Topic 9

The non-carious lesions occurring before teeth eruption

Dental fluorosis
Fluorosis is a systemic violation of the development of the hard tissues due to fluoride
intoxication resulting from the consumption of drinking water and food with its high content. In
significant concentrations fluorine is capable to affect the human bony skeleton. Many authors
consider that fluorosis is hypoplasia of specific origin which is caused by excess fluorine in drinking
water.
CODE upon ICD-10 - К00.30 Endemic mottling of enamel (fluorosis).
Endemic teeth fluorosis or "mottled teeth" are found on all continents. When the content of
fluorine in water of 0.8 – 1 mg/l the prevalence of dental fluorosis among the population is 10-12%, at
a concentration of 1.0 – 1.5 mg/l - 20 - 30%, when the content of fluorine in water of 1.5 – 2.5 mg/l
fluorosis is found already in 30-40% of the population and when the concentration is more than 3 mg/l -
more than 50% of the population.
The intensity of fluorosis depends on fluorine content in drinking water and on climate. In the
hot regions water consumption is more, then in the regions with cold climate. So, total fluoride intake
can be more in hot regions.
According to WHO, minimal concentration of fluoride, which can cause dental fluorosis, is 1-1,5
mg/l.
The adult person in average receives per day is 0.5 – 1.1 mg of fluorine with food and 2.2 – 2.5
mg with water.
Pathogenesis
Fluorine (F) is the active element from the group of Halogens. More often the fluorine occurs as
fluorine in combination with metals.
The effect of fluorine on enamel is associated with its toxic effect on enameloblasts leading to
improper formation of the enamel. Fluorine reduces the activity of the phosphataze that negatively
affects on the mineralization of the enamel. Fluorine, penetrating into the blood, affects on thyroid
activity that result in disorders of enamel mineralization.
Clinical picture
Generally fluorosis is presented on the permanent teeth at the moment of their eruption, if the
child lived in endemic region during first 3 years of his life.
WHO recommends to use the following classification of dental fluorosis (also known as Dean’s
index):
0 – normal enamel
1 - questionable fluorosis - barely noticeable white flecks or spots are appeared on enamel (less
than 10% of enamel surface);
 2 – very mild fluorosis is characterized by the presence of bands and small opaque white spots
which represent from 10% to 25% of the enamel surface;
3 – mild fluorosis - white opaque multiple, well-defined chalky, sometimes, confluent spots in
tooth enamel which gradually becomes a normal enamel, with a smooth, shiny surface, covering from
25% to 50% of the enamel;
4 - moderate fluorosis is characterized by the presence of brown spots and rounded enamel
defects which have uneven edges, dirty-gray or brown bottom;
5 -severe fluorosis - all of tooth surface are affected, there are vast areas of brown staining and
destruction of the enamel in the form of pits and erosions.

In the domestic classification of fluorosis suggested by B. K. Patrikeev (1956) five forms are
distinguished:
Dashed form – the elements of the lesion have the form of strips and small spots of white color.
They occupy less than 25 % of the area of the tooth crown. Oftenthey appear
whendryingthetoothsurface
Spotted form–is appeared by the presence of large chalky spots located on all teeth surfaces of
the teeth (less than 50% of the surface of the tooth crown). The intensity of white color of spots
disappears from the center to the periphery. Changed portions of enamel gradually returns to normal
enamel. Sometimes ill-defined light yellow pigmentation is revealed.
Chalky-pitted –white shining and mat spots are observed, areas of spot pigmentation from
light- to dark-brown color. Sometimes small rounded defects of enamel – pits – are detected. Their
bottom is light-yellow or dark color. This form can go with quick erasing of enamel with exposure of
pigmented dentin.
Erosive form is characterized by significant pigmentation and destruction of enamel in the form
of pits and erosions. Destructive form is characterized by changes in the shape of crowns of the teeth
due to the gradual destruction of the tooth enamel and the erasure of hard tissues. Teeth tissues are very
fragile, can be broken off easily. But thanks to deposition of substitution dentin the tooth cavity is not
opened.

