|

|
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u According to Tencate -
´Dentin is the hard tissue portion of the pulp-dentin complex
and forms the bulk of the tooth.µ

u According to Berkovitz and Holland -

´Dentin is a rigid but elastic tissue consisting of large number
of small parallel tubules in a mineralized collagen matrix.µ

u According to „

 

  


´Dentin is a calcareous material similar to but harder and
denser than bone that composes the principal mass of a
tooth.µ
 V



 
u Ônce the tooth is erupted and fully formed, dentin
can undergo a number of changes.
u These changes are either related to:
1] Age
2] In response to stimulus applied to the tooth.
(such as Caries or attrition).
^ith regard to physiological age changes
u Secondary dentin &
u Translucent dentin are considered

^ith regard to response of dentin to stimuli

u Tertiary dentin.
u Sclerotic dentin.
u Dead tracts are considered.
 Õ




 
u It·s the most conspicuous age related change in
dentin.
u It represents the continuous, but slowed
deposition of dentin
u It is very similar to primary dentin, and it is
difficult to differentiate between them.
u However, Primary & secondary dentin are often
delineated as a result of a change in direction of
the dentinal tubules.
u Also it contains fewer tubules than primary dentin.
 


 
u ›specially seen in root dentin.
u Here the tubules can become
completely occluded with
3
 
  
u ^ith age, translucent dentin is
particularly pronounced at the

3  .
u It increases linearly with the age.
u For this reason it is used in
J
   
 to help determine
the age of the person from the
teeth.
  



 
u It is also called
3
  
3  

 
  
u Induced by certain (noxious stimuli) stimuli
such as the following :
1. Temperature (extreme heat and extreme cold)
2. Carious lesions
3. Chemical agents (calcium hydroxide and
sodium fluoride)
4. Demineralized tooth matrix.
u Is produced only by the odontoblasts
directly affected by the stimulus.
u The main function of the reparative dentin is to
protect the pulp from the inward spread of
noxious materials along the dentinal tubules
(like bacterial toxins etc.).

u This protection is accomplished by the ´ 

JJµ of those involved dentinal tubules so that

their potentially harmful contents do not reach
the dental pulp.
 FÔ
ATIÔ :

u As a result of the stimuli the majority of the

odontoblasts are degenerate.

uThose odontoblasts that are killed are replaced by the

migration of undifferentiated cells arising in the deeper
regions of the pulp ²dentine interface.

uIt is believed that these new odontoblasts origin from the

cells in the  
  
3

  deeper in pulp.
Y   
   
u This term refers to dentin
forming in response to an
insult in which, although
some damage has been
sustained and some
odontoblasts die. Y 3
 
  
u The existing odontoblasts uThis term refers to dentin
recover and continue to forming after a stimulus in
form dentin. which the original
odontoblasts in the associated
region have been completely
destroyed.
uew calcified tissue
(reparative dentin) is formed
by newly differentiated cells
referred as ´odontoblast- like
cellsµ.
 Õ  





 
u It is suggested by some researchers that the drying or
dead processes induce, or otherwise enhance
mineralization resulting in the formation of collagen
fibers and apatite crystals within the dentinal tubules.

u The calcified tubular space assumes a different refractive

index becoming transparent. This calcified Predentin and
process space of the tubule is known as sclerotic or
transparent dentin.

u Hardness tests and oentgen ay studies indicate these

areas to be more highly mineralized than the other
regions of the dentin.
u Increased hardness and density and
decreases permeability.
u Characterized physically by
increased transparency with
transmitted light
u Sclerotic dentin is frequently found
beneath worn enamel such as occurs
in the incisal area of anterior teeth of
the teeth in elderly people.
u Sclerotic dentin may also be found
under slowly progressing caries. In
such cases blocking of the tubules
may be considered or defensive
reaction of the dentin, sclerotic
dentin is also found beneath tomes
granular layer in the cervical area of
older teeth where the cervical
cementum has been exposed to the
oral cavity as a result of recession of
the gingival.
 |




