anatomy histology enamel of teeth

1. GOOD
MORNING…..

2. 2
GROWTH AND
DEVELOPMENT OF
ENAMEL,DENTIN AND PULP

4. CONTENTS
●Introduction
●Physical Characteristics Of
Enamel
●Chemical Properties Of
Enamel
●Structure Of Enamel
●Development Of Enamel
●Amelogenesis
●Stages In Ameloblastic Life
Cycle
●Structural features of

5. INTRODUCTION
●Enamel is a hard, acellular, nonvital,
insensitive tissue, which forms a protective
covering of variable thickness over the
entire surface of crown of a tooth
●Ectodermal in origin formed by the enamel organ
●Enamel forming cells - Ameloblasts
●Hardest calcified tissue in human body
●Helps teeth to withstand masticatory forces.
●Lacks reparative & regenerative properties

6. PHYSICAL PROPERTIES
●Extremely Hard
●Brittle - elastic modulus: 19×10 6
●Translucent - yellowish white to
grayish white
●Specific gravity - 2.8
●Selectively permeable

7. ● Density - 3 gm/ ml
● Thickness incisal edge :2mm
premolar :2.3-2.5mm
molar-2.5-3mm
cervical –knife edge
CHEMICAL PROPERTIES
Solubility – acid soluble
- fluoride ions decrease acid solubility

8. CHEMICAL COMPOSITION
●Inorganic component : 96% approx
▪Consists of Ca - P- CO2-
mineral phase
with inclusion of lower concentration of
Na+
, Mg+
, K+
& large number of trace
elements
●Organic components : 4 %
▪Mainly protein 58%, lipid 40%
& rest water
TYPES OF PROTEINS
▪Amelogenin – 85% ▪ Enamelin ▪Amelin

9. ● Hydroxyappatite crystal
▪Organized into basic structural unit – prism
● Fluoroappatite crystal
▪Replacement of dipolar hydroxy groups by fluoride ions
● Carbonate hydroxyappatite
▪Important for enamel maturation
▪More liable & preferentially lost along with Mg+
during
chemical erosion & carious destruction

10. STRUCTURE OF ENAMEL
●Enamel rod
●Inter rod
substance
● Rod sheath

11. ENAMEL ROD
●Basic structural unit of
enamel
●Diameter - 4 μm at DEJ ; 8 μm
at surface
●Crown of incisor - 5 million rods
●Crown of molar - 12 million rods
●Rods are arranged at
different angles (30-90 degrees
- cross section)

12. ●Arranged perpendicular to the external surface
●Cross section- fish tail ( key – hole) pattern , with
body towards occlusal / incisal surface & tail cervically

13. ●Interrod substance
Light microscopy-
cementing substance b/n
rods
Electron microscopy-
extension of adjacent rods
● Rod Sheath
Interrod space rich in
organic matrix devoid of
apatite crystals

14. DEVELOPMENT OF ENAMEL
●Epithelial Enamel Organ(derived from
stratified epithelium of stomodeum )
At bell stage it consist of four distinct layers:
▪ Outer enamel epithelium
▪ Stellate reticulum
▪ Stratum intermedium
▪ Inner enamel epithelium (ameloblastic layer )

15. DEVELOPMENT OF TOOTH – BELL
STAGE

17. AMELOGENESIS
2 Step Process
● First step:
▪organic matrix formation
● Second step:
▪ Maturation / Calcification

18. ● Differentiation of
ameloblasts begins at the
cusp tips
● Dentinogenesis precedes
differentiation
● Reciprocal induction

19. ●During dentinogenesis
odontoblasts retreat
centrally, leaving behind
formed dentin
●Ameloblasts retreat in a
peripheral direction

20. LIFE CYCLE OF AMELOBLAST
●Morphogenic Stage
●Organizing Stage
●Formative Stage
●Maturation Stage
●Protective Stage
●Desmolytic Stage

21. MORPHOGENIC STAGEMORPHOGENIC STAGE
● IEE- cuboidal or low columnar cells
● Large centrally placed nuclei
● Golgi apparatus & centriole are located in
proximal end of cell
● Mitochondria scattered throughout
the cell

