DENTAL

DISEASES
DENTAL CARIES
 Definition
Dental caries is a microbial disease of the calcified
tissues of the teeth ,characterized by demineralization
of the inorganic portion and destruction of the organic
substance of the tooth
 Theories of dental caries

1. Early Theories
The legend of the worm
2. Endogenous theories
 Humoral Theory
 Vital theory

3. Exogenous theories
 Chemical (Acid) theory - Parmly (1819)
 Parasitic or Septic theory – Dubos (1954)

 Miller`s Chemico-parasitic (Acidogenic)

theory
 W.D.Miller (1882) most widely accepted
 Evidence for Acidogenic theory

 Acid was present within deep carious lesions

 Bread/sugar with saliva could decalcify teeth
 Correlation between no. of cariogenic bacteria & caries
 Inoculation of acidogenic bact. induced caries
 pH of cavities was lower than those of normal teeth

 The Proteolytic theory- Gottlieb (1944)

 The Proteolysis chelation theory- Schatz(1955)
DISEASES OF THE PULP &
PERIAPICAL TISSUE
ETIOLOGY OF PULPAL
INFLAMMATION(PI)
 MECHANICAL DAMAGE
 THERMAL INJURY
 CHEMICAL IRRITATION
 BACTERIAL EFFECTS
MECHANICAL DAMAGE
May be due to ---
 traumatic accidents
 cracked tooth syndrome
 iatrogenic damage from dental procedures
 attrition
 abrasion
 barometric changes-
 AERODONTALGIA--a condition clinically simulating
pulpitis ( toothache)--reported at WORLD WAR 11.
 Seen in aircrew flying at high altitutes, astronauts,sub-
marines crew & in deep sea divers
 The pain is due nitrogen bubbles formation due to
decompression in BV & pulp tissue of recently filled teeth
 Aerodontalgia -happens due to inadequate pulp protection
ie caries etc
THERMAL INJURY
 Severe thermal stimuli can be transmitted through
large UNINSULATED METALLIC restoration
 may occur during over rapid cavity prep or without
sufficient coolant
 polishing of filling
 exothermic chemical reactions of dental materials-cold
cure resins
CHEMICAL IRRITATION
 MAY OCCUR FROM EROSION
 INAPPROPRIATE USE OF ACIDIC DENTAL
MATERIALS-irritant travels through dentinal tubule. mild
irritant--sclerosis or reparative dentin
 when two dissimilar metallic restorations are present saliva
acts as an electrolyte & galvanic current is formed. This
acts as irritant--pulpitis
BACTERIAL EFFECTS
 Bacteria can damage the pulp through toxins or
directly after extension of caries .
 Through transportation via the vasculature -
BACTERMIA OR SEPTICEMIA
 ANACHORETIC PULPITIS--bacteria circulating in
the blood stream tend to settle in areas of pulpal
inflammation (due to chemical or mechanical injury)
 Anachoresis is the phenomenon by which blood borne
bacteria, dyes ,pigment, metallic substance, foreign
protein are attracted to site of inflammation.
 Occurs in clinically insignificant number.
 PULPAL & PERIAPICAL DISEASES

Pulpal Diseases

Pulpitis Pulpal Degeneration &

Necrosis
Acute Chronic
-Reversible -Reversible Pulp Others
-Irreversible -Irreversible Calcifications -External
•Hyperplastic resorption
Pulpitis -Pulp Stones
•Internal
resorption
 REVERSIBLE PULPITIS
Mild inflammation of the tooth pulp caused by caries
encroaching on the pulp.

 Clinical Features:    hypersensitive to thermal (hot or cold)

or sweet stimulus which rapidly disappears when stimulus is
removed   localized increase in intrapulpal pressure
  threshold stimulation for A-delta nerve fibers is lowered 
 Treatment:    no treatment other than time for the tooth pulp
to heal 
 IRREVERSIBLE PULPITIS
Progresses from reversible pulpitis, a severe inflammation of
the pulp.
 Clinical Features:    hypersensitive to thermal stimulus
(hot or cold) which produces a pain which lingers for
minutes when stimulus is removed   pain is severe, persistent
and poorly localized   pain may radiate to ear, temple, eye or
neck  
 Treatment: root canal treatment or extraction.
FOCAL REVERSIBLE PULPITIS
 Was also called pulp hyperaemia (which could also
occur artefactually from the pumping action during
tooth extraction).
CLINICAL FEATURES OF FOCAL
REVERSIBLE PULPITIS
 Sensitive to thermal changes --cold eg pain occurs
after application of ice
 pain disappears on removal of the stimuli
 tooth responds to stimulation by the electric pulp tester
at a lower level of current--indicating a LOWER PAIN
THRESHOLD THAN A NORMAL TOOTH
 Teeth in this condition exists in DEEP CARIOUS
LESIONS, LARGE METALLIC RESTORATION
WITHOUT ADEQUATE INSULATION OR WITH
LEAKING MARGINS
TREATMENT & PROGNOSIS
 Condition is REVERSIBLE --provided the irritant is
removed before pulp is severely damaged .
 Decay must be restored soon
 delay results in extensive pulpitis -death of the pulp
 tooth shd be kept under observation
ACUTE PULPITIS
 It is the sequela of focal reversible pulpitis
 Also occur as an ACUTE EXACERBATION OF
Chronic pulpitis
C.F OF ACUTE PULPITIS
 Even in the early stages when I is under the carious
lesion --severe pain in presence of COLD or hot.
 Pain PERSISTS when stimulus is removed
 open acute pulpitis pain is less
 pulp of the individual tooth are not precisely
represented on the sensory cortex--referred pain.
 As Infection increases -intra pulpal abscess are formed
-pain becomes more severe -lancinating or throbbing
type
 pain lasts 10-15 mins or may be continuous
 intensity increases in lying down position
 HEAT may cause an acute exacerbation of pain
 Tooth responds to electric pulp vitality tester at a lower
level of current than adjacent normal teeth --due to
increased sensitivity of pulp
 non vital pulp- sensitivity is lost
 SEVERE PAIN is present in CLOSED PULP -due to
EXUDATE build up + pain producing substances released.
 Rapid spread of Infection--pain & necrosis
 When infection or necrosis spreads beyond the pulp
tissue--pain on percussion occurs
 In open pulpitis-pain is dull, throbbing sensitive to
thermal changes—no infection build up--mobility
absent , POP absent
TREATMENT
 ACUTE PULPITIS--May enter CHRONIC stage( pt
with high resistance & low virulence micro-organism)
 Very initial stage -pulpotomy+Ca(OH)2 dressing
 BEST CHOICE--RCT
CHRONIC PULPITIS
 May be chronic on onset
 May occur through quiescence of a previous acute
pulpitis
 Signs & symptoms are milder
 May be open or closed
CLINICAL FEATURES
 INTERMITTENT MILD ,dull pain may be present
 Reaction to thermal change is dramatically reduced
 Threshold for stimulation by electric pulp tester is
often increased due to degeneration of nerve tissue in
the pulp
 Pulp may become totally necrotic without pain
 Pulp may bleed on probing-but without pain
TREATMENT & PROGNOSIS
 RCT or EXTRACTION
CHRONIC HYPERPLASTIC
PULPITIS (PULP POLYP)

