Vous êtes sur la page 1sur 118


First year MDS
 History
 Introduction
 Stages of tooth development
 Physical properties
 Composition
 Dentinal tubules
 Peritubular dentin
 Intertubular dentin
 Predentin
 Dentino-enamel junction
 Odontoblasts
 Primary denin

 Secondary dentin
 Tertiary dentin
 Incremental lines
 Interglobular dentin
 Granular layer
 Innervation of dentin
 Age and functional changes in dentin
 Dentinal fluid
 Clinical considerations
 Developmental disturbances
 New study,facts and evolution

 1771 – John Hunter →hard tissue.

 1775 – Anton Von Leeuwenhoek: Described tubular structures.

 1837 -Purkinje and Retzius explained about Dentinal Tubules.

 Cuvien gave the name “Ivory” to Dentin

 1867 – Neuman gave the term Neuman’s sheath

 1891 – Von Ebner gave the term – Ebner’s growth lines or Imbrication lines .

 1906 – Von Korff gave the term – Korff’s fibres


 Second layer of the tooth Structure that provides the bulk and
form of the tooth

 Since it begins to form slightly before

the enamel, it determines the shape of
the crown, including the cusps and
ridges and also the number and size
of the roots.
 Dentin  Physically and chemically, it closely resembles

 Said to be a living tissue since the tubules present in it

contains processes of specialised cells, the

 Main morphologic difference between bone and dentin

is that some of the osteoblasts exists on the surface of
the bone and when one of the cells becomes enclosed
within its matrix, it is called an osteocyte

 Teeth develop in distinct stages that are easily

recognizable at the microscopic level.

 Hence, stages of tooth development (odontogenesis)

are described by the histologic appearance of the tooth

 The stages are described as the lamina bud, cap, early

bell and late bell stages of tooth development

 First morphologic sign of tooth development

 Visible at approximately 6th week of human gestation.


 At this stage, the cells in the dental epithelium and the

underlying ectomesenchyme are dividing at different
rates, the latter more rapidly
 The dental lamina continues to grow and thicken to form bud Cells of
the ectomesenchyme and proliferate and condense to form the dental

 At this stage, the inductive or tooth forming potential is transferred from

the dental epithelium to the dental papilla


 The tooth bud assumes the shape of a cap that is surrounded by the
dental papilla.

 Ectodermal compartment of the tooth organ is referred to as the dental

or enamel organ.

 Dental organ assumes the shape of a bell as cells continue to divide but at
differential rates.

 A single layer of cuboidal cells called the external or outer dental epithelium,
lines the periphery of the dental organ

 Cells that border the dental papilla and are columnar in appearance form the
internal or inner dental epithelium.

 The inner epithelium gives rise to the ameloblasts, cells responsible for
enamel formation and outer enamel epithelium leads to the formation of
mineralised dentin.

 These cells secrete high levels of alkaline phosphatase.

 In the region of the apical end of the tooth organ, the internal and external
dental epithelial layers meet at a junction called the cervical loop.

 These extends apically to form the Hertwigs Epitheial root sheath which
forms the root dentin

 The dental lamina that connects the tooth organ to the oral epithelium
gradually disintegrates at the late bell stage.

 Cells of the internal dental epithelium continue to divide at different rates to

determine the precise shape of the crown
 In summary, development of the tooth rudiment from the
lamina to the late bell stages culminates in the formation
of the tooth crown.

 As root formation proceeds, epithelial cells from the

cervical loop proliferate apically and influence the
differentiation of odontoblasts from the dental papilla as
well as cementoblasts from the follicle mesenchyme.

 This leads to the deposition of root dentin and



 Young age - light yellow

 With advancing age - becomes darker


 Elastic and resilient

 Harder than bone but softer than enamel

Tensile strength : 40mpa

Compressive strength : 266mpa


 Dentin has 35% organic, 65% inorganic and water by

weight .

