4. Developmental un-carious lesions of teeth that appears before teeth eruption. Classification, pathomorphology, clinic, diagnosis, differential diagnosis and treatment of un-carious lesions. Classification of dental fluorosis

4. Developmental un-carious lesions of teeth that appears before teeth eruption. Classification, pathomorphology, clinic, diagnosis, differential diagnosis and treatment of un-carious lesions. Classification of dental fluorosis

 

Classification of un-carious lesions:

I. Lesions that occur in the stage of dental follicle development, before eruption:

         1. hypoplasia;

         2. hyperplasia of enamel (enamel pearls);

         3. endemic fluorosis;

         4. developmental disturbances and disorders of eruption;

         5. genetic disturbances of tooth development.

II. Lesions that occur after teeth have been erupted:

         1. tooth wear: attrition, abrasion, wedge-shaped defect;

         2. erosion;

         3. necrosis of hard tooth tissues;

         4. hyperesthesia;

         5. trauma of teeth;

         6. fluorosis;

 

Disturbed Tooth Eruption

Tooth eruption comprises the movement of teeth through the soft tissues of the jaw and the overlying mucosa into the oral cavity involved biological processes are not yet entirely elucidated, but the importance of the dental follicle  has  been  established  beyond  doubt.  Teeth may erupt too early, too late, not in the proper position,  or  not  at  all.  In  the  latter  event,  one speaks of impaction. It is most often seen in lower 3rd molar teeth.

Premature Eruption

Both deciduous as well as permanent teeth may erupt into the oral cavity at a too-early age. Because the roots are not yet well developed at that time, the fixation of the tooth in the jaw may be compromised and the subsequent root development  may  be  disturbed,  resulting  in  teeth  with malformed and/or too-short roots.

 Sometimes, the teeth exfoliate spontaneously due to lack of a well-formed root and periodontal ligament. Premature eruption may occur as one of  the  abnormalities  of  the  Hallermann-Streift syndrome.

 

Developmental tooth anomalies

Developmental disturbances of the teeth may be inherited or they may be acquired and the result of environmental disturbances. In all cases the disturbances occur during the period of tooth formation which may be either before and/or after birth. Developmental disturbances which occur early in tooth development affect the shape (form) of teeth, their number or size. Those which occur later during the formation of the dental hard tissues result in disturbances of tooth structure.

 

Disturbances in the number of teeth

Hypodontia

Hypodontia is a decrease in the number of teeth  compared with normal and is relatively common in the permanent dentition (although rare in the primary dentition). The most common missing teeth are:

■ Lower third molars.

■ Upper lateral incisors.

■ Lower second premolars.

In some cases there is a hereditary trait but many cases appear sporadically.

Fig. Congenital absence of lateral incisors with spacing of the

anterior teeth.

Anodontia

Anodontia is a total absence of teeth and is very unusual. It usually occurs in association with a hereditary genetic condition, hypohidrotic ectodermal dysplasia. The condition is caused by a gene defect in which patients have very few or no teeth, and absence of hair and sweat glands.

Supernumerary teeth

An additional tooth in the arch is known as a supernumerary tooth. They are more common in the permanent than the primary dentition and affect females more  than males. Supernumerary teeth may occur at any site but are more common in the anterior maxilla and the  premolar region of the mandible. Different types of supernumerary teeth are recognised. These are:

■ Mesiodens – a supernumerary tooth that develops between the upper central incisors. This is the most common type of supernumerary tooth.

■ Paramolar – an additional molar tooth.

■ Supplemental teeth – additional teeth that resemble normal teeth.

Fig. Two mesiodens: supernumerary teeth in the midline

between the upper central incisors. Note the marked crowding.

Clinical importance

Supernumerary teeth may prevent the eruption of a  permanent tooth and should always be considered if  a tooth fails to erupt. Similarly, a supernumerary tooth may cause displacement or malposition of teeth and, if unerupted, may resorb teeth.

