Non-carious lesion of dental hard tissues in children: hypoplasia, fluorosis.
Etiology, clinical manifestations, diagnosis, differential diagnosis, treatment and prevention.
Hereditary defects of dental hard tissues.
Symptoms, diagnosis, tactics child’s dentist
Non-carious lesion of dental hard tissues in children in a quantitative sense is not very large, but diverse clinical manifestations and the origin of the group of diseases. Most have not been sufficiently studied, which complicates their treatment and prevention too.
Depending on the occurrence of non-carious lesion of dental hard tissues are divided into two groups (MI Hroshykov, 1985):
1st – those that occur during follicular development tooth – hypoplasia, hyperplasia, fluorosis and hereditary lesions (dysplasia Kapdepona, imperfect Amelie and dentynohenez, marble disease, etc..)
2nd – damage arising after the eruption of the tooth – pathological tooth wear, wedge-shaped defects, necrosis, erosion of hard tissue, tooth hypersensitivity, trauma.
In practice children’s dentist often con-sterihayutsya non-carious lesions of the 1st group. On the 2nd group primarily occur injury permanent and deciduous teeth.
According to the classification of T. Vinogradova (1987), will highlight ¬ tion groups such non-carious lesions of teeth:
– Hereditary anomaly caused by the imperfection of the structure of the tissues that form
the enamel and dentin (enamel or imperfect dentynohenez syndrome Steyntona-
Kapdepona);
– Structure abnormalities and malformations tissues that arise as a consequence of
-systemic illness in the body of the child (amber teeth as a result of osteogenesis
imperfecta, Hutchinson teeth due to congenital syphilis, gray-blue and brown teeth
in hemolytic syndrome, aedentia, hipodentiya and shylopodibni ectodermal
dysplasia with teeth , with pituitary dwarfism mikrodentiya et al.)
– Structure abnormalities and malformations tissues, caused by the influence of the factors
– fluorosis, “tetracycline” teeth and so on.
Еnamel hypoplasia
Enamel hypoplasia – a malformation of the enamel, which is characterized by its lack of formation and mineralization. Etiologic factor that contributes to the development of enamel hypoplasia is insufficient or delayed function ameloblastiv, arising from metabolic around the body under the influence of various diseases due to metabolic or in some follicles under the influence of mechanical trauma, infections, increased radiation etc.
Depending on the cause of the violation may occur in the group of teeth are formed in the same period (systemic hypoplasia), located next to several other teeth or different periods of development (focal hypoplasia) on one tooth (local hypoplasia).
Etiology and pathogenesis of the disease. When changing hypoplasia building protein matrix of enamel and dentin , and disturbed mineralization . Bookmark deciduous teeth starts at 4 – 8 weeks of intrauterine growth retardation , their differentiation – at 12 – 14 weeks , mineralization – 17 – 18 weeks . When the system hypoplastic primary teeth etiological factor is metabolic disorders in pregnant women ( especially water and salt , protein metabolism ). These disorders are often associated with disorders such as toxemia of pregnancy, nephropathy, rheumatism , endocrine pathology, Rhesus -conflict , as well as the influence of environmental factors , etc.
Formation of sixteen permanent teeth comes from the fifth month of fetal development, the beginning of mineralization – during the nine months of fetal development to nine months of life. The emergence of permanent teeth hypoplasia associated with late toxemia of pregnancy and child with diseases in the first year of his life (indigestion, rickets, infectious diseases, neonatal asphyxia, diseases of the endocrine system, etc..).
Yuri Fedorov, V. Drozhzhina in his works noted that 60% of hypoplasia defects develop in the first 9 months of life, when adaptive mechanisms are still poorly defined. In this regard hypoplasia is most common on the incisors, canines and first molars.
Premolars and second molars are beginning to emerge later – in terms of 2 to 3 years. And the common diseases of children aged 3 – 4 years old can promote hypoplasia in these teeth.
Concomitant lesions of teeth which are formed in the same terms, is defined as systemic hypoplasia. The level of affection of the same teeth the same. For example, cutters – cutting edge, the first molars – the surface of the hills. This feature is defined as a symmetrical hypoplasia
If there is a change of the entire crown of a certain group of teeth, it indicates a long course of suffering a common disease. The severity of the disease determines the general suffering varying degrees of lesions – with mild pathology enamel determined spots in severe disease marked hypoplasia of enamel until its absence.
System hypoplasia of enamel lesions characterized by groups of teeth vnutrishnoschelepna mineralization which occurs simultaneously. Most often affected first permanent molars and incisors of the upper and lower jaws
Pic.1. Systemic enamel hypoplasia of permanent teeth came in child ¬ us because of heavy flow of measles in the age of two
Pic.2. Systemic enamel hypoplasia of permanent teeth
The occurrence of hypoplasia associated with metabolic disturbances in the body of the child during vnutrishnoschelepnoho tooth formation, which adversely affects the functioning ameloblastiv.It is believed that the development of enamel hypoplasia system is closely related to violation of calcium homeostasis in the body. Low levels of calcium in the blood serum during enamel formation is a determining factor in the development of hypoplasia. Decreased levels of calcium in the blood serum occurs at deficiency of vitamin D, many perinatal disorders.
According to many authors, hypoplasia occurs after an in childhood rickets , severe infectious diseases due to indigestion ( dyspepsia ), failure of the endocrine glands (especially parathyroid ) in children with metabolic disorders. Very often cause enamel hypoplasia of permanent teeth is parenteral antibiotics dihyam 1st year of life. Antibiotics prescribed their children for health reasons (for example, in the treatment of pneumonia), can inhibit the function ameloblastiv , which interferes with the formation as well as the mineralization of enamel and causes hypoplasia of varying severity.
Hypoplasia observed both permanent and temporary teeth, but the latter – much less. This is due to the fact that the formation and mineralization of deciduous teeth ation occurring in utero. Therefore, hypoplasia of deciduous teeth occurs only in case of complications during pregnancy, severe toxicosis and severe illness of the mother during the second half of pregnancy. In premature babies signs of hypoplasia can be found in canines, neck cutters chewing surfaces of molars temporary.
Much more hypoplasia occurs pa permanent teeth , due to the fairly common disease of children 1 year of life.
Through a chronological history can be detected dependence of hard tissue lesions occasionally carried diseases and their severity. For example, if a child was sick in the first 1-3 months of life , the enamel defects are found only in the first molar , and if the disease originated in 5-10 months , it also damaged front teeth . Premolars and second permanent molars mineralizuyutsya ranging from 2-3 years when metabolic processes are consistent, and hypoplasia observed only during prolonged severe illness in children.
According to the clinical manifestations are three forms of systemic hypoplasia:
1. – Change the color of the enamel (spotted form);
2. – Change the structure of hard tissues:
a) wavy;
b) point;
c) grooved;
3. – Lack enamel (aplasia).
Change the color of the enamel is found in a different form, symmetrically arranged spots of white teeth in under the same title. These spots are often localized on the vestibular surface and not accompanied by any discomfort. A characteristic feature spots in hypoplasia is that the outer layer of enamel is smooth, shiny, not stained with methylene blue. Over the life size, shape and color patches do not change.
Insufficient development of the enamel is more severe hypoplasia her . Clinical manifestations are different – wavy , pointed , striated enamel. Often there is a pointed shape enamel hypoplasia system . Enamel defects have the form of point depressions located on the vestibular and lingual surfaces at different levels in different groups of teeth. Initially after prorizuvanim teeth enamel in places depressions has normal color , then gradually pigmented . But always it is thick, smooth and shiny . Hypoplasia can occur as a single transverse grooves on the crown . This recess may be significant , and the crown is noticeably reduced ( interception ). This form of enamel hypoplasia was called striated . Such fissures may be few, they alternate with intact tissues.
Sometimes there is a complete absence of enamel (aplasia) in a certain area of the crown.
System hypoplasia of the enamel. Dot shape, complicated caries.
System hypoplasia of the enamel. Cupped.
Histologically for all forms of hypoplasia detected thinning enamel, increasing mizhpryzmovyh, expansion Rettsiusa lines, reducing the definition of contours of enamel prisms. The degree of histological abnormalities depends on the severity of the process. In the field of hypoplastic enamel defects in children often occurs caries.
Local enamel hypoplasia
Local enamel hypoplasia – often observed at low molar teeth of the upper and lower jaws, sometimes on a permanent incisors
Local hypoplasia of permanent maxillary incisors arising from injury temporary incisors
1-2 affected teeth. The development of this form of hypoplasia is often caused by injury (dislocation scored a temporary tooth that causes damage to the permanent tooth follicle) or inflammation in periodontal temporary tooth predecessor. Light damage to the enamel apparent change in color of a single tooth (white, yellow, brown spots).
Local hypoplasia of permanent maxillary incisors (as spots) on the vestibular surfac of the central incisors.