 The organic matrix of dentin is collagenous

 It provides resiliency to the crown which is necessary to

withstand the forces of mastication

 The principle inorganic component of dentin is

hydroxyapatite crystals The high mineral content of
dentin makes it harder than bone and cementum but
softer than enamel .The knoop hardness for dentin is
approximately 68
Organic substances:

 Type I collagenous fibrils  Type V collagenous fibrils (minor)

Non collagenous proteins:

 •Dentin phosphoprotien (DPP)

 •Dentin matrix protein 1 (DMP1)
 •Dentin sialoprotein (DSP)
 •Bone sialoprotein (BSP)
 •Osteopontin, Osteocalcin

 Proteoglycans  Phospholipids

Growth factors:

 •Bone morphogenetic proteins (BMP)

 •Insulin like growth factors (IGFs)
•Transforming growth factors β (TGF- β)

Inorganic substances: •Calcium hydroxy appatite crystals

Type I collagen is the principal type of collagen found in dentine
 The course of the dentinal tubules follow a gentle curve in the crown
where it resembles an S shape

 Starts at right angles at the pulpal surface, the first convexity of this
doubly curved course is directed towards the apex of the tooth 
These tubules end perpendicular to the DEJ & CDJ

 It is almost straight near the root tip and along the incisal edges and

 Dentin thickness ranges from 3-10mm or more

 Ratio btwn outer and inner surfaces of dentine is about 5:1

 No. of tubules per square millimeter varies from 15000 at the DEJ
to 65000 at the pulp – density and diameter increases with depth

 There are more tubules per unit area in the crown than in the root 

 The dentin that immediately surrounds the dentinal tubules is termed

peritubular dentin

 Highly mineralised than intertubular dentin

 Twice as thick in outer dentin(approx. 0.75µm) than inner dentin(approx.


 Calcified tubule wall has an inner organic lining termed the Lamina Limitans
which is high in glucosaminoglycans

 Located between the zones of peritubular dentin

 One half of its volume is organic matrix, specifically collagen fibres

 The fibrils range from 0.5-0.2µm in diameter and exhibit crossbanding at

64µm intervals  HA crystals are formed along the fibres with their long axis
oriented parallel to the collagen fibres
Well mineralised , Provide tensile strength to dentin

 Located adjacent to the pulp tissues  2-6µm, depending on the activity of


 First formed dentin and is not mineralised

 The collagen fibres undergo mineralization at the predentin – the

predentin then becomes dentin and a new layer of predentin forms

 The DEJ is a complex and critical structure uniting these

two dissimilar calcified tissues and acts to prevent the
propogation of cracks from enamel into dentin.

 The DEJ has a three level structure, 25-100 µm scallops

with their convexities directed toward the dentin and
concavities toward the enamel; 2-5 µm micro scallops
and a smaller scale structure.
 The convexities of the scallops are directed towards the dentin. The
concavities are directed towards the enamel. The surface of the
dentin at DEJ is pitted.

 Cytoplasmic extensions of the odontoblasts

 The odontoblasts reside in the peripheral pulp at the pulp-predentin

border and their processes extend into the dentinal tubules

 The processes are largest in diameter near the pulp and taper further
into dentin  The odontoblast cell bodies are approximately 7µm in
diameter & 40µm in length 37

• Dentin that is formed prior to eruption of a tooth(before root completion)

• Classified as Orthodentin, the tubular form of dentin lacking of cells

found in teeth of all dentate mammals

• Secreted at a relatively higher rate 

• Constitutes major part of the dentin in the tooth



 Mantle dentin is the first formed dentin in the crown underlying the DEJ

 Regular in structure

 less mineralised and provides cushioning effect to the tooth

 It is the outer or most peripheral part of the primary dentin and is about
150µm thick

 Circumpupal dentin forms the remaining primary dentin or the bulk of the

 The collagen fibrils are much smaller in diameter and are more closely
packed together

 Slightly more mineral content than in mantle dentin


 Formed after root completion

 Narrow band of dentin bordering the pulp

 Contains fewer tubules than primary dentin

 There is usually a bend in the tubules where primary and

secondary dentin interface

 Appears in greater amounts on the roof and floor of the

pulp where it protects the pulp from exposure in older

Localized formation of Dentin At pulp –Dentin Border in response to

noxious stimuli- Caries, Trauma Attrition , Cavity Prep. Etc.

