Noncarious Diseases of Teeth Hard Tissues

Home , Abfraction, Dental fluorosis, Dentin hypersensitivity, Enamel hypoplasia, Hard tissue, Tooth discoloration

The Classification of Noncarious Diseases of Teeth

Depending on their origination period the noncarious diseases of teeth hard tissues are divided into two basic groups (V.Patrikeev, 1986):

1. Diseases of teeth hard tissues, which are originated during a tooth development or before the tooth eruption a) Enamel hypoplasia b) Enamel hyperplasia c) Dental fluorosis d) Hereditary disturbances of the tooth development

2. Diseases of teeth hard tissues, which are originated after the tooth eruption a) Tooth discoloration and dental plaques b) Tooth wear, attrition, abrasion c) Abfraction d) Dental erosion e) Dental necrosis f) Tooth traumas f) Dental sensitivity

Classification of Noncarious Diseases of Teeth Hard Tissues accepted by WHO in 1997

I Disorders of Tooth Development and Eruption 1. Anomalies of the tooth dimensions and shape- teeth coalescence, fused teeth, splited teeth, enamel drop (nodule, pearl), tooth in tooth. 2. Stained teeth- dental fluorosis 3. Teeth forming disorders- enamel hypoplasia (prenatal and neonatal, Terner’s teeth). 4. Hereditary disorders of teeth structures - indefinite amelo- and dentinogenesis, teeth changes because of indefinite osteogenesis. 5. Congenital syphilitic symptoms: screwdriver molars, Hutchinson’s teeth. 6. Other disorders of tooth development: color changes which are caused by Rh-conflict, congenital anomalies of the biliary system, porphyria and tetracycline usage in big quantities.

II Other Diseases of Teeth Hard Tissues 1. Tooth wear 2. Abrasion ( loss by wear of dental tissue, caused by abrasion by foreign substance e.g., toothbrush with tooth powder; abfraction because of bad habits, harmful professional materials and habits influences) 3. Dental erosion: professional, idiopathic, are conditioned by diet, medicaments and vomiting. 4. Dental calculi: colored plaque (dark, green, orange and plaque which is conditioned by smoking and betel chewing) generalized soft plaque, white deposit (materia alba), supra- and subgingival calculi. 5. Teeth hard tissues’ discoloration after eruption, caused by metals, presence of metal combinations, pulp bleeding, any habits which may be contributing to the condition, including tobacco use. 6. Other Specified Diseases of Teeth Hard Tissues: hypersensitive dentin, enamel changes, which are caused by the irradiation

III Destructions, poisonings and other after-effects, caused by the influence of external factors 1. Tooth fracture 1.1. Tooth enamel fracture 1.2. Crown fracture without a pulp trauma 1.3. Crown fracture with exposed pulp 1.4. Root fracture 1.5. Crown and root fracture 1.6. Multiple fractures of tooth 2. Tooth dislocation: luxation, extrusion or intrusion, exarticulation

Enamel Hypoplasia Enamel hypoplasia (EH) is a tooth enamel defect that results in lessening of the quantity of enamel. The defect can be a small pit or dent on the tooth, or can be so widespread that the entire tooth is small and/or misshaped. A critical manifestation of the hypoplasia is the aplasia, i.e. a congenital absence of the enamel or the tooth. Etiology and pathogenesis: Hypoplasia is caused by metabolic processes disturbances in the teeth embryos. This can be occurred under the influence of mineral and albuminous exchange disturbances in embryos or child organism, or local reasons, influencing on the teeth embryos. When enameloblasts development is affected only, enamel hypoplasia is occurred, but when odontoblasts metabolism is also affected, the enamel hypoplasia is accompanied by dentin formation disturbances. Some scientists think that hypoplasia is caused, because of the enameloblasts formation disturbance (A. Abrikosov, 1914). According to the point of view of another group of scientists (I. Lukomsky, 1953, S. Vays, 1965), hypoplasia is a defect of the tooth tissues mineralization, in case of their proper forming. Z. Sharaevskaja (1954), I. Novikov (1961), A. Ribakov 1961) point out, that these two processes are interconnected. They think that teeth hard tissues’ hypoplasia is caused by both: disturbance of the enamel formation by ameloblasts and the suppression of the mineralization of the enamel prisms. Hypoplasia origination causes: a) Local harmful affect on the tooth embryo b) Metabolic disturbances in an embryo’s or a child’s organism during rachitis, infectious diseases, dyspepsia, functional disorders of the endocrine glands, etc. During hypoplasia the enamel changes are irreversible. Hypoplasia of primary teeth is mainly connected with the disorders in pregnant woman’s organism (toxicosis, etc). Hypoplasia of primary teeth is found rarely than hypoplasia of permanent teeth, which is connected with metabolic disorders in children’s organism. Hypoplasia of permanent teeth is caused by different diseases children have during the teeth formation and mineralization: rachitis, acute infectious diseases, diseases of gastroenteric path, toxic dyspepsia, alimentary dystrophy, disorders of endocrine system, congenital syphilis, cerebral disorders, etc. The location of the hypoplasia on the tooth crown and the extension of damage depend on the age of the child, when he/she undergone mentioned diseases. For example, in case of the diseases during first months after birth the incisal edges of the incisors and the cusps of the molars are affected. The size of the affected area indicates the long duration of the disease. Classification: According to the etiological factors there are systemic and local hypoplasias. Systemic hypoplasia is noted at teeth, which are formed at the same period. The hypoplasia of one tooth is called local.

Systemic hypoplasia: Clinically 3 types of systemic hypoplasia are distinguished: - change of the enamel color - enamel underdevelopment - enamel absence Clinical symptoms The enamel color change is displayed as white or yellow spots, which have precise verges and the same size. The spots are usually found out on the vestibular surface of the teeth and aren’t accompanied by hypersensitivity. During the lifetime the size, the form and the color of the spot isn’t changed. Enamel underdevelopment is the maximal severe form of the systemic hypoplasia. It can appear with wavy (rough), spotted (pitted) or grooved surface. Wavy enamel is appeared after drying the crown surface with cylinders shape. There is unchanged enamel between cylinders in looks of the pits. The spotted changes of enamel are located on the both oral and vestibular tooth surfaces and have natural color after tooth eruption. These spots change the color later, though the enamel is still strong and smooth. This is the most widespread type of the hypoplasia. The grooved surface gives evidence of the isolated or multiple grooves on the tooth surface. If the whole crown has a lot of grooves it is called a “stepped”. In all the above stated examples the wholeness of the enamel isn’t broken.