Disturbances of tooth size

Tooth size is determined by genetic factors and abnormally large or small teeth may occur. Usually the entire dentition is affected but sometimes only a few teeth may be excessively large or small. Small teeth may occur in association with missing teeth; for example, one missing upper lateral incisor may be associated with a small peg-shaped lateral incisor on the other side.

Disturbances in tooth form

Variations in the form of crowns or roots of teeth are relatively common and may present as dilacerated teeth, double teeth, dens invaginatus and enamel pearls.

Fig. Anhidrotic ectodermal dysplasia showing conical teeth, giving an undesirable, Dracula-like appearance.

Fig. A dilacerated upper central incisor. There has been an abrupt change in the direction of root growth after approximately one-third of the root was formed

Fig. Den invaginatus. Dens in dente or mild invaginated odontome. In this radiograph the enamel-lined invagination and its communication with the exterior at the incisal tip are clearly seen. The pulp is compressed to the periphery.

Enamel pearls

Enamel pearls are uncommon, minor abnormalities, which are formed on otherwise normal teeth by displaced ameloblasts below the amelocemental junction. Enamel pearls may consist of only a nodule of enamel attached to the dentine, or may have a core of dentine containing a horn of the pulp. The pearls are usually round, a few millimetres in diameter, and often form at the bifurcation of upper permanent molars. They may cause a stagnation area at the gingival margin, but, if they contain pulp, this will be exposed when the pearl is removed.

 

Fig. Enamel pearl. There is a small mass of enamel at the root

bifurcation

Disturbances in the structure of teeth

Disturbances in the structure of teeth may affect the enamel or dentine or sometimes both. Those which affect the enamel are more obvious clinically.

 

DISTURBANCES OF ENAMEL

Developmental disturbances of enamel are relatively common and are usually the result of a localised or generalised environmental disturbance occurring during tooth development. Only a few are the result of a genetic defect. The causes are summarised below:

■ Genetic disturbances

– Amelogenesis imperfecta.

■ Local disturbances:

– Infection.

– Trauma.

– Idiopathic.

■ Generalised disturbances:

– Infections.

– Fluorosis.

– Neonatal events, e.g. premature birth, rhesus incompatibility.

 

Amelogenesis imperfecta

This is the name given to a group of inherited disorders which result in defective enamel formation. Most are the result of defects in genes which code for either enamel matrix production or the mineralisation of enamel.

Fig. Amelogenesis imperfecta of the hypoplastic type. Tooth surface shows pitting (a) or irregularities (b)

indicating abnormal enamel formation. The hardness of the enamel is normal

 

The clinical features are variable and depend on which gene is defective:

■ In some forms the teeth appear normal on eruption but, because the enamel is poorly mineralised, it is soft and soon wears away. The remaining enamel becomes stained and the teeth appear yellow–brown.

■ In other forms the enamel is reduced in amount and the teeth are pitted and appear yellow–brown in colour.

■ Some forms are carried on the X chromosome and boys are affected more severely than girls.

■ The teeth are often sensitive, especially where the enamel is thin or has chipped away.

Hypomaturation amelogenesis imperfecta

The enamel is normal in form on eruption but opaque, white to brownish-yellow. The teeth appear similar to mottled fluoride effects. However, they are soft and vulnerable to attrition, though not as severely as the hypocalcified type. There are several variants of hypomaturation defects such as a more severe, autosomal dominant (type 4) of hypomaturation combined with hypoplasia.

 

Fig. Amelogenesis imperfecta, hypomaturation type. Tooth

morphology is normal but there are opaque white and discoloured

patches.

 

Hypocalcified amelogenesis imperfecta

Enamel matrix is formed iormal quantity but poorly calcified. Wheewly erupted, the enamel is normal in thickness and form, but weak and opaque or chalky in appearance. The teeth tend to become stained and relatively rapidly worn away. The upper incisors may acquire a shouldered form due to the chipping away of the thin, soft enamel of the incisal edge. There are dominant and recessive patterns of inheritance.