 UNIQUE FORM OF PULPITIS --where pulp reacts by

excessive & exuberant proliferation
 It occurs as a chronic lesion from the onset or as a
chronic stage of a previous acute pulpitis
CLINICAL FEATURES
 Occurs exclusively in children & young adults --with
high degree of tissue resistance & reactivity --readily
responds by forming proliferative lesions
 Mostly involves teeth with large ,open carious lesions--
deciduous teeth & 1st permanent molars with excellent
blood supply due to large root apical foramen.
 PULP POLYP appears as a pinkish -red globule of tissue
protruding from the pulp chamber & not only fills the
carious defect but extends beyond
 It contains few nerves --insensitive to
manipulation(sometimes large no. of nerves may be
present )
 Lesion may or may not bleed-depending on degree of
vascularity
 Sometimes gingival tissue proliferates into the carious
tooth-resembles pulp polyp
 Careful examination is done to study the connection
with pulp or gingiva
DISEASES OF THE PERIAPICAL
TISSUES
 PULPITIS(acute & chronic)--APICAL
PERIODONTITIS (acute & chronic)

 periapical abscess
(Acute or chronic)

periapicalgranuloma

Periodontal cyst
osteomyelitis
APICAL PERIODONTITIS
 THIS IS INFLAMMATION OF THE PERIODONTAL
LIGAMENT AROUND THE APICAL PORTION OF
THE ROOT
 There may be resorption of periapical bone & root
apex
 POP- symptom
 May be ACUTE OR CHRONIC depending upon the
virulence of microorganism involved & the severity of the
stimuli(physical or chemical) & host resistance
 CAUSES
 Spread of infection following pulp necrosis
 occlusal trauma from a high restoration
 RCT-overinstrumentation,chemical irritation,pushing of
infected tissue
ACUTE APICAL PERIODONTITIS
 History of previous pulpitis
 Tooth feels slightly elevated-due to edema in PDL
 TENDER to touch--POP( external pressure forces the
edema fluid against already sensitised nerve endings
 Radiographic appearance is essentially normal
except slight widening of the PDL space
TREATMENT
 Occlusal trauma is relieved
 pulpal infection spread is controlled with RCT
 EXTRACTION
CHRONIC APICAL
PERIODONTITIS
 (PERIAPICAL GRANULOMA)
 It is a localised mass of chronic granulation tissue
formed in response of infection
 It is a low grade infection --most common sequelae of
pulpitis or acute periapical periodontitis´.( acute phase
is exudative response --chronic is proliferative)
 Lateral canals leads to lateral granuloma
CLINICAL FEATURES
 Tooth is usually NON VITAL
 Slightly tender to percussion--due to hyperaemia &
edema & I of PDL
 Dull sound due to presence of granulation tissue
around the apex
 Slightly elongated in its socket
 May be symptomless
 Usually no perforation of overlying bone or fistula
formation
TREATMENT & PROGNOSIS
 EXT
 RCT
 RCT with apicoectomy
 if left untreated --apical periodontal cyst
APICAL PERIODONTAL CYST
 Also called radicular cyst,periapical cyst, root end cyst
 MOST COMMON CYST -TRUE CYST
 periapical granuloma-> cyst
 always associated with caries
C/F OF PERIAPICAL CYST
 Mostly ASYMPTOMATIC
 seen bet ages of 20-60 yrs
 deci teeth involvement is common
 max anterior most commonly involved
 associated teeth are non-vital or show DCL
 LESS chances of bone destruction & bone expansion
 May undergo acute exacerbation(due to loss of tissue
resistance) ->abscess->cellulitis->draining fistula
TREATMENT & PROGNOSIS
 RCT followed with apicoectomy
 ext followed by curettage
 Does not recur
 ameloblastomatous transformation is NOT
seen,epidermoid carcinoma is rare
 if untreated -increases in size with bone resorption but
seldom expansion of cortical plates is seen.
RESIDUAL CYST
 This is an I odontogenic cyst present in edentulous
jaws
 Occurs after extraction where periapical pathology is
left behind untreated or incomplete removal of a cyst
or granuloma
 Appears as a radiolucent lesion occasionally
dystrophic calcification (radio-opaque) may be present
 History & examination is done to rule out cysts, tumors &
metastatic lesions.
 If it gets infected - purulent discharge thru a sinus is seen
 Treatment
 Curettage & lining is sent for histopathological exam
 Does not recur if etio is removed
PERIAPICAL ABSCESS
 It is an acute or chronic suppurative process of the
periapical area
 may develop from acute PA periodontitis or PA
granuloma
 acute exacerbation of chronic PA lesion ---phoenix
abscess. It may arise in DCL ,TRAUMATIC
INJURY,irritation of PA tissue during RCT(Mechanical
or chemical)
CLINICAL FEATURES
 Acute I of apical periodontium--tenderness of the tooth
often relieved by application of pressure
 Later it becomes extremely painful & is slightly
extruded from the socket
 Regional lymphadenitis & fever may be present
 Extension of the abscess to adjacent marrow spaces
produces osteomyelitis( swelling & extreme pain)
 chronic PA abscess is mild, & has well circumscribed
area of suppuration
 Treatment
 drainage ( RCT OR EXT)
 If it spreads it leads to osteomyelitis, cellulitis,bacteremia
& fistula tract .
 Cavernous sinus thrombosis in extreme situation.
 DENTINE
HYPERSENSITIVITY
 Dentine is a mineralized tissue
that forms the bulk of the tooth.

 It is rigid but elastic,consisting

of many parallel tubules called
dentinal tubules.