22. DIFFERENTIATION STAGEDIFFERENTIATION STAGE
●Cells of the inner dental epithelium elongate and induce
underlying connective tissue cells to differentiate into
odontoblasts
●Odontoblasts lay first layer of dentin
●IEE cells become tall & nuclei shift proximally
●Golgi complex increases in volume
●Increased RER in proximal region

23. MORPHOGENETIC STAGEMORPHOGENETIC STAGE

24. ●Ameloblasts are cut off from their original source of
nourishment
●The reversal of nutritional course is carried out by
proliferation of capillaries of dental sac
●Gradual disappearance of stellate reticulum
●Decrease in distance b/n ameloblast layer &capillaries

25. SECRETORY STAGESECRETORY STAGE
●Ameloblast enters their formative stage after first layer of
dentine is formed
●First apparent change – development of blunt cell processes
● As an initial enamel layer is formed, amelobalsts migrate
away from the dentine surface – permits formation of Tomes
Process
●Initial layer of enamel does not contain enamel rods

26. MATURATIVE STAGE
●Enamel maturation occurs after most of the thickness of
enamel matrix has been formed
●Ameloblasts are slightly reduced in length & are closely
attached to enamel matrix
●During maturation ameloblasts display microvilli at their
distal extremities & cytoplasmic vacuoles – indicating the
absorptive function of these cells
●Ameloblasts with ruffled border have leaky proximal &
tight distal jns thus endocytotic activity occurs along sides

27. RUFFLE - ENDED
AMELOBLAST
SMOOTH- ENDED
AMELOBLAST
●Smooth ended ameloblasts have leaky distal jn &
tight proximal jn thus degradation products of
matrix leak through distal jn

28. PROTECTIVE STAGE
● Enamel – completely developed & calcified
● Ameloblasts cease to arrange in well defined layer &
cannot be differentiated from cells of stratum intermedium
& outer enamel epithelium
● These cell layers form stratified epithelial covering of
enamel – Reduced enamel epithelium which
Protects mature enamel by separating it from connective
tissue until the tooth erupts

29. ● The REE proliferates & induces atrophy of connective
tissue separating it from oral epithelium.
● Premature degeneration of REE may
▪ prevent tooth eruption
▪ cause resorption of enamel
● Remaining REE:
JUNCTIONAL EPITHELIUM
DESMOLYTIC STAGE

30. FORMATION OF ENAMEL MATRIX
●Islands of enamel matrix are deposited along the predentine
● A thin continuous layer of enamel is formed along dentine
– Dentino enamel membrane
● Interdigitation of cells & enamel rods
● Projections of ameloblast into enamel matrix are called
Tome’s processes which have characteristic Picket fence
appearance
● 90% of the initially secreted protein is lost during enamel
maturation & remaining envelopes around individual
crystals

31. MINERALIZATION
2 stages :
●First stage: immediate partial mineralization occurs in
matrix segments & interprismatic substances – 25 to 30%
of total mineral content
●Second stage:
▪Maturation starts from height of crown & progress
cervically
▪Begins at dentinal end of rods, before matrix has reached
its full thickness

32. ENAMEL GENES &
PROTEINS
●There are hundreds to potentially over 10,000 genes
involved in the formation of enamel which are expressed
in a highly regulated fashion at specific times and locations.
●Genes produce proteins that regulate gene expression, cell
function and can be secreted from the ameloblasts to form
the matrix or template for the developing enamel. Some of
the proteins secreted from ameloblasts regulate the size,
shape and orientation of the growing enamel crystallites
and thus contribute to the ultimate structure and compo-
sition of the enamel.

33. ENAMEL GENES & PROTEINS
● Amelogenin:
▪product of AMELX and AMELY genes located on the X
and Y chromosomes is the most abundant protein in
developing enamel
▪Its exact role in enamel formation is not fully understood,
it is thought to be crucial for regulating the size and
shape of the mineralizing enamel crystallites
▪Multiple human mutations in the AMELX gene are
associated with different AI types . There are no known
AMELY mutations and it is thought that only about 10%
of amelogenin mRNA transcripts comes from the AMELY
gene

34. ●Ameloblastin:
Product of AMBN gene located on chromosome 4 is another
enamel associated protein that appears to be the second most
abundant enamel matrix protein .it is considered to be assoc-
-iated with some AI types & promotes mineral formation
& crystal formation.
●Enamelysin:
MMP20 gene located on chromosome 11 is a proteinase that
cleaves amelogenin and is thought to be the major proteinase
involved in processing the enamel matrix proteins

