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1. Malocclusion and endocrinal disturbances
INDIAN DENTAL ACADEMY
Leader in continuing dental education
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2. Contents
Introduction
Pituitary gland
Thyroid gland
Parathyroid gland
Adrenal gland
Pancreatic hormone -insulin
Sex hormones
Role in the etiology of malocclusion
Role during orthodontic tooth movement
Role after orthodontic treatment
Conclusion
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3. Endocrine glands
These are the glands which secrete their products into the
interstitial fluid surrounding the secretory cells rather than into
ducts.So they are known as the ductless glands.
-
The secretions called the hormones diffuse into capillaries and the
blood carries them away to the site of action.
Required in very small amounts.
Several organs and tissues not endocrine glands exclusively but
contain cells that secrete hormones-the hypothalamus,thymus
pancreas,liver,stomach,git,skin ,heart,ovaries,testes,placenta.
Nomenclature
Classical hormones-thyroid,parathyroid,adrenals,hypophyseal
Ovarian,testicular
Local hormones-
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4. Local hormones-
They act locally on neighbouring cells or on the same cell that
secreted them without entering the blood stream.
Paracrine-on neighbouring cells.
Autocrine-on the same cell.
Chemical nature
-steroid hormones…corticosteroids and sex hormones
-protein hormones…pituitary,parathyroid and the pancreas.
-derivatives of tyrosine…thyroid,adrenal medullary hormones.
Chemical classes
-lipid soluble…steroid and the thyroid
-water soluble…peptide hormones,catecholamines
and all pituitary hormones.
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5. Control of hormone secretion-
Hormones are one of the fundamental agents of achieving
homeostasis.Exactly that much hormone is released for
circulation which is needed by the body neither more or less .
That is only the eustate of secretion is permitted, not the hyper or
hypo secretion when the healthy stable state is maintained.
There are 2 feedback mechanisms-
negative feedback
positive feedback
Hormone secretion is regulated by
-chemical changes in blood
-signal from the nervous system
-other hormones
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6. HYPOTHALAMO-HYPOPHYSEAL PORTAL SYSTEM
Vascular connection that exists between the hypothalamus and
the anterior pituitary is a portal system i.e starts in the
hypothalamus as capillaries and ends in the anterior pituitary as
capillaries.
Many hormones called the hypothalamic releasing hormones are
produced by the hypothalamic neurons which enter the capillaries
of the hypothalamus and reach the capillaries at the level of the
anterior pituitary.They then come out of the blood vessels to
enter the cellular masses of the anterior pituitary..
In this way a forward flowing blood flow of hypothalamic
hormones reach the anterior pituitary and either inhibit or
stimulate their cells..
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8. PITUITARY GLAND
Hypopituitarism- deficient secretion of the anterior lobe of the
pituitary..
In infancy ---pituitary dwarfism,lorain levy syndrome,infantilism
In adults ---simmonds disease.
Hyperpituitarism- an excessive secretion of the anterior lobe of
the pituitary
Gigantism ---excessive growth hormone before the union of the
epiphyseal plates
Acromegaly ---excessive growth hormone secreted after the
fusion of epiphyseal plates
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9. Pituitary insufficiency in children
DWARFISM,INFANTILISM
-rare,congenital,reduced production of growth hormone or a
reduced capacity of the tissues to respond to growth hormone.
-affected patients are much shorter than normal.(3 feet)
-body proportions are generally appropriate.
-deficiencies in other hormones such as thyroid and cortisol are
also detected in patients with primary pituitary disorders.
-when sexual development is subnormal for the patient’s age the
term infantilism is often used.
-mental status is normal.
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10. Dental manifestations
-the size of the skull is within normal limits…but as the facial
skeleton does not keep pace with the skull the face is usually
smaller than normal.
-maxilla and mandible are smaller in both length and vertical
dimensions
-teeth are normal in size suggesting that they have separate genetic
determinations.
-teeth show delayed patterns of erruption.the delay of erruption
ranges from 1-3 yrs for teeth that normally errupt during the
1st decade of life and from 3-10 yrs for teeth that normally errupt
in the 2nd decade of life.
-Shedding of deciduous teeth delayed by several years.
-development of the roots of the permanent teeth are also delayed.
-third molars also show lack of development.
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11. Studies by kosowicz ,rzymski(ooo 44:853,1977) showed delayed
shedding of the deciduous teeth,marked delay in the erruption of
permanent teeth and their retention in maxillary and mandibular
shafts..underdevelopment of the apical parts of the roots of the
retained teeth.