 These tubules run from the

pulpal surface to enamel-dentine
& cementum -dentine junction.
 Dentine hypersensitivity is characterised by short,
sharp pain arising from exposed dentine in response to
stimuli, typically thermal , tactile, osmotic (sweet or
sour food) or chemical and which cannot be ascribed to
any other dental defect or pathology
 Females have a higher incidence than males
 Range in age -20 to 40 yrs
 Commonly seen in cervical zones of permanent teeth
 Canines ,first premolar, incisors, second premolars and
molars. (descending order )
MECHANISM
 HYDRODYNAMIC THEORY : This
theory was proposed by
BRANNSTROM which postulates that
rapid shifts, in either direction, of the
fluids within the dentinal tubules,
following stimulus application, result in
activation of sensory nerves in the
pulp/inner dentine region of the tooth.
 Studies performed in vivo revealed that the response
of the pulpal nerves was proportional to the pressure
and therefore the rate of fluid flow
 Stimuli, such as cold,
which cause fluid flow
away from the pulp
produce more rapid and
greater pulp nerve
responses than those,
such as heat, which
cause an inward flow.
 Differences between sensitive and non sensitive
dentine :
 There are more and wider open dentinal tubules in
sensitive dentine
COMMON CAUSES :
1.Enamel loss :a)
Attrition
b) Abrasion
c) Erosion
2.Gingival recession
3.Prominent roots
4.Crown preparation
SYMPTOMS
 Tooth sensitivity to hot and cold
 Tooth pain
 Tingling of the tissues
DIAGNOSTIC TOOLS :
 Air /water syringe (thermal )
 Dental explorer (touch )
 Thermal tests (ice cube )
 Percussion testing
 Assessment of occlusion
 Tooth brush abrasion ,chemical erosion ,thin
enamel ,gingival recession .
MANAGEMENT :
 Incorrect toothbrushing appears to be an aetiological
factor in dentine hypersensitivity, instruction in proper
brushing technique can prevent further loss of dentine
and the resulting hypersensitivity. Excessive force,
hard toothbrushes, highly abrasive toothpastes should
be avoided
  PROPER BRUSHING
TECHNIQUE

TILT THE BRUSH AT A 45°

ANGLE AGAINST THE
GUMLINE AND SWEEP OR
ROLL THE BRUSH AWAY
FROM THE GUMLINE
 Dietary acid has a very clear role in the initiation of
dentine hypersensitivity, dietary counselling is an
important factor for the management of the condition
advice should be directed towards reducing the
quantity and frequency of acid intake.
 Other suggestions have been to, drink something neutral or
alkaline after consuming acids such as water or milk, avoid
sipping, use a straw, chill the drink which can reduce its
erosive potential and finally, avoid acids as a snack just before
bed time or during the night
 If intrinsic erosion is suspected as a factor in tooth
wear and dentine hypersensitivity, Rinsing the mouth
with liquid antacid, especially after vomiting or
regurgitation, is advised. In severe or chronic cases,
fabrication of an occlusal splint to be inserted at high
risk times can reduce the insult to the teeth. If the
splint is loaded with an alkali such as sodium
bicarbonate, it may further neutralise the effect of
gastric acids. Non-acidulated fluoride gels may also be
useful within the splint.
 Professional treatment :dentine sealers
 Dental restoration : composite /glass ionomer
restoration
 Crown replacement
 Root canal treatment
 Periodontal surgical procedure that covers the exposed
dentine
 Home treatment :
 Potassium nitrate containing tooth paste
 Solutions ,gels ,pastes containing fluoride in varying %
and compounds, Sodium monofluorophosphate .
DEVELOPMENTAL
DISTURBANCES OF
TEETH
I. NUMBER II. SIZE
1. Hypodontia
1. Microdontia
2. Hyperdontia
2. Macrodontia

III. SHAPE
3. Gemination IV. STRUCTURE
4. Fusion 3. Amelogenesis imperfecta
5. Concrescence 4. Dentinogenesis
6. Accessory cusps imperfecta
7. Dens invaginatus 5. Dentin dysplasia type I
8. Ectopic enamel
6. Dentin dysplasia type II
9. Taurodontism
7. Regional odontodysplasia
10. Hypercementosis
11. Dilaceration
 DEVELOPMENTAL
ALTERATIONS IN THE
NUMBER OF TEETH
 Anodontia- total lack of tooth development.

 Hypodontia- lack of development of one or more teeth

 Oligodontia (a subdivision of hypodontia)- lack of

development of six or more teeth.

 Hyperdontia- development of an increased number of teeth

and the additional teeth are termed supernumerary.
 Genetic control appears to exert a strong influence on the
development of teeth.

 Numerous hereditary syndromes have been associated with both

hypodontia and hyperdontia. In all of these syndromes, there is an
increased prevalence of hypodontia or hyperdontia, but the strength
of the association varies.

 Many non syndromic numeric alterations of teeth demonstrate a

strong genetic correlation.
Pathogenesis:
 Hyperdontia caused by the development of excess dental lamina,
which presumably leads to the formation of additional tooth germs.
 Hypodontia caused due to the absence of appropriate dental lamina.
 Loss of the developing tooth buds in most instances appears to be
genetically controlled.
 Environment most likely influences the final result or, in some
cases, may be responsible completely for the lack of tooth
formation.
 The dental lamina is extremely sensitive to external stimuli, and
damage before tooth formation can result in hypodontia.
 Trauma, infection, radiation, chemotherapeutic medications,
endocrine disturbances, and severe intrauterine disturbances have
been associated with missing teeth.
Hypodontia:
1. Prevalence of 3.5% to 8.0% (excluding third molars).
2. Female predominance of approximately 1.5:1 is reported.
3. Anodontia is rare, and most cases occur in the presence of hereditary
hypohidrotic ectodermal dysplasia.
4. Hypodontia is uncommon in the deciduous dentition (less than 1% of
the population) and, when present, most frequently involves the
mandibular incisors.
5. Missing teeth in the permanent dentition are not rare, with third molars
being the most commonly affected (20% to 23% of the population).
6. After the molars, the 2nd premolars and lateral incisors are absent most
frequently.
7. Hypodontia is associated positively with microdontia, reduced alveolar
development and retained primary teeth.
Hyperdontia:
1. The prevalence of supernumerary teeth in Caucasians is between
1% and 3%, with a slightly higher rate seen in Asian populations.
2. Single- tooth hyperdontia occurs more frequently in the
permanent dentition and approximately 90% present in the maxilla,
with a strong predilection for the anterior region.
3. The most common site is the maxillary incisor region, followed by
maxillary fourth molars and mandibular fourth molars, premolars,
canines, and lateral incisors.
4. Although supernumerary teeth may be bilateral, most occur
unilaterally.
5. In contrast to single-tooth hyperdontia, non syndromic multiple
supernumerary teeth occur most frequently in the mandible. These
multiple supernumerary teeth occur most often in the premolar
region, followed by the molar and anterior regions, respectively.
 A supernumerary tooth in the maxillary anterior incisor region is
termed a Mesiodens
 An accessory fourth molar is known as Distomolar or Distodens.
 A posterior supernumerary tooth situated lingually or buccally to a
molar tooth is termed a Paramolar.
 Accessory teeth may be present at or shortly after birth.
 Teeth present in newborns is called as Natal teeth
 Those arising within the first 30 days of life are designated as
Neonatal teeth. Although some authors have suggested that these
teeth may represent pre deciduous supernumerary teeth, most are
prematurely erupted deciduous teeth (not supernumerary teeth).
 Approximately 85% of natal teeth are mandibular incisors, 11% are
maxillary incisors, and 4% are posterior teeth.
Treatment and Prognosis:

In Hypodontia:- depends on the severity of the case.

