Maloccln & endocrine /certified fixed orthodontic courses by Indian dental academy


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Maloccln & endocrine /certified fixed orthodontic courses by Indian dental academy

  1. 1. Malocclusion and endocrinal disturbances INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 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
  3. 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-
  4. 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.
  5. 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
  6. 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. 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
  9. 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.
  10. 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.
  11. 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 .
  12. 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.
  13. 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.
  14. 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.
  15. 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. 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.
  20. 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.
  21. 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. 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.
  24. 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. 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.
  27. 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 .
  28. 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.
  29. 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.
  30. 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.
  31. 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. 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
  34. 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. 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.
  40. 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
  41. 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. 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. 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
  46. 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.
  47. 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. 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
  50. 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.
  51. 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.
  52. 52. -calcitonin also plays an important role in maintaining calcium 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
  53. 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
  54. 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.
  55. 55. -studies by Nicozisis 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 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.
  56. 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.
  57. 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
  58. 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.
  59. 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.
  60. 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.
  61. 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
  62. 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)
  63. 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
  64. 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.
  65. 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.
  66. 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 synthesis and the degree and rate of orthodontic tooth movement. Kehoe M J,Cohen S M. A .O.1996;66:339.
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