Also known as:

 Reactive Dentin,
 Reparative Dentin,
 Irritation Dentin,
 Replacement Dentin,
 Adventitious Dentin,
 Defense Dentin

There is ↓ Dentin permeability.

Quality Depends on : •Intensity of stimulus. •Vitality of pulp.

 The incremental lines of Von Ebner or imbrications lines appear as

fine lines or striations in dentin

 Run at right angles to the dentinal tubules.

 The course of the lines indicates the growth pattern of the dentin

 These lines reflect the daily rhythmic, recurrent deposition of dentin


 Some of these incremental lines are accentuated because of
disturbances in the matrix and remineralization process.

 Such lines are known as Contour lines of Owen

 These lines represent hypocalcified bands

 In the deciduous teeth and in the first permanent molars, the
prenatal and postnatal dentin is separated by an accentuated
contour line, this is termed the Neonatal line.


 Sometimes mineralization of dentin begins in small globular areas

that fail to fuse into a homogenous mass.

 This results in zones of hypomineralisation btwn the globules.

 These zones are called interglobular dentin.

 Forms in crowns of teeth in the circumpulpal dentin just below the

mantle dentin

 There is a zone adjacent to the cementum that appears granular

known as Tome’s granular layer

 It slightly increases in amount from the CEJ to the root apex

 Caused by coalescing and looping of the terminal portions of the

dentinal tubules

 Highest concentration of calcium and phosphorous


 Nerve fibres were shown to accompany 30-70% of the odontoblastic

process and these are referred to as intratubular nerves

 These nerves and their terminals are found in close association with
the odontoblasts process within the tubule


 Direct neural stimulation

 Transduction theory
 Modulation theory
 “Gate” control / Vibration theory
 Hydrodynamic theory

 According to which nerves in the dentin get stimulated.

 Drawbacks: The nerves in dentinal tubules are not commonly seen
and even if they are present, they do not extend beyond the inner

 Topical application of local anaesthetic agents do not abolish

sensitivity  Hence this theory is not accepted


 According to which the odontoblasts process is the primary structure

excited by the stimulus and that the impulse is transmitted to the nerve
endings in the inner dentin.

 Drawbacks: Since there are no neurotransmitter vesicles in the

odontoblast process to facilitate the synapse or synaptic

 Most accepted theory

 Various stimuli such as heat, cold, airblast dessication or

mechanical or osmotic pressure affect fluid movement in the
dentinal tubules.

 This fluid movement either inward or outward, stimulates the pain

mechanism in the tubules by mechanical disturbance of the nerves
closely associated with the odontoblast and its process

 Thus these endings may act as mechanoreceptos as they are

affected by mechanical displacement of tubular fluid

Vitality of dentin

 Odontoblasts and its processes are an integral part of dentin

 And so vitality is understood to be the capacity of the tissue to react

to physiologic and pathologic stimuli, dentin must be considered a
vital tissue

 Dentinogenesis is a process that continues through out life

 Although after the teeth have erupted and have been functioning for
a short time, dentinogenesis slows and further dentin formation is at
a slower rate. This is secondary dentin Pathologic changes in dentin
such as dental caries, abrasion, attrition or the cutting of dentin in
operative procedures cause changes in dentin. They are the dead
tracts, sclerosis and the addition of reparative dentin

 By pathologic process or operative procedures, the odontoblastic

processes are exposed or cut, the odontoblasts die or survive,
depending on the extend of injury

 If they survive, dentin that is produced are called reactionary or

regenerated dentin

 Killed odontoblasts are replaced by the migration of undifferentiated

cells arising in the deeper layers of the pulp to the dentin interface

 This newly differentiated odontoblasts then begin deposition of

reparative dentin to seal off the zone of injury as a healing process
initiated by the pulp,  Resulting in resolution of the inflammatory
process and removal of dead cells
 This type dentin produced by a new generation of odontoblast-like
cells in response to appropriate stimulus after the death of original
odontoblasts is called Reparative dentin

 This reparative dentin has fewer and more twisted tubules than
normal dentin

 Histological difference between reactionary and reparative dentin is
that reactionary dentin is deficient in acid proteins so it doesn’t stain.