The absence of enamel or aplasia is the most severe type of the hypoplasia and it is rarely met. In this case apart from the aesthetic defects the feeling of the pain can be present because of the irritant affect. The pain is eliminated after the stimuli removing. The Hutchinson’s, Furner’s and Pfluger’s teeth are the variety of the systemic hypoplasia. Hutchinson’s teeth (screw-driver, notched teeth): the teeth of congenital syphilis in which the incisal edge is notched and narrower than the cervical area. Furner’s teeth are the same with Hutchinson’s teeth without half-moon notches. They occur because of the congenital syphilis and smallpox. Pfluger’s teeth are the first molars, with the conic crown shape (the cervical area is wider than occlusal surface) and have under developmental cusps. “Tetracycline” teeth: This is a type of the systemic hypoplasia. Tetracycline is an antibiotic. It's a fairly powerful antibiotic that kills a broad spectrum of bacteria. However, when it is taken while teeth are forming, it deposits in the dentin and enamel of the teeth and creates a permanent gray or brown stain. It can be a uniform discoloration of the entire tooth or can occur in the form of horizontal bands of stain of varying intensity. They can range from mild to very dark. As a result, tetracycline is forbidden for pregnant women, because it can penetrate through the placenta. A tetracycline tooth stain is irreversible. That’s why tetracycline should be appointed for children and pregnant women only if it is necessary for life.

Local hypoplasia is the defective or incomplete development of the enamel. Local hypoplasia of permanent teeth can be a result of injury or inflammation of the precedent primary tooth. Clinical symptoms It is characterized by pits and chalky spots (of color from white to brown) on the entire tooth surface. Sometimes it happens that all enamel or a part of it is missing. These teeth are called Turner’s teeth. More often the local hypoplasia is met on the premolars, which embryos are located between primary teeth (between primary incisors and canines, which are affected by caries and periodontitis very often). Pathological anatomy During histological investigations the decreasing of the enamel width, widen interprismal spaces, a smoothing prisms’ borders, a widening of the calcification lines of Retzius etc. are found. On the spotted type the changes of the dentin occur as well. In this case the interglobular spaces are increasing, the intensive producing of the secondary dentin in the pulp is formed and the quantity of the cells is being reduced.

Differential diagnosis Enamel hypoplasia should be differentiated from fluorosis and caries in spot stage. Table 1 DISEASES Hypoplasia Fluorosis Caries in spot stage Eruption period before tooth before tooth after tooth eruption eruption eruption Affected teeth mainly the greatly the both the permanent teeth permanent teeth permanent and (rarely the primary teeth primary teeth) Location vestibular and vestibular and natural pits and oral (not typical oral (not typical fissurs, contact for caries) for caries) surfaces, cervical parts Spots quantity often solitary a lot solitary, sometimes more Permeability of not increased not increased considerably dye increased Spot’s outcome doesn’t disappear can disappear disappears with ages, but seldom, a often stays during superficial caries whole life is originated in its place 3

Content of doesn’t matter is originated in an affection is fluoride in the case of high increasing in case water density of the of deficiency in fluoride in the the fluoride in the water water Luminescent luminescence luminescence light diagnostics extinguishing extinguishing extinguishing in isn’t noted isn’t noted carious spots’ areas

Treatment Treatment options depend on the severity of the EH on a particular tooth and the symptoms associated with it. The most conservative treatment consists of bonding a tooth colored material to the tooth to protect it from further wear or sensitivity. In some cases, the nature of the enamel prevents formation of an acceptable bond. If there are patient complaints of the aesthetic lacks, an operator can do the following procedures: a) Enamel micro abrasion - perform minimal reduction of tooth enamel superficial layer, which is discolored. The abrasive creams containing hydrochloric acid (“Prema”) b) remove demineralized enamel and restore with composite c) If there are esthetic concerns, direct or indirect composite or porcelain veneers may be bonded to the affected tooth. Less conservative treatment options, but frequently it is necessary to include using of stainless steel or porcelain crowns, permanent cast crowns or extraction of affected teeth and replacement with a bridge or implant. Prevention of the systemic hypoplasia It is necessary to prevent the origination of the systemic hypoplasia, which causes metabolic disturbance. Prevention of the local hypoplasia: Caries of the primary teeth should be prevented, and after its origination the proper and on time treatment must be done.

ENAMEL HYPERPLASIA (ENAMELOMA)

Enameloma is a developmental anomaly in which there is a small nodule of enamel below the cement-enamel junction, usually at the bifurcation of molar teeth (enamel drop, nodule, pearl). The diameter of enameloma ranges from 1mm to 2-4mm. A dentin can be found under the enamel layer; sometimes the cavity filled with pulp may be inside the nodule. There aren’t any clinical symptoms and physiological disturbances. If there are no esthetic complaints, no treatment is needed.

DENTAL FLUOROSIS

Dental fluorosis is an irreversible condition caused by excessive ingestion of fluoride during the tooth forming years. Dental fluorosis occurs because of the excessive intake of fluoride either through naturally occurring fluoride in the water, water fluoridation, toothpaste, or other sources. The damage in tooth development occurs between the ages of 6 months to 5 years, from the overexposure to fluoride. Teeth are generally composed of hydroxyapatite and carbonated hydroxyapatite; when fluoride is present, fluorapatite is created. The excessive quantity of fluoride can cause yellowing of teeth, white spots, and pitting or mottling of enamel. Consequently, the teeth become unsightly. Fluorosis cannot occur once the tooth has erupted into the oral cavity. At this point, fluorapatite is beneficial because it is more resistant to dissolution by acids (demineralization). Etiology and pathogenesis Fluorine is one of the most active halogen chemical elements and is widely spread in nature. Adults receive 3mg F per day (0.5-1.1mg with food and 2.2-2.5mg with water). Fluoride from food is assimilated by human organism less than from water. According to clinical analyses the limited allowed concentration of fluoride in drinking water is 1-1.5mg per liter. In this case a fluorosis can meet rarely, and there is the caries resistance. A fluoride concentration of more than 6mg/l can affect the erupted teeth. Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste use, consuming food with high fluoride content, or consuming fluoride supplements. In those counties where the temperature 4 is high due to hot weather fluorosis is present even in the event of concentration 0.5-0.7mg per liter. It is related to high quantity water use. Fluoride is present in food, water, air, and most tissues of the human body. The chemical action of Fluoride on teeth is to resist dissolution of the enamel by acid-producing oral bacteria. The proper origination mechanisms are not studied in details. Fluoride causes dental fluorosis by damaging the enamel-forming cells, called ameloblasts in stage of tooth development known as “enamel organ”. It is supposed that the damage of the enamel-forming cells results in a mineralization disorder of the teeth, whereby the porosity of the sub- surface enamel is increased. Fluorosis basically affected children’ permanent teeth, who live in fluorosis areas from birth or to 1-4 years old. Classification and clinical symptoms In affected parts the tooth enamel loses its shine and transparency, becomes dim, and yellowy-brown spots appear on it. According to WHO classification 5 degrees of fluorosis affection exist, meanwhile V. K. Patrikeev classifies 5 main forms of affection.

