ENDOCRINOLOGY

IN ORTHODONTICS

DR . HIBA ABDULLAH
DEPT. OF ORTHODONTICS AND DENTOFACIAL ORTHOPAEDICS
JSSAHER
Contents:
 INTRODUCTION
 CLASSIFICATION OF HORMONES
 FUNCTION OF HORMONES
 MECHANISM OF ACTION
 HORMONE SECRETION , TRANSPORT , & CLEARANCE FROM THE BLOOD
 ROLE OF HORMONE IN ORTHODONTICS
 GROWTH HORMONE
 INSULIN
 THYROID HORMONE
 PARA THYROID HORMONE
 CALCITONIN
 VITAMIN-D
 ADRENAL GLANDS HORMONE
 PROSTAGLANDINS
 ESTROGEN
 ARTICLES RELATED
 CONCLUSION
 Introduction:
• The activities of various organs in our body are controlled by two
systems - nervous system and endocrine system.

• The endocrine system constitutes endocrine glands which is

situated in different parts of body.

• The functions of these glands are mediated by chemical

substances which are called chemical messengers or chemical
mediators or first messengers or hormones.

• The endocrine glands are also called as ductless glands because

the hormones secreted by them are directly release into blood.
• In June 1905, Ernest Starling, a Professor of Physiology at University college London,
UK, first used the word ‘hormone’.

• Starling(1905) defined the word, derived from the Greek meaning ‘to arouse or excite’,
as “the chemical messengers which speeding from cell to cell along the blood stream,
may coordinate the activities and growth of different parts of the body”.

• Hormones have an important influence on the rate of tooth movement, and

information on their consumption is essential to adequately discuss treatment
planning with patients.

• This is especially important in dentistry because many of the patients attending dental
clinics face stressful situations. Awareness is therefore necessary on the risks and
difficulties that may arise during the dental and orthodontic management of patients
with endocrine disorders and most common oral manifestations.
 Classification of Hormones:

• Catecholamines • Post . pituitary • Glucocorticoids • Act by binding to intracellular

• Mineralocorticoids receptor & mediate their actions
(epinephrine & hormone
• Sex steroids via formn of hormone receptor
norepinephrine) ( antidiuretic
• T4 & T3 • Vit D complex
hormone &
oxytocin) • Eg : steroid retinoid & thyroid
• Insulin hormones
• Glucagon • They involves second messengers to
• parathormone mediate their effect.
• Further divided to 4 subgroups
FUNCTIONS OF HORMONE :
1. Regulation of biochemical reactions by:
 Stimulate / inhibit the rate and magnitude of biochemical reactions by controlling enzymes
causing morphologic, biochemical and functional changes in target tissues.
 Modulate energy producing processes and regulate circulatory levels of energy-yielding
substances( eg: glucose ,fatty acids, etc)

2. Regulation of bodily processes:

 GROWTH
 MATURATION
 DIFFERENTIATION
 REGENERATION
 REPRODUCTION
 BEHAVIOUR
• thus maintaining homeostasis in an internal environment.
MECHANISM OF ACTION
Based upon chemical nature of second messengers:

*ANF- Atrial natriuretic peptide *PDGF- parathyroid hormone

HORMONE SECRETION,
TRANSPORT, AND
CLEARANCE FROM THE
BLOOD
Hormone Secretion After a Stimulus and
Duration of Action of Different Hormones:
• Some hormones, such as norepinephrine and epinephrine,
are secreted within seconds after the gland is stimulated and
may develop full action within another few seconds to minutes

• the actions of other hormones, such as thyroxine or growth

hormone, may require months for full effect.

• Thus, each of the different hormones has its own

characteristic onset and duration of action—each tailored to
perform its specific control function.
Concentrations of Hormones in the Circulating
Blood and Hormonal Secretion Rates:
• concentrations of hormones in the blood range from as
little as 1 picogram (which is one millionth of of a gram) in
each milliliter of blood up to at most a few micrograms (a
few millionths of a gram) per milliliter of blood.