u Ôdontoblastic cell processes in the
dentinal tubules when degenerate, leave
behind empty, air-filled tubules.
u The emptied tubules in these areas and
the dentin are referred to as ´dead
tractsµ.
u They are expectedly less sensitive than
those in which the processes are present
in the tubules.
u ^hen ground sections are examined
with reflected light, the air-filled tubules
are light and unaffected tubules are dark.
u ^ith transmitted light, however, the
tubules are dark and the remaining
dentin light.
uDead tracts generally extend from the
dentinoenamel junction to the
corresponding area of the dentin-pulp
interface.
uIn most instances, the dead tracts are
sealed at their pulpal aspect by the
forming of reparative dentin.
uDead tracts are often encountered on
the tips and cusps that have been
subjected to abrasive forces sufficient
in intensity to cause attrition and they
appear to a greater extent in older
teeth.
uDear tracts are probably the initial
step in the formation of 

  
 |



 

 

| 
Developmental disorder of Jaw:
CL›DÔC AIAL DYSPLASIA
u Hereditary disorder
u Skull, clavicle, dentition affected.
u Prolonged retention of primary teeth
and delayed eruption of permanent.
u 
  
J
   3
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u 




3 


3 3
   3  
Developmental disturbance of teeth:

G›
IATIÔ :
u Hereditary and familial tendency.

u Partial development of two teeth from a 

tooth bud following incomplete division .

u Teeth size is larger than normal.

u ›      J  
  

3 3   3 J 

u Common pulp canals present.

      
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u Also called as ¶à
 
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u Three types:
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u     
 

u !,- .
‰
ultiple bone #
‰ Hyper extensible joints.
‰ Blue sclera.

u      .
‰ Deciduous teeth are more commonly affected.
‰ Teeth are brownish violet to yellowish brown
in
color.
‰ Amber translucency seen.
‰ ›namel is lost and dentin undergoes rapid
attrition.
‰ Scalloping of D›J absent.
‰ Anterior teeth are nearly square.
‰ Bicuspids and molars are flatter than normal
‰ Appearance of the posterior may be
described as 3
"*+›  .
u Inherited as autosomal dominant
trait.
u Both dentition are affected
u All other c/f are same except they
are more sever and not associated
with osteogenesis imperfecta.

"*+›  .
u It is also inherited as autosomal
dominant trait.
u Ôpalescent color bell shape crowns
are seen.
Y$/Y+à! -›"0Y› .
u Constriction of cervical portion of tooth
that gives bulbous appearance.
u Slight or market attrition.
u partial or complete obliteration of pulp
chambers.
u oots canals may be absent or thread like
or blunted.
à›

"››"à.
In Brandywine (type 3) DI, enamel of the
tooth appears normal but the dentin is
extremely thin and the pulp chambers are
enormous.
oots are extremely short.
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u dentin is composed of irregular tubules, of with large areas
of uncalcified matrix.
u Cellular inclusions like odontoblast are present which
degenerate rapidly.
u Tubules are larger in diameter, less numerous than normal

„1/›„›1".
u Cast metal crown ² posterior teeth
u Jacket crowns - anterior teeth
   
3
u Y   
u are disturbance of dentine formation characterized by normal
but atypical dentine formation with abnormal pulpal
morphology

 2 3 J  
J  .
u "3  (radicular dentinal dysplasia)
u "3  (coronal dentinal dysplasia)

›   
u Hereditary- autosomal dominant

,J.
"3 -both dentition affected
u Slight bluish-brown translucency apparent
u ormal eruption but characteristically exhibit extreme mobility
and exfoliate prematurely by minor trauma as a result of their
short roots
"3 deciduous teeth have yellow or bluish
grey opalescent appearance.