1. No treatment may be required for a single missing tooth
2. Prosthetic replacement often is needed when multiple teeth are
absent.
3. Therapeutic options include traditional fixed prosthodontics,
resin-bonded bridges, or osseointegrated implants with associated
prosthetic crowns.
4. For children and young adults, a resin-bonded bridge often is
appropriate while waiting for full dental maturation.
In Hyperdontia:-
1. Early diagnosis and treatment often are crucial in minimizing the
aesthetic and functional problems of the adjacent teeth.
2. Only 7% to 20% of supernumerary teeth exist without clinical
complications, the standard of care is early removal of the accessory
tooth. Complications created by anterior supernumerary teeth tend to be
more significant than those associated with extra teeth in the posterior
regions.
3. A consequence of late therapy includes:
a. Delayed eruption or resorption of the adjacent teeth
b. Displacement of the teeth with associated crowding, malocclusion, or
diastema formation.
c. Supernumerary teeth also predispose the area to sub acute pericoronitis,
gingivitis, periodontitis, abscess formation, and odontogenic cysts.
Natal teeth:- must be approached
individually.
1. The erupted teeth in most cases
represent the deciduous dentition
and removal should not be
performed hastily.
2. If the teeth are mobile and at risk
for aspiration, removal is indicated.
3. If mobility is not a problem and the
teeth are stable, they should be
retained.
4. Traumatic ulcerations of the
adjacent soft tissue (Riga-Fede
disease) may occur during breast-
feeding.
 DEVELOPMENTAL
ALTERATIONS IN THE SIZE OF
TEETH
 Tooth size is variable among different races and between the sexes.
 The presence of unusually small teeth is termed microdontia
 Presence of teeth larger than average is termed macrodontia.
 Although heredity is the major factor, both genetic and
environmental influences affect the size of developing teeth.
 The deciduous dentition appears to be affected more by maternal
intrauterine influences; the permanent teeth seem to be more
affected by environment.
Clinical Features:
Microdontia:
1. The term microdontia should be applied only when the teeth are
smaller than usual.
2. Normal-sized teeth may appear small when widely spaced within
jaws that are larger than normal. This appearance has been
historically termed relative microdontia, but it represents
macrognathia (not microdontia).
3. Diffuse true microdontia is uncommon but may occur as an
isolated finding in Down syndrome, pituitary dwarfism.
4. The maxillary lateral incisor is affected most frequently and
typically appears as a peg- shaped crown overlying a root that often
is of normal length. The mesiodistal diameter is reduced, and the
proximal surfaces converge toward the incisal edge.
5. The reported prevalence varies from 0.8% to 8.4% of the
population
Macrodontia:
1. Term macrodontia should be applied only when teeth are larger
than usual and should not include normal-sized teeth crowded
within a small jaw (previously termed relative macrodontia).
2. In addition, the term macrodontia should not be used to describe
teeth that have been altered by fusion or gemination.
3. Diffuse macrodontia has been noted in association with pituitary
gigantism and pineal hyperplasia with hyperinsulinism.
4. Macrodontia with unilateral premature eruption is not rare in
hemifacial hyperplasia. The unilateral bone growth resulting from
this condition may also affect developing teeth on the altered side.
Treatment and Prognosis:
Treatment of the dentition is not necessary unless
desired for aesthetic considerations.
Maxillary peg laterals often are restored to full size by
porcelain crowns.
 DEVELOPMENTAL
ALTERATIONS IN THE
SHAPE OF TEETH
 GEMINATION AND FUSION
 Gemination- defined as a single enlarged tooth or joined (i.e..
double) tooth in which the tooth count is normal when the anomalous
tooth counted as one.

 Fusion- defined as a single enlarged tooth or joined (i.e., double)

tooth in which the tooth count reveals a missing tooth when the
anomalous tooth is counted as one.
Clinical Features:
Gemination and fusion:
1. Double teeth (gemination and fusion) occur in both the primary
and permanent dentitions, with a higher frequency in the anterior
and maxillary regions.
2. Prevalence- 0.5% in the deciduous teeth and 0.1% in the
permanent dentition.
3. Bilateral cases are seen less frequently, with a prevalence of
0.02% in both dentitions.
4. Gemination and fusion appear similar and may be differentiated
by assessing the number of teeth in the dentition.
5. Some authors have suggested that gemination demonstrates a
single root canal. Separate canals are present in fusion, but this
does not hold true in all cases.
 CONCRESCENCE
Concrescence- defined as the union of two teeth by cementum without
confluence of the dentin.
 Unlike fusion and gemination, concrescence may be developmental
or post inflammatory.
 When two teeth develop in close proximity, developmental union by
cementum is possible.
 In addition, areas of inflammatory damage to the roots of teeth are
repaired by cementum once the inciting process resolves.
 Concrescence of adjacent teeth may arise in initially separated teeth
in which cementum deposition extends between two closely
approximated roots in a previous area of damage.
Clinical Features:
Concrescence:
1. Is noted more frequently in the posterior and
maxillary regions.
2. The developmental pattern often involves a second
molar tooth in which its roots closely approximate
the adjacent impacted third molar.
3. The post inflammatory pattern frequently involves
carious molars in which the apices overlie the
roots of horizontally or distally angulated third
molars.
4. This latter pattern most frequently arises in a
carious tooth that exhibits large coronal tooth loss.
5. The resultant large pulpal exposure often permits
pulpal drainage, leading to a resolution of a
portion of the intrabony pathosis. Cemental repair
then occurs.
Treatment and Prognosis:
1. The presence of double teeth (i.e., gemination or fusion) in the
deciduous dentition can result in crowding, abnormal spacing, and
delayed or ectopic eruption of the underlying permanent teeth. So
it should be monitored closely by careful clinical and radiographic
observation.
2. Extraction may be necessary to prevent an abnormality in
eruption.
3. In most cases of surgical division, endodontic therapy was
performed.
4. Selected shaping with or without placement of full crowns.
5. Concrescence often require no therapy unless the union interferes
with eruption then surgical removal may be warranted.
 ACCESSORY CUSPS

Three distinct patterns are:

1. Talon cusp
2. Cusp of Carabelli
3. Dens evaginatus
 CUSP OF CARABELLI
 The cusp of carabelli is an accessory
cusp located on the palatal aspect of the
mesiolingual cusp of maxillary molar.
 Cusp may be seen in permanent or
deciduous dentition.
 Varies from a definite cusp to a small
pit or fissure.
 More pronounced in on 1st molar, and is
less obvious on 2nd and 3rd molars.
 An analogous accessory cusp is seen
occasionally on mesiobuccal cusp of a
mandibular permanent or deciduous
molars called as PROTOSTYLID.
Clinical significance:
1. When it is present, the remaining permanent teeth are larger than
normal mesiodistally
2. Deep grooves if present may cause caries.