35. ●Kalikryn 4: KLK4 gene located on chromosome 19 is
a proteinase that is secreted predominantly during the
maturation stage of enamel development & could be
responsible for processing any proteins not cleaved by
enamelysin

37. STRIAE OF RETZIUS
● Incremental growth lines
● Concentric circles in cross
section attributed to
▪variation in organic structure
▪disturbance in rhythm of
mineralization
▪alteration of rod’s course
● Hypomineralized area-increases
lateral spread of caries

38. NEONATAL LINE
Separates pre & post- nataly
produced enamel
●Deciduous
●1st
molar
Prenataly formed enamel is
more homogenous & rich
in organic content

39. ●“IMBRICATION LINES OF PICKERILL”
a series of grooves / troughs formed by lines
of Retzius which don’t complete the arc
●PERIKYMATA
External manifestations of striae
Approx 30 perikymata/ mm in CEJ region
& 10 perikymata / mm in occlusal region

40. CROSS STRIATIONS
● Human enamel is formed at
rate of 4чm/day
● Ground section of enamel reveals
periodic bands at 4μm intervals called
cross-striations
●Formed due to
▪Diurnal rhythmicity in rod
formation
▪Areas of disturbed calcification
▪Optical effect due to crystal

41. ENAMEL CUTICLE ( NASMYTHS
MEMBRANE )
● Delicate membrane covering the entire
crown of newly
erupted teeth.
● Removed by mastication
● Types:
Primary:
▪Formed by ameloblast
▪ Calcified

42. Secondary :
▪Product REE
▪Do not calcify
▪ Forms outer most layer

43. BANDS OF HUNTER -
SCHREGER
●Series of alternating light & dark bands
in enamel orginating from DEJ , passing
outwards & ending at some distance from
enamel surface(Inner 4/5th
of the enamel)
●Formed due to
▪ Optical phenomenon
▪ Variation in permeability & organic
content

44. GNARLED ENAMEL
● Enamel rods appear twisted around eachother
over the cusp tips
● The rods undulate back & forth within the rows
● Provide strength & resistance

45. GNARLED ENAMEL

46. ENAMEL TUFTS
● Narrow ribbon like
structure arising
from DEJ
● Seen in transverse
ground sections
● Resemble tuft of grass
● Consists of
hypocalcified
enamel rods & interrod
substance-facilitate
caries

47. ENAMEL LAMELLAE & ENAMEL
TUFTS

48. ENAMEL LAMELLAE
● Thin leaf like structure extends from
enamel surface towards dej
● Develops in plane of tensions
● Rich in organic material
● May represent defect on enamel
forming a path for bacteria & caries
initiation

49. ●Types :
▪ Type A : poorly calcified rods
▪ Type B : degenerated cells
▪ Type C : cracks are filled with organic matter from
saliva

50. ENAMEL SPINDLES

51. ENAMEL SPINDLES
● Trapped odontogenic processes between
ameloblasts
● Commonly seen in tips of cusps & incisal edges
●May serve as pain receptors thus causing enamel
sensitivity during tooth preparation

52. DENTINO - ENAMEL JUNCTION
● Scalloped with convexity
facing dentin
● Dentin at DEJ is pitted
&rounded projections of
enamel fit into these pits
● More pronounced in coronal
dentin
Thickness : 30microns
● Prevents shearing of
enamel

53. CEMENTO - ENAMEL JUNCTION
3 Possible variations may exist at CEJ
● Cervical enamel covered by cementum-60%
● Cementum meets enamel at a sharp line-30%
● Cementum & enamel separated exposing dentin-10%

54. AGE CHANGES
● Permeability decreases
● Color becomes darker - due to increase thickness of dentin
● Enamel loss on occlusal & proximal surfaces due to
attrition
● Loss of perikymata
● Localized increase in nitrogen & fluorine
● Resistance to decay increases

56. CLINICAL CONSIDERATIONS
 DEVELOPMENTAL
 PATHOLOGIC
 CAVITY PREPARATION
 ACID ETCHING
 REMINERALISATION
 ENAMEL RESTORATIONS

