Hormones and periodontium

1. 57
Good morning

2. Effect of endocrine on periodontium
Presenter:
Shashwati Paul
Post Graduate Student

3. CONTENTS
• Introduction
• Central endocrine system
• Peripheral endocrine system
• Effect of endocrine hormones on periodontium
adrenal gland hormones
thyroid hormones
parathyroid hormones
sex hormones
pancreatic hormones
• Conclusion

4. INTRODUCTION
• Periodontitis is a type of chronic inflammatory disease affecting people
worldwide, which is characterized by the loss of periodontal connective
tissue and alveolar bone, eventually leading to tooth loss.
• Hormones secreted by endocrine system play an important role in
periodontitis..

5. ENDOCRINE SYSTEM
• Hormones  chemical messengers which
travel through the body
• Effects the target cells in other organ.

6. CENTRAL ENDOCRINE GLANDS
• Hypothalamus
• Pituitary gland

7. HYPOTHALAMUS
• Homeostasis
• Regulation
• Hormones

8. PITUITARY GLAND
• Regulation
• Hormones

9. PERIPHERAL ENDOCRINE GLANDS
• ADRENAL GLAND
• THYROID GLAND
• PARATHYROID GLAND
• GONADS
• PANCREAS

10. EFFECT OF CENTRAL ENDOCRINE GLAND
HORMONES ON THE PERIODONTIUM
• Britto et al 2011….
• M. Partovi et al in 2002…. In vitro studies… effect of dopamine on
human periodontal ligament cells…
• Pituitary hormones…two case control studies…

11. MECHANISM PROPOSED
L- DOPA
Stimulates
Dopaminergic systems in the anterior position of hypophysis
To release Growth hormone
Promoter of healing process

12. EFFECT OF PERIPHERAL ENDOCRINE
GLAND HORMONES ON THE PERIODONTIUM

13. The hormones produced by the adrenal cortex include
• Mineralo-corticoid hormones e.g., Aldosterone,
• Glucocorticoid hormones e. g., cortisol,
• Gonadal hormones e. g., dehydro-epi-androsterone
ADRENAL GLAND HORMONES

14. EFFECT OF ADRENAL GLAND
HORMONES ON THE PERIODONTIUM
Association between elevated cortisol levels and periodontitis were demonstrated by
clinical studies by Rosania et al and Rai et al in 2009 and 2011.
By
Potential psycho-neuro-immunologic mechanism
Potential behavioural mechanism

15. POTENTIAL PSYCHO-NEURO-IMMUNOLOGIC
MECHANISM
Negative emotion
Hypothalamus releases corticotropin realeasing hormone..
….. releases Adreno corticotropic hormone from pituitary
Adrenal cortex release Cortisol

16. • Short term elevations of cortisol reduce inflammation and mobilize
immune components
Glucocorticoids(cortisol) decreases immunocompetency by inhibition of
IgA, IgG and neutrophil function.
• Leads to increased biofilm colonization and reduced ability to prevent
connective tissue invasion.
• After periods of chronic elevation, cortisol loses its ability to inhibit
inflammatory responses  chronic periodontitis

17. POTENTIAL BEHAVIOURAL MECHANISM
The higher cortisol and β endorphin concentrations significantly up regulates expression of
MMP-1,2,7,11 and TIMP-1 in human gingival fibroblasts
Increased periodontal breakdown
Periodontitis
Patricia et al 2007

18. • Various kinds of psychologic stress activate HPA(hypothalamus Pituitary
Adreno cortical) system and SM(sympathetic adrenal medullary) system and
consequently induce significant increases in salivary cortisol and
catecholamine levels respectively

19. Thyroid hormone
Effect of thyroid hormone on periodontium:

20. • 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. • Thyroid diseases may affect the status of periodontal diseases, especially
in hypothyroid conditions.
• Uncontrolled thyroid disease may lead to destruction of periodontium.
• Limited evidence till now.
• Periodontal treatment is safe in controlled conditions(meta analysis by
Wang and Cohen , 2011)