Histologically in all forms of hypoplasia detected thinning enamel , increasing mizhpryzmatychnyh spaces , loss of definition of enamel prisms , lines Rettsyusa expanded. In more severe forms of significant changes in dentin . Thus, in dotted- form hypoplasia increases interhlobulyarnoho dentin zone , there is an intense fat, degenerative changes in the nerve cells.
At the electron microscopic study of enamel prisms detect changes in width , disorientation hydroxyapatite crystals . In dentin broken orientation of crystals of hydroxyapatite, restructured dentinal tubules.
Clinic and diagnostics of enamel hypoplasia : patients complain of the defect hard tissues as amended enamel colors or patterns – depending on the form of hypoplasia. Of pain there. Only in the absence of enamel on the entire crown or in part – in the field furrows, grooves may experience pain from stimuli that passes after their removal.
The diagnosis of hypoplastic placed on the basis of complaints, anamnesis, objective data and additional diagnostic testing. From the history it appears the time of appearance of the defect (to teething) and the stability of motion, ie, hypoplastic areas did not increase with time throughout life.
An objective examination takes into account the number of injuries – several of them, systematic and symmetrical lesions. Localized areas of hypoplasia on the vestibular and lingual surface affects the hills, cutting edge tools, equator crown. The surface defect shiny-looking, smooth, firm and painless in probing has clear boundaries. Spots will not colored when applied methylene blue solution, and fluorescent lights provide intense luminescence compared to healthy enamel.
Patchy form hypoplasia differentiate caries in stage spot, fluorosis, initial acid necrosis. Wavy point and grooved shape of the surface to be distinguished from caries, fluorosis, hereditary disorders ameloheneza. Changes in the form of tetracycline pigmentation teeth differentiated with enamel imperfect amelohenezom, dysplasia
Treatment depends on the severity of hypoplasia.
Spotted hipoplazia form caot be treated. If the stain is causing a cosmetic defect, it can be removed by dissection and sealing of composite materials.
In dotted and striated form of enamel hypoplasia applied restoration technique : an anatomic shape of teeth restored using composite materials and special celluloid caps. In places where the enamel layer greatly thinned or not at all, should be used with insulating gasket or glassionomer phosphate cement. Prior to the restoration work in the treatment of enamel hypoplasia recommended ( A. Fedorov et al. , 1997) prior remineralizuyuchoyi the course of therapy to replenish the mineral composition of infant enamel. This is due to the fact that adhesion ¬ compositions are materials to enamel defects in areas hipoplaziynyh reduced due to its inferior structure.Holding remineralizuyuchoyi treatment by conventional methods is also recommended to prevent tooth decay in children with enamel hypoplasia .
Total remineralizing therapy includes receiving the following drugs:
1) calcium glycerophosphate
2) ” Klamin ” 1 table. per day ( 10- older ) for 15 min. before meals for 1 month ( preparation contains biologically active substances – hlorofilin , polinasycheni fatty acids , phytosterols , macro -and micronutrients , and others. , normalizes mineral and lipid metabolism , has immunostimulant , hepatoprotektornymm properties;
3) multivitamin complexes as ” Complivit ” or ” Kvadevita ” 2 tablets ( 10 and over) per day for 1 month.
In patchy form hypoplasia general treatment is given for 1 month , then take a break for 3 months. All 3 of the course is conducted over 1 year.
Local remineralizing therapy:
1) oral health education , monitoring its implementation ;
2) Appointment fosfatvmisnyh toothpaste (”
3) 3) electrophoresis of 2.5 % solution of calcium glycerophosphate (patients older than 10 years) to the area with lots of teeth hypoplasia, 10 sessions. After the procedure, it is advisable to handle teeth 1% sodium flyuoryda for 10-15 seconds. Electrophoresis is carried out 3 times a year between the rates of total therapy
Remineralizuyuchu dental treatment carried out by different methods , resulting in recovery of the affected surface layer of enamel. Currently, created a number of drugs , which include ions of calcium, phosphorus , fluorine caused remineralization of tooth enamel . The most widespread solution hlyukanatu 10% calcium , 2% sodium fluoride solution , 3% solution Remodent , fluoride varnishes and gels.
To this day remains a popular method of restoring enamel on a method Leus – Borowski.
Tooth surfaces thoroughly cleaned of plaque mechanically brushing with toothpaste . Then treated with 0.5-1 % hydrogen peroxide solution and dried air stream. More on the area of altered enamel impose cotton swabs moistened with a 10% solution of calcium gluconate for 20 minutes, change tampons every 5 minutes. Then follows the application of 2-4% sodium fluoride solution for 5 minutes. After the procedure is not recommended to eat within 2 hours. Course remineralizuyuchoyi therapy consists of 15-20 applications that spend every day or every other day. Efficacy of treatment was determined by the disappearance or reduction of foci of demineralization . For a more objective assessment of treatment may be the method of staining sections with 2% solution of methylene blue . At the same time as the remineralization of enamel surface layer affected the intensity of staining decrease. At the end of treatment recommended fluoride varnish is applied to the tooth surface thoroughly dried brush, a single dose of less than 1 ml , always in heated form.
VK Leontiev proposed to use for applications of 1-2% sodium fluoride gel in 3% agar- agar. After professional tooth cleaning gel heated at spyrtivtsi brush applied to dried teeth. After 1-2 minutes it freezes into a thin film . Treatments 5-7 applications.
RP Rastinya successfully applied the 3% solution Remodent for applications .
Treatment Remodent is as follows: the surface of the teeth thoroughly cleaned mechanically toothbrush with toothpaste . Then the teeth treated with 0.5 % hydrogen peroxide solution , dried with a stream of air. Further areas of altered enamel impose a cotton swab dipped remineralizuyuchym Remodent solution for 20-25 minutes, change tampons every 4-5 minutes. Treatments 15-20 applications.
During follow-up examinations should be determined index hygiene as thoroughly clean teeth of soft plaque is a prerequisite for successful treatment.
In the presence of enamel defects is conducted one-month course remterapiyi complex , and tissues of teeth restored using filling materials. Children under 16 composites with mordant enamel is not recommended . It is better to use glass ionomer cements . Adult patients are advised to conduct bleaching or restoration of modern photocomposite , applying veneers , laminates. Extensive defects treated by orthopedic methods.
During follow-up examinations should be determined index hygiene as thoroughly clean teeth of soft plaque is a prerequisite for successful treatment.In the presence of enamel defects is conducted one-month course remterapiyi complex , and tissues of teeth restored using filling materials. Children under 16 composites with mordant enamel is not recommended . It is better to use glass ionomer cements . Adult patients are advised to conduct bleaching or restoration of modern photocomposite , applying veneers , laminates. Extensive defects treated by orthopedic methods.
Prevention hypoplasia is to strengthen the body’s defenses , preventing somatic diseases in children , pregnant women and mothers during feeding. For this purpose, shall be carried out sanitary- educational work in women’s and children’s clinics. Pregnant women and children should be administered tetracycline only for health indications .
The combination of hypoplasia of enamel and dentin can manifest in changing the shape of crown. An example of this pathology is Hetchynsona teeth, Fournier, Pfluger. Teeth Hetchynsona – a barrel shape and vykrutkopodibna first upper incisors (11, 21) with venous tenderloin on the cutting edge (neck of tooth size larger than the cutting edge
Teeth of Hetchynson, Fournier incisors, molars Pfluger
Fournier teeth have the same shape, but without notch along the cutting edge. Teeth Pfluger – a conical shape first molars (16, 26, 36, 46), when the size of the neck of the tooth more than the chewing surface and undeveloped hills converge and form a cone.
“Tetracycline” teeth
Among the species isolated hypoplasia tetracycline teeth – tooth discoloration as a result of taking tetracycline ( oxytetracycline dihydrate, metatsyklinu hydrochloride dioksytsyklinu hydrochloride monotsyklinu hydrochloride morfotsyklin ) during tooth formation and mineralization. It should be noted that when injected into the body of small doses of the drug may develop pathology in the form of discoloration , the introduction of very large doses – enamel hypoplasia in conjunction with a change in color crown.This is due to the fact that tetracycline preparations formation ¬ form a complex with calcium and therefore deposited in bones, teeth and their rudiments violate protein synthesis , which hinders the development and growth of bones and teeth. When commissioning body even small doses of drugs tetracycline teeth are formed, painted in yellow color. The intensity of the color is different – from light yellow to dark addition , depending on the number of introduced tetracycline.
Treatment of pregnant women drugs tetracycline storage ¬ movlyuye color of deciduous teeth in a child
The color of deciduous teeth due to tetracycline treatment of the mother during pregnancy
Intense staining of permanent teeth yellow because of the child’s treatment withtetracycline (“tetracycline” teeth)
It is believed that tetracyclines cross the placental barrier. The blood from the umbilical cord, its concentration is 10-15% of the level in the mother’s blood. Tetracycline is excreted in mother’s milk, in which it is as much in the serum.