Differential diagnosis:
Mild and moderate fluorosis should be differentiated from carious white spot which is
characterized by a single lesion in a typical caries areas.
Mild forms of fluorosis are also similar to spotted form of hypoplasia of enamel.
Severe forms of fluorosis following by the formation of erosions and other defects of the tooth
crown. It should be distinguished from caries and other non-carious lesions of teeth: erosions, necrosis,
wedge-shaped defect and etc.
 Prognosis: in case of mild or moderate form of fluorosis the spots stay stable during the whole
life. In case of severe form destruction of enamel is possible, also caries development in the enamel
defects can occur.

Treatment. The choice of fluorosis treatment method depends on the shape of clinical
implications. Under mild and moderate forms of dental fluorosis the bleaching and micro-abrasion are
used. In case of severe form of lesion it is necessary to use veneers or artificial crowns.

Prevention.
Preventive measures are divided into collective and individual prevention measures.
Collective prevention measures provide purification of drinking water from an excess of fluorine
by salts of aluminum, magnesium hydroxide or calcium phosphate in defluorination facilities. It is
possible to reduce the concentration of fluorine in drinking water by replacing the water source.
Individual prevention measures include: breast feeding; refusal from early introduction of
complementary foods; introduction to food vitamins C and D, calcium gluconate; delete (restrict) intake
of products containing fluorine (in marine fish, butter, spinach, etc.); the annual export of children for
the summer period from endemic area, use of bottled water.

Enamel hypoplasia
Hypoplasia - is a defect of development consisting of hypoplasia of tooth or its tissues. An
extreme case of hypoplasia is aplasia - congenital absence of a tooth, part or all of the enamel.
Hypoplasia of tooth enamel is the most common lesion of teeth of non-carious origin, occurring in the
practice of a dentist.
The occurrence of hypoplasia is associated with impaired metabolic processes in the body of a
fetus or child or topically acting on the germ of the tooth factor. If in this case the activity of
ameloblasts is affected then the enamel’s hypoplasia is developed : if the violation at the level of
odontoblasts takes place some of the most severe cases of hypoplasia occur, accompanied by
abnormalities of the dentine and pulp of the tooth.
Hypoplasia of primary teeth occurs when the child's illness in the first weeks and months of his
life, which is reflected in the formation of the incisors, canines and molars. Premature children with
congenital allergy, suffered a birth trauma or hemolytic jaundice resulted from the incompatibility of
mother’s and fetus’s blood for rhesus factor, born in asphyxia also have hypoplasia.
Primary teeth hypoplasia can develop in utero. Children, whose mothers during pregnancy have
suffered the diseases such as rubella, toxoplasmosis and toxemia have hypoplasia of primary incisors.
 Hypoplasia of the permanent teeth is developed under the influence of various diseases when 5-
6 month life children are in the period of formation and mineralization of these teeth.
Hypoplasia is detected in children who had rickets, tetany, acute infectious diseases, diseases of
the gastrointestinal tract, toxic dyspepsia, nutritional dystrophy with diseases of the endocrine system,
brain disorders, congenital syphilis. About 60% of hypoplastic defects of the permanent teeth occur in
the first year of a child's life when adaptive and compensatory abilities of the body are weak.
Hypoplasia of the tooth crown (as and group membership of affected teeth) broadly depends on
the age at which the child suffered the disease. So, in the event of illness in the first months of life
hypoplasia is developed in the cutting edge of the central incisors and dental tubercles of first molars,
as their formation starts in 5-6 month after birth.
On the 8-9th month of life the second incisors and canines are formed. In the case if a child has
the desease in this period the areas of hypoplasia will be localized at the cutting edge of the lateral
incisors and canines while as at the central incisors and 6-th tooth the underdeveloped areas of the
enamel will occur approximately at the level of the equator (since half of the crown already formed).
Some children have an uneven structure of the enamel throughout the crown of a certain group
of teeth.
Hypoplasia of hard tissues of the teeth (which are formed in the same period of time) is named
as system hypoplasia. If hypoplasia of a single tooth – local hypoplasia.