Studies by salzmann and stanley(ajo,38:1952) cited the following
Features –abnormally dense calcifications of dentine
-small sized roots,parallel pulpal walls,retardation in
closure of apical foramen,wide pulps.
-tendency towards deep bite as there is deficiency of
vertical development of the face
-crowding of teeth is not pathognomonic .
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12. Pituitary insufficiency in adults
SIMMONDS DISEASE
-rare condition in adult females
-striking features of atrophy of most of the viscera,low bmr,loss of
hair,pale , dry and coarse skin.
-there is rapidly developing senile decay,due to which a 30yrold
may look like a 60yr old.
-there are no significant oral or dentofacial changes.
-also called pituitary cachexia.
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13. Hyperpituitarism
GIGANTISM
-rare condition,abnormally tall individuals.
-the individuals who exceed the mean height by more than 3 sd
may be considered candidates for endocrinologic evaluation.
-markedly accelerated growth during childhood irrespective of
normal growth spurts.
-enlargement of facial soft tissues.
-teeth are usually normal sized.
-structure of teeth are normal though there can be
hypercementosis in older patients.The roots may be longer
than normal..
-radiographic evaluation of the skull often shows an enlarged
Sella as a result of the presence of a pituitary adenoma.
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14. ACROMEGALY
-it is due to excess production of growth hormone after the closure
of the epiphyseal plates in affected patients.
-continued endochondral ossification at the condyle with some
appositional bone deposition results in a prominent growth of the
mandible.
-as the length of the masseter muscle is little changed,there is a
marked increase in the angle of the mandible becoming obtuse 130
degrees.
-in an attempt to keep the teeth in articulation there is continued
alveolar growth and teeth erruption.The arch widens distally and
is connected to the body of the mandible by a thin plate which
exaggerates the prominence of the chin.
-The profound growth occurring in the condyle and ramus results in
a class III skeletal tendency.
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15. -teeth tend to flare out,tilt labially resulting in spacing.
-tongue is increased in size.
-paranasal sinuses are enlarged
-hypertrophy of the soft tissues of the lips,tongue and nose.
-there can be an anterior open bite.
-all these changes produce a simian appearance.
-hypertrophy of the soft palatal tissues may cause sleep apnoea.
-these patients have mandibular prognathism as a result of
increased growth of the mandible which may cause apertognathia.
-the affected enlarged bones are more radio opaque than the normal
-the sella turcica is enlarged when seen on lateral cephalograms.
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19. Studies by ronald e hampton (jada may1997) cited myofacial dys-
function secondary to mandibular overgrowth..the downward and
anterior positioning of the mandible to provide an airway space
and loss of stable occlusion as a result of the enlargement of the
mandible appear to be a contributing factor possibly leading to the
development of a TMJ disorder and myofacial pain.
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20. THYROID GLAND
It stimulates basal metabolism and controls general metabolism
by secreting thyroglobulins directly into the blood stream.
Follicular cells ….t3 and t4
Parafollicular cells … calcitonin
-deficiency of thyroid hormones results in hypothyroidism
infants …congenital hypothyroidism,cretinism
adults …myxedema
-primary hypothyroidism -the thyroid is abnormal
-secondary hypothyroidism-the pituitary does not produce
enough TSH.the thyroid is normal.
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21. Congenital hypothyroidism
-bones of cartilaginous origin.
-cranial base is disturbed and arrested in growth.
-length of cranial base is shortened.
-retardation in the development of tooth buds in the foetus.
Childhood hypothyroidism(CRETINISM)
-manifestations present at birth or within a few months after birth
-skeletal growth is more affected than soft tissues.
-neonatal jaundice,stunted growth with coarse features such as a
broad flat nose,protruding tongue,widely set eyes,sparse hair,dry
skin.
-mentally retarded child.
-skull is brachycephalic.
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23. Dental manifestations
-dental retardation parallels endochondral ossification which is
extremely delayed.
-delay in ossification of tooth buds is more significant.
-Jaws are underdeveloped.
-lips may appear thickened because of the accumulation of glyco-
saminoglycans.
-diffuse enlargement of the tongue occurs for the same reasons.
-the large tongue may cause flaring of teeth.
-the primary dentition may not errupt as late as the 3rd year and
there is a delay in shedding.The 2nd dentition may errupt
alongside the retained deciduous dentition.
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24. JUVENILE MYXEDEMA
-hypothyroidism after 6 yrs and before puberty
-retardation in the normal rate of deposition of ca++ in bones and
tooth buds.