22. Parathyroid gland hormone
• Hormones- parathormone

23. Calcium regulation
The resorption of calcium from bones by PTH is by
• Rapid phase
• Slow phase

24. RAPID PHASE
After reaching bone
PTH gets activated to receptors on cell membrane of osteoblasts and osteoclasts
Hormone receptor complex
Increases permeability of membranes of these cells for ca-ions
Accelerates ca-pump mechanism
Ca-ions move from bone cells into blood at faster rate

25. SLOW PHASE
When Osteoclasts are activated by PTH
Lysosomes release enzymes and citric acid and lactic acid
These substances dissolve organic matrix of bone releasing ca ions
Ca ions release to plasma

26. EFFECT OF PARATHYROID GLAND
HORMONE ON PERIODONTIUM
.
• Primary hyperparathyroidism, resulting principally from adenomas, and secondary
hyperparathyroidism, 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.
• 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.
• ( Frankenthal S,2002)

27. • In an effort to elucidate the relationship of parathyroid hormone with destructive periodontal
disease, recent clinical studies have examined the effects of parathyroid hormone on the
periodontium.
• More specifically, this research has shown decreased cortical bone density, increased
incidence of tori, as well as a positive correlation between serum parathyroid hormone levels
and periodontal ligament space width in patients suffering from primary
hyperparathyroidism when compared with the control group.
• However, there were no alterations in clinical periodontal parameters in the parathyroid
hormone group, suggesting that parathyroid hormone-reduced bone density does not
predispose individuals to alterations in the soft tissue attachment apparatus.
• In spite of the absence of positive hormone-induced effects on the periodontium noted in
hyperparathyroidism patients, the novel use of parathyroid hormone has been suggested as a
therapeutic aid in the prevention of destructive periodontal diseases

28. • LPS produced by various periodontopathogens such as P. gingivalis and
Actinobacillus actinomycetemcomitans induce a local inflammatory response that
ultimately leads to periodontal bone resorption (Fletcher et al., 2001).
• In the periodontium, LPS may promote an inflammatory reaction through the
induction of several cytokines (Kondo et al., 2001; Nagasawa et al., 2002), known to
be produced by several cell types, including gingival fibroblasts and recruited
leukocytes (Nagasawa et al., 2002).
• PTH administration neutralizes LPS-mediated inflammation.
(S.P.Barros, Journal of Dental Research 2003)

29. SEX STEROID HORMONES
• Women’s life cycle changes present unique challenges to the oral health
care profession.
• Hormonal influences associated with reproductive process alter
periodontal and oral tissue responses to local factors.
• Different phases of female life cycle: puberty, menses, pregnancy and the
effect of oral contraceptives

30. ACTION OF SEX STEROID HORMONES ON
PERIODONTIUM
• Increased Sex hormones  increased synthesis of prostaglandin 
Increases the gingival permeability  leads to the alteration of
microvasculature increase in inflammation
Kalkwarf, 1972

31. PROPOSED MECHANISMS
• Sex steroid induced increase in specific microbiota
kumare et al in 2013
• Immune endocrine interactions exaggerate periodontal responses
Shiau, Reynolds in 2010
• Specific populations of fibroblasts and epithelial cells are modulated by sex steroid hormones:
Mariotti. In 1994

32. SEX STEROID HORMONES AND THE CELLS OF
PERIODONTIUM
Hormone Fibroblasts
Androgens (testosterone &
hydrotestosterone)
Decrease proliferation
Decrease IL-6 production
Progesterone Decrease proliferation
Decrease protein synthesis
Decrease cytokine production
Estradiol Increase proliferation
Increase cytokine production

33. Factors influencing sex hormones on
periodontium
• Gender
• Age
• Hormone supplements

34. Gender
• Studies by Lau et al 2001 showed that gender plays an important role in
changes associated with bone density throughout the entire skeleton.
• It was showed that 80% of decreased bone density patients were females.