Table 2 Classification of the fluorosis by WHO Classification of the fluorosis by V.K.Patrikeev I degree: very mild-almost no changes of enamel color II degree: mild- small opaque, paper white Linear type: more frequently is present on areas covering less than 25% of the tooth the vestibular surfaces of the upper incisors surface and characterized by present of the small chalky lines, which are feebly marked III degree: moderate- opaque white areas Spotted type: there are strongly expressed covering less than 50% of the tooth surface chalky spots. The enamel surface in spots’ areas is smooth and glossy. IV degree: middle heaviness- all tooth Chalky-speckled form, there are strongly surfaces affected; marked wear on biting expressed chalky spots in this case. An surfaces; brown stain may be present enamel surface in spots’ areas is smooth and glossy. V degree: severe- all tooth surfaces are Erosive form, which is characterized by affected; discrete or confluent pitting; erosions, up to the dentin uncovering brown stains present Destructive type: both the enamel and dentin are affected

Pathologic anatomy The nature of the changes depends on the clinical type. Striae of Retzius and Hunter-Shregers lines appear vividly. The enamel surface is rough in some parts. The dentin-enamel junction has the cogged shape. The interprismal spaces are enlarged because of the partial resorption of the enamel prisms. The hypo- and hypermineralized zones are originated the latter give watered appearance to enamel. Differential diagnosis Fluorosis should be differentiated from superficial caries, caries media, enamel hypoplasia, abfraction and enamel chemical necrosis (see the table). Treatment The treatment depends on the stage of pathological process. Tooth bleaching, microabrasion, and conservative composite restoration or porcelain veneers are commonly used treatment modalities. Generally speaking, bleaching (20- 30% hydrochloric and phosphoric acids) and microabrasion are used for superficial staining, while the conservative restorations are used for erosive and destructive forms. Also, as a preventative measure, dentists recommend that children should not receive topical fluoride treatment until the age of three or at the earliest time that a determination can be made about a child's total flouride exposure. Prevention Prophylactic procedures are: 5

1. public 2. individual Public procedures are usually used for decreasing the fluoride quantity in drinkable water by following: a) the change of water source b) mixing the different water sources c) water cleaning with salts of Aluminum, Magnesium hydroxide or Calcium phosphate There are some individual preventive methods: a) natural nutrition b) non usage of foods additive in the daily food of a child from the early age c) addition of the vitamins C, D, Ca gluconate in daily food d) the limitation or exclusion of F-contain products from the daily meal (for example, sea fish) e) children evacuation from endemic areas during their holidays.

ANOMALIES OF TEETH DEVELOPMENT AND ERUPTION

1. Eruption delay. This arises under the action of general and local factors. The general etiologic factors are the rickets, tuberculosis, defeats of nervous and endocrine systems. The local etiologic factors are the wrong arrangement of the teeth rudiments, periodontitis of primary teeth and wrong development of the jaws. More often the third molars and canines of the top jaw have eruption delay. 2. Premature eruption. It is considered, that the reason is the acceleration. It meets very rarely. Cases of children birth with already erupted teeth (which are necessary to remove at once) were described. 3. Supercompleted teeth. Such teeth can be erupted both in the tooth arch, and out of it. They often have wrong form, rarely - normal. 4. Reduction of total quantity of the teeth - adentia. It is characteristic for the second incisors of the upper jaw and the third molars. Very rarely meets complete absence the teeth - complete adentia. 5. Changes of the form of the teeth. It is characterized by adhesion and merge of the next teeth.

HEREDITARY DISORDERS OF TEETH DEVELOPMENT

AMELOGENESIS IMPERFECTA

Amelogenesis imperfecta (AI) is a hereditary disease at which the normal development of ectodermic cells is affected, and as a result not only enamel is affected, but also other organs, which have epithelial origin - hair, nails, perspirative and sebaceous glands, etc. Clinical symptoms 4 clinical forms of amelogenesis imperfecta are distinguished: 1. Changes are not much expressed, the teeth are of normal form and size, but have yellow or brown shade. 2. 1-3 years after the eruption the enamel become matte, then is painted in brown color becomes rough, cracks appear on it. Then the enamel completely or partly lost. Dentin is dense, brown, has normal structure. 3. The teeth have normal form and size at eruption. The enamel is white, but is covered by a considerable quantity of grooves. Enamel on all teeth quickly disappears and brown dentin is bared, which have normal structure. 4. The teeth have normal form and size at eruption, but enamel is already chalky, matte, is absent in some places. Enamel easily separates from dentin at mechanical influence. Hypersensitivity of the teeth is observed. It is necessary to note, that at all forms of amelogenesis imperfecta the roots of the teeth have normal structure, which testifies about normal dentinogenesis. Pathologic anatomy Under an electronic microscope it is possible to find out roughness of the dentin-enamel junction, and quantity increase of organic substance of the enamel. The orientation of enamel prisms is broken, zones without prisms are found out, which are filled with amorphous substance. Dentin has a usual structure. Treatment In some cases the remineralization of the tooth enamel could be needed. Sometimes prosthetic treatment is necessary.

DENTINOGENESIS IMPERFECTA

Dentinogenesis imperfecta is a hereditary disturbance of dentin development. Crowns of the teeth have normal form, size and color. Roots of the teeth are involved into the pathological process. They either are underdeveloped, or have sharpened form, and sometimes are completely absent. The X-ray shows shortening of roots length of all teeth, and also absence of tooth cavities and root channels. Teeth are mobile and early drop out. Treatment Prosthetic treatment is necessary.

STEPTON-KAPDEPON’S DISPLASIA

This is a hereditary disease which is based on the dentin formation disorders. Primary and permanent teeth is amazed. The eruption terms and teeth quantity are not broken. Crowns of the teeth have normal form and size, but roots are short and narrow. Crowns of the teeth have grey shade. Right after the eruption the enamel is lost, transparent dentin is bared, which is used up very quickly. Hystologically disorders of the prism arrangement are found out in enamel, and shortened and expanded dentin tubules are observed in dentin.

MARBLE-BONE DISEASE

Marble disease (or Albers-Sheinberg’s disease) is a congenital family osteosclerosis. The basic symptom of the disease is the sclerosis of spongy substance of the bones. The bone X-ray shows white centers of sclerosis, reminding marble drawing. Because of the bone sclerosis, there is an eruption delay. Right after the eruption the teeth enamel has chalky shade, and then becomes friable and is quickly lost. The teeth are destroyed very quickly. Treatment Prosthetic treatment is necessary.

