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14 Tooth Abnormalities
14 Tooth Abnormalities
Hasham Khan
Head Deptt. of Paediatric Dentistry
Khyber College of Dentistry
Peshawar
Tooth Abnormalities
1. Abnormalities of Number
2. Abnormalities of Form
3. Abnormalities of Size
4. Abnormalities of Structure
5. Abnormalities of Colour
6. Odontomes
7. Abnormalities of Eruption and Exfoliation
8. Chemical and Physical Injuries
9. Resorption
Abnormalities of Tooth Number
(Tooth Formation)
• Genetic factors.
Decrease in Root Number
Clinical Features:
• Occur in multi-rooted teeth.
• Any molar tooth may have single tapering root but more
frequent in 2nd and 3rd permanent molars.
Associations:
• Reduction in root number may occur together with
taurodont root forms.
• Reduction in root number is associated with
hypodontia.
Aetiology:
• May arise from a failure of the invagination of Hertwig’s
root sheath.
• Probably polygenic in nature.
Abnormalities of Tooth Form
– Invaginated teeth
– Evaginated teeth
– Double teeth
– Taurodontism
– Dilaceration
– Enamel projections and pearls
– Accessory cusps (Talon and Carabelli)
– Hutchinson’s incisors and Moon’s molar
Invaginated Teeth
Dens in dente’ – Tooth within a tooth – a misconception.
‘
Clinical Features:
• May occur in any tooth but the palatal surface of maxillary lateral incisor is more commonly
affected.
• Carious destruction of tooth tissue within the invagination may lead to pulpal exposure, acute
facial cellulitis or acute dentoalveolar abscess.
Prevalence
Associations:
Significant association between supernumerary and
invaginated teeth. So check radiograph for invagination
when a supernumerary is present or vice versa.
Aetiology:
Arises as a result of an invagination of the enamel
epithelium into the dental papilla of the tooth germ.
Appears to be largely genetically determined.
Clinical Implications and Treatment
Clinical Features:
Prevalence:
• Prevalence in Mongoloid races – 4.8 % (southern
Chinese)
• Rare in Caucasians.
Associations:
• A peculiar idiopathic resorption of dentine may
sometimes be an associated feature.
Aetiology:
• This anomaly of tooth form is thought to result from an
outward folding, or evagination, of the enamel organ. It
is probably a largely genetically determined anomaly.
Treatment
Treatment is directed at preventing the complications
associated with exposure and death of the pulp.
1. If no occlusal interference, seal the occlusal surface with a
filled composite resin and flow it around the tubercle and
over the adjacent fissures.
Taurodontism describes
teeth (molars) in which the
body of the tooth
containing the pulp
chamber is vertically
enlarged at the expense of
the roots.
Clinical Features
• After about 4.5 years of age, when the roots of the permanent incisors are
forming and the teeth are moving over the primary incisor roots, injury to
the primary incisors will most likely cause labial dilaceration (of root) and
there will be no enamel hypoplasia.
• Dilacerated teeth not associated with trauma are gently curved from
crown to root; the crown is bent labially from the crown-root junction and
there is no enamel hypoplasia.
Treatment
Enamel Projections:
These are irregularities of the enamel margin in molars in the
furcation area.
• Seen on deciduous second molars and all permanent molars.
• Occur more often on mandibular than maxillary teeth and more
common on the buccal aspect of tooth. May be predisposing factor
to periodontal disease.
• Prevalence range is from 6 – 24 %. Higher in Mongoloids.
• Enamel projections and enamel pearls tend to occur together.
• Often occurs bilaterally, suggests it is due to systemic rather than
localized factors.
Enamel Pearls:
• Pearls containing dentine vary greatly in size. Enamel pearls may be extradental or intradental (included in
dentine).
• Enamel pearls are not seen in deciduous dentition.(but enamel projection seen in decidous second molars
oly)
• In permanent dentition, molars are most often involved, often bilaterally symmetrical and the enamel is
poorly mineralized.
• Enamel pearls are probably indicative of some disturbance in the function of Hertwig’s root sheath. Some
pearls may be due to trauma.
Accessory Cusps
• Talon cusps
• Shovel-shaped incisors
• Cusp of Carabelli
Talon Cusp
Hutchinson’s Incisor:
The term ‘barrel-shaped’ is often applied to the typical
Hutchinson’s incisor. It is narrower at the incisal edge than at the
cervix, has rounded incisal angles and may have a notch of the
incisal edge.
Moon’s Molars:
Moon and Lus described the characteristic first permanent molar
defect, with a reduction of the crown form towards the occlusal
surface.
Mulberry Molar:
The so-called ‘mulberry molar’ of congenital syphilis is due to a
marked enamel hypoplasia affecting the first permanent molar.
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Dental changes are seen in approximately 40 – 70 % of patients
with congenital syphilis (caused by spirochaete, Treponema
Pallidum).
Abnormalities of Tooth Size
– Crown size
• Megadontia
• Microdontia
Clinical Features:
• Sometimes associated with increased complexity of form.
Clinical Features:
• Microdont teeth may be small but of normal form or may be both of small
dimensions and of tapering (conical or peg) form.