35. • Regarding periodontal anatomic differences:
Residual ridge height was lower in women compared to men +
decreased amount of estrogen in post menopausal women was associated
with decreased crestal bone density

36. Age
• With regard to age, females undergo more biologic changes (hormonal
imbalances) compared to males such as during puberty, menstrual cycle,
pregnancy, menopause

37. Hormone supplements
• These are common used drugs that stimulates a state of pregnancy to
prevent ovulation.
• Hormone supplements has helped in overcoming bone loss in menopausal
women, it also has been associated with side effects like cancer

38. PUBERTY
• Increased production of sex hormones(estrogen and progesterone)
• Increased prevalence of gingivitis without an increase in amount of plaque
• P. intermedia uses ovarian hormone as a substitute for vitamin K growth
factor( Kornman and Loesche,1979)

39. Longitudinal studies have examined the transformation of subgingival flora from pre puberty to puberty and have
demonstrated a significant increase in
• Prevotella intermedia,
• Capnocytophaga species ,
• Prevotella nigrescens,
(Delancy and Kornman)

40. Clinical findings
• Erythematous tissue
• Nodular hyperplastic lesion with increased deposits
• Bleeding on probing

41. PREGNANCY
….Old saying…
• In 1877, Pinard recorded the first case
• Characterised by erythema, hyperplasia and gingival bleeding.
• Periodontal status prior to pregnancy influences the progression or severity of
disease.
• Increased pocket depth, increased mobility
• Mostly seen in anterior region of mouth.

42. • Pregnancy granuloma or granuloma gravidarum or pregnancy epulis
• Female sex hormones  increased local synthesis of angiogenic factors
• Periodontal disease alters systemic health  effects the well being of fetus
Risk of low birth weight, preterm infants
• Periodontal infection.. Releases endotoxin.. Enters circulation..

43. ETIOLOGY OF GINGIVAL RESPONSES TO ELEVATED
ESTROGEN & PROGESTERONE DURING PREGNANCY
• Subgingival plaque composition
B.melaninigenicus
P.intermedia……
P.Gingivalis
Campylobacter rectus
• Maternal immuno-response.
Decreased neutrophil chemotaxis, depression of cell mediated immunity with increase in progesterone.(Raber-
durlacher,1993)
Down regulation of IL-6 Production due to progesterone decreased resistance of gingiva

44. • Sex hormone concentration
Progesterone reaches 100 ng/ml
Estrogen regulates cellular proliferation, differentiation and keratinisation
Progesterone influences the permeability of microvasculature, alters rate of
collagen production, increases metabolic breakdown of folate

45. ORAL CONTRACEPTIVES
• These mimics the hormone levels of pregnancy… clinical manifestations are
similar..
• Increased response to local irritants.
• Increased prostaglandin synthesis with increase in sex steroids  results in
inflammation
• Gingival melanosis

46. PANCREATIC HORMONES
• Effect of pancreatic hormones on periodontium
The metabolic disturbances and the resulting disease of
diabetes mellitus are ultimately the result of a complete or
partial reduction in insulin secretion from the β cells, impaired
insulin action OR the destruction of the cells.

47. 1997, American Diabetis Association classified into:
• Type 1 Diabetes
• Type 2 Diabetes
• Gestational Diabetes
• Other types

48. COMPLICATIONS OF DIABETES MELLITUS
Five classic complications
• Retinopathy
• Nephropathy
• Neuropathy
• Macrovascular disease
• Altered wound healing and sixth one is
• Periodontal disease

49. ORAL MANIFESTATIONS
Oral changes described in diabetic patients including
• Cheilosis
• Mucosal drying
• Cracking
• Burning mouth and tongue
• Diminished salivary flow
• Altered oral cavity flora

50. • Diabetes – risk factor
• Diabetes – increased gingival inflammation – bacterial plaque(Gusberti
1983)
• This response-level of glycemic control
• Presence of poor glycemic control- risk of less favourable response
• Prevalence of attachment loss and bone loss greater in diabetic patients…

51. MECHANISMS OF DIABETIC INFLUENCE
ON PERIODONTIUM
These are primarily related to changes in
GCF glucose level
Periodontal vasculature
Collagen metabolism.
The subgingival microbiota
Host response

52. • Increased thickness of capillary endothelial cell basement membrane and
walls of small blood vessel may be seen in diabetes.
• This thickening Impairs oxygen diffusion and nutrient provision across
membrane  alters normal periodontal tissue homeostasis.