Treatment:
3. No therapy.
4. If a deep groove is present on mesiolingual cusp, then it is sealed to
prevent caries.
 TALON CUSP

 Also called as dens evaginatus of anterior tooth

 It is a well delineated additional cusp that is located on the surface of
an anterior tooth and extends at least half the distance from the
cementoenamel junction to the incisal edge.
 3/4th of all reported talon cusp are located in permanent dentition.
 Usually found on
-permanent maxillary lateral incisor (55%)
-maxillary central incisor (33%)
-mandibular incisors (6%)
-mandibular canine (4%)
 Mostly , talon cusp contains a pulpal
extension.

 Radiographically, cusp is seen

overlying the central portion of the
crown and includes enamel and
dentin.

 No sex predilection.

 Seen in patient with:

-Rubinstein Taybi syndrome
-Sturge Weber syndrome
Clinical significance:
 Talon cusps present on maxillary teeth interferes with occlusion.
 Caries
 Periodontal problems
 Irritation to adjacent soft tissues

Treatment:
 Talon cusp on mandibular teeth require no therapy.
 If present on maxillary teeth, then it may interfere with occlusion
and should be removed by periodic grinding.
 DENS EVAGINATUS
Definition:
 Cusp like elevation of enamel
located in the central groove or
lingual ridge of the buccal cusp of
permanent premolars or molar
teeth.

Clinical features:
1. Mostly occurs on premolars
2. Cusp consists of enamel, dentin
and pulp.
3. Radiographically , the occlusal
surface exhibits a tuberculated
appearance, often a pulpal
extension is seen in cusp.
4. May be seen in association with shovel shaped incisors.
5. Affected incisors demonstrate prominent lateral margins creating a hollowed
lingual surface that resembles the scoop of shovel.

Clinical Significance:
 Occlusal problems
 More prone to fracture
 Pulpal exposure

Treatment:
 Removal of enamel tubercle
 Placement of Ca(OH)2 dressing to stimulate the odontoblasts to produce reparative
dentin.
 If it involves pulp then endodontic procedures are carried out.
 ECTOPIC ENAMEL
Ectopic enamel- refers to the presence of enamel in unusual locations,
mainly the tooth root, called as enamel pearls.
 Enamel pearls are hemispheric structures that may consist entirely of
enamel or contain underlying dentin and pulp tissue.
 Cause: Mostly project from the surface of the root and are thought
to arise from a localized bulging of the odontoblastic layer. This
bulge may provide prolonged contact between Hertwig’s root sheath
and the developing dentin, triggering induction of enamel formation.
Clinical and radiographic features:
1. Mostly found on roots of maxillary molars, then mandibular molars.
2. Majority occur on roots at furcation area or near CEJ.
3. Radiographically, pearl appear as well defined, radiopaque nodules
along the root’s surface.

Treatment:
Due to more plaque retention ,meticulous oral hygiene should be
maintained to prevent loss of periodontal support.
 DENS INVAGINATUS
 It is a deep surface invagination of the crown or root that is lined
by enamel.

 Two forms
1. Coronal
2. Radicular

 Mostly affect maxillary teeth.

Coronal dens invaginatus:-

 Type1- Invagination confined

to crown

 Type2- Invagination
extending below CEJ and
ends in a blind sac that may
or may not communicate with
the adjacent dental pulp

 Type3-Extends through the

root and perforates in the apical or
lateral radicular area without any I II III
immediate communication with
pulp.
 Invagination may be large
resembling tooth within a tooth
called as DENS IN DENTE.
 Radicular dens invaginatus is
rare.
 It arises secondary to proliferation
of hertwig’s root sheath, with the
formation of strip of enamel that
extends along surface of root.
 Altered enamel forms a surface
invagination into the dental papilla.
 Radiographically, affected tooth
shows enlargement of root.
Treatment:
 In TYPE 1 opening of invagination should be restored upon
eruption to prevent caries.

 In larger invaginations, contents of lumen must be removed and

Ca(OH)2 base is placed.

 In cases with pulpal communication, root canal therapy is needed.

 TYPE 3 with periradicular inflammatory lesions requires root canal

therapy.
 TAURODONTISM

Taurodontism- is enlargement of body and pulp chamber of a

multirooted tooth with apical displacement of the pulpal floor and
bifurcation of roots.

 This pattern of molar formation has been found in ancient

Neanderthals, and the overall shape of taurodont resembles that of
molar teeth of cud chewing animals.(Tauro= Bull, Dont= Tooth)
Clinical and radiographic features:
1. Affected teeth tends to be rectangular, exhibits pulp chambers with
an increased apico-occlusal height and a bifurcation is close to
apex.
2. Taurodontism has been classified according to the degree of apical
displacement of pulpal floor:
a. Mild (hypo taurodontism)
b. Moderate (meso taurodontism)
c. Severe (hyper taurodontism)

3. May be unilateral or bilateral

4. Affects permanent teeth more than primary
5. No sex predilection
Conditions associated with taurodontism:
1. Klinefelters syndrome
2. Tricho dento osseous syndrome
3. Down syndrome

Treatment:
 No specific therapy
 If endo therapy is required, shape of pulpal chamber increases the
difficulty of locating instrumentation and obturating the pulp
canals.
 HYPERCEMENTOSIS
Hypercementosis is a non neoplastic deposition of excessive cementum
that is continuous with normal radicular dentin.

 Factors associated with hypercementosis:

Local factors: Systemic factors:
 Abnormal occlusal trauma Acromegaly
 Adjacent inflammation Calcinosis
Paget’s disease of bone
 Unopposed teeth (eg impacted)
Thyroid goitre
Vitamin A deficiency
Clinical and radiographic features:
1. Occurs predominantly in adulthood

2. May be isolated, or involve multiple teeth

3. Mostly involves premolars

4. Radiographically , affected teeth shows a thickening or blunting of root,

but exact amount of increased amount of cementum is difficult to
ascertain because cementum and dentin shows
similar densities.

Treatment:
 No treatment

 Problem may arise during extraction due to

thickened root.
 If the tooth is carious, endo treatment should be performed carefully.
 DILACERATION

 It is an abnormal angulation or bend in the root, less frequently the

crown of a tooth.