DISEASES OF TEETH HARD TISSUES ORIGINATED AFTER THE TOOTH ERUPTION a) Tooth discoloration and dental plaques b) Tooth wear, attrition, abrasion c) Abfraction d) Dental erosion e) Tooth necrosis f) Tooth sensitivity

TOOTH DISCOLORATION

In norm healthy teeth has white color with various shades from bluish-white (primary teeth) to white-grey and even yellow (permanent teeth). Change of the teeth color is caused by many factors, both external and internal. The internal factors are: - Hard proceeding viral hepatitis or cholera can cause tooth coloring into pink color (the change of the tooth color is a result - of hemorrhages in the pulp). - A number of general diseases (for example, during liver diseases pigments bilirubin and biliverdin are collected in hard tissues of the teeth, which give yellow or brown shades to the teeth). - Reception of antibiotics of Tetracycline series by children under 12 years or by pregnant women during last 6 months of pregnancy - Pulps necrosis The external factors are: - Food pigments (coffee, tea, some berries) - Some medicaments, used for the oral cavity rinsing (chlorhexidine gluconate, potassium permanganate (KMnO4), Etacridine, Lactate, Iodine containing solutions) - Some pastes for the root canas filling (resorcin-formalin paste, paratsin, which paint a tooth in orange color)

- Oxidation of broken endodontic tools or silver pins in the root channel - Smoking, this can cause dense brown or black plaque on the teeth Treatment The dense tooth plaque and the plaque of smokers should be removed by excavators or scalers. Then clearing of the teeth by special brush with abrasive paste and rubber cups is done. For correction of teeth color bleaching of vital or devital teeth is spend or ceramic veneers are prepared.

TOOTH STRUCTURES’ WEAR

Wear is a loss of substance or a diminishing through use, friction, or other destructive factors. Wear is a physiologic process occurring during all life. There are physiologic and abnormal occlusal wear. Physiologic wear is an attrition or abrasion of tooth substance occurring as a result of the conditions such as the abrasive consistency of the normal diet or the slight buccolingual movement of the teeth possible in the masticatory process. It does not include the wear produced by such influences as habits or occlusal prematurities. Wear degree depends on the men age. In the range the loss of tooth enamel is seen on the cusps at the age of 40, and the considerable enamel wear of cusps and incisors crowns shortening is expressed at the age of 50-60. Abnormal occlusal wear is the early, in young age, and strongly expressed decrease of firm tissues, which can be seen on one tooth, on the group of teeth, or on all teeth. Etiology and pathogenesis Deformation of tooth structure results from three basic physical and chemical mechanisms that can act alone or in combination. a) stress results in compression, flexure, and tension. It can produce microfracture and abfraction as a dental manifestation; b) friction includes abrasion from exogenous material and attrition, which is endogenous and results from empty mouth bruxing and parafunction. The end point of both is wear of tooth surfaces; c) corrosion is the result of chemical or electrochemical degradation. The wear rate of enamel, called attrition, is 8 micrometers a year from normal factors. A common misconception is that enamel wears away mostly from chewing, but actually teeth rarely touch during chewing. Furthermore, normal tooth contact is compensated physiologically by the periodontal ligaments (pdl) and the arrangement of dental occlusion. The truly destructive forces are the parafunctional movements, as found in bruxism, which can cause irreversible damage to the enamel. Other nonbacterial processes of enamel destruction include abrasion (involving foreign elements, such as toothbrushes), erosion (involving chemical processes, such as lemon juice), and possibly abfraction (involving compressive and tensile forces). So, there are many factors, which are occlusion, occlusal overloading because of the missing teeth, bad prosthesis, the influence of professional harmful factors, endocrine glands disorders (thyroid gland, parathyroid gland, hypophysis), incomplete formation of tissues structures, etc. Classification According to clinico-anatomical classification by M.Groshikov (1985) there are 3 degrees: I degree- the slight wear of cusps and incisal edges II degree- wears of cusps and incisal edges up to the dentin exposure III degree- enamel and dentin wears to teeth cavity. Clinical symptoms Depends on the wear degree, the patients complain of hypersensitivity from thermal, physical and chemical stimuli. Though due to renewing function of pulp (secondary dentin formation) the hypersensitivity can eliminate or be feebly marked. The clinical appearance of attrition: matching wear on occluding surfaces; enamel and dentin wear at the same rate; possible fracture of cusps or restorations. The clinical appearance of abrasion: lesions are more wide than deep; usually located at cervical areas of teeth; premolars and cuspids are commonly affected. The teeth crowns shorten by 1/3-1/2 of their height; EPT is 6-20mA. The incisal edges became flat planes, and the cusps of premolars and molars are completely worn. The delayed treatment can cause malocclusion, shorten vertical dimension, which can cause TMJ disorders. TMDs lead to pain and burning of the oral mucous membrane, decreased hearing and origination of fold in mouth angles. Pathologic anatomy Oral pathology depends on the wear degree: I degree characterized by the secondary dentin in place according to place of wear. II degree characterized by the pronounced origin of secondary dentin, obliteration of dentinal tubules, changes in pulp (decreased quantity of odontoblasts and their vacuolation). III degree characterized by the sclerosis of the dentin; almost the whole crown is filled with secondary dentin; the pulp is resorpted.