57. DEVELOPMENTAL ABNORMALITIES OF
ENAMEL
 Acquired disturbances
 Focal
 Systemic
 Hereditary disturbances
 Amelogenesis imperfecta
 Dens invaginatus
 Dens evaginatus
 Enamel pearl

58. AMELOGENESIS IMPERFECTA
 Represents a group of hereditary defects of enamel
unassociated with any other generalized defects.
 Entirely an ectodermal disturbance.
 Development of normal enamel occurs in three
stages-
 Formative stage
 Calcification stage
 Maturation stage

59. CLINICAL FEATURES
 HYPOPLASTIC TYPE –when matrix formation of enamel
is affected during odontogenesis, enamel not formed to
full thickness.
 HYPOCALCIFIED TYPE- mineralisation of enamel is
affected, enamel is soft and can be easily removed by
blunt instrument.
 HYPOMATURATIVE TYPE –when maturation of enamel
get disturbed,is of normal thickness, can be pierced by an
explorer, can be lost by chipping.

60. HYPOPLASTIC AMELOGENESIS IMPERFECTA

61. HYPOCALCIFIED AMELOGENESIS IMPERFECTA

62. HYPOMATURATIVE AMELOGENESIS
IMPERFECTA

63. FLUOROSIS
Fluoride is often called as double edged sword as
inadequate ingestion is related to caries &
excessive intake is related to fluorosis.
Dental fluorosis is an endemic disease in
geographic areas where the content of fluoride is
>2ppm
It is a developmental disturbance in tooth
formation caused by excessive fluoride ingestion
during amelogenesis.

64. No further fluorosis can be induced by additional
intake of fluoride once the crown of the tooth has
formed .
Most commonly affected teeth are premolars
followed by 2nd
molars.maxillary incisors,canine,1st
molar & mandibular incisor.

65. DENTAL FLUOROSIS

66. DENS INVAGINATUS
Developmental anomaly which arises as a result of
invagination in the surface of a tooth before calcification has
occurred.
●Most commom maxillary lateral incisor(unilateral/bilateraly )
●Prevalence-0.25 to 6.9%
CLASSIFICATION
●Bhaskar’s – Coronal
Radicular

67. RADIOGRAPH OF DENS INVAGINATUS
Radiographically appears as a pear shaped
invagination of enamel &dentin within chamber

68. LONGITUDINAL SECTION OF A
DENS INVAGINATUS TOOTH

69. DENS EVAGINATUS
●Dev anomaly characterized by presence of globule of
enamel or extra cusp on occlusal aspect of
premolars(Leong’s premolar)
●Most commonly - mandibular premolars
●The incidence of dens evaginatus is predominant in Asians
●Etiology is unknown

70. ●Cinical significance : Sometimes causing occlusal
interference. The cleaning of the area between the nodule and
the tooth is difficult, leading to caries & when the
evagination is worn or fractured, pulp exposure can occur,
leading to pulp necrosis
TREATMENT
● Pulp capping or partial pulpotomy vital tooth
treatment when pulp exposure is encountered following the
sterile removal of the tubercle
●When pulp exposure is not encountered, preventive resin
composite sealing of the dentin or class I amalgam
cavity preparation would be the treatment of choice.

71. Enamel pearl is localized
mass of enamel that develop
ectopically, typically over the root
surface, in close proximity to the
cemento- enamel junction
●Most commonly seen in maxillary
molar ,near the bifurcation or
trifurcation of roots near CEJ.
●It may contain a small core of
dentin & sometimes of strand of
pulp.
●Can result in periodontal problems.

72. PATHOLOGICAL
ΦCARIES
ΦEROSION
ΦABRASION

73. Dental caries is defined as an infectious microbiological disease of
tooth that results in localised dissolution and destruction of
calcified tissues.