• Similarly, the rates of secretion of the various hormones

are extremely small,
• usually measured in micrograms or milligrams per day.
REGULATION OF HORMONE SECRETION
(1) Direct control :
• Hormone secretion is regulated by blood concentration of the
substances which are directly controlled by the hormone
themselves.
• Example:
Insulin secretion from pancreatic β-islets of Langerhans is
promoted by a rise in blood glucose level and glucagon
secretion from α- cells by a fall in blood glucose level.
These responses keep the blood glucose levels within narrow
limits inspite of variations in carbohydrate intake in the diet.
(2) Nervous control:
• Hormonal secretion from endocrine glands is largely controlled by
the CNS.
• It occurs by three mechanisms:
I. Direct innervation via ANS
II. Neurosecretory neurons control of the posterior pituitary
III. Neurosecretory neurons control of the anterior pituitary
FEEDBACK CONTROL OF HORMONE SECRETION:

 Negative Feedback Prevents Overactivity of Hormone Systems.

 Surges of Hormones Can Occur With Positive Feedback.

*TRH:thyrotrophin releasing hormone, *CRH: corticotrophin releasing hormone ,

Cyclical Variations Occur in Hormone Release:
• Superimposed on the negative and positive feedback control of
hormone secretion are periodic variations in hormone release that are
influenced by seasonal changes, various stages of development and
aging, the diurnal (daily) cycle, and sleep.

• Eg: secretion of growth hormone is markedly increased during the

early period of sleep but is reduced during the later stages of sleep.

• In many cases, these cyclical variations in hormone secretion are due

to changes in activity of neural pathways involved in controlling
hormone release.
 Measurement of Hormone Concentrations
in the Blood :
• hormones present in the blood are as low as one billionth of a milligram
(1 picogram) per milliliter.

• Therefore, it was difficult to measure these concentrations by the usual

chemical means.
• An extremely sensitive method that was developed about 50 years ago
revolutionized the measurement of hormones, their precursors, and
their metabolic end products. This method is called radioimmunoassay.

• More recently, additional methods, such as enzyme-linked

immunosorbent assays, have been developed for accurate
measurements of hormones.
TRANSPORT OF HORMONES IN THE BLOOD:
• Water-soluble hormones (peptides and catecholamines) are
dissolved in the plasma and transported from their sites of
synthesis to target tissues ,
where they diffuse out of the capillaries, into the interstitial
fluid, and ultimately to target cells.

• Steroid and thyroid hormones, in contrast, circulate in the blood

while being mainly bound to plasma proteins.

• Usually less than 10 percent of steroid or thyroid hormones in

the plasma exist free in solution.
• However, protein-bound hormones cannot easily diffuse across the
capillaries and gain access to their target cells and are therefore
biologically inactive until they dissociate from plasma proteins.

• The relatively large amounts of hormones bound to proteins serve

as reservoirs, replenishing the concentration of free hormones
when they are bound to target receptors or lost from the circulation.

• Binding of hormones to plasma proteins greatly slows their

clearance from the plasma.
Clearance of Hormones From the Blood :

Two factors can increase or decrease the concentration of a hormone

in the blood

Rate of secretion Rate of removal of

into the blood hormone from blood
(Metabolic clearance rate)
expressed in terms of the number of milliliters of
plasma cleared of the hormone per minute
• To calculate this clearance rate, one measures
(1) The rate of disappearance of the hormone from the plasma
(e.g., nanograms per minute)
(2) The plasma concentration of the hormone (e.g., nanograms
per milliliter of plasma). Then, the metabolic clearance rate is
calculated with use of the following formula:

Metabolic clearance rate = Rate of disappearance of

hormone from the plasma/Concentration of hormone
Hormones are “cleared” from the plasma in several ways,
including
(1) metabolic destruction by the tissues.
(2) binding with the tissues.
(3) excretion by the liver into the bile.
(4) excretion by the kidneys into the urine.
HORMONE RECEPTORS AND MECHANISM OF ACTION :
 All hormones acts through specific receptors which are large proteins
present in hormone sensitive target cells.
• CHARACTERISTICS OF HORMONE RECEPTORS:
1. RECEPTOR SPECIFICITY
2.CHANGE IN RECEPTOR NUMBER
 No. of receptors vary according to different situations
 It is regulated by 2 mechanisms:
A. DOWN REGULATION B. UP REGULATION

o Refers to decrease in o Increase in number of

number of active receptors active receptors on a cell
o Occurs to regulate hormone o Occurs to regulate hormone
sensitivity when present in action when its
excess concentration is less
 MECHANISM
OF ACTION OF
HORMONES

via CHANGE IN via EFFECT ON via TYROSINE

via SECOND
MEMBRANE GENE KINASE
MESSENGERS
PERMEABILITY EXPRESSION ACTIVATION
1. Action through change in membrane potential :

Opening and Movement of

Hormones bind Conformational
closing of ion ions causes
with extracellular changes in
channels( Na+,K+, subsequent
receptors protein receptors
Ca2+ channels) target effect

*adrenaline, noradrenaline acts by this mechanism

2. Action through effect on GENE EXPRESSION :

• Hormone carried to target tissue on serum-

1.TRANS
PORT binding protein

• Lipophilic hormone diffuses through plasma

2.INTER
NALIZAT
ION
membrane

3.RECEP
• Hormone binds to specific receptor inside
the cell( forms RHC)
TOR-
HORMO
NE
COMPL
EX

*RHC- Receptor Hormone Complex

4.CONFO
• Occurs in the receptor protein leading to its activation
RMATIO
NAL
CHANGE

5.ACTIVA
TED R-H
• Activated RHC diffuses into nucleus and binds to specific
COMPLE
X
DIFFUSE
areas on DNA (HRE) and initiates gene transcription
INTO
NUCLEU
S

• Binding of RHC alters rate of transcription of messenger

6.BINDIN
G OF R-H
COMPLE
X TO
RNA
DNA

• And promotes translation at the ribosomes to produce

7.mRNA
diffuses
into
cytoplas
specific proteins
m

*HRE-Hormone Responsive Element

• Group I hormones such as steroids, retinoids and thyroid
hormones acts by this mechanism
 3. Action through SECOND MESSENGERS

GROUP II hormones acts exclusively via second messengers

It is mediated by GTP binding proteins called G proteins. Then coupling of Gproteins which lead to changes in
the cellular concentration of secnd messengers . Secnd messenger system that are activated through coupling
of HRC . Like Adenyl cyclase – C amp , guanyl cyclase C gmp calcium- calmodulin system.
4. Action via TYROSINE KINASE activation

GROUP II-D hormones such as insulin, growth hormone ,etc

acts via this mechanism
Activation of tyrosine kinase can occur by two mechanisms

Hormone receptors Hormone receptors NOT

possessing intrinsic possessing intrinsic
tyrosine activity tyrosine activity
ROLE OF HORMONES IN ORTHODONTICS:
(1) Growth Hormone:
• GH is a protein hormone, secreted by the acidophils of the anterior pituitary gland.

• GH secretion is pulsatile, secretory bursts occurring especially at early hours of sleep and
throughout the night.

• Craniofacial development is hampered and leads to immature facial appearance, small facial dimensions
and profile convexity.

• GH has no specific target organ. It is an anabolic hormone to which every organ system responds.

• Apparently, it has no direct action upon bones, acting through a substance called somatomedin.