Treatment The factors of etiology and pathogenesis, degree of wear should be taken into account during treatment planning. In case of I and II degree the goal of treatment is to stabilize the process. For this purpose the inlays, onlays and full metal crowns are made on the antagonists (generally for molars). If the number of the missing teeth is great the fixed or removable dentures are used. In case of III degree the main aim is to restore vertical dimension. Prosthetic treatment is needed (by fixed or removable dentures). The direct indication to it are complaints of pain in the TMJ area, burning and pain of tongue, that is a result of change of position of the articulate head in the articulate pit. Usually the treatment is long and accompanied with the construction of appliances used to provide therapeutic effect. These appliances give opportunity to restore the rest position of TMJ components. For treatment of wear in case of tooth sensitivity see Tooth sensitivity. Tooth wear, leading to the loss of enamel or root surface may result from abrasion or attrition. Attrition is tooth- to-tooth contact, which results from occlusal function or parafunction, such as bruxism, and can cause loss of tooth structure on the occlusal surfaces and incisal edges. Neither abrasion nor attrition usually results in hypersensitivity due to the force-created smear layer, which obdurate dentin tubules. Both of these gradual traumatic processes stimulate the development of natural protective measures, such as secondary dentin and sclerosis. This can be observed in older individuals who show more exposed dentin, but less sensitivity than their younger counterparts. Tooth Abrasion Tooth abrasion is the permanent loss of tooth structure that can occur on the tooth's cutting surface, the outer enamel layer, exposed root surfaces, and non-enamel surfaces. It is caused primarily by improper brushing - usually overly vigorous or horizontal brushing. The damage can also be caused by abrasive toothpaste, or habits such as chewing on hard objects or using teeth as a cutting tool. Tooth abrasion is most common in people suffering from gum disease whose gums have pulled away from their teeth. The root surface that is then exposed is not as wear-resistant as enamel. If the abrasion occurred gradually, body's natural ability to repair itself enabled new dentin to be deposited on the damaged portions of the tooth. This will prevent the pulp (the portion that contains, among other cells, the nerves and blood vessels) within the tooth from being severely or even irreversibly damaged. However, if the abrasion occurred quickly, it's likely that patient will suffer pulp damage, which can cause tooth sensitivity, infection, pain, and possible loss of that tooth. Tooth Attrition Tooth attrition is the loss of tooth structure that can result from tooth-to-tooth contact during biting or chewing. It occurs primarily on the biting or chewing surfaces of teeth, but it can also occur on what we call the proximal areas, where the teeth are in contact with adjacent teeth. The changes resulting from tooth attrition can range from small points of increased wear to a reduction of the tooth's height and a flattening of the chewing surfaces (the cusps). Generally, tooth attrition is commonly met among elderly people and it often showed up as smooth, polished surfaces on the tooth. The condition can be influenced by the texture of the foods you eat, gum chewing, use of tobacco products, or bruxism, an abnormal clenching and grinding of the teeth. Attrition can also be caused by abrasive dust in the atmosphere. The attrition can be severe if the patient suffers from amelogenesis imperfecta or dentinogenesis imperfecta - conditions in which the tooth's enamel or dentin does not form properly.

ABFRACTION

Abfraction is a loss of tooth surface at the cervical areas of teeth caused by tensile and compressive forces during tooth flexure. It is a mechanism that explains the loss of dentin tissue and tooth enamel caused by flexure and ultimate material fatigue of susceptible teeth at locations away from the point of loading. The breakdown is dependent on the magnitude, duration, frequency, and location of the forces. (Studies needed to prove this hypothetical phenomenon). Abfraction generally occurs on the teeth of patients of average age and elder people and is accompanied with periodontosis. Location: Affects buccal/ labial cervical areas of canines and premolars. These are deep, narrow V-shaped notches. They can be single and multiple, on the symmetric teeth. Commonly affects single teeth with excursive interferences or eccentric occlusal loads. Etiology and pathogenesis There are two general theories - mechanical and chemical, which explains the origination of the so-called abfraction lesions. According to the first theory the accepted characteristics of abfractions as wedge-shaped lesions with sharp line angles is actually characteristic of toothpaste abrasion because of vigorous tooth brushing.

Abfraction lesions more often occur on the canines and premolars, which has more vestibular position, and that’s why are more affected with mechanical overload. This fact is explained by mechanical theory. It is clinically established, that at right-handed persons, defects are located generally at the left side, as they clean their left-side teeth more intensively. At lefthanders who clean the teeth of the right-side more intensively, defects are more expressed on the right. But there are some facts, which leave doubt, that cervical lesions are the result of mechanical influence, for example the presence of abfraction on animal teeth and that of the patients who doesn’t brush their teeth. Another theory (chemical) isn’t convincing. Further studies indicated that acid penetrates the microcracks and undermines tooth surfaces that are then more susceptible to mechanical deformation. Some investigators have claimed that diseases of endocrine glands, disorders of gastrointestinal tract and nervous system. Clinical symptoms Cervical lesions, caused by occlusal stresses, lead to weakening of the cervical tooth structure and can cause enamel, cementum or dentin to chip away from the cervical aspect of the tooth. The appearance of the lesion is a V- shaped cervical notch. In the first stages the lesions are superficial scratches. And then they are increased and resizes to the regular shape. Walls of lesions are smooth, hard and shiny. Abfraction is most likely a co-factor with abrasion or erosion in tooth structure loss, since abfraction has not been identified as a sole cause of hypersensitivity. In fact, enamel loss rarely results from a single agent but rather from a combination of two or three contributing factors (thermal, mechanical and chemical). The patients complain of aesthetic defects. They usually don’t have pain or hypersensitivity, because the cervical lesions are developed slowly, and the secondary dentin is originated. As a rule an exploration isn’t painful. Different stimuli can cause pain in cases of fast development of abfraction. Defects can penetrate hard tissues up to the pulp, which is never exposed. Abfraction is often accompanied with gingival recession. Pathologic anatomy The contraction of enamel interprismal spaces, obliteration of dentinal tubules, and atrophy process in pulp are found. Differential diagnosis Abfraction should be differentiated from dental erosion, cervical necrosis of the enamel, superficial and medial caries of the teeth (see the table). Treatment There are two directions of treatment: local and general. The purpose of general treatment is a strengthening the structure of teeth hard tissues by using vitamins and microelements. The local treatment provides eliminating the teeth sensitivity (10% solution of calcium gluconate, 2% solution of fluoride of sodium (Na), tooth pastes containing 75% F), restoration of the defect (by composites, etc.), and in case of deep lesions the artificial crowns are indicated. It is necessary to remove affecting factors (use of rigid bristles toothbrushes, horizontal movements during tooth brushing) to prevent defect’s development and further deepening. It is advised to use toothpastes with fluoride or glycerophosphates.

DENTAL EROSION

Dental erosion is defined as irreversible loss of dental hard tissue by a chemical process that does not involve bacteria. It is located on vestibular surfaces of the teeth and has a form of a plate. Etiology and pathogenesis The mechanism of erosion is incompletely known, but there are some points of view. Dissolution of mineralized tooth structure occurs upon contact with acids that are introduced into the oral cavity from intrinsic (e.g., gastroesophageal reflux, vomiting) or extrinsic sources (e.g., acidic beverages, citrus fruits). Exposure to acid over a long period of time leads to progressive loss of enamel with the effect that the tooth “shrinks” and crumbles at the biting edge. Eventually the dentine is exposed leading to pain and sometimes death of the tooth. Y. M. Maksimovsky (1981) thought that an important role in dental erosion pathogenesis have endocrine disturbances and, in particular, the thyroid gland hyperfunction. One of the symptoms of this disease is the increase of saliva secretion and decrease of the oral liquid viscosity that should affect the teeth hard tissues. Location