74. STRUCTURAL PREDISPOSING
FACTORS OF CARIES OF ENAMEL
● Deep pits and fissures
● Dental lamellae
● Plaque deposits

75. EFFECT OF FLUORIDE ON
ENAMEL
Forms fluorapatite which is caries resistant
Ca10(po4)6(OH)2 +2F Ca10(po4)6F2 +2OH
●Replaces soluble salts that were lost during bacteria
●Prevents activity of glucosyl transferace
●Exerts toxic effect on S.mutans

76. ATTRITION
●The physiologic wearing away
of tooth structure as a result of
frictional contact b/w adjacent or
oppossing teeth.
●Wear can be found on occlusal,incisal
or interproximal surfaces.
●With time it may lead to a reduction
in both height & length of the arch
●Usually caused by bruxism
●Severe occlusal wear-reverse cusping
TREATMENT: Correction of
parafunctional habits & crown.

77. ABRASION
●Pathologic wearing away of the tooth structure
due to frictional force between teeth & external
object or b/n contacting teeth components in
presence of abrasive medium.
●Most commonly occurs due to a combination of
improper toothbrushing &abrasiveness of the
dentrifice.
●Tooth surfaces typically exhibit notching that is
horizontally oriented.
●More severe on the opposite side of the
dominant hand.
●May also occur on incisal or proximal surfaces,these
patterns may be related to habits or occupations eg; nail
biting ,bobby pins ,tooth picks ,tobacco pipes .

78. TOOTH BRUSHING ABRASION

79. EROSION
●Pathologic loss of tooth
structure as a result of
chemical action without
bacterial involvement
ETIOLOGY
1.Intrinsic
●chronic
Vomiting(anorexia nervosa
and bulimia nervosa)
●Regurgitation
●Rumination

80. 2.Extrinsic
●Occupational ( electroplating, fertilizer,battery)
●Diet ( acidic drinks , fizzy drinks and
fresh fruit juices)
●Medicaments (vit C, asprin, iron tonics)
Clinically - shallow spoon shaped depressions
on tooth surface

81. PERIMOLYSIS
●One of the pattern of erosion in bulimics is known as
perimolysis which demonstrates loss of enamel on the
occlusal surfaces with eventual relative elevation of any
occlusal amalgam above the surface of remaining tooth
structure

82. CAVITY PREPARATION Structural
requirements
 The enamel must rest
upon sound dentin.
 The rods which form
the cavosurface angle
must have their inner
ends resting upon
sound dentin.
 When inner ends of
the rods rest upon
sound dentin, the
elasticity of dentin
gives the enamel a
certain degree of
elasticity,but the
enamel itself without
this support isbrittle.

83. NARROW CLASS 1 CAVITIES ,WALLS INCLINED
TOWARDS THE
CENTER
CLASS 5 CAVITY WALLS ARE DIVERGING
TOWARDS OUTSIDE
Direction of the cavity walls as guided
by the direction of enamel rods

84. In class 2 amalgam cavity enamel portion of the gingival wall
is beveled as the direction of enamel rods inclines apically

85.  When the fissure is no deeper than ¼ to 1/3 the thickness of the
enamel enameloplasty is indicated rather than further extension of
the outline form of the cavity.
 Thus it refers to elimination of the developmental fault by
making it saucer shaped, using a flame shaped diamond stone
bur leaving a smooth surface which is self cleansible.
 It does not extend the outline cavity form.
 During carving amalgam should be removed from areas of
enameloplasty.
 Enameloplasty is not indicated if a centric contact is involved.

86. ACID ETCHING
 Dr. Michael Bunoncore envisioned the use of
acid to etch enamel for sealing pits & fissures in
1955,since then acid etching has revolutionized
the practice of restorative dentistry.
 The ability of the clinician to bond restorative
materials to enamel has fundamentally changed
such diverse areas as cavity preparation ,caries
prevention & esthetic treatment options.

87. ●A new safe and natural alternative for patients who do not
wish to have flouride treatment on their teeth. It is derived
from the milk protein caesin.
●GC Tooth Mousse Plus provides a superior form of
fluoride ions & CPP-ACP
G C TOOTH MOUSSE

88. ●The active ingredient is Recaldent®
CPP-ACP (Caesin
Phosphopeptide - Amorphous Calcium Phosphate) a water
based, sugar and fluoride free crème.
●Tooth Mousse works by neutralizing acidic saliva, one of the
major causes of tooth decay and erosion. It rehydrates and
rebuilds early enamel decay lesions and stops further
progression of the decay thus often eliminating the need for a
filling.
●Tooth Mousse comes in five delicious flavours. Strawberry,
mellon, vanilla, mint and tutti frutti. the flavour of the tooth
mousse will help to stimulate saliva flow.