• GH stimulates the liver to secrete somatomedin and is the main regulator of childhood and
adolescent growth.
• Cephalometric analysis in males reveals an increased posterior facial height, short cranial
base, mandibular length, total facial height and a retrognathic facial type

• In addition, the mandibular ramus heights and corpus lengths have also been found to be
reduced

• Females were found to have short anterior and posterior cranial base lengths and
mandibular ramus heights

• patients treated with growth hormone replacement therapy have significant improvements
in overall facial dimensions with improved mandibular ramal and basal lengths

• orthodontic intervention did not contribute to significant improvements in the craniofacial

skeleton and plays a greater role in alleviating dental malocclusion due to micrognathia
Growth Hormone Effect on Cartilage and Bone Growth:

(1) Increased deposition of protein by the chondrocytic and osteogenic

cells that cause bone growth.
(2) Increased rate of reproduction of these cells.
(3) A specific effect of converting chondrocytes into osteogenic cells,
thus causing deposition of new bone.
Growth Periods
• Two periods of rapid growth occur the first in infancy and the second in late puberty
just before growth stops
.
• The first period of accelerated growth is partly a continuation of the fetal growth
period.

• The second growth spurt, at the time of puberty, is due to growth hormone,
androgens, and estrogens, and
the subsequent cessation of growth is due in large part to closure of the epiphyses
by estrogens

• Since girls mature earlier than boys, this growth spurt appears earlier in girls.

• It is interesting that at least during infancy, growth is not a continuous process but
is episodic or saltatory.
 Catch-Up Growth

• Following illness or starvation in children, A

period of catch-up growth takes place during
which the growth rate is greater than normal.

• The accelerated growth usually continues until

the previous growth curve is reached, then
slows to normal.
• The mechanisms that bring about and control
catch-up growth are unknown.
Growth curve for a normal boy who had an illness beginning at age 5 and ending at ag
7. Catch-up growth eventually returned his height
to his previous normal growth curve.
Effects of Growth Hormone on Craniofacial Growth:

Growth Hormone Deficiency:

• The length and depth of the face are inappropriately small for the
child’s age, with the face maintaining childlike convexity.

• Many studies have reported mandibular total length (Gn-Cd) is

reduced, primarily as a result of the small ramus height (Cd- Go).

• In addition, the maxilla is significantly reduced, and there may be

a comparable degree of reduction in the mandible. The maxilla is
often retrognathic but is affected less than the mandible.
*Gn – gonion *Cd - condylion
• Concerning cranial base size, many studies have reported that
the posterior cranial base length is smaller than the anterior
cranial base (N-S) length.

• By contrast, facial convexity decreases with GH replacement

therapy, and its main effect seems to be on condylar growth.

• Cantu et al found that catch-up growth with GH therapy affects

the anterior facial height, posterior facial height, and posterior
cranial base.
PITUITARY DWARFISM:
 Diminished production of GH by the anterior pituitary gland or reduced capacity of the tissues to GH

 CLINICAL FEATURES
 Short stature

 Face is small

 Exception is seen in skull size which is usually normal

 ORAL CHANGES
 Maxilla and mandible are smaller

 Size of teeth is reduced in proportion to other anatomic structures

 Teeth show a delayed pattern of eruption,

 Shedding of deciduous teeth is delayed by several years

 Root development of permanent teeth is also delayed

 Lack of development of third molars

 Radio immunoassay for GH shows levels that are markedly below normal
Hyper secretion of Growth Hormone
GIGANTISM
This is caused due to the increased production of GH usually related
to a functional pituitary adenoma.
Increased production takes place before the closure of the epiphyseal
plate and the affected persons grows at a much more rapid pace.
CLINICAL FEATURES
Extreme height (7 ft tall)
ORAL CHANGES
Enlargement of facial soft tissues
Enlargement of the mandible
True generalized macrodontia
 ACROMEGALY
 Excess production of GH after the closure of the epiphyseal
plate in the affected patient. Usually due to functional pituitary
adenoma.
• CLINICAL FEATURES
Renewed growth in the small bones of the hands and feet and in
the membranous bones of the skull and jaws
Soft tissue is affected producing a coarse facial feature
• ORAL CHANGES
Hypertrophy of the soft tissues of the palate which may cause or
accentuated sleep apnea
Mandibular prognathism as a result of increased growth of the
mandible which may cause Apertognathia (anterior open bite)
Growth of the jaws may cause spacing of the teeth and lead to
Diastema formation
Soft tissue growth often causes macroglossia
 Effect on Dental Development :
• Dental delay is always less pronounced than height or bone
delay.