Etiology:
 An injury that displaces the calcified portion of tooth germ and
remainder of the tooth is formed at an abnormal angle.
 The bend may develop secondary to adjacent cyst, tumour or
odontogenic hamartoma.
Clinical and radiographic features:
1. Most frequently involved teeth are permanent maxillary incisors,
followed by mandibular anterior dentition.
2. Occasionally deciduous teeth are involved
3. Altered maxillary anterior teeth frequently demonstrate the bend in
the crown or coronal half of the root, failure of eruption seen
4. Affected mandibular incisors shows involvement of crown or the
superficial portion of root, but more
frequently they erupt into full occlusion.
5. Many of the affected tooth, are non vital
and associated with periapical
inflammatory lesions.
Clinical significance:
 Associated with periapical inflammatory lesions
 Difficulty in extraction
 During endo treatment, perforation may occur.

Treatment:
 Patients with minor dilaceration of permanent teeth require no
therapy.
 Teeth that exhibit delayed or abnormal eruption may be exposed and
orthodontically moved to new position.
 Grossly deformed require surgical removal
 DEVELOPMENTAL
ALTERATIONS
IN THE STRUCTURE OF TEETH
 AMELOGENESIS IMPERFECTA
 At least 14 different hereditary subtypes of amelogenesis imperfecta
exist, with numerous patterns of inheritance and a wide variety of
clinical manifestations.

 The most widely accepted classification is given by Witkop.

 Witkop’s classification relies on the phenotype and pedigree (i.e.,

clinical appearance and apparent pattern of inheritance). Classification
by clinical appearance is problematic, because different phenotypes
have been noted within a single affected family.

 The formation of enamel is a multistep process, and the defect may

arise in any one of the steps.
 The development of enamel can be divided into three major stages:
1. Elaboration of the organic matrix
2. Mineralization of the matrix
3. Maturation of the enamel
 The hereditary defects of the formation of enamel also are divided
along these lines: hypoplastic, hypo calcified, and hypo maturation.
 Etiology of amelogenesis imperfecta is related to the alteration of
genes involved in the process of formation and maturation of the
enamel. The defective gene is linked to the locus DXS85 at Xp22
which encodes for amelogenin, a principal protein in developing
enamel.
Clinical and Radiographic Features:
 The estimated frequency of amelogenesis imperfecta in the population
varies between 1:718 and 1:14,000.
 Both the deciduous and permanent dentitions are diffusely involved.
I) Hypoplastic amelogenesis imperfecta: characterised by inadequate
deposition of enamel matrix. Any matrix present is mineralized
appropriately and radiographically contrasts well with the underlying
dentin.
 Pinpoint-to-pinhead- sized pits are scattered across the surface of the
teeth and do not correlate with a pattern of environmental damage.
 The buccal surfaces of the teeth are affected more severely, and the pits
may be arranged in rows or columns.
 Staining of the pits may occur.

 Variable expressivity is seen

within groups of affected patients.
The enamel between the pits is of
normal thickness, hardness, and
coloration.
 Both dentitions or only the primary teeth may be affected.
 The autosomal recessive type (type IC) is more severe and typically
demonstrates involvement of all teeth in both dentitions.
 In the autosomal dominant smooth pattern, the enamel of all teeth
exhibits a smooth surface and is thin, hard, and glossy
 The absence of appropriate enamel thickness results in teeth that are
shaped like crown preparations and demonstrate open contact points.
 The color of the teeth varies from opaque white to translucent brown.
 Radiographically, the teeth exhibit a thin peripheral outline of
radiopaque enamel.
Lyonization effect:
 On approximately the 16th day of embryonic life in all individuals
with two X chromosomes, one member of the pair is inactivated in
each cell. As a result of this event, females are mosaics, with a
mixture of cells, some with active maternal X chromosomes and
others with active paternal X chromosomes. Usually the mix is of
approximately equal proportions.
 If one X were to direct the formation of defective enamel and the
other X were to form normal enamel, the teeth would exhibit
alternating zones of normal and abnormal enamel.
 Males with the X-linked dominant smooth pattern exhibit diffuse thin,
smooth, and shiny enamel in both dentitions.
 Enamel agenesis demonstrates a total lack of enamel formation.
 The teeth are the shape and color of the dentin, with a yellow-brown
hue, open contact points, and crowns that taper toward the incisal-
occlusal surface.
 The surface of the dentin is rough, and an anterior open bite is seen
frequently.
 Radiographs demonstrate no peripheral enamel overlying the dentin.
Hypo maturation amelogenesis imperfecta:
 In this enamel matrix is laid down appropriately and begins to
mineralize, however, there is a defect in the maturation of the
enamel’s crystal structure.
 Affected teeth are normal in shape but exhibit a mottled, opaque
white-brown- yellow discoloration.
 The enamel is softer than normal and tends to chip or fracture from
the underlying dentin.
 Occasionally, the surface enamel may be affected severely and be
similar in softness to that of
hypo calcified patterns. These
cases often demonstrate extensive
calculus deposition.
 The snow-capped patterns exhibit a zone of white opaque enamel on
the incisal or occlusal one quarter to one third of the crown.
 The altered areas do not exhibit a distribution that would support an
environmental origin, and the surface lacks the iridescent sheen seen
with mild fluorosis.
 The affected teeth often demonstrate an anterior to posterior
distribution and have been compared with a denture dipped in white
paint.
 Both the deciduous and permanent dentitions are affected.
 Most cases demonstrate an X-linked pattern of inheritance.
 Radio graphically, the affected enamel exhibits a radio density
that is similar to dentin.
Hypo calcified amelogenesis imperfecta: In this type the enamel
matrix is laid down appropriately but no significant mineralization
occurs.
 In both patterns of hypo calcified amelogenesis imperfecta, the teeth
are appropriately shaped on eruption.
 The enamel is very soft and easily lost.
 On eruption the enamel is yellow- brown or orange, but it often
becomes stained brown to black and exhibits rapid calculus
apposition.
 With years of function
much of the coronal enamel
is removed, except for the
cervical portion that is
occasionally calcified better.
 Both patterns are similar, but the
autosomal recessive examples
are generally more severe than
the autosomal dominant cases.
 Radio graphically, the density of
the enamel and dentin are
similar.
 Before eruption the teeth are
normal in shape; however, after
a period of function much of the
cuspal enamel is lost, with the
occlusal surface becoming the
most irregular.
A B C