-delayed carpel and epiphyseal calcification.
-disharmonies in the erruption of teeth.
-incomplete unfolding in the nasal area and inadequate
development of the maxilla.
-mesio or disto occlusion of teeth and crowding.
-malposed maxillary and mandibular incisors and canines with
loss of proximal contact.
-irregularities of tooth arrangement and open bite may be present
-prolonged retention of deciduous teeth,permanent teeth are
slow to errupt..
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26. Dental treatment in hypothyroid patients should be carried out
under strict medical supervision.The use of sedatives or analgesics
may prove to be dangerous as these agents tend to precipitate
coma in patients with hypothyroidism.
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27. Hyperthyroidism
-thyrotoxicosis/ graves disease
-it is a condition caused by excessive production of thyroid
hormones.
-signs can be attributed to an increased metabolic rate resulting in
nervousness,heart palpitations,heat intolerance,ocular involvement
-there is alveolar bone atrophy.
-premature shedding of deciduous teeth
-accelerated erruption of permanent teeth
-hyperthyroidism is rare in children,but when it occurs the
primary teeth may be present at birth.
-bones are comparatively fragile.
-osteoporotic condition results in decreased density of alveolar
bone.THIS CONDRAINDICATES ORTHODONTIC
TREATMENT .
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28. -in patients with uncontrolled hyperthyroidism a definite risk
exists with respect to inappropriate release of large amounts of
thyroid hormone at one time.A thyroid storm may be precipitated
by infection,trauma,stress.The clinician should be aware of the
potential for this problem and such patients should ideally have
the condition under control.
- These patients have increased sensivity to epinephrine and are
usually hypertensive. They make very poor dental patients.
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29. PARATHYROID GLAND
-The parathyroid glands secrete the parathormone which maintains
a normal plasma ca++ level (9-11mg/100ml).When this level falls
these glands are stimulated resulting in PTH secretion,and an
increase in this level inhibits PTH secretion and thus a reciprocal
relationship exhibits between them.
-deficiency of PTH leads to hypoparathyroidism.
-normal PTH but defective biochemical pathways results in
pseudohypoparathyroidism/ALBRIGHT HEREDITARY
OSTEODYSTROPHY.
-an increased production of PTH results in hyperparathyroidism
or OSTEITS FIBROSA CYSTICA.
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30. HYPOPARATHYROIDISM
-blood ca++ may fall as low as 7mg/100 ml ,hypocalcemia.
-Tetany is a striking feature of this condition (repeated convulsive
muscular contractions)
-Chvosteks sign – tapping at the angle of the jaw stimulates the
facial nerve resulting in muscle twitching.
-Carpopedal spasm-peculiar spasm of the hand muscles.
Dental manifestations
-can affect the mouth at any stage during tooth development.
-if it develops early in life during odontogenesis a pitting
enamel hypoplasia and failure of erruption may occur.
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31. -If it develops during tooth development,there is delayed erruption
and resorption of the roots of the primary teeth and retarded
erruption of the permanent teeth.
-Enamel defects usually follow tetany,the teeth have a white
appearance but later turn brown due to staining.They are brittle,
show opaque areas and are fractured easily because of poor
calcification.
-large pulp chambers and irregularities of occlusion in permanent
dentition have been reported.
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33. Pseudohypoparathyroidism
-rare condition,is a disorder in which normal PTH is present in
adequate amounts but the biochemical pathways responsible for
activating the target cells are not functioning properly.
-dental manifestations include
-general enamel hypoplasia
-oligodontia
-delayed erruption
-blunting of the apices of teeth
-pulpal calcifications dagger shaped
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34. HYPERPARATHYROIDISM
-excessive production of PTH producing increased blood ca++
levels.
-pathological fractures may be the first sign of the disease.
-a giant cell tumour or cyst of the jaw may be detected on
radiographs.skeletal lesions can be seen in the skull, jaws.
-due to ca++ and po4 disturbance generalised osteoporosis with
abortive attempts at bone repair and new bone formation.The
new bone may be resorbed and the resorption may lead to
Pseudocyst formation,the extent depending on the intensity
and duration of the disease.
-also called the Brown tumours.
-generalised loss of lamina dura surrounding the roots of the teeth
-ground glass appearance can be seen on radiographs.
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39. -in growing children there may be interruption of tooth
development producing marked effect on dentine formation in the
form of deeply stained contour lines,formation of osteodentine and
Osteocementum.