 

Fig. Amelogenesis imperfecta, hypocalcified type. The soft chalky

enamel was virtually of normal thickness and form but has chipped away

during mastication.

Acquired disturbances of enamel formation

HYPOPLASIA

 

Most acquired enamel defects result in areas of hypoplasia, which may be due to either a defect in matrix production or a defect in mineralisation. If only a single tooth is affected these are classified as localized disturbances, but if several teeth are affected then they are referred to as generalized.

Fig. White spot on labial surface of right first incisor

tooth indicates transient period of hypocalcification

Localised defects most commonly affect the upper incisor teeth or premolars and usually form as a result of infection (follicles of premolars are placed between roots of temporary molars that are very often have apical periodontitis) or trauma to the deciduous predecessor. This affects the ameloblasts of the developing tooth, resulting in the production of enamel which may be yellow–brown, pitted or irregular. These teeth are sometimes referred to as Turner teeth.

Fig. Turner tooth. The upper central incisor is markedly hypoplastic and brown in color.

 

Enamel opacities are opaque white spots sometimes seen particularly on the upper central incisors. They may become stained with time. The cause of these opacities is not known but they are relatively common.

Generalised defects are sometimes referred to as chronological hypoplasias and most are the result of a generalised or systemic infection or disturbance occurring during tooth development. The disturbance affects enamel formation and results in a linear horizontal band of hypoplasia. This may be characterised by ridging or grooving or pitting on the enamel surface and the teeth that are affected are those which were forming at the time of the disturbance. Hypoplastic defects that are localized on incisal edge of maxilla central incisors, canines and cusps of 1-st molars and lateral mandible incisors as well –  could justify the disturbance in mineralisation  at the age from 6 month until 1 year of life. Thus with a knowledge of the times of crown formation it is possible to predict at what age a patient was systemically unwell. The overwhelming majority of chronological hypoplasia as is the result of disturbances in the first 10 months of life and the teeth affected are:

■ The first permanent molars.

■ Upper central incisors.

■ Lower lateral incisors and canines.

Fig. Chronological hypoplasia due to metabolic upset. Unlike the

hereditary types of amelogenesis imperfecta, defects are linear and

thought to correspond to a short period of amelogenesis disturbed by a

concurrent severe illness.

 

However, disturbances may occur before birth or during the neonatal period. Common causes of disturbances are viral infections, such as measles and mumps, and excess fluoride ions. In the prenatal period, diseases affecting the mother may be important.

Enamel hypoplasia is a defect that occurs when dental enamel doesn’t form completely, usually because of  malnutrition or disease. Enamel hypoplasia is identified as a horizontal line, a series of pits or grooves along the outer surface of the tooth. These lines mark points at which the bone’s growth was resumed after it had stopped. The degree of  hypoplasia is proportional to the length of time the growth was arrested. Hypoplasia does not form in individuals who are chronically ill or malnourished;  it only occurs in healthy individuals.

Hypoplasia is most common in the permanent teeth and represents episodes of arrested  growth in infancy or childhood while these teeth were still developing. Once the enamel forms, it caot longer be affected.

Hypoplasia in deciduous or baby teeth is extremely rare since the fetus is usually well nourished in the womb. A case of hypoplasia in the baby teeth is generally a sign that the baby was born prematurely  or was nurtured in the womb of a very sick woman.

Hypoplasia in young children’s teeth is usually an  indication that the mother was malnourished while pregnant or nursing.

Conditions preceding EHP

• Malnutrition

• Low birthweight

• Prematurity

• Maternal illness

• Smoking

• Drug abuse

• Liver disease

• Other systemic diseases

Infection

Congenital syphilis

 One of the forms of systemic hypoplasia is Hutchinson’s teeth.  Prenatal syphilis, the result of maternal infection, can cause a characteristic dental deformity, described by Hutchinson in 1858.  If the fetus becomes infected at a very early stage, abortion follows. Infants born with stigmata of congenital syphilis result from later fetal infection, and the permanent teeth are affected. The characteristic defects are usually seen in the upper central incisors.