Treatment with tetracycline baby in the first months of life causes the color of crowns of deciduous teeth. When tetracycline was administered from 6 months of age, the stain is not only temporary molars and partially permanent teeth formed at this time.
Over time, under the influence of light color of the teeth, especially on the vestibular surface of yellow turns to gray , gray- yellow or reddish- brown . To prevent the development of ” tetracycline ” teeth , remember that antibiotics tetracycline absolutely contraindicated pregnant women, nursing mothers and children under the age of 8 years.
Discoloration of deciduous teeth to yellow , gray- yellow , dark brown , yellow- green, blue seen in children who have had Rh disease . Products converting indirect bilirubin deposited in the tissues, causing their color, can influence the histogenesis , causing development hypoplasia. In this case necessarily combined with hypoplasia of tooth discoloration .
Hyperplasia of enamel or enamel drops
The condition manifests itself in the form of excessive tissues during its development. Observed in 1.5 % of patients , areas of hyperplasia often placed in the neck of the tooth enamel and on the verge of cement or bifurcation region roots. The diameter of from 1 to
Hyperplasia of enamel
In dentin enamel drops can be found in the cavity preparation when forest area is defined by tougher dentin. Near the necks enamel drop seen in retraction of the gums , root – with X-ray .Treatment only be near the necksenamel drops – they cut down, polished piece of fabric and prescribe daily fluoride toothpaste application within 7-10 days.
Fluorosis (endemic fluorosis )
This disease is associated with excessive intake of fluoride in the human body. Early signs of fluorosis – damage teeth. In 1900, Italian physician Chyyya found in the outskirts of Naples residents known to the change of teeth and called them black , accounting for the influence of this phenomenon on the teeth of drinking water contaminated by volcanic emissions. Later, similar lesions of teeth observed in the U.S. and other countries. Almost 3 decades the cause of this lesion was unknown. Only in 1931 was found to be the etiological factor is the high content of fluoride in drinking water. Fluoride is an active element in the free form not found in nature , it is part of the more than 100 minerals. Enrichment of soil fluorine occurs as a result of the eruption of volcanic rocks , mineral fertilizers , emission of fluoride products. Under the influence of rainfall fluoride minerals dissolve skoplyuyutsya in deep artesian wells. The waters of rivers and lakes may also contain large amounts of fluoride salts . With water and soil fluorine enters the plant and hence to animals and humans. Especially in his many marine fish , cabbage, meat products, chicken eggs, plants. The concentration of fluoride in fruit relatively small. However, products that contain fluoride, fluorosis does not cause , they are complementary source of this element in the body. With food a person receives an average of 0.5-1.1 mg of fluoride per day. Major source of fluoride in the body – water (up to 2.5 mg per day), it is in its use of fluoride in the body is fixed more than when you receive it with food or air. In the body, fluoride is delayed children much more than adults. Therefore fluorosis affects mainly the permanent teeth of children living in endemic foci from birth to 3 – 4 years when their teeth are in the stage of formation of incomplete and unfinished mineralization. 3ahvoryuvannya does not occur in people who have come into focus of endemic fluorosis after eruption of teeth. However, the concentration of fluoride in water less than 6 mg / l , may cause changes in teeth that are formed, and when the content of fluoride in water 20 mg / l and above can be affected by fluorosis teeth adults ( Acting Novick ).
Fluoride is included in all organs , but mostly found in the bones and teeth. Fluoride in saliva , gingival fluid, dental plaque . Most of fluoride excreted by the kidneys and sweat glands , and a smaller portion is retained in the body. The frequency and severity of fluorosis depends on the concentration of fluoride, the individual characteristics of the organism ( individual sensitivity , kidney , central nervous system , parathyroid glands , etc.) , age , climate, water content of calcium. When the concentration of fluoride in water 1.0 – 1.5 mg / l fluorosis was observed in 30 % of the population , with 1.5-2.0 mg / l – 30% – 40% , with 2.0 – 3.0 mg / l – 80 % – 90 % of the endemic areas ( VK Patrikyeyev ). In areas with a hot climate , where many of potable water is used , it may naholoshuvatysya expressed at moderate fluorosis fluoride content in water ( 0.5 – 0.7 mg / l).
When fluorosis changes in hard tissue of teeth due to over ¬ residual intake of fluoride , especially in drinking water. Fluorosis – a kind of enamel hypoplasia that occurs as a result of excess fluoride ions that inhibit ameloblasty period in jaw formation and mineralization of teeth. According to national standards acceptable concentration of fluoride in drinking water is 1.5 mg / l. Increasing the concentration of fluoride in drinking water (2 mg / L and above) promotes dental fluorosis and increased severity of its course . If the concentration of fluoride in drinking water is greater than the allowable (1.5-2 mg / l ), the 30-40 % of the population is affected dental fluorosis mainly I and II degree. The use of water with the concentration of fluoride may be temporarily allowed in terms of the local water supply. In the case of centralized water supply should be carried out or dilution water defluorination .At high concentrations of fluoride in drinking water ( 2.6 mg / l) population fluorosis prevalence is 30-90 %, and 10-50 % of them turns fluorosis III-IV degree. Among children often there are cases backlog growth and bone mineralization . These violations by drinking water containing 2.3 mg / l of fluoride are temporary. In some people who drink water containing fluoride 4.6 mg / L, revealed an increase in bone density and disturbance of conditioned reflex activity. In experimental animals, especially if the fluoride concentration greater than 3 mg / L , there are minor changes in the activity of certain enzymes, functional changes in the nervous and endocrine systems , changes in the intensity of metabolism of calcium and phosphorus , minor pathomorphological and histochemical changes in the bones , liver, kidneys , brain and some other organs. Must defluorination or dilution water.At very high concentrations of fluoride in drinking water ( 6-15 mg / L) 90-100 % of the population affected by the prevalence of dental fluorosis severe , significantly increased abrasion , brittle teeth. Children often find themselves developmental disorders and bone mineralization in adults – changes in the bones of the type of osteosclerosis . Observed inhibition of thyroid function , changing the activity of certain enzyme systems levels, changes in the myocardium (according to ECG) , inhibition of bio ¬ electrical activity of the brain, as well as violations of other internal organs (such as liver) , detected during functional studies . Given the hot climate and poor nutrition possible severe fluorosis skeletal ossification of the spinal ligaments and severe disorders of the peripheral nervous system and internal organs. It is mandatory water defluorination .
Based on clinical observations revealed that the optimal concentration of fluoride in drinking water is 0.8-1.2 mg / l. With such a concentration of fluoride fluorosis is almost not there, but there is a significant effect kariyesstatychnyy.Fluorosis affects permanent teeth (temporary rare) children who are in an area endemic fluorosis from birth or from 3 to 4 years of age. In Ukraine there is endemic fluorosis in some parts of the Poltava region.
To determine the degree of severity of fluorosis I.Myullyera use classification recommended by WHO ( 1975).
I- a questionable fluorosis : the enamel appear subtle white dots or spots.
II- stage – very weak fluorosis : white opaque spots occupy less than 25 % of the surface enamel.
I- moderate fluorosis : opaque white spots on tooth enamel more , but affected no more than 50 % of the surface enamel.
II- moderate fluorosis : the entire surface of the affected tooth enamel color as brown spots , the presence of abrasion , which changes the surface of the enamel.
III- heavy defeat : the entire surface of the tooth is fully damaged, marked a significant area brown , destruction of enamel.
Depending on the clinical manifestations of dental fluorosis distinguish the following forms : dashed , spotted, speckled kreydopodibno – erosive , destructive . The first three forms are not accompanied by loss of tooth structure , erosive and destructive lead to loss of tooth structure .
Dashed form of fluorosis is characterized by the appearance of small strips kreydopodibnyh – strokes that are located in sub-surface layer of enamel. They are almost invisible , appear on drying enamel located on the vestibular surface of the incisors of the upper and lower jaws .
Spotted shape fluorosis is characterized by kreydopodibnyh spots located on all surfaces of the tooth crown . There may be overwhelmed by all the teeth , but often – cutting the upper and lower jaws. Sometimes the color of the lesion areas – spot becomes yellowish- brown. Feature of tsiyey form fluorosis is that enamel spots in the area smooth , firm, brilliant.
As chalk– spoted form of fluorosis is characterized by a great variety of forms. The enamel on all surfaces of the tooth has a matte shade, and on this background are well -defined pihmetovani spots. Sometimes enamel yellowish , with numerous spots, dots , sometimes it found minor defects. For this form of experienced rapid abrasion of enamel exposing dentin pigmented dark brown.Electron microscopic studies of affected dental fluorosis showed that in the area of spots in the enamel extended mizhpryzmovi spaces, weakened the link between structural formation of enamel , indicating a reduction in its strength. In more severe forms of dental lesions observed blurred boundaries enamel prisms and even pockets of decay, alternating with amorphous structures in the enamel. All this indicates a violation of the strength and resistance of teeth.