The erosions are more often broad concavities of different shapes at the cement-enamel junction on the vestibular surfaces of upper incisors, upper and lower canines and premolars in symmetric parts. Erosions aren’t seen on the surfaces of the molars and mandibular incisors. Classification There are 2 clinical stages of erosion: active and stabilized, though it is a chronic disease by its course. The active stage is characterized by quickly progressing decrease of the tooth hard tissues that is accompanied by hypersensitivity of the amazed site to various external stimuli (the phenomenon of hypersensitivity). The stabilized stage of erosion is characterized by slowed down and quieter current. Other sign is the absence of the teeth hypersensitivity. There are 3 degrees according to depth: I degree (superficial) - the superficial enamel layers are affected. II degree (middle) – the entire enamel is affected up to the dentin-enamel junction III degree (deep) - the superficial dentin layers are affected Clinical symptoms The enamel is less susceptible to erosion than the cement, since it is thicker and more highly mineralized. At the area of the cement-enamel junction there may be only a thin layer of enamel, making this area particularly susceptible to loss of tooth structure. Because the layer of the cementum is thin and not highly mineralized, it easily can be abraded or eroded in this area. Erosion is thought to be the major source of tooth wear, and has been defined as tooth dissolution by acids that are not of bacterial origin. Erosion from dietary acids is thought to work in combination with abrasion from tooth brushing and toothpaste, leading to more loss of tooth structure than would be possible with either effect alone. At the first stage the insignificant defect is originated and step-by-step increased up to the dentin. The surface of the erosion cavity is hard and smooth. Sometimes the brown-yellowish shade is possible. Considerable loss of tooth structure and increased hypersensitivity are characterized for the active form of erosion, and the stabilized form is characterized by relatively slow course and no tooth sensitivity. Pathological anatomy There is widening of the enamel interprismal spaces, enamel superficial demineralization, obliteration of dentin tubules. Differential diagnosis Enamel erosion should be differentiated from superficial caries and abfraction. Erosion differs from caries by location, by defeat form, and by surface (at erosion it is smooth, and at caries it is rough). Abfraction differs from erosion by defeat form, by localization at the neck on the enamel-cement junction (see the table). Treatment The process is irreversible and requires cosmetic dentistry to restore function and appearance. The activity of process, disease’s character, etc should be considered. Common treatment purpose is to put into organism vitamins, medicaments, containing Ca (calcium) and P (phosphorus). The restoration with filling material is usually not effective (according to Y. M. Maximovsky) because of the failure of edge fit of inlay and origination of secondary defects around restoration. The remineralization with Ca and P before dental fillings and restorations are recommended to avoid of failure. Composites, compomers or glass ionomer cement are used as filling materials. Fillings containing fluoride are more preferable. In case of big defects the prosthetic treatment is advised.

NECROSIS OF TOOTH HARD TISSUES

Necrosis of hard tooth tissues is severe disease, which sometimes causes tooth loosening. There are cervical and chemical necroses. Etiology and pathogenesis There are internal and external causing factors. The internal factors are pathologic processes of endocrine glands, chronic discolorations, and hereditary disorders of tooth development. The influence of local or external factors causes chemical necrosis of the teeth, which is met among the people working in chemical factories. The presence of different organic and inorganic acids’ steams (chlorine, sulfuric, nitric,

11 hydrochloric acids) in the environment of the factory can cause decalcification, because these acids penetrate to oral cavity and are dissolved in saliva, which pH is became acid. Clinical features Cervical necrosis is mainly located in cervical part of central teeth on the vestibular surfaces. The chief complaint of patient is pain to thermal, chemical, mechanical substances. The pain is quickly passed when stimuli are removal. A small, shiny, chalky spots are seen in first stage and then these spots loose their brilliance, became dark brown. The softening in the centre of hearth is found during examination; enamel is very fragile and can be exfoliated by excavator. It is peculiar to necrosis, that necrotic part is spread in width (breadth) much more than in depth. This property is very important in differential diagnosis of caries and necrosis (pathologic hearth is spread in depth when the caries joins to necrosis). The feeling of tender and sensitivity to thermal and mechanical agents are first signs of the chemical necrosis. Sometimes the sense of adherence is originated during teeth contact. The enamel (generally of frontal teeth) is chalky, rough and sometimes is discolored; the wear is strongly pronounced. In first stage the mentioned changes of teeth are originated on the vestibular surfaces, and then the process is spread on the oral surfaces as well. Crowns shorten and take the shape of wedge. Pathologic anatomy The origination of superficial demineralized locuses is typical for cervical necrosis. Differential diagnosis Dental necrosis should be differentiated from abfraction, dental erosion and caries (see the table). Treatment The aim of treatment is to eliminate the tooth hypersensitivity and fill the cavity. In case of severe wear of tooth structures the prosthetic treatment is indicated.

TOOTH HYPERSENSITIVITY

Hypersensitivity is an adverse reaction to contact with specific substances in quantities that usually produce no reaction in normal individuals. Tooth sensitivity is tooth discomfort after eating cold or hot foods or drinking liquids or even breathing cold air, means increased sensitivity to thermal, chemical and physical substances. It can cause by caries, non-carious disease, periodontal disease, in case of disorders of the nervous, digestive, endocrinal systems, metabolic and climacteric disorders, etc. Tooth sensitivity can be caused by the following factors: - Brushing too hard or with too much pressure which removes gum tissue. 2 of 3 people brush too hard. - Aging, sensitivity is highest between the ages of 25-30 - Using a hard tooth brush instead of a soft one - Poor oral hygiene which leads to plaque build-up around the teeth and gums. This plaque hardens into tartar. The bacteria that live in plaque cause gum disease and gum recession - The exposed roots contain small pores or tubules which lead directly to the nerve of the tooth. Pain, pressure and cold stimuli can travel down the tubules and trigger the tooth nerve causing pain and discomfort - Stimulation from hot beverages or foods. - Tooth whitening - often beautiful, but sometimes uncomfortable at least for a few days Hypersensitivity - Cracked teeth - Grinding teeth - Long term use of mouth wash such as Listerine or Oraldene damage dentine and cause dentin sensitivity and reverse the beneficial effects of toothpaste - Enamel erosion by acidic foods - Root sensitivity can occur after having your teeth cleaned, following root planning, crown placement, or even having fillings. - People with sensitivities to sight, hearing, taste, smell and touch also usually have sensitive teeth. - Decreased saliva flow-simple test is to invert the lower lip, dry the mucous membrane off and see how long it takes for small droplets of saliva to flow from the minor salivary glands. If it takes more than a minute, the saliva flow is down. - PH test resulting in an "acidic mouth" - Dental treatments-simple cleanings, orthodontics or restoration - Dehydration due to diuretics such as alcohol beverages, caffeine-containing drinks like coffee. Many other causes exist, some of which can require a more comprehensive treatment plan:

- Broken, chipped or fractured teeth - Nerve damage in the root, cant' sleep at night-root canal - Grinding and/or clenching the teeth-mouth guard - Gum disease-begin a comprehensive oral hygiene regimen - Receding gums-gum disease and/or oral habits Classification (by Y.Fedorov) a) According to the localization: 1. Limited hypersensitivity (because of some separate teeth caries or abfraction) 2. Generalized hypersensitivity (increased sensitivity of the majority of teeth because of periodontal diseases, attritional wear, etc) b) According to the origin: 1. Hypersensitivity related with the loss of tooth structure (caries and non-carious diseases) 2. Hypersensitivity without loss of tooth structure (in case of periodontal and systemic diseases) c) According to the clinical signs: 1. I degree- the state of responsiveness of teeth to external influences, such as heat- thermal sensitivity, EPT 5-8mA; 2. II degree- increased sensitivity to thermal and chemical stimuli, EPT 3-5mA; 3. III degree- increased sensitivity to all types of stimuli, EPT 1.5-3.5mA; Clinical appearance Hypersensitivity has been referred to as an enigma for a variety of reasons, including difficulty in determining the etiology, the numerous treatment approaches, variability in pain relief, and because in vivo objective clinical trials are difficult to conduct. Dentin hypersensitivity has been defined as short or transient sharp pain of a rapid onset that arises from exposed dentin. It usually occurs in response to stimuli—typically thermal, evaporative, tactile, osmotic, or chemical—and cannot be ascribed to any other dental defects or pathology. It can also be described as a response from a non-noxious stimulus and characterized as a chronic condition with acute episodes. Tactile (i.e., instrumentation-dental explorer), thermal (i.e., hot or cold water) and chemical (i.e., cotton small balls are impregnated with 4% glucose) stimuli are non-noxious. Differential diagnosis It should be differenced from the acute pulpitis, as there is acute pain in both conditions, and the patients mention the painful tooth with difficulty in both cases. A pain during pulpitis is long-term and became severe in the night, EPT 20mA and more. In case of hypersensitivity EPT is 2-6mA as in normal condition. Treatment It depends on the factors, causing sensitivity. Remineralizing therapy is indicated in all cases. If the sensitivity is a result of the caries or non-carious diseases a dental fillings of cavities are felt. It is much more difficult to fight against postoperative tooth sensitivity. So it is necessary to prevent it by keeping the rules of acid-etching techniques, using proper adhesives for desensitization, avoiding of excessive dentin drying, etc. And the treatment of sensitivity, caused by the cervical exposure or exposure of the root cementum. In these cases the chemical desensitization is the most common method of treatment: - Ca containing medicaments, such as 10% solution of the Ca gluconate. - Fluoride containing medicaments: 2% solution of the sodium fluoride, fluoride varnish? etc. - Surface sealers or self etch primers: “Fortify” (Bisco), Seal & Protect/Clearfil SE Bond (Dentsply) etc.

TEETH INJURIES

Teeth injuries may include damage to teeth as a result of falls, accidents and other mishaps. These injuries can cause teeth to become chipped, cracked, partially displaced or completely dislodged from the socket in the mouth. The severity of a dental injury (fractured, displaced, or avulsed tooth) may not be immediately apparent. Often dental injuries are associated with other head and neck injuries, such as fractured facial bones, concussions, abrasions, bruises, soft tissue lacerations with bleeding, and jaw-joint problems. After medical concerns are addressed, the extent of the dental injury should be evaluated. Any dental injury has the potential of being serious, and complications may arise weeks or years after the incident. Patients who suffer a tooth injury often have symptoms such as bleeding in the area, pain or increased sensitivity in the tooth injuries are caused by mechanical trauma. According to factors and date of injury origination there are acute and chronic damages. The acute injuries are usually resulting of simultaneous mechanical influence of comparable big

13 force (shock), and chronic damages are caused from long-term influence of the little mechanical force (bad fillings, prosthesis, etc.). Classification 1. Acute injuries: (by M.Groshikov 1985) Contusio dentis - with or without the damage of neurovascular bundle 2. Luxation, delocation dentis a) Subluxation: Injury that causes a tooth to become loose in the socket but is not knocked out of position (with or without the damage of neurovascular bundle) - with the tooth crown movement to occlusal surfaces - with the tooth crown movement to vestibular surfaces - with the tooth crown movement to the adjacent teeth - with the tooth crown movement palatal movement - with rotation along its long axis - combined. b) Intrusive luxation: injury that causes the tooth to be pushed deep into the socket, sometimes to the point that the tooth is no longer visible. The tooth may appear knocked out. c) Extrusive luxation: Injury that displaces the tooth from its position. These teeth require immediate treatment to keep them from becoming permanently fixed in this position. 3. Tooth fracture- fractura dentis a) tooth’s crown fracture - within enamel - within enamel and dentin with or without tooth cavity’s exposure b) cervical fracture - upper the gingival sulcus - below the gingival sulcus c) root fracture, with or without pulp trauma, (with or without displacement of the fragments), in apical, in cervical and in the middle part of the root - longitudinal - transverse - oblique - multiple 4. Combined injuries 5. Tooth embryo injuries

CONTUSIO DENTIS

It is an insult or damage to the tooth and its investing structures produced by trauma. During first hours patients suffer from chronic pain in rest condition. The pain is increased during biting. Sometimes lesions include damage of neurovascular bundle and pulp necrosis, because of periodontal apical ligament’s mechanical pressure. In case of pulp necrosis the tooth after some time changes its color (grey or black), and the symptoms, which are typical for chronic periodontitis, are appeared (bone resorption, fistula origination, etc). EPT should be done in 2-3 days to determine the degree of vitality of the pulp tissue. Differential diagnosis Contusio dentis should be differentiated from root fracture. The root fracture is visible on the x-ray film. Treatment It is necessary to provide rest condition of injured tooth by avoiding eat hard food and eliminating any contact with antagonist. If the pulp cannot be saved it may need to be removed. In case of damage of neurovascular bundle pulpotomy should be done. If there is a tooth discoloration the tooth bleaching must be done before root filling.

LUXATION

Luxation-(Luxatio, delocatio dentis) - dislocation or displacement of a tooth because of trauma in case of vertical or lateral forces. In case of periodontal diseases, if there is bone resorption, luxation can occur even during mastication of hard food. Luxation can be isolated or accompanied with fractures of root, alveolar bone or mandible.