D E
Hypo maturation/ Hypoplastic amelogenesis imperfecta:
This type of amelogenesis imperfecta exhibits enamel hypoplasia in
combination with hypo maturation.
 Both the deciduous and permanent dentitions are involved diffusely.
 Two patterns are recognized that are similar but differentiated by the
thickness of the enamel and the overall tooth size.
 In the hypo maturation- hypoplastic pattern, the predominant defect
is one of enamel hypo maturation in which the enamel appears as
mottled yellowish white to yellow-brown.
 Pits are seen frequently on the buccal surf aces of the teeth.
 Radio graphically, the enamel appears similar to dentin in density,
and large pulp chambers may be seen in single-rooted teeth in
addition to varying degrees of taurodontism.
 In the hypoplastic- hypo maturation pattern the predominant
defect is one of enamel hypoplasia in which the enamel is thin; the
enamel that is present demonstrates hypo maturation.
 Except for the decrease in the thickness of the enamel, this pattern is
radio graphically similar to the hypo maturation- hypoplastic
variant.
 Both patterns are seen in the systemic disorder, tricho-dento-
osseous syndrome.
Treatment and Prognosis :
1. The clinical implications of amelogenesis imperfecta vary
according to the subtype and its severity, but the main problems are
aesthetics, dental sensitivity, and loss of vertical dimension.
2. In addition, in some types of amelogenesis imperfecta there is an
increased prevalence of caries, anterior open bite, or associated
gingival inflammation.
3. Types ID, IE, IG, IIA, IIIA, IIIB, and IVB demonstrate very thin
enamel or highly defective enamel, which leads to rapid attrition.
4. These variants require full coverage as soon as is practical; if the
treatment is delayed, a loss of usable crown length occurs.
5. In those patients without sufficient crown lengths, full dentures
(over dentures in some cases) often become the only satisfactory
approach.
6. In some cases, only aesthetic appearance is the prime
consideration.
7. Many less severe cases can be improved by the placement of full
crowns or facial veneers on clinically objectionable teeth.
8. In some cases a lack of good enamel bonding of veneers occurs
and does not result in a durable restoration.
9. The use of glass ionomer cements with dentinal adhesives often
overcomes this weakness.
 DENTINOGENESIS IMPERFECTA
(HEREDITARY OPALESCENT DENTIN;
CAPDEPONT’S TEETH)
 Dentinogenesis Imperfecta is a hereditary developmental disturbance
of the dentin.

 Similar dental changes may be seen in conjunction with the systemic

hereditary disorder of bone, Osteogenesis imperfecta.

 Like amelogenesis imperfecta, the disorders of dentin also involve

disagreements in classification. Two systems, one by Witkop and the
other by Shields, are well accepted but not totally satisfactory.
 It is evident that the third type of dentinogenesis imperfecta (Shields’
type III or Witkop’s Brandywine isolate) is not a separate disease and
merely represents a variation of expression of Shields’ type II.
 The best nomenclature system was suggested by Levin.
 Analogous to amelogenesis imperfecta, the diagnosis of
dentinogenesis imperfecta should be reserved for defective dentin
formation with opalescent teeth (deciduous and permanent) in the
absence of systemic disease.
 Dentin defects associated with
the systemic bone disease are
termed osteogenesis imperfecta
with opalescent teeth.
Clinical and Radiographic Features :
1. The disorder is autosomal dominant and occurs in about 1:8000
whites in the United States.
2. The dental alterations in dentinogenesis imperfecta and
osteogenesis imperfecta with opalescent teeth are similar clinically,
radiographically, and histopathologically.
3. All teeth in both dentitions are affected.
4. The severity of the dental alterations varies with the age at which
the tooth developed.
5. Deciduous teeth are affected most severely, followed by the
permanent incisors and first molars, with the second and third
molars being least altered.
6. The dentitions have a blue-to-brown discoloration, often with a
distinctive translucence
7. The enamel frequently separates easily from the underlying
defective dentin.
8. Once exposed, the dentin often demonstrates significantly
accelerated attrition .
9. Radiographically, the teeth have bulbous crowns, cervical
constriction, thin roots, and early obliteration of the root canals and
pulp chambers
10. The enamel abnormality is thought
to be a secondary defect and not a
direct expression of the
dentinogenesis imperfecta gene .
12. Although the pulps are usually obliterated by excess dentin
production, some teeth may show normal- sized pulps or pulpal
enlargement (shell teeth).
13. Shell teeth demonstrate normal-thickness enamel in association
with extremely thin dentin and dramatically enlarged pulps .
14. The thin dentin may be present on the entire tooth or be isolated to
the root. This rare abnormality has been seen most frequently in
deciduous teeth in the presence of dentinogenesis imperfecta.
12. In the isolated variant, slow but progressive root resorption occurs.
13. Initially, this pulpal enlargement was discovered in the large
Maryland Brandywine isolate and thought to be a new variant of
dentinogenesis imperfecta (type III or Brandywine isolate).
14. Current evidence strongly supports the Brandywine isolate
representing nothing more than variable expressivity of the gene
for dentinogenesis imperfecta.
Treatment and Prognosis :
 The root canals become threadlike and may develop micro
exposures, resulting in periapical inflammatory lesions.
 The success of full coverage is best in teeth with crowns and roots
that exhibit close to a normal shape and size.
 Overlay dentures placed on teeth that are covered with fluoride-
releasing glass-ionomer cement have been used with success in some
cases.
 In patients with extensive attrition, the vertical dimension has been
rebuilt by placing non precious metal castings with adhesive luting
agents on teeth that have received no preparation and are not subject
to significant occlusal stress.
 The newer composites combined with a dentin-bonding agent have
been used in areas subject to occlusal wear.
 DENTIN DYSPLASIA
 Dentin dysplasia was initially categorized in 1939.
 There are two major patterns: type I and type II.
 Dentin dysplasia should have no correlation with systemic disease or
dentinogenesis Imperfecta.
 An unusual combination of type I and type II dentin dysplasia has been
reported, but these cases represent variable pulpal anatomy that has
been documented well in dentin dysplasia type I.
 Systemic Diseases Correlated with Dentin Dysplasia-Like Alterations
:
1. Calcinosis universalis
2. Rheumatoid arthritis and vitaminosis D
3. Sclerotic bone and skeletal anomalies
4. Tumoral calcinosis
Clinical and Radiographic Features:
Dentin dysplasla type I. (radicular dentin dysplasia; rootless teeth)
 Referred to as rootless teeth because the loss of organization of the
root dentin often leads to a shortened root length.
 The process exhibits an autosomal dominant pattern of inheritance.
 The enamel and coronal dentin are normal clinically and well
formed, but the radicular dentin loses all organization and
subsequently is shortened dramatically.
 Wide variation in root formation is produced because dentinal
disorganization may occur during different stages of tooth
development. If the dentin organization is lost early in tooth
development, markedly deficient roots are formed: later
disorganization results in minimal root malformation.
 The variability is most pronounced in permanent teeth and may vary
not only from patient to patient but also from tooth to tooth in a
single patient.
 Because of the shortened roots, the initial clinical signs are extreme
tooth mobility and premature exfoliation, spontaneously or
secondary to minor trauma.
 The radicular strength of the dentin is reduced, with the teeth being
predisposed to fracture during extractions.
 Radiographically, the deciduous teeth are affected severely, with little or
no detectable pulp and roots that are markedly short or absent.
 The permanent teeth vary according to the proportion of organized
versus disorganized dentin.
 With early disorganization, no pulp can be detected and the roots are
extremely short or absent.
 With somewhat later disorganization, crescent or chevron-shaped pulp
chambers can be detected overlying shortened roots that exhibit no pulp
canals.
 Late disorganization results in
normal pulp chambers overlying
roots, each of which exhibits a
large pulp stone.
 SEVERE MILD