Erosive form of fluorosis on the background of severe pigmentation enamel defects observed various forms – erosion, where no enamel ;Notable abrasion of enamel and dentin.
Destructive forms characterized by impaired forms of teeth due to erosive destruction and erasure of hard tissue . Observed in areas where the concentration of fluoride in drinking water is greater than 5 mg / l. For this form of tooth brittle , easily breaking off , but the tooth cavity is not opened due to the formation of dentin substitute.
The pathogenesis of dental fluorosis is not fully understood.
There are several assumptions:
– Fluoride toxic effect on enameloblasty and this leads to an incorrect formation of enamel;
– Fluoride as enzymatic poison prolonged his admission reduces phosphatase activity and thereby violates the mineralization of enamel;
– According to IG Lukomsky (1940) fluorosis results from the interaction of large amounts of fluoride that comes from outside, calcium, magnesium, manganese and other elements, thereby disrupting the processes of mineralization of dental hard tissues.
So hypoplasia and fluorosis at various etiological factors have similar pathogenesis , ie enameloblastiv lesions and disturbances of mineralization of hard tissues of teeth during their development. Therefore, according to some authors, who conducted the study , fluorosis is a hypoplasia of specific origin, caused by excess fluoride in drinking water.YA Fedorov, VA Drozhzhina (1997 ) suggest that a change in the thyroid gland is the most likely explanation for the unfavorable effects of fluoride on mineralization of enamel as fluoride in oral as well as topical administration quickly into the bloodstream and blocks the thyroid gland, affecting its activity.The widespread use of fluoride in toothpaste composition , nutritional supplements, water fluoridation to prevent tooth decay caused the recent increase in the prevalence of mild fluorosis iatrogenic origin in some European countries and the U.S..Histopathological changes in fluorosis depend on the form of clinical manifestations. The surface layer of enamel is well mineralyzovanyy in subsurface zone vidmichayetsyayetsya hipomineralyzatsiya . In kreydopodibno rebirth enamel increased mizhpryzmatychni spaces marked reduction in the density of enamel , increasing its permeability in areas of spots. With this tie enamel pigmentation resulting penetration in her coloring foodstuffs (tea, coffee, tobacco , etc.). . In mild lesions observed clarity crystal structure of hydroxyapatite , with severe clarity decreases structures , are pockets of complete disintegration of the enamel. Dentin – enamel compound has notched shape. The structure of the basic substance sealed dentin , dentinal tubules expressed around the area hiperkaltsynatsiyi , increased microhardness of dentin.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of dental fluorosis and similar hard tissue lesions of teeth is carried out using the traditional scheme of clinical examination of patients ( find out complaint , history, physical examination data , etc.).Due to the fact that dental fluorosis has a lot in common with other diseases of hard tissues of teeth ( especially in its early stage of development ) in the differential diagnosis , we will comply with strict schema parsing stuff.
The scheme has the following differential- diagnostic features :
– Pathogenesis of the disease ;
Hours lesions of teeth;
Any damaged teeth ;
– Localization of the lesion ( of glass kreydyanopodibni we and other signs );
-Characteristic spots during the inspection ;Ratio to the living room painting;
Fluorescent – stomatoskopiya ;
Conductivity – hard tissue of teeth;Speaker of the disease;Description of the destructive stage , and other indicators.The greatest difficulty in the differential diagnosis of dental fluorosis occurs with patchy form hypoplasia (A. Fedorov , VA Drozhzhinov , 1997).Clarifying the pathogenesis of these diseases, it should be remembered that the basis of the mechanism of dental fluorosis as hypoplasia , are disturbances of mineralization of dental hard tissues . Dental fluorosis is caused by overly getting fluoride from drinking water during the formation of ( zvapnyuvannya ) tooth germs. System hypoplasia occurs in the same period of life ( zvapnyuvannya tooth primordia are ) influenced by disturbances of mineral metabolism in the body of a child due to illness (simple and toxic dyspepsia, spazmofilii , rickets , etc.). Perhaps that is why some authors (PA Leus ) dental fluorosis attributed to specific varieties hypoplasia that occurs as a result of known factors ( excess fluoride ).When fluorosis and hypoplasia with lesions occurring during tooth calcification of dental primordia 1-2 – 3 year of life , and therefore permanent teeth erupt are the changes in the enamel, which emerged in the period of development in jaw teeth.In systemic hypoplasia , as in fluorosis, affects ¬ BY mainly permanent teeth ( deciduous teeth strike ¬ be rare).Cretaceous fluorosis stains when placed in a custom field to decay ( mouth and tongue tooth surface near the hillocks and the cutting edge of the crown ). When hyperplasia spots are also located atypical for brown places ( convex surface of the teeth , areas of hillocks etc.).When fluorosis stains are placed symmetrically on most teeth or even all teeth. When you move in en demichnu area for 2 – 3 year of life ( after the end the period of mineralization front group of teeth ) affected mostly premolars and second molars . If the child was born and lived until 2 – 3 years of age in the center fluorosis , and her parents left the endemic zone – are affected , usually front teeth and first permanent molars. In marked hypoplasia strict symmetry and systematic lesions of teeth under the terms of mineralization. Moreover, the validity of the adverse factors that led to disturbances of mineral metabolism in the body , usually short because of hard tissue lesions of teeth with hypoplasia is more often localized . On examination flyuorozni spots pearly white , shiny , painless in probing gradually moving in unchanged form in the enamel. When hypoplasia spot light in chain that girded around the crown of the tooth, not tight painless in probing , brilliant . Limits spots are usually well defined.Cretaceous spots in fluorosis , as with hypoplasia without zafarbovuyutsya 2% solution of methylene blue or other dyes.In the UV rays chalk stains fluorosis was reflected in a light blue glow and do not differ from the fluorescence of intact teeth. When hypoplasia was reflected spots pale yellow glow. Lots of pigmentation regardless of the intensity of fluorosis was reflected in the red- brown glow. When pi ¬ hmentatsiya hypoplasia of enamel can be traced in the recess , the furrows in areas of plaque accumulation , it is more rotten ¬ but not so pronounced and was reflected in the UV rays. In severe forms of fluorosis of teeth with brown paint marked or fragmented , or total fluorescence quenching of primary enamel. When borozemnniy and destructive forms of hypoplasia fluorescence affected areas light yellow, as in patchy form hypoplasia, fluorescence quenching primary enamel were observed.Spots by fluorosis relatively constant and stable in its development. Accommodation for the child in areas with optimal and low fluoride content in drinking water spot size may eventually diminish or disappear altogether.
In destructive forms hypoplasia occur deep transverse grooves that cover the crown of the tooth furrows often placed on the central and lateral incisors and the first molars. They strictly symmetrical and clearly coincides with the period of mineralization of the enamel crown. In areas with destruction hypoplasia developing tooth decay, so the first molars in adult patients often absent.
Differential diagnosis of dental fluorosis with initial caries is based on these differences.
Initial caries focal demineralization of dental hard tissues occurs when dental plaque formed in the teeth. Teeth usually erupt on the surface of intact enamel. Cavities are affected equally as temporary and permanent teeth. Favorite place in localization caries – fissure, aproksymalni surface area of the cervical tooth crowns.
Carious spots occur on different groups of teeth in people who are prone to tooth decay. Because focal demineralization almost always multiple and combined with other, more expressive stages of caries (superficial, medium and deep).
On examination carious spot light kreydyanopodibna, matte, opaque, supple and sensitive in probing. In chronic course of caries – a dense, painless, no shine, intensely colored. When processing areas affected by caries 2% solution of methylene blue or other dyes (magenta) colored chalk spot.
In the UV rays observed fluorescence quenching of primary carious spots, its degree related to the rate of destruction of the enamel. In acute during brown ¬ yesu fluorescence quenching primary enamel clearly.
Conductivity chalk stains with caries, unlike ¬ mine spotted forms of fluorosis, sharply increased. Hard tissue resistance to electric current significantly decreases.
Cavities in stage spots or progresses to form brown ¬ oznoyi oral or delayed in their development (light stain darkens over time, becoming yellow-brown or even black at all, caries becomes chronic course.
The differential diagnosis of dental fluorosis should be conducted with other non-carious lesions of the hard tissue of origin (wedge defect, erosion of dental hard tissues, cervical and acid (chemical) necrosis).
In the differential diagnosis of dental fluorosis wedge defect should use the following differential-diagnostic feature.
Etiology and pathogenesis of wedge-shaped defect so far not well understood. The disease occurs in persons in violation of the organic substance of the tooth (Znamenskii). There are proponents of mechanical impact (tooth brushing) and chemical factors (demineralization of enamel in the cervical area influenced by the fermentation of food residues). In the literature, there are also indications of the role of endocrine disorders, diseases of the central nervous system and gastrointestinal tract.