Avulsion refers to a tooth being knocked out of the mouth. Subluxation. Injury that makes a tooth become loose in the socket but is not knocked out of position. It is accompanied by rupture of some periodontal fibers. The tooth can be displaced in different directions, what is visible and is determined by the tooth position in dentition. Radiographically, evidence includes the narrowing of the periodontal membrane space or it’s absent on the side of displacement. And on the opposite side the periodontal membrane space become wide. In case of vestibular movement of tooth the crown and root apex are being displaced in opposite directions. On the x-ray film the root of this tooth is appeared shorter. In case of occlusal movement the crown of moved tooth is appeared elongated. There is empty space in apical part of alveolus on the x-ray film. Intrusive luxation. Injury that makes the tooth be pushed deep into the socket, sometimes to the point that the tooth is no longer visible. The tooth may appear knocked out. Extrusive luxation. This is an injury that displaces the tooth from its position. These teeth require immediate treatment to keep them from becoming permanently fixed in this position. In case of luxation the patients complain of one or group of teeth pain and teeth mobility. Patients indicate the exact reason and duration. Treatment First of all it is necessary to determine an expediency of saving the tooth. The main criterion is the condition of bone in the region of tooth root. The tooth should be saved if the bone structure is maintained not less than half of root length. A dentist often can determine the severity of the injury based on whether or not the tooth is loose and whether or not the tooth is tender to the touch. In some cases, X-rays may be helpful in determining the extent of the injury. If the injured tooth is still in the mouth, the dentist will determine whether the tooth needs to be realigned or removed. In some cases, the tooth can be pushed into place or reimplanted without having to perform major restoration work. However, some injuries may be severe enough to put the tooth’s pulp at risk of infection or death. In such instances, the main purpose of treatment is to keep the pulp of the tooth intact. If the pulp cannot be saved it may need to be removed. So EPT is used for determining the condition of pulp. If data of EPT is 2-3mkA, so the neurovascular bundle is damaged. Notice: the data of EPT can be decreased during first 3-5 days because of the response of tissues to injury. In such cases it is necessary to check up the pulp condition in dynamics (repeatedly). If the tooth at repeated inspection reacts to the current of 100mkА and more, it indicates the pulp necrosis, and the tooth is necessary to remove. Treatments that may be performed when the pulp is compromised include: Direct pulp capping: Placement of a cement base under a deep filling to protect the pulp from infection. Pulpotomy. This is a removal of the top part of the pulp, which results in partial removal of the nerve. It is mostly often used on primary teeth. Pulpectomy. Complete removal of the pulp. This is usually the start of root canal. After the pulp is removed, the hollow area within the tooth is usually filled and sealed. Extraction. This is a removal of the entire tooth from its socket in the jaw. Extraction may be used when the tooth is too damaged or diseased to be saved. Dental restoration procedures, including cosmetic dentistry, may be recommended to improve the appearance of cracked or chipped permanent teeth. If the tooth is pushed into maxillary sinus, soft tissues, or the inflammation of tissues around tooth step-by-step becomes severe, so this tooth must be extracted. Intrusive luxation is always accompanied by rupture of a neurovascular bundle. In this case the tooth must be fixed in correct position, and the necrotic pulp should be removed at once. The pulpectomy is recommended to do as soon as possible, in order not to admit disintegration and coloring of the tooth crown into black. Treatment of extrusive luxation consists in tooth reimplantation. This operation can be successful if the parodontal tissues are not changed. It is spend in the following sequence: the tooth trepanation, pulp removal and canal sealing. After the root and the socket is treated with antiseptic solutions, put the tooth into its place and fix it by splintage (in some cases splintage is unessential). In case of complaints absence to pain, supervision and the radiological control are spent. The success of reimplantation depends on how quickly after the trauma it has been spent. A tooth root, reimplanted in the first 15-30 mines after a trauma, is resorpted insignificantly, and the tooth remains for a long time. If reimplantation is spent in later terms, the root resorption is defined by X-ray within the 1st month after the operation. The root resorption progresses, and by the end of a year, a considerable part of it is already becomes resorpted.

TOOTH FRACTURE

It is a traumatic injury to a tooth that manifests itself as a chip, crack, or break. Manifestations may also include dislocation or complete displacement of a tooth. There are various types of fractures. Fractures may involve the tooth’s crown, root or both. In some cases, the pulp can be damaged. This type of damage is most likely to cause pain. Teeth that are fractured cause various symptoms depending on the extent of the fracture. For example, fractures of the enamel and dentin may lead to increased sensitivity of tooth to cold foods or drinks, or to air. Fractures that go beyond the enamel and dentin and reach the pulp may cause bleeding around the tooth or formation of a small red spot.

Crown fracture does not represent difficulty for diagnostics. The volume and character of medical intervention depend on loss of tissues. At fracture of a part of a crown, without opening the pulp chamber, it is restored by composites. If conditions are insufficient for seal fixing, parapulpar pins are applied. If during a trauma the tooth cavity is opened, then first of all anesthesia and pulp removal or its amputation (for non generated root) is done. Then the canal is sealed. For the purpose of improvement of seal fixing conditions, a pin which is fixed in the canal can be made. The lost part of the crown is restored by composites. Also, inlays or artificial crowns can be made. At full fracture of crowns it is necessary to solve the question of possibility of root preservation. After that the root channel is treated and sealed up. Then various pin teeth are made.

Root fracture It is a microscopic or macroscopic cleavage of the root in any direction. There are longitudinal, transverse, oblique, multiple fractures. Treatment will vary depending on the type of fracture that occurs, and is found due to x-ray examination. Clinical symptoms are like the clinical appearance of the tooth contusion or luxation. The treatment of the longitudinal, multiple and diagonal oblique fractures are the most unfavorable. Transverse root fractures’ treatment depends on the fracture line level. If the line of the fracture is on 1/4 - 1/3 or in the middle of the root, the pulpectomy must be done, and 2 fragments are joined together with special pins. If the line of the fracture is on apical ¼, only the sealing of the big fragment is sufficient. Apical part of the root can remain without treatment. After the channels sealing it is important to restore the correct position of the tooth and except the trauma at jaws closing. Surgical intervention is used in case of emergency.

CHRONIC INJURY

Chronic injury can be conditioned by the influence of professional factors or bad habits (the concave depressions on the central incisors of the tailors, who cut a thread by teeth, the shoemakers, holding nails by teeth, glass-blowers, etc. Generally the patients don’t complain on pain. Treatment The tooth defect must be removal by microabrasion or filling. It is necessary to eliminate the harmful factor.

TOOTH EMBRYO INJURIES

Tooth embryo injuries are most often seen in permanent teeth, since it is conditioned by the influence of deciduous teeth or by mechanical injury of jaws. Trauma of primary teeth (especially intrusive luxation) can cause the injury of permanent tooth embryo, which is expressed by discoloration of permanent tooth after its eruption, pulp necrosis, hard tissues resorption, etc.