• The commonest affected teeth are the permanent maxillary lateral incisor
and the third molar.
All tissues
Enamel defects
Dentine defects
Cementum defects
Discolourations
All Tissues
– Odontodysplasia
Arrest of Development of a Tooth Germ
Treatment:
Removal of the affected teeth and replacement.
Enamel defects
• Several classifications.
Posterior Teeth:
• Stainless steel crowns (conservation of the primary molars ensure that
the 1st permanent molars erupt in their normal positions and normal height).
Anterior Teeth:
• Strip crowns
• In severe cases extraction is justified.
Treatment for Permanent Teeth with AI
Anterior Teeth:
Small areas of hypomineralized labial enamel do not require
treatment because it may not be of concern to the child and
parent.
Posterior Teeth:
Localized:
1. Infection
2. Trauma
i. Mechanical trauma
ii. Extraction of deciduous teeth
iii. Fracture of the jaw
iv. Cleft lip / palate ( defects attributed to surgical repair)
3. idiopathic
Generalized
Environmental influences may be:
Prenatally
Endocrine disturbances (e.g; hypoparathyroidism)
Infections (e.g; rubella)
Drugs ( e.g; thalidomide)
Nutritional deficiencies (e.g; rickets)
Haematological and metabolic disorders (e.g; hyperbilirubinaemia
associated with Rhesus incompatibility and erythroblastosis fetalis)
Perinatally
Early childhood
Viral exanthematous diseases (common in early childhood) suggested
(not proved), if these can than what about gastroenteritis and
pneumonia?
Excessive chronic ingestion of fluoride in the drinking water.
Tetracycline chelates calcium to form a tetracycline – calcium
orthophosphate complex.
Hypothyroidism
Idiopathic hypoparathyroidism
Nephrotic syndrome
Idiopathic
Dental Fluorosis
• Dental fluorosis is a developmental disturbance of enamel
caused by excessive fluoride intake during tooth development
(leading to hypomineralization of enamel and increased
porosity).
• Fluoride is a double-edged sword because a deficiency of
fluoride intake leads to dental caries while excessive
consumption leads to dental fluorosis.
Risk Factors:
High fluoride concentration in drinking water or fluoridated
water and caries preventive measures like fluoride containing
dentifrices, fluoride supplements, gels, mouth rinses and
varnishes are risk factors.
Food habits such as consumption of tea, fish and fluoride
containing trona or formula are also the risk factors for
fluorosis.
Clinical Features & Treatment
• Diagnosis of dental fluorosis require clean and dry teeth
surfaces.
• Clinically dental fluorosis is presented as bilateral diffuse
opacities (unilateral or discrete or demarcated opacities are
not related to fluoride). The white opacities may coalesce to
form white patches. In more severe forms of fluorosis,
enamel may become discolored and/or pitted.
Indices Used to Measure Fluorosis in Community:
Dean’s Index, Thylstrup and Fejerskov Index, DDE and
Modified DDE Index.
Treatment:
Include external bleaching, microabrasion, veneers
(composite or porcelain), crowns or a combination of
methods.
Molar – Incisor Hypomineralization (MIH)
• MIH is a common developmental dental condition that presents in
childhood world-wide (term introduced in 2001).
• It is defined as hypomineralisation of systemic origin, presenting as
demarcated, qualitative defects of enamel of one or more first
permanent molars (FPMs) frequently associated with affected
incisors.
• Etiological factors are systemic conditions (e.g. frequent childhood
diseases) or environmental insults during the child's first 3 years of
life.
• Prevalence: 2.8 – 40.2 %
• Clinical Problems Posed by MIH to Dentist & Child:
• Rapid caries development
• Inability to anaesthetize MIH molar for treatment
• unpredictable behaviour of apparently intact opacities
• The child experience pain & sensitivity (e.g. on brushing)
• Child complaining of appearance of incisor teeth
Clinical Features
• MIH is a hypomineralized defect of the first permanent molars,
frequently associated with affected incisors (defects could affect any
primary or permanent tooth – a more recent note).
• The porous, brittle enamel easily chip off under masticatory forces and
then it may resemble hypoplasia.
Differential Diagnosis
Incidence:
• Type I DI: 1 : 20,000
• Type II & III DI: 1 : 8000
• Type I DI appears in 20 – 40 % of patients with Osteogenesis
Imperfecta.
• Both sexes are equally affected.
• Both the primary and the permanent dentitions are affected.
Classification
Shields et al proposed the following classification of DI, which is
based upon the clinical appearance of various forms of DI:
•
IMPERFECTA
Enamel is normal but the ADJ is weak and cracking within
enamel / at ADJ can occur.
• Amber-brown or blue-grey discolouration of teeth with an
opalescent sheen.
• Radiographically crowns are bulbous with marked cervical
constriction and short, blunt roots are seen with partial or
total obliteration of the pulp chambers and root canals by
dentine.
Type – III DI: Brandywine Isolate
Primary Dentition:
• Stainless steel crowns for primary molars.
• Anterior teeth may be restored with composite (strip crowns).