Lesions of teeth with wedge-shaped defect often occurs in adulthood, in patients suffering from periodontal disease. Affected, usually premolars and molars of the upper and lower jaws, sometimes – front teeth.
The disease begins slowly, with a gradual decrease in the thickness of enamel in the cervical area. The presence of spots is not characteristic wedge-shaped defect. ¬ You Polytones different manifestations of the disease are in the shape of a wedge, hence the name – wedge-shaped defect. The bottom and sides of the defect dense, shiny, not colored dyes.
In the UV rays of the lesion area was reflected pale blue glow, no different from the intact enamel. Electrical conductivity affected teeth replaced due to a decrease of their thickness.
Cuneiform defects gradually progressing up to expose the dentin and pulp. As a result of chronic irritation of the pulp cavity of the tooth forms a thick layer of secondary dentine. In chronic disease patients tend to present a complaint. However, with bare tooth pulp possible sensitivity to the action of stimuli.
Erosion of dental hard tissues – a gradual, progressive disappearance of the enamel sufficiently identified etiology. Most authors point to the role of the chemical (lemons and other citrus fruits and their juices) and mechanical (brushing teeth) fac ¬ tors in causing disease. Some authors emphasize the role of the neuropsychiatric disorders, gout. M. Maksimovsky believes that erosion occurs in individuals with a dash ¬ toxicity.
In the differential diagnosis of erosion and fluorosis should be aware that hard tissue lesions with erosion occurring in the teeth formed in middle-and old pohy ¬ logo, not during the growth and development of teeth.
Erosion occurs only in permanent teeth bite. Affected the central and lateral incisors of the upper jaw, at least – canines and premolars. On the lower front teeth erosioever occurs.
The disease begins with erasing the equatorial areas of central vestibular enamel surface and lateral maxillary incisors. In a distinct cases you ¬ formed funnel defect with smooth shiny sides and bottom, which gradually turns into intact enamel.
Designated lesions not colored dyes.
In the UV rays of the teeth lesion area was reflected pale blue glow.
The conductivity varies as hollow defect by changing the thickness of the hard tissues.
The process progresses, usually slowly, to form a deep funnel (bowl-shaped) grooves. At slow flow erosion patients usually do not complain of pain. Ulcerative disease form ¬ ing dissatisfaction with the cosmetic result in sick. In the differential diagnosis of dental fluorosis of dental hard tissue necrosis (necrosis of cervical) should use the following differential-diagnostic feature.
Necrosis of hard tissues – a demineralization li ¬ senting in the cervical area of the tooth with the rapid progress that occurs in adults on a background of dysfunction of endo ¬ krynnyh glands ts.n.s, chronic intoxication ¬ th, Ray and others.
Cervical necrosis occurs in existing teeth. Affected different groups of teeth (incisors, canines, premolars, mo ¬ lares).
As with caries, the disease begins with a mo ¬ hnyschevoyi demineralization of enamel in the cervical area. -Not having demineralizuvatysya, enamel prisms vidtorhuyutsya exposing at a not yet destroyed, no pigment ¬ mentovanyy, light dentin, which repeats the shape of the crown. Patients, as always, there are defects in various stages of development: the focal demineralization you in the form of ¬ chalk smudges, chalk stains from enamel prisms annexations and naked light yellow dentin defects pryshyykovi funnel with indentations that resemble a tooth surface more.
Cretaceous spots and destructive forms of lesions stained with methylene blue.
In the UV rays, as well as in acute caries, areas cheer ¬ tions are the primary quenching of fluorescence.
Electrical conductivity of solid tissue increased to ¬ priorities would need very different from intact teeth.
The process usually progresses rapidly to form cavities.
Acid (chemical) necrosis of the dental hard tissues – it acquired a total demineralization of enamel due to changes in the pH of oral fluid after a single action as a result of adverse concentrated acids at work.
Often affects the enamel of the front group of teeth (incisors, canines), much less – premolars and molars.
Unlike dental fluorosis, not for Acid necrosis characterized by spots. On examination of the teeth enamel surface has a matt appearance, dull, with a pronounced roughness, well painted dyes. Patients often skarzhat ¬ subsequent to oskomyny feeling in his mouth.
In the UV rays of the affected surface enamel has the ability to put out the initial fluorescence. When zishlifovuvanni rough surface enamel is a light-yellow fluorescence. Electrical conductivity of solid tissue virtually unchanged. However, under intense pressing the electrode probe conductivity values vary due to susceptibility of enamel and increase the area of the active electrode.
With prolonged exposure to acid on enamel process progresses. Prior to joining the above attributes are set on edge and feeling sleep, there are long, aching pain in the teeth. In severe forms of the acid necrosis enamel rozm’yakshuyet ¬ Xia, becomes brittle, and easily vidkolyuyetsya erased.
To summarize this section, it should be emphasized that the diagnosis of dental fluorosis and especially the initial stages of the important role played by the differential diagnosis of such lesions of dental hard tissues for clinical signs. In addition, the differential diagnosis are important laboratory techniques. Laboratory Methods).
Well-conducted dental fluorosis diagnosis based on the form and severity of the disease and the influence of environmental factors assists the physician in the choice of rational treatment.
Diagnosis is based on subjective and objective data analysis, additional methods of examination . It should take into account the importance of such information , as the absence of pain in sensing of the stimulus ( the pain can occur only when erosion forms ), the presence of a smooth , shiny enamel lesions in areas , stains do not stain with a solution of methylene blue , depth and area of the lesions sometimes increases (except for destructive forms when observed decline sharply expressed altered tissue under erasure ) is defined endemicity area of residence of the patient.Treatment of the various manifestations of dental fluorosisTreatment of dental fluorosis should be done comprehensively considering the severity of the disease , in ¬ tween total body state and the impact of endemic factors.”The overall effect on the body and teeth affected by fluorosis should include (quoted in PT Maksymenko , AK Nikolishynym , 1976 ):Stopping or at least limit access to the child’s body elevated concentrations of fluoride to drinking with water and food.a) 3 for this purpose for drinking and cooking is recommended to use water from nearby reservoirs with low fluorine content . In the absence of such a possibility (technical or otherwise ) should partially ¬ ve zneftoryuvannya water used for drinking and cooking, by her 5 -10- minute boil followed by settling .b) Restrictions in the diet of fish dishes cooked with sea fish or strong brewed tea -like products with a high content of fluorine.Reducing the toxic effects of elevated concentrations of fluoride in the body as a whole and dental tissues , including traveling power ¬ Hom purpose of rational diet and drugs.a) Due to the fact that children who suffer ¬ flyuo development , therapeutic diet is not fully developed , they generally denote by ¬ physiological diet, determined for different age groups, with some adjustment dial Har ¬ chovyh products. To prepare the meat varieties recommended fresh lamb, beef , pork , and river fish . Since dairy products are recommended milk for ¬ Smet , cheese , butter , yogurt, yogurt , and various sorbent ¬ thou cheese : the Dutch , Swiss , yaroslavs ¬ cue fused and others. These foods contaiot only .Treatment of dental fluorosis depends on the severity of the injury and may include bleaching, restoration of modern filling materials , the use of facets , veneers or orthopedic treatment . Apply general and local treatment. For a general treatment appointed phosphorus – calcium preparations and vitamins. Eliminates excessive amounts of fluoride from drinking water is limited to the use of products that contain fluoride. If you change the color of the enamel recommendations in most cases reduced to bleaching pigmented areas of different acids ( phosphoric, citric acid) with subsequent neutralization with alkaline agents and the use of applications of a 10% solution of calcium gluconate for 10 – 15 minutes. The course of treatment consists of 10-15 procedures. After 6-8 months, made repeated courses of general and local treatment. Appointed toothpaste with the content of minerals.Treatment of erosive and destructive forms of fluorosis is to eliminate defects using tissue filling materials , facets , and in some cases – by making artificial cosmetic crowns. YA Fedorov , VA Drozhzhina (1997 ) propose to treat dashed , blotchy and kreydopodibno – speckled forms fluorosis in the same way as the spotted form hypoplasia ( rates remineralizuyuchoyi comprehensive therapy for 6 months. – 2 years). A more complex and heavier forms of dental fluorosis – by filling defects after previous month course of general and local remineralizuyuchoyi therapy. Thus , dental fillings in children should be using glass ionomer cements , which then can be partially replaced by composites .To apply individual home whitening bleaching gels of kappa containing 10% hydrogen peroxide were ¬ tion of calcium , phosphorus , and various trace elements, tu ¬ Tamino and, most importantly , the poor in fluorine. This is necessary to alleviate toxic effects of elevated concentrations of fluoride and normalization of phospho -calcium metabolism substances ¬ wines.Therefore, children living in endemic fluorosis stake , instead of water administered to 0.5 –
Device for bleaching tooth enamel affected by fluorosis
The device consists of from 1 , which is made from strumoneprovidnoyi mass, such as plastics , in which the bottom side and soldered needle 2 and C, which are used for input and output whitening liquid. Above from 1 individual fixed mark 4 with the upper jaw , which is made from stomalhinu or other alginate impression mass, where mass impression on the area of the affected tooth is removed from the edges of the gums d “o from 1 to create a cavity 5 , which includes needle 2 and 3. electrode 6 , which is mounted in the cavity 5 is made of food steel in plate.The method is performed as follows.The patient in the dental chair sadovlyat zaprokynutoyu back of his head. In the mouth injected plastic huboutrymuvachi . On the vestibular surface of the upper front teeth , which are subject to bleaching, 3-5 minutes impose swab moistened with 10-20% HCl solution . Neutralize acid 1-2 % solution of sodium bicarbonate . After that, the mouth and the patient is injected device clamps its teeth. After 2 needle with a syringe into the cavity 5 input device bleaching solution. The device is connected to the unit U -2 and act on the oxide ¬ vach direct current from the power of 30 – 50 mA with exposure of 20-25 minutes. During the procedure, periodically changing the polarity of the current.