• The root is flared at the site of the stone, and the canal is constricted
apical to the stone.
• The inflammatory lesions appear secondary to caries or spontaneous
coronal exposure of microscopic threads of pulpal remnants present
within the defective dentin.
 DENTIN DYSPLASIA TYPE II
 Dentin dysplasia type II (coronal dentin dysplasia) exhibits
numerous features of dentinogenesis imperfecta,
 Autosomal dominant inheritance is seen.
 In contrast to dentin dysplasia type I, the root length is normal in
both dentitions.
 The deciduous teeth closely resemble those of dentinogenesis
imperfecta.
 Clinically, the teeth demonstrate a blue-to-amber- to-brown
translucence.
 Radiographically, the dental changes include bulbous crowns,
cervical constriction, thin roots, and early obliteration of the pulp.
The permanent teeth demonstrate normal clinical coloration:
however, radio graphically, the pulp chambers exhibit significant
enlargement and apical extension.
 This altered pulpal anatomy has been described as thistle tube-
shaped or flame-shaped .
 Pulp stones develop in the enlarged pulp chambers.
 A similar but unrelated disorder is pulpal dysplasia.
 This process develops in teeth that
are normal clinically.
 Radiographically, both dentitions
exhibit thistle tube- shaped pulp
chambers and multiple pulp stones.
Histopathologic Features:
 In dentin dysplasia type I, the
coronal enamel and dentin are
normal.
 Apical to the point of
disorganization, the central portion
of the root forms whorls of tubular
dentin and atypical osteodentin.
 These whorls exhibit a peripheral
layer of normal dentin, giving the
root the appearance of a “stream
flowing around boulders”.
 In dentin dysplasia type II, the deciduous teeth demonstrate the
pattern described in dentinogenesis imperfecta.
 The permanent teeth exhibit normal enamel and coronal dentin.
 Adjacent to the pulp, numerous areas of interglobular dentin are
seen.
 The radicular dentin is atubular, amorphous, and hypertrophic. Pulp
stones develop in any portion of the chamber.
Treatment and Prognosis :
 In Dentin dysplasia type I, preventive care is of foremost
importance.
 Perhaps as a result of short ended roots, early loss from periodontitis
is frequent. In addition, pulp vascular channels extend close to the
dentino enamel junction; therefore, even shallow occlusal
restorations can result in pulpal necrosis.
 If periapical inflammatory lesions develop, the therapeutic choice is
guided by the root length. Conventional endodontic therapy requires
mechanical creation of canal paths and has been successful in teeth
without extremely short roots.
 Teeth with short roots demonstrate pulpal ramifications that
eliminate conventional endodontic treatment as an appropriate
therapeutic option.
 Dentin dysplasia type II demonstrates similar
problems, and meticulous oral hygiene must be
established.
 In the permanent teeth, an increased risk of periapical
inflammatory lesions is also seen. Because the pulp
canals are not usually obliterated completely,
endodontic therapy is accomplished more readily.
 REGIONAL ODONTODYSPLASIA
(GHOST TEETH)
 It is a localized, nonhereditary developmental abnormality of teeth with
extensive adverse effects on the formation of enamel, dentin, and pulp.
 Most cases are idiopathic, but a number have been related to various
syndromes, growth abnormalities, neural disorders, and vascular
malformations.
 Pathoses noted in association with regional odontodysplasia:
1. Ectodermal dysplasia
2. Epidermal nevi
3. Hypophosphatasia
4. Ipsilateral facial hypoplasia
5. Neurofibromatosis
6. Vascular nevi
Proposed Causations for Regional Odonlodysplasia
1. Abnormal migration of neural crest cells
2. Local circulatory deficiency
3. Local trauma or infection
4. Malnutrition
5. Medication used during pregnancy
6. Radiation therapy
7. Somatic mutation
 Most popular theory revolves around an alteration in the vascular
supply.
 Several cases have occurred in patients with vascular nevi of the head
and neck; in addition, similar changes have been induced in animals by
restricting the vascular flow to an area of the jaws
Clinical and Radiographic Features :
 Regional odonto dysplasia is an uncommon finding that occurs in both
dentitions and a slight female predominance (1.4:1).
 There is a maxillary predominance (2.5:1) and a predilection for the
anterior teeth.
 Ipsilateral involvement of both arches and bilateral changes in the
same jaw have been reported.
 Involvement of more than two quadrants is rare.
 Involvement of the deciduous dentition is typically followed by
similarly affected permanent teeth. In the area of altered teeth, the
surrounding bone often exhibits a lower density.
 Many of the affected teeth fail to erupt. Erupted teeth demonstrate
small irregular crowns that are yellow to brown, often with a very
rough surface.
 Caries and associated periapical inflammatory lesions are fairly common.
Because of dentinal clefts and very long pulp horns, pulpal necrosis is common
(often in the absence of an obvious cause).
 Radio graphically, the altered teeth demonstrate extremely thin enamel and
dentin surrounding an enlarged radiolucent pulp, resulting in a pale wispy
image of a tooth; hence the term ghost teeth
 There is a lack of contrast between the dentin and the enamel with an indistinct
or “fuzzy” appearance of the coronal silhouette.
 Short roots and open apices may be seen.
 The enlarged pulps frequently demonstrate one or more prominent pulp stones.
 The most common presenting signs and
symptoms include delayed or
failure of eruption, early exfoliation,
abscess formation, malformed teeth, and
non inflammatory gingival enlargement.
Treatment and Prognosis :
 The basic approach to therapy of regional odonto dysplasia is
directed toward retention of the altered teeth, whenever possible, to
allow for appropriate development and preservation of the
surrounding alveolar ridge.
 Endodontic therapy on nonvital teeth that have sufficient hard tissue
to allow restoration has been performed successfully.
 Unerupted teeth should remain untouched, restoring function with a
removable partial prosthesis until the skeletal growth period has
passed.
 Erupted teeth can be covered with etched-retained restorations or
stainless steel crowns until final restorations can be placed after the
completion of growth.
 Because of the fragile nature of the coronal hard tissue and the
ease of pulp exposure, tooth preparation is contraindicated.
 Severely affected and infected teeth often are not salvageable and
need to be removed.
 Although vitality of the abnormal dentition often is difficult to
maintain, such efforts may bring significant rewards.
 In cases followed for many years. the teeth lost their ghostly
appearance and revealed a resultant decrease in pulp size, a
significant increase in dentin thickness, and ultimate relative
normalization of the radicular anatomy.
 In contrast, the enamel remained hypoplastic.
 The surrounding bone became well developed and lost its
diminished density.