 Reactionary dentin appears as either osteodentin type or orthodentin


 Reparative dentin has structure-less mineralisation as in bone.


• Presence of irritating stimuli -Caries, Attrition, Erosion, Cavity

Preparation → Deposition of Apatite Crystals & Collagen in
Dentinal Tubules.

• Blocking of tubules- Defensive reaction.

• Filled with H. A - Obliteration of Lumen- Peritubular Dentin.

• Refractive indices are equalized- Transparent

• Elderly people – Mostly in Roots

• Also seen- slowly progressing Caries.

• Reduced Permeability
• Prolonged pulp vitality
• Resistant to Caries
• Free fluid occupies 1% of superficial dentin and 22% of total volume of
deep dentin

• Ultrafiltrate of blood from pulp capillaries

• Contains plasma proteins

• Serve as a sink from which injurious agents can

diffuse into the pulp producing inflammatory response

• Also serve as a vehicle for egress of bacteria from a necrotic pulp into
periradicular tissue
“Exposure of Dentinal Tubules”

 Tooth wear, fractures, caries, cavity cutting procedures etc. lead to

exposure of Dentinal tubules.

 1 mm of Exposed Dentin → Damage to 30,000 living odontoblasts.

 Exposed Tubules- Should not be insulted!!

 Sealed- Bonding agents, varnishes or Restorations.


Irritants from Restorative Materials- Pulpal Damage

• Thermal Protection- Bases below Restoration

on Dentin

• Chemical Protection- Cavity liners and varnishes


 Unusual symptom of Pulp- Dentin Complex.

 Sharp Pain- easily localized.

 Etiology- Exposure of Dentinal tubules loss of enamel- Attrition,

abrasion, erosion etc. loss of cementum- scaling and RP, Gingival

 Best Explained by the Hydrodynamic Theory.

 Management - Block The Dentinal Tubules!!! • Desensitising

toothpastes-AgNo3, SrCl2, fluorides, Bonding Agents, lasers etc.

 Smear Layer - term most often used to describe the grinding debris
left on dentin by cavity preparation

 Cutting debris when forced into dentinal tubules, it forms plugs

known as smear plugs

 Smear layer : 1-3 µm  Smear plug : 40 µm 

 Significance - Lowers the permeability of dentin surface and

occludes it

 Disadvantage: prevents the adhesion of restorative materials in the


 Due to increased Permeability of dentin by tubules,it acts as a

pathway of various kinds of micro organisms

 Rapid spread of Caries Through Dentin

 ZONE 1 – Normal dentin

 ZONE 2 – Sub transparent

 ZONE 3 – Transparent dentin

 ZONE 4 – Turbid dentin

 ZONE 5 – Infected dentin


 Infected dentin is that part of dentin which is contaminated and contains

the microorganism with their toxins, and demineraliaed dentin.
 Brownish black in colour
 Can be scooped off
 Should be removed

 Affected dentin is not occupied by microorganism it just contains the

toxins produced by microorganisms of the infected dentin, and also there is
 Light brown in colour
 Cannot be scooped off
 Not necessary to remove completely
 Have a chance of remineralisation

 • AVOID- Excessive Cutting Heat Generation Continuous Drying

 • USE : Air- Water Coolant. Sharp hand Instruments- most


 Tungsten Carbide Burs to Cut vital Dentin,Less Heat generation.

 Dentin- Treated with care during op.

instrumentation to prevent damage to
the odontoblasts

 Cavity Floor → Dentin

 Dentin is RESILIENT → Absorbs and Resists Forces of Mastication

and deformation – Grips the rest. material.


 Grooves, coves, pins etc –

completely in Dentin.

 The reparative Dentin Formation can be stimulated by cavity lining

materials (such as Calcium hydroxide)

 Materials like Mta,Biodentine - can be used as a substitute to

dentin(capable of inducing reactionary dentin by stimulating
odontoblastic activity and repairative dentin by induction of cell

 Includes Direct and Indirect pulp capping • Results in formation of

reparative dentin .