The spent solution is released through a needle in 3 substituted threadlike tray. Not removing the device from the mouth, bleaching solution is replaced with a new every 5-7 minutes. Total processing time takes 20-25 minutes teeth .The device is removed from the mouth , rinse your mouth with water and 30-40 minutes in the vestibule of the mouth injected cotton rolls, well moistened with a solution of 3-5% Remodent . After 10-15 minutes rollers moisturize SRI ¬ zhoyu liquid. Pi ¬ slya teeth removal rollers dried and coated medical glue MK -2. The advantage of the method is that acid acting on the teeth , enhances the diffusion of atomic oxygen , which is formed in sealed containers with okyslvacha under DC, which is several times enhances the effect of whitening. Action Remodent after acid promotes remineralization of enamel. For a multitude ¬ teeth enamel remineralization process covering medical glue MK- 2, which is fixed on the teeth for a long time (average 12-14 days).Teeth Whitening in sealed containers should be used in children older school- age children and adults with very severe forms of fluorosis of primary total quenching of fluorescence and total enamel paint .Monitoring the treatment of patients with various manifestations of dental fluorosis is made by clinical signs ( color change , as measured by an optical wedge ) of changes in electrical resistance of dental hard tissues and study the fluorescence characteristics of enamel.We have treated patients using you – schezaznachenyh techniques. The nearest and long-term results were followed up in 350 patients with a period of 0.5 to 15 years.The data show that in the course , individual di- ferentsiyovanomu treating patients , taking into account the severity, reactivity and age of patients , and the condition of strict compliance with the doctor’s recommendations in all cases achieved a positive effect. However, as a rule, was observed a steady increase show ¬ ers of electrical resistance, decreasing the degree of fluorescence quenching of primary enamel. Intensity painted enamel ¬ ing a 10-point tonal range of 8.10 to ¬ businessman decreased to 1-2 scale graduations , indicating a relatively high efficiency of the proposed medical con ¬ sobiv bleaching the enamel. Relapses painting in strict compliance with the recommendations of your doctor (especially in the first 2 weeks after application of the acid bleaching method ) have been observed . To illustrate the positive outcomes of patients present pictures before and after treatment.
Dental fluorosis severe renal patient dark brown color and destruction of enamel
a) before treatment (in the rays of the visible spectrum and in the light of initial fluorescence);
b) 3 years after treatment (in the rays of the visible spectrum and in ¬ SRI initial background fluorescence).
Modern methods of professional and home teeth whitening gel solutions using foreign firms
For professional (in the doctor’s office ) whitening enamel used concentrated ( 30-35%) gel solution of hydrogen peroxide or concentrated ( 1-10 %) gel dissolution ¬ us carbamide peroxide ( urea peroxide )Methods of professional whitening tooth enamel affected by fluorosis , as follows.To protect the gums and other parts of the oral mucosa before whitening on front teeth of the upper jaw puts koferdam or minidam . On the vestibular surface of the teeth, as in the previous methods , place a cotton roll , which moisturize bleaching liquid ( gel concentrated solution of hydrogen peroxide or carbamide peroxide ).For a more intense penetration of the oxidant in the tooth enamel before applying the gel solution is applied to the surface of the enamel solution or a gel with organic or inorganic acids. In recent years, the enamel more ” pickled ” 37 % phosphoric acid gel (exposure of 30 to 60 sec. ).Effect of bleaching on deep pigmentation of the enamel, as when using the above methods, incomplete and therefore need to re- visiting the patient.In addition to professional whitening ( in a dental office ), foreign firms offer to conduct a home tooth whitening using 1-6% solution of carbamide peroxide gel mixed with Carbopol . For longer retention in the mouth gel solution of carbamide peroxide bleaching is carried out at night time using individual or standard cap.
Koferdam, as recorded in the patient’s mouth
Custom mouthguards are made in a dental laboratory elastic material. The gel is applied to Capua under projection prints teeth (in the individual capital) or it is applied to the inner surface of a standard capacitor. The patient keeps the mouthguard in the mouth for 2-5 hoursIt is believed that saliva slows down at night, so the gel kept much longer and is better able to act on your teeth. For positive results of this method should be used within 1 – 2 weeks.
The standard cap for home teeth whitening (a set of Plus + White Ultra made in USA).
Errors and complications in the course of serving enamel fluorosis patients teeth.
After contact with the mucous membrane of the mouth bleaching solution it is necessary to immediately neutralize 1% soda solution and, if necessary , to use anesthetic and antiseptic.Phenomena hyperesthesia of hard tooth tissue that occur in the presence of microcracks in the enamel, increasing exposure concentration or bleaching solution, the lack of neutralization of oxidant are usually the second or third day without any further intervention by remineralizuyuchyh properties of the components of saliva. To speed up the disappearance of phenomena hyperesthesia can cover the crown of the tooth or apply adhesive application calcium supplements , anestezynovoyi slurry or other anesthetic.If you violate recommendations for food hygiene especially during the first week after bleaching the enamel may cause its pigmentation in different colors – depending on the nature of the food (jam of black currants, blueberries, strong brewed tea, black coffee , etc.). Food pigmentation that while there is usually easily removed by polishing the teeth with pumice glycerin, or other polipastom ¬ Shimi milkodyspersnymy abrasives .In some cases, after bleaching may be gray (with Lights ) in the presence of enamel pigmentation in the mouth substandard seals of different materials , the oxidation of lead electrode , the presence of metallic structures orthodontic appliances and more. In order to prevent the appearance of pigmentation of the enamel should be guided by the following rules:1. Before applying the acid enamel whitening method should replace all metal and so -called ” combined ” ( cement with sawdust silver ) fillings on the other seal materials (cement, composite materials or light chemical hardening method )
Prevention of dental fluorosis is held collectively and individually.- Change in water sources ;
– Water purification from excess fluoride ;
– Natural breastfeeding a child;
– Replacement Water juices and milk ;
– Appointment of vitamins D and C
;- Prescribing calcium and phosphorus two-week course ;
– Limiting the intake of foods containing fluorine ;
– Removal of the children in the summer of endemic areas .