89. Clinical Applications for Tooth Mousse
● White spot prevention /removal (during/after orthodontic
bracket treatment).
● Post bleaching.
● Post scaling and root planing.
● Dentinal hypersensitivity.
● Treatment of erosion and incipient carious lesions.
● Caries prevention.
● Promote fluoride uptake.

90. A new toothpaste that has been specifically
formulated for those at risk of acid erosion
&works in a number of ways:
●helps re-harden tooth enamel, making
it more resistant to further acid attack
● has low abrasivity to limit further enamel
wear during the process of toothbrushing
●Its pH neutral (non-acidic) to be kind to
tooth enamel
●specifically formulated for people with
sensitive teeth (this can be a sign of acid erosion).
SENSODYNE PRONAMEL

91. TOPACAL C - 5
●derived from milk proteins and hence boost
the natural ability of saliva to repair and protect
teeth by remineralizing tooth structure which
has been damaged as the result of acid attack.
●Fluoride and Topacal C-5 are synergistic rather
than competitive.
●Should not be used by anyone with a known or
suspected allergy to milk or milk products
●Topacal C-5TM is a thixotropic tooth surface
coating cream which contains Phoscal
a phosphoprotein-calcium phosphate
complex

92. SYNTHETIC TOOTH ENAMEL
● An alternative to the conventional acid etching of
the dental enamel for the retention of an adhesive system
is a revolutionary method of crystal growth on the surface of
the enamel2
. This technique is called "synthetic enamel" or
crystals adhesion
● It involves the application of a gel paste based on
calcium/phosphateions in acid medium onto the surface of
the enamel, promoting the crystal growth directly from the
tooth enamel inorganic structure . As a result, the coating
adheres firmly to the enamel by chemical retention and
promotes a physical - chemical interconnection with the
adhesive

93. WILL ENAMEL RESTORATIONS BE
POSSIBLE SOON ?????????
 Researchers at school of dentistry ,SOUTH CALIFORNIA are close to making
tooth enamel .
 They have identified tiny spheres that regulate the form & organization of
tooth enamel by controlling the crystalline growth called as NANOSPHERES
 The are called so as they are only 20 nm in diameter,these structures are
formed by a naturally occurring family of tooth specific proteins called
amelogenins.
 These spheres are also a component of synthetic amelogenin first cloned at the
school of dentistry Center for Craniofacial Molecular Biology.
 Tooth enamel begins to form in the human embryo when specialized layer of
cells called ameloblasts in embryogenic tooth bud secrete amelogenin
proteins.
 The amelogenin self assemble to form the extra cellular matrix within which
the inorganic crystals of mineral start to form.

94. This recombinant protein has since been shown to self
assemble to make nanosphere structures identical to those
seen in the mouse & other animals including humans.
Thus in the near future we can expect to replace the
current restorative materials with dental restorations
which will be very similar to natural tooth enamel.

95. DR.

96. TO START WITH……………..
(Mosby’s Dictionary 4th
ed.)

97. Dentin: the chief material of teeth, surrounding
the pulp and situated inside of the enamel and
cementum. Harder and denser than bone, it
consists of solid organic substratum infiltrated
with lime salts.
Pulp: any soft, spongy tissue such as that
contained within the spleen, the pulp chamber
of tooth……
(Mosby’s Medical and Allied Health Dictionary 4th
ed.)

98. WHY PULP-DENTIN COMPLEX?
Dentin and
Dentin and pulp-
embryologically
and functionally
the same tissue
and therefore are
considered as a
complex

99. Common embryonic
origin – Cephalic
neural crest –
Ectomesenchyme –
Dental Papilla

100. • Remain in an intimate relationship
throughout the life of the vital tooth
• Anything that affects dentin will affect pulp
and vice-versa
• Physiologic and pathologic reactions in one
of the tissues will also affect the other
• Interstitial fluid of pulp and dentinal tubules
forms a continuum

101. The pulp lives for the dentin and the dentin lives by
the grace of pulp. Few marriages in nature are
marked by a greater affinity.
Alfred L. Ogilvie