-studies by Silverman,Ware (ooo aug 1968) have revealed dental-
structure changes of loss of lamina dura,giant cell tumors and
demineralization.Involvement of jaw bones appears to be a late
change and the least sensitive indicator of parathyroid overactivity
as compared to hypercalcemia.These are late signs of
hyperparathyroid bone disease which itself is a late complication
of primary hyperparathyroidism.
-teeth tend to become loose,pathological migration is seen.
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40. THE ADRENAL GLAND
The adrenal gland consists of the inner medulla and the outer
Cortex.
Medulla ----adrenaline and noradrenaline
Cortex ----3 classes mineralocorticoids.
glucocorticoids.
sex hormones.
-the major are cortisol,aldosterone ,androsterone.
-these hormones are released under the influence of ACTH from
the anterior pituitary .
-acute adrenocortical insufficiency/Waterhouse Friedrichear
Syndrome.
-chronic insufficiency of the adrenal gland/ADDISONS DISEASE
-hyper functioning of the adrenal gland/CUSHINGS DISEASE
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41. ADDISONS DISEASE
-a chronic insufficiency of the adrenal gland results in this .
-a generalised hyper pigmentation of the skin occurs classically
described as bronzing.
-hyperpigmentation of the buccal or labial mucosa is seen(due to
increased levels of beta-lipoprotein).
-diffuse or patchy brown,grey macular pigmentations of the oral
mucosa can be seen.
-often oral mucosal changes are the first manifestations with skin
hyperpigmentation occuring late.
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43. CUSHINGS DISEASE
-it is due to excessive secretion of glucocorticoids,in particular
cortisol.
-redistribution of fat in the body,water and salt retention leads to
edematous appearance of the face.(moon face)
-extremities of body are thin.
-truncal obesity,facial broadening and periorbital edema.
-decrease in intestinal calcium absorption leads to loss of bone
tissue, osteoporosis and nontraumatic fractures.
-bone becomes susceptible to fracture.
-due to immunosupression ,patients are susceptible for infection.
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45. Pancreatic hormone –insulin
-The endocrine function of the pancreas is performed by the islets
of langerhans which secrete the hormone insulin.
-insulin is the hormone regulating the metabolism of carbohydrates,
fats and proteins.
-it plays a vital role in maintaining the blood sugar level.
-Diabetes mellitus is a condition with elevated blood sugar level
assosciated with other manifestations.
-type 1DM/ JUVENILE DIABETES-absence of beta cells
-insulin dependent
-type 2 DM/MATURITY ONSET -normal level of insulin
-defective insulin receptors
-non insulin dependent
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46. Clinical manifestations
-the usual symptoms are hyperglycemia,polyuria,polydypsia,
polyphagia.
-the progression of diabetes is assosciated with atherosclerosis,
diabetic nephropathy,neuropathy and atherosclerosis.
-oral manifestations include Median rhomboid glossitis,reported
to be prevalent in diabetics.
-other oral conditions that may be exacerbated by diabetes are
gingivitis,periodontal disease,oral candidiasis,localized osteitis
(dry socket)after extraction.
-burning tongue.
-oral candidiasis.
-reasons for the assosciation of diabetes and candidiasis includes
increased genetic susceptibility,altered immune response and
candida colonization in the oral environment.
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47. -regarding measures pertaining to dental treatment the following
should be considered.
-it is advisable to use local anaesthetics without epinephrine in
dental surgical procedures.(epinephrine elevates blood glucose
levels,increases the incidence of dry socket particularly with
mandibular extractions.)
-antibiotic prophylaxis to prevent subsequent infection is
recommended .
-no complicated procedures should be performed in uncontrolled
diabetics.
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49. Studies by Tarek El Bialy,Samir (AJO :118, 2000) have cited
the craniofacial morphology and skeletal maturation in diabetic
juveniles.The results show decreased skeletal maturation,and
decreased linear and angular cephalometric measurements as
compared to the controls.These results should be considered
when diabetics require orthodontic or orthopedic treatement
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50. Sex hormones
-Male sex hormones-there are no specific oral changes seen with
variation in the male sex hormones.
-Female sex hormones-the oral aspects due to variation in these
hormones are as follows.
-the prevalance and severity of gingival disease are increased
in puberty suggesting an exaggerated response of the gingival
tissues to local irritants such as plaque and calculus.
-in pregnancy ,gingival response to local irritants may be
accentuated so as to cause clinical lesions.pregnancy acts as a
modifying factor and is not the cause of gingival pathology.
-tumour like lesions called the pregnancy tumour can also be
observed.