1. System hypoplasia.
The main factors, which can cause system hypoplasia of permanent teeth:
- Nutritional deficiency: deficiency of vit A, C, D, Calcium and Phosphorus.
- Exanthematous diseases: measles, chicken pox, scarlet fever
- Congenital syphilis
- Hypocalcaemia (tetany)
- Tetracycline intake

Clinically there are 3 forms: color change; hypoplasia (underdevelopment); the lack of enamel.
The color change (opacity) of the enamel is a weak degree of the enamel hypoplasia; it is
characterized by spots of white, less frequently yellowish.
The spots are usually localized on the vestibular surface and not accompanied by any unpleasant
feeling. Typically, the outer layer of enamel remains smooth, shiny and not colored by coloring
agents. The elements stay stable during the life. The thickness of the enamel in the spot area is the same
as on the area of intact enamel next to it. On x-ray picture this form of hypoplasia is not normally
revealed.
 Hypoplasia (incomplete formation) of enamel is the most severe form of its hypoplasia which
can be detected by different ways (wavy, spotted, striated enamel).
Wavy enamel is discovered after drying of teeth in the shape of aggers and small grooves
between them.
Pitted grooves is the most wide-spread form of hypoplasia. In time the enamel in areas of
grooves gradually is colored but it remains thick and smooth.
Linear form is detected in the shape of single lateral groove on the crown. Such grooves may
be few. They are alternated with unaltered tooth tissues. Rarely grooves are revealed along the entire
height of the teeth crown of some groups. This form is called a ladder hypoplasia. The integrity of
enamel (when severe forms take place) is not broken. In recent years the mixed forms of hypoplasia
are more typical when all the above mentioned forms are detected on individual teeth and even within
one tooth.

The lack of the enamel (aplasia) on the definite area is the most severe and rarely occurred
form of hypoplasia. When this form takes place the pain senses can be if impact of thermal,
mechanical and chemical irritants exists. After elimination of irritants the pains will disappear.
Clinically this form appears as lack of enamel on the part of crown or on the bottom of cup-shaped
recess or in the groove covering the tooth crown.

Differential diagnosis. Hypoplasia of enamel differs from caries at the stage of «white spot».
When caries takes place, the white spot usually is single and located at the neck of the tooth. And when
hypoplasia takes place the white spots are usually multiple and localized on any area of the crown and
not colored by 2% solution of methylene blue. Hypoplasia is characterized by symmetry of lesion, the
surface of enamel is smooth and doesn’t stain by methilen the blue.

System hypoplasia due to congenital syphilis

Hutchinson’s teeth (code upon ICD - A50.51) - upper central incisors, which are smaller and
more widely spaced than normal and which have notches on their cutting edges.
Mulberry molars (code upon ICD - А50.52) – first molars characterized by multiple rounded
rudimentary enamel cusps on the occlusial surface.
Moon’s molars - dome-shaped first molars.

Treatment of system hypoplasia

Depending on the clinic manifestations the row of medical actions are recommended:
1. Micro-abrasion.
2. Micro-invasive composite restoration
 2. Direct or indirect veneers.
4. Full crowns.

Prevention. Prevention of system hypoplasia consists of prevention of system deseases

following by severe abnormality of metabolic processes.

Tetracycline teeth - one of the type of system hypoplasia and characterized by change of color in
the result of the reception of tetracycline during the period of formation and mineralization of tooth
tissues. Tetracycline is deposited in the enamel and dentin of developing teeth as well as in the fetus
bones in case of tetracycline introduction in the body of a pregnant woman or a child as therapeutic
agent when different deseases take place. Tetracycline can cause not only coloring of teeth but
hypoplasia of enamel.

2. Local hypoplasia (Turner’s teeth) – damage of permanent teeth formation as the result of
inflammation or physical trauma of tooth’s germ.
Clinical picture is characterized by the presence of chalky spots or pits on the tooth surface. In
severe cases the aplasia occurs.
Treatment:
- direct restoration;
- prosthetic treatment;
Prevention: prevention or early treatment of primary teeth caries.