Fig. Congenital syphilis; Hutchinson’s teeth. The characteristics

are the notched incisal edge and the peg shape tapering from neck to tip.

 

The incisors (Hutchinson’s incisors) are small, barrel-shaped, and taper towards the tip. The incisal edge sometimes shows a crescentic notch or deep fissure which forms before eruption and can be seen radiographically. An anterior open bite is also characteristic. The first molars may be dome-shaped (Moon’s molars) or may have a rough pitted occlusal surface with compressed nodules instead of cusps (mulberry molars). These defects are now largely of historical interest.

Pathology

The effects are due to infection of the dental follicle by Treponema pallidum. The postulated consequences are chronic inflammation, fibrosis of the tooth sac, compression of the developing tooth and distortion of the ameloblast layer. T. pallidum causes proliferation of the odontogenic epithelium which bulges into the dentine papilla causing the characteristic central notch.

Tetracycline Discoloration

Tetracycline is taken up by calcifying tissues, and the band of tetracycline-stained bone or tooth substance fluoresces bright yellow under ultraviolet light. The teeth become stained only when tetracycline is given during their development, and it can cross the placenta to stain the developing teeth of the fetus. More frequently, permanent teeth are stained by tetracycline given during infancy. Tetracycline is deposited along the incremental lines of the dentine and, to lesser extent, of the enamel. The more prolonged the course of treatment the broader the band of stain and the deeper the discolouration. The teeth are at first bright yellow, but become a dirty brown or grey. The stain is permanent, and when the permanent incisors are affected the ugly appearance can only be disguised. When the history is vague the brownish colour of tetracycline-stained teeth must be distinguished from dentinogenesis imperfecta. In dentinogenesis imperfecta the teeth are obviously more translucent thaormal and, in many cases, chipping of the enamel from the dentine can be seen. In tetracycline-induced defects the enamel is not abnormally translucent and is firmly attached to dentine. In very severe cases, intact teeth may fluoresce under ultraviolet light. It is no longer necessary to give tetracycline during dental development. There are equally effective alternatives and it should be avoided from approximately the fourth month to 12th year of childhood. Nevertheless tetracycline pigmentation is still seen.

Fig. Tetracycline staining. Note the chronological distribution of

the dark-brown intrinsic stain.

 

Trough  binding  to  calcium,  tetracyclin  is  deposited together with calcium in any tissue undergoing mineralisation. After its incorporation during mineralisation, it can be demonstrated in teeth and bones in ultraviolet light, showing up as fluorescent yellow bands. Grossly, tetracyclin causes a greyish-black discoloration of the tooth  crown (Figs. a–c).

Fig. Tetracyclin discoloration; a. Outer view showing grey discoloration of crown and yellow discoloration

of upper part of the root. b. Cut surface showing the band-like appearance of the discoloration indicating several

administrations of the drug.  c. Ground section also illustrating the band-like discolorations in the enamel and a tiny

yellow line in the dentin.

 

When making ground sections of these teeth, the tetracyclin bands can be observed  under  UV  light  illumination  both  in dentin as well as in enamel, each band indicating  a  time  point  of  tetracyclin  administration. After decalcification the tetracyclin has been lost together with the calcium and therefore, in decalcified paraffin sections, this fluorescence is not present anymore.

TREATMENT OF HYPOPLASTIC DEFECTS

Hypoplastic teeth can be disguised by restorative procedures such as veneers or jacket crowns. The latter should be delayed until adult life. The young pulp is large, is easily damaged during preparation of the tooth, and injuries are more frequent than in older persons.