-oral symptoms in menopause are less frequent.commonly
occuring are dry mouth and burning tongue.
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51. Calcium metabolism
Calcium levels are maintained within very small tolerances in
the blood.control of calcium is complicated and involves several
organ systems and multiple hormones.
-control of calcium homeostsis is dependent on PTH .PTH acts
directly on bone,intestine and kidney to conserve calcium.
on kidney –active reabsorption of ca++.
on intestine-PTH stimulates conversion of vit D hormone into the
active metabolite diOHD3.this increases calcium reabsorption.
on bone –the vit D metabolite increases the enzyme activity in the
bone resorbing cells so that more calcium is released.
-this feedback loop of calcium is closed by by the increased conc-
entration of calcium in the bloodstream,which signals the para-
thyroid glands to decrease the PTH secreted.
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52. -calcitonin also plays an important role in maintaining calcium
level.it decreases the blood calcium level and thereby counter
acts the actions of PTH.
BONE
PLASMA
CA++
INTESTINE
KIDNEY
calcitonin
PTH
25 OH D3
1,25 diOHD3
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53. LOCAL HORMONES
-Local hormones are the substances released from tissues or
produced in the blood.
-they are produced in an inactive state and may be activated
under certain conditions and produce some action in the
immediate neighbourhood.
-are classified into 2 types
• Those synthesised in the tissues-prostaglandins
thromboxanes
leukotrienes
prostacyclines
• Those synthesised in the blood – seratonin
bradykinin
angiotensinogen
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54. HORMONES DURING AND AFTER TOOTH MOVEMENT
Studies by Dennis stewart,Paul sherick(Annals N Y Acad Scien
2005) have cited the use of a naturally occurring hormone
Relaxin,to biochemically augment tooth movement and retention.
This hormone is best known to help in relaxing the uterine
muscles during pregnancy by softening the collagen and elastin in
tissues.The collagen and elastin fibres resist the force of
orthodontic treatment applied to move the teeth and when the
force is removed the elasticity of the tissues springs the tooth
back into position.
-the study will test the hormone as an orthodontic therapy and
it is hoped that the drug could cut the treatment time by half and
eliminate the need for retainers after the braces are removed.
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55. -studies by Nicozisis et.al(Clin Ortho Research 2000) have cited
potential indications for the use of relaxin which include instances
of sutural and soft tissue adaptation of orthopedic expansion in
non growing patients by a reduction in tension of the stretched
soft tissues .
-Michael Ashcraft et.al(AJO1992) have studied the effects of
corticosteroid on orthodontic tooth movement and relapse.the
results of their study indicated that subjects with corticosteroid
induced osteoporosis undergo significantly more rapid
orthodontic tooth movement and subsequently less stability
of the final treatment resulting in more amount of relapse.
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56. Shirazi M, Dehpour A R. ( J Clin Pedi Dentistry 1999, spring 23)
have studied the effects of thyroid hormone on orthodontic tooth
movement.Thyroid hormones are major regulators of bone
development and remodelling and changes in thyroid function
are assosciated with alteration in bone metabolism.The administr-
-ation of L-thyroxine showed to reduce bone density which in turn
accelerated orthodontic tooth movement and thereby decreased
force induced root resorption.
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57. -studies by Efstratios (A.O.1994) have studied the relation of
thyroid function and force induced root resorption.
-the study found that thyroxine administration seems to lower the
frequency of root resorption .
-this was due to a decrease in the resorptive lesions ,altered bone
remodelling and different alkaline phosphatase activity
-administration of thyroxine should be considered especially in
some patients who begin to show root resorption or those who
have low thyroid function
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58. Yamasaki K ,Shibata Y.( AJO1984;85) have studied the clinical
application of prostaglandins PGE1,upon orthodontic tooth
movement.It was administered in clinical cases of tooth movement.
It was seen in canine retraction cases that the rate of distal canine
movement was almost 1.6 fold on the side of PGE1 injections as
compared to the vehicle injected site.
Macroscopically and roentgenographically ,no side effects were
observed in the gingiva.
The results of this study show that local injection of PGE1 may be
a safe, effective and clinically applicable method of accelerating
tooth movement.
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59. The role of leukotrienes in tooth movement was studied by
Mohammed A H,Tatakis D N.(AJO 1989 march95).
The leukotrienes played a role in mediating / modulating tooth
movement and interacted with the prostaglandins.