• Dentition seems to be harmoniously delayed, so that all

studied components of dental development (primary root
resorption, secondary tooth formation and eruptive
movement) display the same degree of retardation

• GH influence on growth starts after 9 months of age, so that

the effect on the growth of primary teeth is very little known.
*Angle Orthodontist, Vol 76, No 6, 2006
(2) Insulin:
• Insulin is a polypeptide hormone secreted by the beta cells of the Langerhans islets
of the pancreas.

• A normal non-obese man secretes approximately 50U/day, with a basal plasma

insulin concentration of 10-50 microns/ml.

• Its main function is to maintain the blood glucose level. Insulin deficiency produces a
clinical state called diabetes mellitus, while its excess leads to hyperglycemia.

• Diabetes Mellitus (DM) is an endocrine disorder characterized by a triad of hyperglycemia,

increased micturition and thirst

• If left uncontrolled or untreated, acute complications such as diabetic ketoacidosis and non-
ketotic coma can occur. Long term chronic complications include cardiac stroke, renal failure,
foot ulcers and eye damage

• Diabetes mellitus is diagnosed in 3-4% of the population treated in day-to-day

orthodontic practice.
• . There are two main categories of DM:
• Type 1 DM (insulin‑dependent diabetes mellitus or juvenile‑onset diabetes)
results from defects in insulin secretion.
The onset is usually before adulthood and accounts for approximately 5%–15%
of all people with DM
• Type 2 DM (noninsulin‑dependent or mature‑onset diabetes) develops as a
result of defects in insulin secretion, insulin action, or both.
There is a link with being overweight.
Type 2 DM usually appears in people over the age of 40, although in South
Asian and African‑Caribbean people, it often appears after the age of 25

Recent studies have been reported that there are three types,
• Type III which has been proposed for Alzheimer’s disease where there is
insulin resistance in the brain
Orthodontic Considerations:
• No orthodontic treatment should be performed in a patient with uncontrolled diabetes.

• A good oral hygiene is especially important when fixed appliances are used, as they may
increase plaque retention, which could more easily cause tooth decay and periodontal
break‑down.

• The orthodontist should educate patients about the potential side effects associated
with orthodontic treatment. This may include microangiopathies that may cause the
patient to experience iatrogenic odontalgia, sensitivity, pulpitis or in rare cases loss of
tooth vitality

Especially in orthodontic treatments involving force application for moving teeth over a
considerable distance, the practitioner should regularly check the vitality of the teeth
involved. It is advisable to apply light forces and not to overload the teeth.
• orthodontic team should be trained to deal with diabetic emergencies.
Hypoglycemia is characterized by initial signs of tremor, nausea, sweating,
anxiety, tachycardia, palpitations, and shivering
• Conscious 50 g of glucose as a drink, tablet, or gel has to be given
• Unconscious 20 ml of 50% Dextrose IV or 1 mg of glucagon should be
administered intramuscularly
• When the patient is cooperative, oral glucose should be given to prevent
recurrent hypoglycemia. If recovery is delayed, the emergency services should be
called.
• In adults, before starting the orthodontic treatment, the orthodontist should
obtain a full-mouth (periodontal) examination and evaluation of the need
for periodontal treatment.
• Patients should be advised to take the medicines prescribed by their
diabetologist. Patients should be appointed in the morning hours and
advised to take their usual meal and medications before arriving at the
dental clinic.
(3) Thyroid Hormone:
Hormones secreted by the thyroid gland maintain physiological
functioning of the brain, heart and various muscles, whereas
altered thyroid function may affect functioning of these organs.
Orthodontic Considerations:
• Orthodontic therapy should be instituted in patients with adequately
managed thyroid disease.

