalance on the periodontal tissues of young dogs results in: Osteoid that forms at a normal rate but remains uncalcified. Failure of osteoid to resorb , which leads to its excessive accumulation. in the width of the PDL space. A normal rate of cementum formation, but defective calcification and some cementum resorption . Distortion of the growth pattern of alveolar bone.

97. Conclusion: The influence of hormones from the endocrine system on health or disease is colossal. Ironically, 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. Medical history and dialogs should include thoughtful investigation of the individual patient needs.

98. 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.

99. References: New men MG, Takei HH, Kslokkevold PR, Carranza FA. Carranza’s clinical periodontology.10 th ed. Elsevier publications; St.Louis , Missouri 2009 Jan Lindhe , Clinical Periodontology and Implant Dentistry 4th ed. Blackwell Publishing Company 2003 Leblebicioglu B, Connors J, Mariotti . Principles of endocrinology , Periodontology 2000, Vol. 61, 2013, 54–68 Armitage G C Bi-directional relationship between pregnancy and periodontal disease . Periodontology 2000, Vol. 61, 2013, 160–176 Corgel G .Dental management of the female patient. Periodontology 2000, Vol. 61, 2013, 219–231

100. S.P. Barros, M.A.D. Silva1, M.J. Somerman and F.H. Nociti , Parathyroid Hormone Protects against Periodontitis -associated Bone Loss J Dent Res 2003 82(10):791-795 Gomez-Moreno G, Cutando -Soriano A, Arana C, Galindo P, Bolanos J, Acuna Castroviejo D, Wang H-L. Melatonin expression in periodontal disease. J Periodont Res 2007; 42: 536–540. Brian L. Mealey &Alan J. Moritz Hormonal influences: Effects of diabetes mellitus and endogenous female sex steroid hormones on the periodontium Periodontology 2000, Vol. 32, 2003, 59–81 Hutton JH. Relation of Endocrine Disorders and Dental Disease. J Am Dent Assoc 1936: 23: 226–236

101. Partovi M et al Mitogenic effect of L-dopa on human periodontal ligament fibroblast cells. J Endod 2002: 28: 193–196. Britto et al Periodontal disease in adults with untreated congenital growth hormone deficiency: a case control study. JCP 2011: 38: 525–531

102. THANK YOU