Y 
3 J  
.
"3 .
u oots of both dentition are
short/abnormally shaped.
u Pulp chamber/root canals completely fill in
before eruption
u 20% teeth has Periapical radiolucencies
associated with intact tooth (characteristic
feature)

"3 :
u Permanent teeth exhibits large pulp
chamber in coronal portion (THISTL›-
TUB›) appearance
u Ôbliteration of pulp chamber & reduction
in caliber of root canal after eruption (5-6
yr.)
u Pulp chambers filled with hypertrophic
dentine giving FLA
› shaped appearance
u
ultiple pulp stones.
 à  
J  
:
u "3
:
ormal dentinal tubule formation
appears to have blocked so that new dentine
forms around obstacles & giving the
appearance of -
u ´
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u Dentine itself normal ,simply disoriented

"3 .
u Atubular dentin in radicular portion
while coronal dentin is normal.

„   .
u Prosthetic replacement
 Y  
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u / 



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u A developmental disturbance of several adjacent teeth in which the

enamel & dentine are thin and irregular and fail to adequately
mineralize.

u Surrounding soft tissue is hyperplasic and contains focal

accumulations of spherical calcifications and odontogenic rests.

!,-.

u Both dentition affected

u Teeth-small &mottled brown
u Susceptible to caries
u Fracture as teeth are brittle
u Central incisors &canines-most affected
u ›ruption delayed or may not erupt at all
à   J  
 .
u
arked reduction in amount of dentin with
widening of predentin
u Large areas of interglobular dentin
u Irregular tubular pattern

Y 
3 J  
.
u
arked reduction in density of teeth, giving
ghost appearance.
u ›namel and dentin very thin.
u Pulp chambers very large with wide root
canal.
u oots are shortened

„   .
u Prosthetic replacement
 !
 
  
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u Dentin has tubular structure.
u Thus there is a possibility of substances applied to its outer surface
being able to reach and affect the dental pulp.
u This depends on various factors like:
- ^hether the dentin surface is exposed due to the pathology like
caries, attrition, abrasion, trauma.
- ^hether the tubules are patent or occluded physiologically by
Intratubular dentin.
- ^hether their outward movement of interstitial dentinal tubule
washes out the cause of irritation.
- ^hether the causative agent can pass through the odontoblast layer
.which acts as a barrier to the molecules of high molecular weight

The most significant material that can travel down the tubules the 
 .
Specially their toxins

Also components of dental material or etchants used with resins can pass
through the dentin n=and damage the pulp.
 Y 3 



 
.
u ›xternal stimuli like eg. Caries, attrition can affect the
dentin.
u The response to these stimuli come from the pulp but is
manifested in the dentin.
u Presence of secondary dentin and its continuous deposition
throughout life , along with tertiary dentin formation act as
barrier function of dentin.
›   
.
u Continuous deposition of secondary dentin and formation
a tertiary dentin leads to the reduction in size of the root
canal
u It may sometimes lead to obliteration of pulp chamber and
root canal too.
u ^hen root canal are small they are hard to locate thus
effective CT becomes difficult and the prognosis is poor.
   

.
u ›xposed dentin is sensitive and is sometimes described as
¶3
   
u Pain of dental origin is the major cause of concern for most of the
people. Dentine hypersensitivity or cervical dentine hypersensitivity
constitute one of the most important factor for dental pain.
u 3 main hypothesis put forward to account for dentin sensitivity are:
1. erves in dentin.
2. The odontoblastic process.
3. Fluid movement in dentinal tubules.

u ›1"1› à*+›Y ›1 "3"*  1 ›1/„ )›1/

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u !  J 3
      .
u ›rosion
u Abfraction
u Gingival recession.
u Attrition
  J
 JJ   3
    
.
u ›namel thickness
u Age- mineralization of pulpal and sclerotic dentine,
decrease number of tubules
u Diameter of the tubule.
u Saliva carrying Ca and phosphate ions obliterating the
tubules.
u Inflamed pulp more sensitive.
 
JJ

  
J
3
   
u Cavity varnishes
u Anti inflammatory agents
u Treatment that partially obdurate dentinal tubule
u Burnishing of dentine
u Silver nitrate
u Zinc chloride-Potassium Ferro cyanide
u 40% Formalin
u Dibasic Ca3 (PÔ4 )2.
u Fluoride compounds
u Sodium silicoflouride
u Iontophoresis
u Strontium chloride
u Potassium oxalate
u estorative resins
u Dentine bonding agents.