• Children with hypothyroidism have dental characteristics such as delayed

tooth eruption, enamel hypoplasia and anterior open bite

• Abuabara reported an increased risk of external apical root resorption

related to hypothyroidism due to low bone turnover.

• Children with hyperthyroidism may suffer from accelerated tooth eruption,

macroglossia and maxillary and mandibular osteoporosis.
• Thyroxin administration lead to increased bone remodeling, increased bone
resorptive activity, and reduced bone density.

• Treatment procedures such as banding and bonding should have brief

appointments and stress management is important for patients who have
hyperthyroidism. Banding should be avoided especially on molars, and
bondable molar tubes can be placed

• The speed of orthodontic tooth movement increases in patients undergoing

such medication. Low-dosage and short-term thyroxin administrations are
reported to lower the frequency of “force induced” root resorption.
• Treatment should be discontinued if signs or symptoms of a thyrotoxic crisis develop
and access to emergency medical services should be available

• After treatment, it is important that patients continue taking their thyroid medication
as prescribed

• • Excessive radiation exposure should be avoided. Thyroid collar should be used while
taking patient X‑rays.
Conclusion:
It seems that the combination of
thyroxine and prostaglandin E2, with a
synergistic effect, would decrease the
root resorption and increase the rate of
orthodontic tooth movement in rats.
(4)Parathyroid Hormone(PTH) :
Parathyroid hormone provides a powerful mechanism for
controlling extracellular calcium and phosphate concentrations.
Hyper function of Parathyroid glands Hypo function of Parathyroid glands
Orthodontic considerations:
• Parathyroid hormone, as a major regulator of calcium and phosphate homeostasis,
has gained particular attention for its paradoxical effects on bone metabolism.

• Relative studies have confirmed that parathyroid hormone could stimulate both
osteoclast-mediated bone resorption and osteoblast-mediated bone formation,
therefore accelerating the bone turnover rate.

• Continuous infusion of parathyroid hormone results in, catabolic effect whereas

intermittent injection leads to an anabolic effect.

• Systemic continuous infusion or local chronic application of parathyroid hormone

could accelerate tooth movement through enhancement of alveolar bone
resorption.

• Under intermittent parathyroid hormone administration, both osteoblast and

osteoclast activities are stimulated.
Conclusion:
Mandibular ramus osteotomy
combined with high-dose PTH
can increase catabolism on the
compressed periodontal tissues,
thereby accelerating remodeling
of periodontal bone and
promoting orthodontic tooth
movement after surgery.
(5)Calcitonin :

• Calcitonin, a peptide hormone secreted by the thyroid gland,

tends to decrease plasma calcium concentration and, in
general, has effects opposite to those of PTH.

• However, the quantitative role of calcitonin is far less than that

of PTH in regulating calcium ion concentration.

• Synthesis and secretion of calcitonin occur in the parafollicular

cells, or C cells, lying in the interstitial fluid between the follicles
of the thyroid gland.
Increased Plasma Calcium Concentration Stimulates Calcitonin
Secretion:
• The primary stimulus for calcitonin secretion is increased plasma calcium ion
concentration.

• This provides a second hormonal feedback mechanism for controlling the plasma
calcium ion concentration.

• Calcitonin inhibits proximal tubular calcium and phosphate reabsorption by direct

action on kidney.

• Calcitonin is used in the treatment of hypercalcemia, osteoporosis and Paget’s

disease of bone.
Effects of Calcitonin on bone and tooth movement:
• Calcitonin inhibits bone resorption by direct action on
osteoclasts decreasing their ruffled surface which forms contact
with resorptive pit.

• It also stimulates the activity of osteoblasts.

• Because of its physiological role, it is considered to inhibit the

tooth movement, consequently delay in orthodontic treatment
can be expected
Vitamin D :
• Vitamin D has a potent effect to increase calcium absorption
from the intestinal tract; it also has important effects on both
bone deposition and bone absorption.
Vitamin D deficiency:
Bone formation is a series of events involving the deposition of osteoid which is later mineralized.
During new bone formation, the failure of the mineralization leads to Rickets
. Bone remodeling brings about change in existing bone and a failure of remineralization in this
process is known as osteomalacia.