 THE DENTINAL BRIDGE repair tissue that forms across the pulpal

 Sign of successful healing.


 Secondary & Tertiary Dentin →obliteration of Pulp Chamber &

Root Canals.

 Endodontic treatment → Difficult.

 Apical Dentin Chip Plug- Dentinal Chips compacted at apex

during Obturation- provides a “biologic seal”

All isthmus must be found,prepared and filled during


 Pic A-reverse filling does not extend coronally to the

height of the bevel,arrows indicate a possible pathway
for fluid penetration
 Pic B - reverse filling extends coronally to the
height of the bevel blocking fluid penetration into
the root canal space

 Significant removal of the isthmus and proper

restoration have significantly reduced the failure of
endodontic surgeries
Ellis classification (Tooth fractures)

 Ellis Class I
Enamel fracture: This level of injury includes crown fractures that
extend through the enamel only. These teeth are usually nontender and
without visible color change but have rough edges.

 Ellis Class II
Enamel and dentin fracture without pulp exposure: Injuries in this
category are fractures that involve the enamel as well as the dentin
layer. These teeth are typically tender to the touch and to air exposure.
A yellow layer of dentin may be visible on examination.
 Ellis Class III
Crown fracture with pulp exposure: These fractures involve the enamel, dentin,
and pulp layers. These teeth are tender (similar to those in the Ellis II category)
and have a visible area of pink, red, or even blood at the center of the tooth.

 Ellis Class IV
Traumatized tooth that has become non-vital with or without loss of tooth

 Ellis Class V
Luxation: The effect on the tooth that tends to dislocate the tooth from the
Teeth loss due to trauma.

 Ellis Class VI

Fracture of root with or without loss of crown structure.

 Ellis Class VII
Displacement of a tooth without the fracture of crown or root.

 Ellis Class VIII

Fracture of the crown en masse and its replacement.

 Ellis Class IX
Fracture of deciduous teeth.

 Simple restorations

 Tetracycline Pigmentation

 Yellow- Brown/grey Discoloration.

 Fluoresce Bright Yellow under U.V light.

 Deposited along Incremental lines of Dentin and to lesser

Extent in Enamel.

 Bevels are angulations which is made by 2 surfaces of a

prepared tooth which is other than 90 degrees.

 They are created to increase the retention and to

prevent marginal leakage

 Hey are given at various angulations depending upon

the type of material used for restoration and the purpose
the material serves

 Sterilization and disinfecting chemicals applied to the dentin produce

odontoblastic injury

 Alcohol &chloroform produce thermal irritation by evaporation and

dehydrate dentinal tubules

 Hydrogen peroxide may travel through dentinal tubules of deep

cavity preparations and into the pulp producing emboli and perhaps
even arresting circulation.

 Classic acid etchant used on dentin de mineralize Peritubular

dentin which widens the tubule increasing permeability.

 The acid should be passively applied for short periods 5-15


 This technique leaves behind smear plugs in tubule apertures

 The intact collagen framework interacts with hydrophilic

priming agents which penetrate through the remnant smear
layer and into the Intertubular dentin and fills the spaces left
by the dissolved apatite crystals.

 This allows acrylic monomers to form an interpenetrating

network around dentin collagen.

 Adhesive resin of the dentin bonding agent micromechanically

interlocks within the inter tubular dentin and surrounding collagen

 Hybrid layer is formed in following manner:-

 1.etching removes smear layer and exposes collagen fibers .It also
removes hydroxy apetite with in the intertubular dentin

 2. Primers penetrate the collagen network.

 3.Adhesive resins along with the primers form resin microtags

within the intertubular dentin .Hybrid layer is also called resin-
dentin interpenetration/ interdiffusion zone

 When dentin is cut, the inorganic hydroxyapatite crystals are broken

up and the collagen is stretched, torn, and smeared over the cut

 The above picture shows how a cut dentin surface is covered with
such a "smear layer."
 This picture shows how the smear layer covers the dentin and form
so called "smear plugs."
 Before any serious bonding attempt can be made, this "smear" layer
must be removed. Such a removal is achieved with a so-called
"conditioner." In most cases, the conditioner consists of an acid.
 Dentin should be etched for 15 - 30 s. During this time, the smear
layer is removed and the outer surface of the dentin is demineralized
leaving a demineralized collagen mesh, attached to the mineralized
dentin located a few microns under the collagen surfaces.