Localised composite resin restorations

Defective enamel can be replaced with a tooth-coloured restoration that bonds to, and blends with, enamel. It is indicated for well-demarcated white, yellow or brown patches. The localised restoration is quick and easy to complete. Despite the removal of defective enamel down to the amelodentine junction, there is often no significant sensitivity and, therefore, no need for local anaesthesia. If the hypoplastic enamel has become carious and extends into dentine, a liner of glass ionomer cement (correct shade) prior to placement of composite resin will be necessary. In these cases, local anaesthesia will probably be required. Advances in bonding and resin technology make these restorations simple and obviate the need for a full labial veneer. Disadvantages are marginal staining, difficulty in achieving an accurate colour match and reduced composite translucency when lined by a glass ionomer cement.

Composite resin veneers

Although the porcelain jacket crown (PJC) may be the most satisfactory long-term restoration for a severely hypoplastic or discoloured tooth, it is not an appropriate solution for children for two reasons: the large size of the young pulp horns and chamber, and the immature gingival contour. Composite veneers may be direct (placed at initial appointment) or indirect (placed at a subsequent appointment having been fabricated in the laboratory). The conservative veneering methods may not just offer a temporary solution but may also offer a satisfactory long-term alternative to the PJC. Most composite veneers placed in children and adolescents are of the ‘direct’ type as the durability of the indirect composite veneers is as yet unknown. Composite veneers are durable enough to last through adolescence. Before proceeding with any veneering technique, the decision must be made whether to reduce the thickness of labial enamel before placing the veneer. Certain factors should be considered:

• increased labiopalatal bulk makes it harder to maintain good oral hygiene; this may be courting disaster in the adolescent with dubious oral hygiene

• composite resin has a better bond strength to enamel when the surface layer of 200-300 µm is removed

• if a tooth is very discoloured, some sort of reduction will be desirable as a thicker layer of composite will be required to mask the intense stain

• if a tooth is already instanding or rotated, its appearance can be enhanced by a thicker labial veneer.

 New-generation, highly polishable hybrid composite resins can replace relatively large amounts of missing tooth tissue as well as being used in thin sections as a veneer. Combinations of shades can be used to stimulate natural colour gradations and hues. The exact design of the composite veneer will vary with each patient. Usually it will be one of four types: intraenamel or window preparation, incisal bevel, overlapped incisal edge or feathered incisal edge.

Indications

• discoloration

• enamal defects

• diastemata

• malpositioned teeth

• large restorations.

Types of veneer preparation, (a) Feathered incisal

edge, (b) Incisal bevel preparation, (c) Intra-enamel or window

preparation, (d) Overlapped incisal edge preparation.

 

DISTURBANCES OF DENTINE

Like defects of enamel, the dentine may be affected by acquired and by genetic defects. However, acquired dentinal defects cause very few problems and only genetic defects are of clinical significance.

Dentinogenesis imperfecta

This genetic disorder is characterised by defective dentine matrix production and two types have been described. Dentinogenesis imperfecta type 1 occurs in association with osteogenesis imperfecta, in which there is defective bone formation. It is very uncommon.

Fig. Dentinogenesis imperfecta. Note the brown color of the dentine and the marked attrition.

 

Dentinogenesis imperfecta type 2 is the commonest form. It has the following features:

■ Both the permanent and primary dentition are affected.

■ The teeth have a normal shape on eruption but appear amber–brown or purple–blue in colour.

■ The enamel shears away from the poorly formed dentine which quickly wears away.

■ The pulps become obliterated with abnormal dentine.

Patients suffer marked attrition and this can cause severe problems. The aim of treatment is to prevent attrition with the restoration of lost tooth substance and the provision of crowns if necessary.

DEVELOPMENTAL STRUCTURAL ABNORMALITIES INVOLVING BOTH ENAMEL AND DENTIN

Odontodysplasia

Odontodysplasia is a developmental disturbance  consisting of both enamel and dentin abnormalities  in  several  adjacent  teeth.  The often-added  suffix “regional” emphasises this usually localised character,  but  a  few  cases  have  been  described with involvement of more extensive parts of the dentition, the abnormal teeth being present bilaterally and in both upper and lower jaw.