Rickets
Orthodontic Considerations :
• Hypophosphatemic vitamin D resistant rickets with 1-α hydroxylase deficiency may
present with muscle weakness, seizures and tetany.

• Dental manifestations include hypoplastic enamel that has yellow to brown

discoloration, defective dentin mineralization, gingivitis and periodontitis.

• Radiographic features include large tooth pulp chambers and shortened roots.

• Vitamin-D3, together with parathyroid hormone and Calcitonin, regulate the amount of
calcium and phosphorus in the human organism

• . It promotes intestinal Ca+2 and PO4-3 absorption. Vitamin- D3 increases bone mass
and thus reduce fractures in osteoporosis patients. Considering its beneficial effects on
bone tissue, it may be assumed that it inhibits tooth movement.
• Nutritional supplementation has been recommended for infants,
children and pregnant females.

• Early diagnosis of this condition is required to prevent the

development of adverse effects.

• Patients with the x-linked disorder are advised good oral hygiene and
may require dental restorations such as crowns.
(6)ADRENAL GLANDS HORMONES:
 Situated on either side at the
• Upper pole of kidney( suprarenal gland)
 Weighs about 5g and consists of
• 2 parts:
• Outer cortex (80-90%)
• Inner medulla ( 10-20%)
Orthodontic Considerations :
• Main effect of corticosteroids on bone tissue is direct inhibition of osteoblastic function and thus the
decrease of total bone formation.

• Corticosteroids increase the rate of tooth movement, and since new bone formation can be difficult in
treated patients, they decrease the stability of tooth movement and stability of orthodontic treatment in
general.

• Short term steroid administration leads to reduced bone turnover and a decrease in orthodontic tooth
movement.
In contrast, long term steroid administration hastens bone turnover leading to increased orthodontic tooth
movement.

• Short term administration is favorable in cases of areas with increased anchorage requirement. Patients
undergoing long term steroid administration should be recalled at a two week interval due to chances of
rapid orthodontic tooth movement.

• Use of a stress reduction protocol and profound local anesthesia minimizes the physical and psychological
stress associated with therapy and reduces the risk of acute adrenal crisis. Hydrocortisone 200 mg (IV/IM
immediately preoperatively or orally 1 h preoperatively) and continue normal dose of steroids
postoperatively
The results from the present study
provide evidence that emotional
stress is also associated with
orthodontic tooth movement.
Animals subjected to stress and
experimental orthodontic
treatment demonstrated reduced
amounts of tooth movement when
compared with controls and non-
stressed orthodontically treated
animals. They also showed the
greatest amount of root resorption
throughout the experimental
period.
(7)PROSTAGLANDINS:

 These are paracrine hormones, i.e. they act only on cells near the point of hormone synthesis
 group of chemical messengers belonging to a family of hormones called eicosanoids
 The three major classes of eicosanoids are prostaglandins, thromboxanes and
leukotrienes.
 Prostaglandins act in many tissues by regulating the synthesis of cyclic AMP.
 As cyclic AMP mediates the actions of diverse hormones, prostaglandins affect a wide range of
cellular and tissue functions:
(1) They affect blood flow, sleep cycle and
response to hormones such as adrenaline
and glucagon.
(2) They elevate body temperature, cause
inflammation and pain.
(3) They stimulate contraction of the smooth
muscle of the uterus
Prostaglandins and orthodontics:
PGs act by increasing the number of osteoclasts, and by promoting
the formation of ruffled borders, thereby stimulating bone
resorption.
Among the PGs that had been found to affect bone metabolism (E1,
E2, A1, and F2-alpha), PGE2 stimulated osteoblastic cell
differentiation and new bone formation, coupling bone resorption in
vitro.
Yamasaki and associates were among the earliest researchers to
investigate the role of prostaglandins in bone resorption associated
with orthodontic tooth movement
Conducted experiments on rats to investigate whether the synthesis
of prostaglandins is induced by orthodontic force, and whether
exogenous prostaglandins can produce bone resorption similar to
orthodontic force.
Conclusion:
1. orthodontic mechanical stress induces the synthesis of PGs by
localized cells, which stimulate osteoclastic bone resorption.
2. Administration of indomethacin, a specific inhibitor of PGs
synthetase, suppressed the appearance of osteoclasts and alveolar
bone resorption that was induced by experimental tooth movement.
Am. J. Orthod., 1984, 85, 508–518.
(8)ESTROGENS:

Estrogen is considered the most important hormone affecting

bone metabolism in women
Inhibits the production of cytokines involved in osteoclastic
activation and bone resorption, such as interleukin-1, tumor
necrosis factor-A
Controls bone remodeling during reproductive life, and
maintenance of maximum bone mass after menarche.
Effect on tooth movement :
• Estrogen inhibits tooth movement by increasing the bone mineral
content and bone mass and by reducing the bone resorption rate.
• Several studies have shown that estrogen deficiency accelerated
tooth movement .
• Estrogen directly stimulates the bone-forming activity of osteoblasts,
so it is reasonable to expect a decrease of the velocity of orthodontic
tooth movement.
• Androgens also inhibit bone resorption and modulate the growth of
the muscular system. Thus, the excessive use of these drugs by
athletes, in an attempt to achieve better athletic scores, may affect
the length and the results of orthodontic treatment.
 It thus can be indicated that the bone
protective effects of estrogen
mentioned may have restraining
effects on OIRR because of the
reduction of bone resorption factors
and differentiation of odontoclasts
and cementoclasts.

*OIRR – orthodontic induced root resorption

CONCLUSION:
• The success of orthodontic treatment lies in identifying the patient’s
needs and concerns and addressing them with the best hardware at
an orthodontist’s disposal. For achieving timely orthodontic
correction, it is imperative that the patient is either disease free or
the disease is in a controlled state. It is essential to understand the
basics of human physiology and the interaction between medicine
and orthodontic science to provide the best treatment outcome with
the least undesirable side effects.
• In the current era, more adults are seeking orthodontic treatment
than before and this age group is affected by complicated medical
conditions and their corresponding drug regimens. A prompt medical
and drug history of the patient allows the orthodontist to know their
patient and focus not only on the dentition and facial esthetics but
also the patient’s overall systemic health
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• Textbook of Medical Physiology – GUYTON AND HALL , 13th Edition.
• Human physiology – Indu khurrana
• BERNE & LEVY PHYSIOLOGY
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JMSCR 2016 VOLUME 04 ISSUE 06 JUNE.
• Endocrine Disorders and their Effects in Orthodontics Sunil Kumar KHARE
et al 2013 VOLUME 17 ISSUE 4 OCTOBER.
• The Implications of Endocrinology in Orthodontics- Literature Review
Adeel Tahir Kamal et al Balk J Dent Med 2020;8-13.
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Dental Journal (2013) 24(5): 503-507.
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76, No 6, 2006
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Sarah MG Braga et al, Eur J Oral Sci 2011;119:7-14.
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on Orthodontic tooth movement and root resorption in rats, Massoud
Seifi et al, J Dent(Shiraz) 2015 Mar;16(1 suppl):35-42.
• Differences in accelerated tooth movement promoted by recombinant
human parathyroid hormone after mandibular ramus osteotomy, Yao Li
et al, Am J Orthod Dentofacial Orthop 2019 May;155(5):670-680.
• Effects of Calcitonin on orthodontic tooth movement and associated
root resorption in rats, Ling Guan et al, ACTA Odontologica
Scandinavica,2017.
• The local use of Vitamin D to increase the rate of orthodontic tooth
movement, Monte K.Collins et al, Orthod Dentofac Orthop 1988;94:278-
284.
THANK
YOU