Freezing and boiling water, use household filters concentration of fluoride in water is not reduced.Congenital malformations of the dental hard tissuesThe condition of the teeth is caused by an inherited disorder of ectodermal and mesodermal functioning of the cellular structures involved in the formation of enamel and dentin. Characteristic lesions are both temporary and permanent teeth.Imperfect amelohenez (amelogenesisimperfecta) ~ is severely impaired enamel formation , characterized by a systemic violation ¬ structure and mineralization of temporary and permanent tooth discoloration and subsequent partial or complete loss of enamel cover. This malformation of enamel has other names: hereditary enamel hypoplasia , aplasia enamel, Brown enamel, Brown enamel hypoplasia , brown enamel dystrophy and others.N.M.Chuprynina (1987) distinguishes four forms of imperfect manifestations amelohenezu .In the 1st form of quantitative and qualitative changes of enamel minor : teeth have a normal shape and size , the enamel is smooth , shiny, but masses of yellowish or korychnevatyy shade.For the 2nd form is characterized by more pronounced changes. Teeth aperture ¬ yutsya time, their crowns initially have normal color. After 1-3 years, the enamel becomes opaque , and then light brown, becoming shorstkuvatoyu.na thickness crack it there , and then it disappears (” cleave “) partially or completely. Dentin tight, light brown or brown.In the 3rd form teeth erupt on time, with normal devel ¬ extent. Enamel white, but with a significant number of furrows without some guidance, all teeth quickly disappears (” cleave “) and exposed dentin brown that has a normal structure.In the 4th form size and shape of the teeth usual , but the enamel during the eruption kreydopodibna not shine , sometimes it’s not at all. As a result of mechanical action is easily separated from the dentin. The absence of enamel and dentin exposure cause tooth response to temperature and chemical stimuli.Microscopically with imperfect amelohenezi enamel disturbances of orientation and location of enamel prisms , increasing gaps between them , sometimes there bezpryzmovi area filled with amorphous substrate. With imperfect AME ¬ lohenezi mesonephral formation ( dentin, pulp ) are not changed , because the roots of the teeth are normal structure, the obliteration of cavities and tooth roots are observed.Likuvannya.U case of hypersensitivity to the irritation dentin ¬ ers spend remineralizuyuche treatment. Prosthetics by conventional methods for cosmetic indications recommended after 16 years in the early destruction of the enamel of permanent teeth they cover orthodontic crowns. It should be noted that the com ¬ Ronco primarily cover the chewing teeth antagonists to fix the height at ¬ bite, then the front teeth of the upper and lower jaws ¬ noyi . When the destruction of teeth crowns using pins , metal cult and others.Imperfect dentynohenez (dentinogenesis imperfecta) – an inherited disorder of dentin. Quite a rare abnormality characterized by the development of tooth roots or ano ¬ Malia their shape. Dental Crowns correct form, of normal size and color. The structure of the enamel is not changed, but its connection with the dentin is weak , making it easy vidkolyuyetsya (. Typical complaints of tooth mobility and early fall . Radiological findings revealed a significant shortening of the roots of all teeth , and complete obliteration of the cavity of the tooth and root canal that is very typical for this type of pathology. ofteear the roots show changes similar to cystic formations with clear contours. Nevertheless, the emergence of these entities is not associated with diseases of the teeth. believed that these changes are the result of violations bone formation , as this pathology is often combined with systemic or focal osteogenesis imperfecta.Treatment. Preferably orthopedic . Before the prosthesis should take X-rays to determine the condition of the roots.Imperfect odontohenez syndrome ( Steyntona – Kapdepona ) is characterized by discoloration of the crown , the early loss of enamel cover and a significant abrasion of hard dental tissues . This issue of dental hard tissues was first described by W. S. Stainton ( 1892) , and subsequently S. Capdepont ( 1905). Later, following the change of teeth got other names: bezkoronkovi teeth , teeth that have lost enamel , brown or ¬ dawn teeth , defective dentynohenez ; mezoektodermalna odontopatiya more. Found that this inherited disorder of teeth is transferred from one parent and half seen in the offspring. Lesion to be not only temporary , but permanent teeth . Syndrome Steyntona – Kapdepona most missing teeth enamel , the color of yellowish- brown, transparent dentin quickly erased. Sometimes the visible contours of the pulp , although complaints of pain are usually absent. Defeat teeth begins with the disappearance (” cleavage “) enamel and dentin exposure . First of all affected incisors and first molars, second molars then . A characteristic feature of the syndrome Steyntona – Kapdepona is normal root formation , but they can be thinner and shorter cavity of the tooth and root canals are narrowed , sometimes completely obliterovani .
Ortopantohrama with imperfect dentynohenezi. X-ray observed shortening of the roots of permanent teeth and tooth cavities obliteration
However, there are signs hipertsementozu cells and the presence of bone thinning near the tops of the roots of teeth that are not affected by caries .During the histological examination of tooth syndrome Steyntona – Kapdepona appear structureless areas of enamel. In other areas there are vast distances between the enamel prisms . Enamel- dentine combination looks like a straight line , according to some authors, is the cause of poor communication with enamel dentin . Dentin has a layered structure , the number of dentinal tubules significantly reduced. At the same time meet the ” giant ” dentinal channel filled with blood , which causes the color of dentin. Interhlobulyarni spaces in the dentin enlarged and filled bilkovopodibnoyu matter. In most cases predentyn missing. Dentin microhardness decreased by about half.
Significant changes in the pulp. The cavity of the tooth and root canals are reduced in size by deposition of dentin substitute . In the layer of odontoblasts observed disorientation of cells, presence of vacuoles present odontoblasts , which have no appendages. In the pulp decreased number of blood vessels and increased collagen content . In most cases elektrozbudzhuvanist pulp dramatically reduced or absent altogether.In cement resorption observed cells along with over-development in some areas of cellular cement ( hipertsementoz ). Pathological tooth wear are the main clinical features of this syndrome , the children have to be under the clinical supervision of an orthodontist , which individually determines the timing and type of prosthesis (protective mouth guards , crowns, dentures ).In dismissing the development of dental zachatikv during embryogenesis, histogenesis observed makrodentiya teeth.
Makrodentiya of teeth
The anomaly is defined as a form due to the reduction of the masticatory apparatus as a result of development phylogenetically
Microdentia
Treatment of inherited disorders that affect the structure of dentin is quite difficult, orthopedic techniques used before which can be performed if indicated remineralizucha therapy.
Hereditary disorders of teeth
Etiologic factor in hereditary diseases are mutations , expression of which is not affected by the environment, but the environment has an impact on the severity of symptoms.
Hereditary diseases are divided into 2 groups: gene and chromosome . Depending on the number of genes involved in the process, monogenic and polygenic distinguish disease. Gene mutations can affect the development of hard tissues – enamel and dentin.
The nature of hereditary monogenic diseases can be divided into 3 groups:
1. autosomal dominant ;
2. autosomal recessive ;
3. linked to the gene .
Occurs amelohenez flawed and imperfect dentynohenez .
Imperfect amelohenez
( inferior enamel formation ).
This is a serious hereditary violation emaleutvorennya , which is expressed in violation of the structure and mineralization of milk and permanent teeth, changing their color and subsequent partial or complete loss of tissue. This pathology is also called hereditary enamel hypoplasia , aplasia.
There are three main groups imperfect ameloheneza milk and permanent teeth:
1. enamel hypoplasia caused by a violation of enamel matrix ;
2. enamel hypoplasia due to violation of maturation of enamel,
3. enamel hypoplasia associated with hipokaltsyfikatsiyeyu enamel.
Enamel hypoplasia caused by a violation of the enamel matrix is expressed in the form of thin enamel on the teeth in the form of pits , vertical and horizontal grooves on the enamel. The teeth on the sides not in contact with each other.
Enamel hypoplasia due to violation of its maturation – amelohenez characterized by defective enamel coated spots and has brownish- yellow. The enamel of normal thickness, but is softer thaormal and has a tendency to cleavage .
Enamel hypoplasia associated with it hipokaltsyfikatsiyeyu ie hipokaltsyfikovanyy defective amelohenez accompanied by such disturbances when all enamel or some parts do not reach normal hardness on the outer surface of the crown of the tooth enamel may be absent (aplasia ) , there is hypersensitivity due to open areas of dentin.
The first group includes the following forms:
1. autosomal dominant point hypoplasia ;
2. autosomal dominant local hypoplastic ;
3. Autosomal dominant smooth hypoplastic ;
4. autosomal dominant rough hypoplasia ;
5. autosomal recessive rough enamel aplasia ;
6. coupled with X-linked dominant smooth hypoplastic .
The second group includes :
1. autosomal dominant hipodozrivannya enamel combined with tavrodontyzmom ;
2. Coupled with X-linked recessive inheritance , hipodozrivannya ;
3. autosomal recessive pigmentation hipodozrivannya ;
7. autosomal recessive rough enamel aplasia ;
8. coupled with X-linked dominant smooth hypoplastic .
4. ” Snow cap ” – an autosomal dominant hipodozrivannya enamel.
The third group includes :
9. autosomal dominant hipokaltsyfikatsiya ;
10. autosomal recessive hipokaltsyfikatsiya .
Autosomal dominant point hypoplasia . Milk and permanent teeth enamel layer of normal thickness, but more on the vestibular surface of enamel defects are defined as points , coloring pigments of these defects food provides dental crowns speckled appearance. Perhaps the defeat of the whole or part of the crown . The disease is transmitted from man to man.
Autosomal dominant local hypoplastic . Most enamel defects occur on the vestibular surfaces of premolars and molars. Defects are arranged horizontally in a linear depressions or pits , usually above or below the equator of the tooth (in the middle third ). Cutting edge and surface interdigitation usually not involved in the process . Maybe lesions milk and permanent teeth , the number of affected teeth varies as the severity of injury. Histological examination revealed lack of maturity of enamel, enamel prisms disorientation .
Autosomal dominant smooth hypoplastic . Teeth that are cut can have a different color – from opaque white to transparent brown. Enamel stonchena , smooth, is 1/ 4 – 1 /2 the thickness of normal enamel. Often it is not present on the surfaces of teeth stulennya and on contact – is white , and these teeth are usually not in contact . There delayed eruption of permanent teeth.
Autosomal dominant rough hypoplasia . Tooth color changed – from white to yellowish- white. Enamel is solid, with a rough , granular surface , it can chip from dentin. Its thickness from 1/ 4 to 1 /8 of the normal thickness of enamel. Affected milk and permanent teeth.
Autosomal recessive rough enamel aplasia . There is an almost complete absence of enamel, the teeth are cut , have a yellow tint. The surface of the crown is rough, granular , resembles frosted glass. The teeth are not in contact . Often there is a delay of eruption of permanent teeth. On radiographs there is resorption of teeth crowns that are not slotted in the alveoli.