Fig. Radiographic appearance of regional odontodysplasia. On one

side of the midline the deciduous incisors have poor root formation with

thin radicular dentine and enamel. A poorly organised spotty calcification

is present at the site of the permanent successors.

 

The teeth are abnormally formed and the covering enamel layer is thin and yellow. The pulp chambers are wide and the amount of dentin is greatly reduced.  The enamel is hypoplastic and the dentin contains large areas of interglobular dentin. Also, the predentin zone is very wide. The dental pulp usually contains large and irregular aggregates of mineralised matrix, the so-called denticles. The condition may be accompanied by gingival enlargement.

Odontogenesis Imperfecta

In  odontogenesis  imperfecta,  both  enamel  and dentin  exhibit  pathologic  changes  in  all  teeth. The enamel is hypoplastic and the dentin shows changes similar to those seen in dentinogenesis imperfecta.

Shell teeth (dentinogenesis imperfecta)

Fig. Shell tooth. In this severe form of dentinogenesis imperfecta

only a thin mantle of dentine is formed and no root develops

 

This rare anomaly is so called because only a thin shell of hard dental tissue surrounds overlarge pulp chambers. Like other types of dentinogenesis imperfecta there is normal, but thin, mantle dentine which covers irregular dentine. The pulp lacks a normal odontoblast layer and consists of coarse connective tissue which becomes incorporated into the deep surface of the dentine.

 

ENDEMIC DENTAL FLUOROSIS

 

Fig. Fluorosis. Moderate effects from an area of endemic fluorosis.

Irregular patchy discolouration.

 

Fluorosis continues to be an endemic problem. The following countries have been identified for the problem of fluorosis: Pakistan, Bangladesh, Argentina, United States of America, Morocco, Middle East countries, Japan, South African Countries, New Zealand, Thailand etc. Children in the age group of 0 to 12 years are most prone to fluorosis as their body tissues are in formative / growth stage during this period. Expectant mothers are also to be protected, as there is growing concern about effects of fluoride on fetus. Acceptable measures of fluorine in water according to hygienic standards is – 0,8-1,2(1,5)mg/l. Fluorosis is the term given to changes in the enamel which are associated with excess ingestion of fluoride. These vary from localised white opacities to more severe brown–yellow mottling on the teeth. The precise effect depends on the dose of fluoride (from all sources), the duration for which it was taken and the age of the patient at the time of ingestion. Fluorosis when very severe (concentrations in the water supply greater than six parts per million) may result in extensive hypoplasia with brown staining.

Fig. Left: Enamel fluorosis of mild to moderate severity is seen across much of this patient’s dentition.

Right: Mild – to – moderate enamel fluorosis is more localized in this patient.

 

Table. Distinctive features of dental fluorosis

Clinical features

Mottling ranges from paper-white patches to opaque, brown, pitted and brittle enamel. Clinically, it may be difficult to distinguish fluorotic defects from amelogenesis imperfect when the degree of exposure to fluoride is unknown. There is considerable individual variation in the effects of fluorides. A few patients acquire mottling after exposure to relatively low concentrations, while others exposed to higher concentrations appear unaffected. Changes due to mottling are graded as shown in Table.

Table. Grading of mottled enamel

• Very mild. Small paper-white areas involve less than 25% of surface

• Mild. Opaque areas involve up to 50% of surface

• Moderate. The whole of the enamel surface may be affected with paper-white or brownish areas or both

• Severe. The enamel is grossly defective, opaque, pitted, stained brown and brittle

 

Fig. Fluorosis. Severe effects from an area of endemic fluorosis.

Closer view showing irregular depressions caused by hypoplasia and

white opaque flecks and patches.

 

Table.   Type and stages of dental fluorosis

Information was prepared by Levkiv M.O.