Permanent Dentition:
• In children, stainless steel crowns for molar teeth. Cast
veneers for premolars (SS crowns for premolars not available).
• Anterior teeth may be restored with composite (strip crowns).
• In adults, bonded porcelain crowns for posterior teeth and
jacket crowns for anterior teeth.
Continues:
Localized
• Injury to the developing permanent tooth germ via the
deciduous tooth interferes with dentine formation:
• A hypoplastic area in the enamel may show a corresponding zone
of interglobular dentine beneath.
• In cases of crown dilaceration and root angulation, the dentine is
always involved.
• Direct trauma to an erupted tooth may result in gradual
pulpal calcification.
• In some cases, post-traumatic irregular dentine formation has
been observed.
• Where a root fracture occurs, a calcific union with tissue
resembling osteodentine may sometimes follow.
Generalized:
• Generalized environmental insults which affect enamel
formation may also affect dentine. Therefore, in dentine,
there is a neonatal line corresponding to that in enamel.
• Factors retarding dentinogenesis in children:
• Tetracycline discolouration of dentine and delay in
dentinogenesis.
• Irradiation.
• Lathyrism or Neurolathyrism
• Hypothyroidism.
Genetically determined
Associated with generalized
defects
Environmentally determined
Genetically Determined Cementum Defects
Associated with Generalized Defects:
Cleidocranial dysostosis
Aplasia or hypoplasia of clavicles.
Brachycephalic skull with pronounced frontal and parietal bossing.
Delayed closure of the cranial fontanelles and sutures.
Numerous wormian bones are formed in the suture lines, especially
lambdoidal sutures.
Presence of large numbers of supernumerary teeth, especially in
the anterior segments of the jaws.
Eruption of many deciduous and permanent teeth may be delayed
or fail completely.
Histologically, there is hypoplasia of cementum, especially affecting
the cellular cementum.
Hypophosphatasia
• Acquired
• Changes in colour with age
Localized
• Developmental
• Trauma (Enamel and dentine defects)
• Infection (Enamel and dentine defects)
• Acquired
• Early and extensive carious lesions • Effects of amalgam
• Some root canal filling materials • Pulpal hemorrhage.
• Pulpal necrosis • Pulpal calcification
• Internal (pink spot) resorption
.
External
• Generalized
• Localized
Numerous external staining agents.
More staining if hypomineralization of enamel, pits or
grooves, or marginal leakage of restorations.
External staining agents include:
Tobacco, betel nuts and medicaments such as iron, iodine,
and silver nitrate.
The stannous ion of topical stannous fluoride preparations
may cause dark staining, particularly of demineralized area.
The products of some of the bacteria found in oral flora may
cause staining in plaque which varies from brown and black to
green.
Odontomes
Odontomes are developmental malformations or tumors
containing enamel, dentine and pulp.
Types:
• Compound odontome
• Complex odontome
Teeth which are present in the mouth at birth are called natal
teeth while teeth which erupt during the 30 days following birth
are called neonatal teeth.
Clinical Features:
The lower first deciduous molar is the most commonly affected tooth
although some studies reported it to be the second primary molar.
• Erosion
• Attrition
• Abrasion
• Irradiation
• Secondary Dentine
• Pulpal Calcification
• Hypercementosis
Tooth Wear
Tooth wear may be caused by attrition, abrasion or erosion, or by
any combination of the three processes.
Extrinsic factors
Intrinsic factors
Extrinsic factors:
• Include consumption of acidic foods and drinks, especially
fruit drinks and carbonated beverages.
• Excessive consumption of acidic foods and drinks is especially
hazardous in the primary dentition because the enamel and
dentine are thinner than in the permanent dentition.
• Certain medicinal preparations may also be highly acidic and
will cause erosion unless used carefully.
• Some occupations, e.g; battery construction, involve contact
with acidic substances. The workers may suffer from erosion
of the labial surfaces of the incisors.
Intrinsic Factors:
• Include recurrent vomiting resulting from an abnormality of
the GIT or from psychological disorders such as anorexia or
bulimia nervosa. Erosion will occur on palatal or lingual
surfaces of teeth.
Treatment
We have to be vigilant to detect minor changes in enamel
indicative of erosion so that appropriate intervention can be
made:
1. Take a careful social, dental and medical history, and ask the parent to
complete a 3-day diet record.
2. If dietary factors are identified, ask the patient to reduce the frequency
of intake of erosive food and drink, to confine drinks to mealtimes, and
use a straw to reduce the erosive effect on anterior teeth (the most
affected).
7. The affected teeth should be restored only when the cause has been
identified and removed, otherwise erosion will continue around the
restorations. For restoration of anterior teeth composite resin or
porcelain veneers may be used. However, if buccal and lingual surfaces of
teeth are affected full coverage crowns may be indicated.
Resorption
• Aetiology of resorption
• External resorption
• Internal resorption
Aetiology of resorption
1. Acute mechanical trauma to the tooth, such as avulsion, subluxation or
root fracture.
5. Teeth which remain completely embedded in the jaws are more prone
than others to undergo resorption.
7. The tumors that produce resorption of the roots of teeth are those with
moderate growth and expansion rates such as ameloblastomas.