It was seen that when a leukotriene inhibitor was used it caused
inhibition of the lipooxygenase pathway which in turn potentiated
the cyclooxygenase pathway and increased production of PGE2
Inspite of the increased PGE2 it was seen that there was a significant
reduction in tooth movement.
The results suggest that leukotriene production is important in the
mediation of tooth movement along with prostaglandins.
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60. The effect of acetaminophen,ibuprofen and misoprostol on PGE2
synthesis and the degree and rate of orthodontic tooth movement
was studied by Kehoe M J,Cohen S M.(AO 1996,66).
Ibuprofen significantly inhibits PGE2 production and assosciated
with this decrease is the decrease in the degree and rate of
tooth movement.
Acetaminophen did not show a significant decrease in the rate and
degree of tooth movement .
Misoprostol on the other hand had an insignificant inhibitory effect
on PGE2 and the degree and rate of tooth movement were enhanced.
By recommending an “over the counter” analgesic which exhibits
minimal adverse effects on PG synthesis ,clinicians may thus reduce
treatment time.
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61. Arif Umit Gurton,Erol Akin (A.O Vol 74 aug 2003) have studied
the effect of prostacycline PGI 2 and thromboxane TXA2 in
tooth movement and osteoclastic action in rats.The results showed
that there was an increase in the number of multinucleate
osteoclasts ,bone resorption and rate of tooth movement.
Soma S,Matsumoto S,Higuchi(J.D.R. sep 799,2000) studied the
effect of local and chronic application of PTH on tooth movement
and found that a local injection of PTH in a slow release formula
increases rate of tooth movement and hence is applicable for
orthodontic therapy
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62. Systemic hormones such as estrogen,androgen, calcitonin are
assosciated with an increase in bone mineral content, bone mass
and a decrease in rate of bone deposition.Consequently they
could delay tooth movement .
On the contrary thyroid hormones,corticosteroids might be
involved in a more rapid tooth movement resulting in a less stable
orthodontic result.
Attention has also been focussed on effects of prostaglandins
and leukotrienes in tooth movement.It seems that they might
have future clinical applications that could result in enhanced
tooth movement.
Tyrovola J.B, SpyropoulousM.N (Quintessence Int2001 may32)
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63. References
- Use of relaxin in orthodontics. Dennis Stewart,Paul Sherick
Annals N.Y Acad Scien 1041:379-387,2005
- Effects of PGI2 and TXA2 analogs and inhibitors in orthodontic
tooth movement.Arif Umit Gurton, Erol Akin .A.O.Vol 74,2003
-Relaxin affects the dentofacial sutural tissues.Nicozisis J.L et al
Clini Ortho Research Nov 2000
-Study of craniofacial morphology and skeletal maturation in
juvenile diabetes.Tarek El-Bialy A.J.O 2000:118;189-195
-Orthodontic tooth movement in the prednisolone treated rat.
Colin K.Ong ,Laurence Walsh. A.O.2000:70:118-125
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64. -Local and chronic application of PTH accelarates tooth
movement in rats.Soma S Matsumoto,S Higuchi. JDR Sep 2000.
-Acromegaly and resulting myofacial pain and temporomandibular
Joint dysfunction.JADA Vol 114, May 1997
-Thyroid function and root resorption.Poumprous.AO,Vol64,1994
-The effect of corticosteroid induced osteoporosis on tooth move-
ment.Ashcraft,Karin. AJO,102:310-9,1992
-Abnormalities of tooth development in pituitary dwarfism
Kosowicz, Rzymski OOO Dec 1977.
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65. -Dental aspects of hyperparathyroidism.Silverman,Ware,Gillooly
OOO Aug 1968
-Dental correlation in pituitary dwarfism.Salzmann AJO;38,1952
-Effect of drugs and systemic factors on orthodontic treatment
Tyrovola JB,Spyropoulous.Quintessence Int may 32,2001.
-Leukotrienes in orthodontic tooth movement.Mohammed A H,
Tatakis D N. AJO,March 95;3. 1989
-The effect of thyroid hormone on orthodontic tooth movement.
ShiraziM,Dehpour AR.(J Clin Pedia Dentistry1999,spring 23;3.
www.indiandentalacademy.com
66. -Textbook of oral pathology.4th edition.Shafer
-Oral and maxillofacial pathology. 2nd edition. Neville,
Damm, Allen and Bouquot.
- Clinical application of prostaglandin E1 upon orthodontic tooth
movement.Yamasaki K, Shibata Y. AJO 1984;85.508-518
-Effect of acetaminophen,ibuprofen and misoprostol on PGE2
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