 The above figure shows how the dentin surface looks after it has
been etched for 15 s.
 As long as this collagen mesh remains moist, it is fluffy. However,
if it is desiccated, the mesh structure densifies.

 Fortunately, it is possible to re-swell the mesh by rubbing the

surface with a water-saturated pellet.
 In order to infiltrate the moist collagen mesh with a primer, one
must use a primer that consists of a molecule that has both a
hydrophilic and a hydrophobic end

 1n the absence of a water spray,coolant,tooth reduction incurs not

only the risk of heat trauma but, also, of
 desiccation of the dentin and aspiration of odonto- blasts into the
dentinal tubu1es.These effects followed an air-cooled cavity prepara-
tion and the prolonged application of an air blast.

 Frictional heat generated dur- ing tooth reduction causes evaporation

and expansion of the tissue fluid in dentin. These phenomena suggest
a loss of tissue fluid at the surface of exposed dentin and an outward
capillary flow.~ Any strong dehydrating agent may produce the same
effect.A dry cavity preparation lasting only a few seconds
or an air blast of more than 20 seconds may induce aspiration of
cells into the tubules.

 Odontoblasts aspirated through exposure to an air blast

disappears within 24 hours by autolysis and further outward

 The dissolution of aspirated cells does not cause inflammation of

the pulp or injure the cells in the cell rich zone

 A reduction in the number of odontoblasts leads to the formation

of repairatve dentin after 1 -3 months

• A restoration placed in a cavity preparation can develop

contraction gaps between the restoration and the cavity wall.

• This gap then fills with fluid from the outflow of tubules or saliva
from external surface.

• An environment is created for

bacterial growth and failure of
restoration .

Anomaly of Mesodermal Portion of the Odontogenic Apparatus.

• TYPE I -Assoc with. O.I

• TYPE II -Not Assoc with O.I
• TYPE III -Brandy wine Type


 Tulip Shaped teeth, Bluish- grey- Yellow/Brown Translucent.

 Enamel Chips away→ Exposed dentin, rapid attrition.

 Amber appearance, Excessive wear, Multiple pulp Exposures.


 Partial/complete obliteration of pulp chamber , root canals

Shell teeth- Normal Enamel, Thin Dentin, short roots.
 In patient with DI, one must first be certain which type he/she are
dealing with.

 Severe cases of DI type 1 associated Osteogenesis imperfecta

can present significant medical management problems. Careful
review of the patient's medical history will provide clues as to the
severity of bone fragility based on the number of previous
fractures and which bones were involved.

 Patients not exhibiting enamel fracturing and rapid wear crown

placement and routine restorative techniques may be used.

 Bonding of veneers may be used to improve the esthetics.

 In more severe cases, where there is significant enamel
fracturing and rapid dental wear,

 the treatment of choice is full coverage crowns.

 However in case of D.I III with thin root are not good cases for
full coverage because of cervical fractures.

 Occlusal wear with loss of vertical dimension – Metal castings

Newer composites.

 Rare Dental Anomaly

 Normal Enamel, Atypical Dentin, Abnormal Pulp Morphology




 Normal Morphology, Amber Translucency. Extreme Mobility and

Premature Exfoliation Primary- yellow /brown- grey.


 Deciduous - pulp chambers completely obliterated, short conical


 Permanent – crescent shaped pulp chambers- Difficulty in locating

canal orifices.Permanent - “thistle tube” appearance

 Calcified / atubular dentin

 Lava flowing around boulders pattern is seen

 Amorphous forms and cascades of dentin


• No treatment

• If periapical pathology arises extraction is advised


 Usually seen in Maxillary Anteriors


 unusually large pulp chambers with thin layers of enamel and

dentin are evident.delay or failure of eruption, irregular shape.