Coupled with X-linked dominant smooth hypoplastic . The clinical picture of enamel lesions in homozygous males is different from that of heterozygous females. In men, teeth yellowish- brown, hard enamel , smooth , shiny, thin. The teeth are not in contact . Marked pathological stertist their tissues. Affected milk and permanent teeth. Electron microscopic examination showed that this form of hypoplasia of enamel prisms No , but determined single crystals of irregular and weak degree of crystallization. In women, there is a different clinical picture of lesions of enamel : the tooth crowns are vertical strips of almost normal thickness of enamel , alternating with strips of hypoplasia.
Autosomal dominant hipodozrivannya combined with tavrodontyzmom . Enamel in these cases, it is rough and dysplastic , various colors – from white to yellow. Tavrodontizm observed in milk and permanent teeth. The cavity of the tooth of the tool in any age of large size . Altered teeth only .
Coupled with X-linked recessive inheritance , hipodozrivannya . Men and women are different clinical lesions of teeth . In men, it is more pronounced. Permanent teeth are mottled yellow and white , with age they become darker due to staining of enamel. The shape of the teeth is not changed. Perhaps reducing the thickness of the enamel, it is softer compared to normal. Pathological abrasion is weak . Histologically, a violation of the outer layer of enamel. Women tooth enamel is composed of vertical stripes. There are cases when the enamel is dull and it shows areas of white enamel.
Autosomal recessive pigmentation hipodozrivannya . Enamel color from milky – gray to pale amber . This altered enamel intensely colored pigments from food. It usually normal thickness may peel . This is the most rare form of the disease.
“Snow cap ” – an autosomal dominant hipodozrivannya . Matte white enamel covering 1/ 3 to 1 /8 cutting or chewing surface of the tooth. Modified enamel usually thick and pigmented , usually affects the permanent teeth . Sometimes all affected incisors and premolars or molars and incisors of all , in mild cases – only the central and lateral incisors . Studies by scanning electron microscopy teeth showed that the structural defect limited bezpryzmennym external layer of enamel, but most normal enamel .
Autosomal dominant hipokaltsyfikatsiya . The enamel of the teeth that are cut , white or yellow , normal thickness on the vestibular surface is very soft and gradually separated from the dentin. Enamel is quickly lost, leaving bare , sensitive dentin, which is colored by pigments food in dark brown. When the disease is often observed retention eruption of individual teeth , teeth that are not slotted , may be subject to resorption. In low-contrast radiograph enamel over dentin . Histologically normal enamel thickness, but its matrix resemble those after dekaltsyfikatsiyi .
Autosomal recessive hipokaltsyfikatsiya . Enamel dark, zluschuyetsya . Clinically , renhenolohichno , histologically – a heavier form of the disease compared with autosomal dominant hipokaltsyfikatsiyeyu .
Imperfect amelohenez should be differentiated from changes crowns of teeth with idiopathic hypoparathyroidism form , psevdoparatyreozi , spazmofilii , severe rickets, with indirect influence of various infectious diseases in the formation of crowns with tetracycline teeth , severe dental fluorosis, marble disease acidic necrosis .
Treatment is imperfect ameloheneza systematic processing solutions remineralizuyuchymy enamel and fluoride preparations , restoration of altered areas of modern filling materials. In a large change in the enamel is made orthopedic treatment .
Hereditary disorder affecting dentin ( defective dentynohenez ).
There are 3 types of defective dentynohenezu :
I type is one of several manifestations of common skeletal diseases, so-called defective bone formation . Transmitted in an autosomal dominant type. There congenital disease ( Frolika ) and late (illness Lobshteyna ) osteogenesis imperfecta First rarer second, more common in boys. Frolika disease detected in fetuses or newborns. Characterized by fractures of long bones , ribs, collarbone. Hands and feet are not affected. Children grow slowly , with a broad , flattened skull.
There is a very slow ossification timyachok delay of growth and weight gain . Mental development age.
The second form ( Lobshteyna disease ) is found in the first year of life or later. Sometimes it is hidden until adolescence . The characteristic blue sclera , deafness and change the structure of the teeth. At the heart disease – lack of salt deposits in the bones that form . X-ray image – stonchennya cortical layer valykocharunkova structure of spongy material. Teeth are normal size, the right shape . The color is uneven bits from gray to blue- gray or yellowish- brown with a high degree of translucence . EDI is normal, except for the teeth, where there is a change in the apex of the root , there is abnormal abrasion. Histologically normal structure of the enamel , but enamel- dentine connection is kind of a straight line. Raincoat dentin correct structure, but towards the pulp dentinal tubules less .
Type II defective dentynohenezu called in the literature an inherited syndrome or dentin opalestsyruyuchym Stanton – Kapdepona .
Syndrome Stanton – Kapdepona
In 1892, Stanton was first described this pathology , in 1905 published Kapdepon more posts by this disease. Affected milk and permanent teeth. The disease is characterized by a change in color of crowns, early loss of enamel cover and marked stertistyu . Teeth erupt in the medium term , jaws develop properly. Most teeth devoid of enamel, with yellow- brown color. The remains of the enamel quickly skolyuyutsya soon after eruption , dentin that bare quickly erased. Pain from thermal stimuli are absent, but worried about pain from injury gingival papillae during chewing. The length of roots and their usual form , but it is thin and short roots. The cavity of the tooth and root canals are reduced in size by deposition of dentin substitute .
Dentinal tubules filled with blood, which makes the teeth are different shades of dentin ( from pink to red- purple). The pulp is found only in certain areas , there’s little vessels, but many of collagen fibers , the number odontoblastov reduced, they are deprived of processes, EDI reduced. In cement resorption foci alternating with hipertsementozom . The water content increased in the teeth , and inorganic substances – decreased.
Treatment. The main type of treatment of this pathology has long been the prosthesis. In recent years, conservative treatment is used , which is to appoint remineralizuyuchoyi comprehensive care for the full annual scheme (described in ” hypoplasia “). Timely application of such a treatment for early diagnosis allows to achieve good results. Defects in glass ionomer cements replaced , if necessary prosthesis .
Type III deficient dentynohenezu characterized by lesions of teeth in type I and II both in color and form. Often clinical signs as opalestsyruyuchoho color of teeth , dome type caps, and so-called tooth ” shells ” which are determined by X-ray (teeth where there is no dentin formation after formation of dentin raincoat ). Affected milk and permanent teeth.
YA Belyakov (1993 ) proposes to allocate several types of inherited disorder of dentin.
1. Dentynohenez imperfecta type I ;
2. Imperfect opalestsyruyuchyy dentin ( Kapdepona dysplasia );
3. Root dentin dysplasia ;
4. Odontodysplaziya ;
5. Focal odontodysplaziya .
At the root dentin dysplasia crowns of teeth changed in color, but have a normal shape. The roots of the teeth short, conical (in one root teeth) or W- like curved (in the multi- teeth). Crown and root of the tooth cavity obliterovani .
Coronal dysplasia is different deciduous teeth change color ( amber with opalestsyrovanyem ) obliteruvannyam tooth cavity and deposition dentykliv it . At the root and crown dysplasia type of autosomal dominant inheritance .
Odontodysplaziya characterized by impaired development of enamel and dentin as milk and permanent teeth. Teeth irregularly shaped, thin enamel and dentin . It can be observed hypoplasia and hipodozrivannya enamel. Increased tooth cavity filled dentyklyamy .
Focal odontodysplaziya – a rare abnormality that occurs in healthy children. Characterized by delayed development and eruption of teeth arranged along several as temporary, permanent, single or different periods of development. Crowns of the teeth reduced by hypoplasia of enamel, are yellow in color and rough surface . On radiographs hard tissues are presented thinned compared with healthy teeth of the same jaw with short back and wider channels of unequal density tissues in different parts of the crown , indicating that the impaired mineralization . The etiology of this disease has not been established ( Chuprinin NM, 1980). To differentiate this type of pathology should be systemic and local hypoplasia and inherited disorder enamel.
Treatment of inherited disorders affecting the dentin, is quite difficult , orthopedic techniques used , for which the evidence may be made remineralizucha therapy.
Used Books:
1. Khomenko LO Preventive dentistry childhood. Kyiv.: Book Plus, 2001. Article. 227 – 241.
2. Kuryakyna NV Terapevtycheskaya Dentistry of child age. – Moscow: Medicine, 1988 –
3. Preventive dentistry / edited. prof.A.K.Nikolishyna.-T.1.-Poltava “dreamland” 2005.-p 179-225.
4. Persyn LS Dentistry age of child Moscow: Medicine, 2003.
5. LM Lomyashvyly, LG Ayupov Artistic modeling and restavratsyya teeth. Moscow: “Medytsynskaya book” 2005.-village-39-41
6. Internet sources.