53. FORMATION OF AGEs
• AGEs  Arterial smooth muscle cell proliferation  increased thickness of
vessel walls
• In capillaries increase in crosslinking of AGE modified collagen  inhibits
normal degradation of proteins  increased thickness of basement membrane.
• Increased LDL….AGE modified collagen bind to LDL  Narrows the lumen

54. • Periodontally diseased sites harbor similar species as in non diabetics
…..host response plays a major role..
• Defects in PMN Adherence, chemotaxis and phagocytosis observed in diabetics..due to hyper-
responsiveness… Oliver and colleagues,1993
• Hyperresponsive monocyte/macrophage phenotype stimulation by bacterial lps  increased cytokine
production(offenbacher,1996)
In vitro studies – decreased chemotaxis of PDL fibroblasts to PDGF when placed in hyperglycemic
environment compared to normoglycemic condition.
Increased GCF level  adversely affects wound healing and local host response to microbial challenge

55. CONCLUSION
• The influence of endocrine hormones in health and in disease is colossal.
• Ironically, still there is limited evidence and our understanding of the
effect of these hormones on periodontium is still incomplete.

56. Source Hormone Target tissue Principle function Periodontium
Hypothalamus Prolactin inhibiting hormone
(dopamine)
Anterior pituitary gland Inhibits prolactin release Stimulates periodontal ligament
cell proliferation
Anterior pituitary Growth hormone (somatotropin) Bone, soft tissues and liver Promotes growth, affects
lipids and carbohydrate
metabolism
Presence of growth hormone
associated with protective effect on
periodontium
Thyroid Thyroid hormones (tri iodothyrosine,
thyroxine)
Most cells of body Regulators of numerous
tissues including cardiac
and brain involved with
growth and metabolism
Deficiency may be associated with
destructive periodontal diseases
Adrenal Cortisol,
Weak androgens and estrogens
Progesterone
Most tissues of body
Sex accessory tissues
Important for glucose,
protein and lipid
metabolism
Low potency of secreted
hormones diminishes
effects on target tissues
Excess cortisol associated with
destructive periodontal diseases
Known effects on periodontal
tissues including growth of
microbiota as well as disease
progression
Pancreas Insulin (β cells) Skeletal muscle, liver,
adipose tissue
Lowers the blood
glucose, fatty acid and
amino acid levels
Decreased insulin production
associated with destructive
periodontal diseases
Parathyroid Parathyroid hormone Bone, kidneys, intestine Increases plasma calcium Decreased cortical bone density
and increased PDL width no effect
on periodontal parameters

57. References
• Carranza’s clinical Periodontology: 10th Ed: Saunders
• Partovi et al. Mitogenic effect of L dopa on human periodontal ligament fibroblast cells:
Jour of Endodontics. Vol 28(3): 193-196
• Periodontal Medicine..Rose Mealey Genco
• Perio 2000, vol 61,2013
• Patricia R Cury et al: hydrocortisone affects the expression of MMP-1,2,3,7,11 and tissue
inhibitor of matrix metalloproteinases TIMP-1 in human gingival fibroblasts: J
Periodontol 2007: 78: 1309-1315
• Peruzzo et al. Systemic review of stress and psychological factors as possible risk factors
for periodontal disease. J Periodontol 2007: 78: 1491-1504

58. • Frankenthal S et al: the effect of the secondary hyperthyroidism and
hemodialysis therapy on alveolar bone and periodontium: J Clin Periodontol
2002: 29: 479-483
• Barros et al: parathyroid hormone protects against periodontitis associated
bone loss: J Dent Res 2003: 83: 791
• Marriotti A: Sex steroid hormones and cell dynamics in the periodontium. Crit
Rev Oral Biol Med 1994:5:27-53

59. • Lindhe et al : influence of sex hormones on gingival exudation in dogs with chronic
gingivitis: J Periodontol Res: 3 :279-283
• Kumare et al: sex and the subgingival microbiome: do female sex steroids effect
periodontol bacteria Perio 2000: 2013: 103
• Shiau, Reynolds: sex differences in destructive periodontal disease: exploring the
biologic basis. J Periodontol 2010: 81: 1505-1517
• Mariotti AJ. Estrogen and extracellular matrix influence human gingival fibroblast
proliferation and protein production. J Periodontol 2005: 76: 1391-1397