Hereditary disturbances of tooth development

1. Amelogenesis imperfecta
Classification of amelogenesis imperfecta according to Witkop (1989)
I type. Hypoplastic - this form is manifested by a variety of crown sizes, ranging from small to normal.
However, the small teeth reveal a lack of proximal contacts. The color of the teeth may vary from
opaque white to normal white to yellow brown. The enamel is noticeably thin and smooth as compared
to the normal thickness of teeth. It also displays pits, grooves and furrows.
- hypoplastic, pitted autosomal dominant
- hypoplastic, local autosomal dominant
- hypoplastic, local autosomal recessive
- hypoplastic, smooth autosomal dominant
- hypoplastic, smooth X-linked dominant
- hypoplastic, rough autosomal dominant enamel agenesis, autosomal recessive
II type. Hypomaturation - the enamel has usually normal thickness, having white, yellow or brown
spots.
- hypomaturation, pigmented autosomal recessive
- hypomaturation, X-linked recessive
- snow-capped teeth, autosomal dominant?
III type. Hypocalcified - the enamel has normal thickness, but it is soft and rough. The teeth break off or
wear away easily.
- autosomal dominant
- autosomal recessive
IV type. Hypomaturation-hypoplastic with taurodontism
- hypomaturation-hypoplastic with taurodontism, autosomal dominant
- hypoplastic-hypomaturation with taurodontism, autosomal dominant

2. Dentinogenesis imperfecta
The Shields' classification is summarised below:
Dentinogenesis imperfecta type I
Individuals with DGI-I also have osteogenesis imperfecta. The teeth of both dentitions are typically
amber and translucent and show significant attrition. Radiographically, the teeth have short, constricted
roots and dentine hypertrophy leading to pulpal obliteration either before or just after eruption.
Expressivity is variable even within an individual, with some teeth showing total pulpal obliteration
while in others the dentine appears normal.
Dentinogenesis imperfecta type II
The dental features of DGI-II are similar to those of DGI-I but penetrance is virtually complete and
osteogenesis imperfecta is not a feature. Bulbous crowns are a typical feature with marked cervical
constriction. Normal teeth are never found in DGI-II. Sensorineural hearing loss has also been reported
as a rare feature of the condition [5]. The color of the teeth varies from brown to blue, sometimes
described as amber or gray, with an opalescent sheen.

3. Odontogenesis imperfecta – hereditary incomplete formation both of enamel and dentine. Early
enamel loss and severe teeth attrition are characterized.

4. Dentine dysplasia - is a genetic disorder of teeth, commonly exhibiting an autosomal dominant

inheritance. It is characterized by presence of normal enamel but atypical dentin with abnormal pulpal
morphology. There are two types. Type I is the radicular type, and type II is the coronal type.
Dentine dysplasia type I
The teeth in DD-I appear generally unremarkable clinically with normal shape, form and consistency.
Radiographically, the roots are sharp with conical, apical constrictions. Pre-eruptive pulpal obliteration
occurs leading to a crescent-shaped pulpal remnant parallel to the cemento-enamel junction in the
permanent dentition and total pulpal obliteration in the deciduous teeth. Numerous periapical
radiolucencies are often seen in non-carious teeth.
Dentine dysplasia type II
The features seen in the deciduous dentition resemble those observed in DGI-II; however, the permanent
dentition is either unaffected or shows mild radiographic abnormalities such as thistle-tube deformity of
the pulp chamber and frequent pulp stones.

5. Shell teeth
Dentinogenesis imperfecta type III
This is a form of DGI found in a tri-racial population from Maryland and Washington DC known as the
Brandywine isolate. The clinical features are variable and resemble those seen in DGI-I and -II but the
primary teeth show multiple pulp exposures and radiographically, they often manifest "shell" teeth i.e.
teeth which appear hollow due to hypotrophy of the dentine.