 “Ghost Teeth.”

 Reduction in amount of dentin

 Widening of pre-dentin layer

 Presence of large interglobular dentin

 Irregular tubular pattern of dentin


No treatment required • Meticulous oral hygiene • Extraction /

Endodontic treatment • Prosthetic rehabilitation

 Dentin & enamel forming tissue invaginate the whole length of a


 Arises due to localised external pressure, focalgrowth

retardation,focal growth stimulation in certain areas of tooth bud

 Pear shaped invagination


 “tooth within a tooth.”

 Food lodges in the cavity to cause caries which
rapidly penetrates the distorted pulp chamber

 Endodontic Treatment Difficult- abnormal Anatomy


 Need for fillings could be reduced in future as study reveals natural

ability of teeth to repair themselves can be enhanced using
Alzheimer’s drug

 The activation of stem cells in the centre of teeth works to repair small
cracks and holes in dentine. Enhancing this ability could allow the
tooth’s own cells to rebuild cavities.

 Dentists have devised a treatment to regenerate rotten teeth that

could substantially reduce the need for fillings in the future.

 The therapy works by enhancing the natural ability of teeth to repair

themselves through the activation of stem cells in the soft pulp at the
 Prof Paul Sharpe, is leading the work at King’s College London,
“Almost In the trial, in mice, the team showed that when defects were
filled with a biodegradable sponge soaked in the drug, the tooth was
gradually able to rebuild itself.

 Restoring the tooth’s original dentine structure is preferable because

dental cements used in conventional fillings weaken the tooth, leave it
prone to future infections – and inevitably erode or detach

 The new treatment would not eliminate the need for the dentist’s drill,
however, since decaying sections of the tooth would still need to be

 The therapy relies on a drug called tideglusib, which has been

assessed as a potential Alzheimer’s treatment, and which is known to
be safe for clinical use.
 the drug stimulates stem cells in the centre of the tooth, triggering
them to develop into odontoblasts (specialised tooth cells) and
boosting the production of dentine, allowing larger defects to be

 In the study, published in Scientific Reports, the scientists drilled

holes into the teeth of mice, inserted a biodegradable collagen
sponge soaked in the drug and sealed the tooth with a dental

When the teeth were examined several weeks later, the sponge
had degraded and been replaced with new dentine. Collagen
sponges are commercially available and clinically-approved. The
dental preparation of the tooth would be almost identical to that
required for conventional fillings, according to the scientists.
 A remaining question is whether the method will scale up
successfully to human teeth, in which cavities can be
significantly larger. The team are currently testing the technique
in rats, whose teeth are about four times larger than those of
mice, and if this is successful plan to apply later this year to
carry out the first clinical trials in patients.

Elephant ivory is solid dentin. The structure of the dentinal tubules

contributes to both its porosity and its elasticity. Elephant tusks are
formed with a thin cap of enamel, which soon wears away, leaving the
dentin exposed. Exposed dentin in humans causes the symptom of
sensitive teeth.
Because dentin is softer than enamel, it wears away more quickly than
enamel. Some mammalian teeth exploit this phenomenon, especially
herbivores such as horses, deer or elephants. In many herbivores, the
occlusal (biting) surface of the tooth is composed of alternating areas of
dentin and enamel. Differential wearing causes sharp ridges of enamel to
be formed on the surface of the tooth (typically a molar), and to remain
during the working life of the tooth. Herbivores grind their molars together
as they chew (masticate), and the ridges help to shred tough plant
A material similar to dentin forms the hard material that makes up dermal
denticles in sharks and other cartilaginous fish

 Orbans’ Oral Histology and Embryology-G.S Kumar – Twelfth


 Pathways of the pulp- Cohen. Hargreaves- eleventh Edition.

 Shafer’s Textbook of Oral Pathology- Shafer,

 The art and science of Operative dentistry- Theodore

Sturdevant- 4th Edition.
 The effect of dentin desiccation and aspirated odontoblasts
on the pulp


 SUMMITS fundamentals of operative dentistry 4th edition