 

  
.
u Calcium compounds
u Sodium fluoride
u Stannous fluoride
   
J



  
u Advances in restorative dentistry are
as a result of restorative material
which adhere to enamel and dentin.
u Adhesion to dentin is more complex
than enamel due to :-
-high inorganic content
-tubular architecture.
u ^hen dentin is cut a smear layer
forms on the surface
u This layer consist of dentinal debris
and bacteria embedded in it.
u Smearing has as advantage that it
occludes the dentinal tubules and
disadvantage of harboring bacteria
which provides a difficult surface to
adhere
u emoving the smear layer id the
prerequisite before applying
bonding agents.
u For this dentin is first etched with
strong acids to remove the smear
layer
u This provides a porous surface that
can be infiltrated by bonding
agent.
u Thus binding agent penetrates the
dentinal tubules and exposed
collagen in the Intertubular dentin.
u In some cases , the smear layer is not removed but rather
dissolved or modified to include it within the bonding
process.
u easons have been cited for retaining the smear layer on the
bonding substrate which are :
u It prevent decrease in bond strength seen with some
bonding systems as deeper dentin is prepared.
u etention of smear layer lowers dentin permeability.
u Greatly lowers the effect of pulpal pressure bond strength.

u
ore recent generation of dentin adhesives involves

modification of smear layer as it greatly improves the bong
strength to dentin.
 „ 
J
  
 
.
)  
 3
  J   .
u Ôccurs through interaction between positive Ca+2 ions on
surface of dentin with negative charges on group X of the
adhesive
u Group X can be Phosphates, Amino acids, Amino alcohols,
or Dicarboxylates .

) 
 3
  J    .
u Ôccurs through interaction with Amino, Amide, Hydroxyl,
Carboxyl groups present in the collagen of dentin.

u  
 J   2     3
      
3

  
    J
      
2
3
       J   
 ›JJ  
J

  

  
.
6 3"„1  .
u 
 .
u Cereal an pulses.
u Green leafy Vegetables .
u
ilk.
u Butter.

u Y 4
  .
u Adult ² 600mcg
u Child ² 350 mcg

u  J  JJ     .
u Defective formation of dentin
u Dentin is too atypical in structure.
u Lacks normal tubular arrangement.
u Dentine contains vascular and cellular bodies

u „   .
u Depending upon deficiency 7500 ² 15000 mcg /day for one
%3"„1

.
u 
 .
u Sunlight.
u Fish and poultry.
u Ghee and butter.

u Y 4
  .
u Adult & child ² 0.01mcg

u  J  JJ     . 3   J 
2 
u Ôccurs at the age of 3 years.
u Developmental anomalies of dentin occurs
u High risk of caries.
„   .
u Dentin is reduced to a thin margin.
u Thus pulp cavity is enlarged.
u%5

  J


 
 
    

u 3 
 
2 .  
u X linked trait
u ^idespread formation of globular hypoclacified dentin seen.
u Clefts and tubular defects seen in the region of pulp horn.
u Gross reduction in the amount of dentin.
u Faulty calcifications and marked Interglobular spaces seen in dentin.
 ›JJ  
J
J


  .
u Improper use of dietary fluoride supplements and ingestion of fluoride
dentifrices by small children, particularly in fluoridated communities, may
result in dental fluorosis.
u Dental fluorosis is defined as hypoplasia or hypomaturation of tooth enamel
produced by chronic ingestion of excessive amounts of fluoride as the teeth are
developing.
u manifested as whitish opacities on the teeth.
u In severe cases, mottled enamel may occur.

u In the dentin, four abnormalities were commonly seen with excess of fluorides:
1. Striations.
2. Hypoplastic defects.
3. Hypomineralized interglobular spaces.
4. Gross deformations of the external outline of the dentin.
u The number and severity of these abnormalities increased with increasing
fluoride levels in the diets, and with increasing time on the diets.
u Both hypo- and hypermineralized striations were seen in the
microradiographs

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