102. DENTIN
• Provide bulk.
• Hard tissue with tubules throughout thickness
• Determines the shape of crown
• Odontoblastic processes within tubules
• Resembles bone
• Odontoblast cell body remain external to dentin and
processes exist within tubules

103. PHYSICAL AND CHEMICAL
PROPERTIES
• Light yellowish
• Viscoelastic
• Harder than bone
• Harder in central part
• Less hard in primary teeth
• Low mineral content – more radiolucent than enamel

104. 35% organic matter
65% inorganic matter
Organic:
Collageneous fibrils, mucopolysaccharides
(proteoglycans, glycoproteins)
Inorganic contents: Hydroxyapatite 3Ca3
(PO4)2.Ca (OH)2
Crystals are plate shaped, much smaller than enamel

105. STRUCTURE
Butler and Ritche:
• Highly specialized cells
• Good vascular supply
• High alkaline phosphatase activity

106. FIBERS
1. Collagen – Type I, V
2. Non-collagen – 5 types

107. NON COLLAGENEOUS FIBERS
1. Principle type – DPP, DSP
2. Ca+ binding- OSTEOCALCIN, BONE
SIALOPROTEIN, SERINE PHOSPHOPROTEIN,
DENTIN MATRIX PROTEIN 1
3. Growth factors – FGF, BMPs.
1. Principle type – DPP, DSP
2. Ca+ binding- OSTEOCALCIN, BONE
SIALOPROTEIN, SERINE PHOSPHOPROTEIN,
DENTIN MATRIX PROTEIN 1
3. Growth factors – FGF, BMPs.

108. DENTINAL TUBULES
• Gentle ‘S’ curve
• More curve in crown and less in roots
• Right angle from pulpal surface, 1st
convexity is apex of
tooth
• Tubules end perpendicular to DEJ, DCJ
• Almost straight at Incisal edge or Cusp tips

111. Coronal dentin
Root dentin

112. • Number vary between 50,000 – 90,000 per sq mm
• More in crown than in roots
• Lateral branches termed as canaliculi or microtubuli
• Few dentinal tubules extend through DEJ into enamel
– Enamel Spindle

113. PERITUBULAR DENTIN / INTRA-TUBULAR
DENTIN
Dentin surrounding dentinal tubules
Forms walls of tubules
Highly mineralized (9%) than intertubular dentin
Twice as thick 0.75um in outer dentin than 0.4um
in inner dentin

114. Peritubular dentin
Dentinal tubules
Intertubular dentin

115. INTERTUBULAR DENTIN
• In between dentinal tubules, zones of
peritubular dentin
• Main body of dentin
• Highly mineralized
but have half part
as organic
• In between dentinal tubules, zones of
peritubular dentin
• Main body of dentin
• Highly mineralized
but have half part
as organic

116. PREDENTIN
Adjacent to pulp tissue
2-6um wide
1st
formed dentin, not mineralized
As collagen fibers undergo mineralization at
predentin-dentin junction, predentin
becomes dentin
Adjacent to pulp tissue
2-6um wide
1st
formed dentin, not mineralized
As collagen fibers undergo mineralization at
predentin-dentin junction, predentin
becomes dentin

117. ODONTOBLASTS – PSEUDOSTRATIFIED
LAYER
Odontoblasts
Predentin
Dentinal tubules

118. CONTENTS OF DENTINAL
TUBULES
• Odontoblastic process
• Odontoblastic Fluid
• Collagen fibers, Minerals
• Nerve endings
• Odontoblastic process
• Odontoblastic Fluid
• Collagen fibers, Minerals
• Nerve endings
JDR 1985

119. ODONTOBLASTIC PROCESS
• Cytoplasmic extensions of
odontoblasts
• Extend into tubules
• Largest diameter near pulp – 3-4um
• Tapered to 1um diameter in dentin
further
• Cell body – 7um in diameter and
40um in length

120. ODONTOBLASTIC FLUID
Composition unknown
Deposits minerals
Sterile fluid contains immunoglobulins
99.8% of s.mutans killed
Quint Int 2001

121. INTRATUBULAR FIBERS
Hahn and Overton
66% of collagen fibers in the tubules
Quint Int 2001

122. Enamel spindles –
extension of
odontoblastic
process to DEJ
Enamel spindles

123. OUTLINE OF STEPS OF DENTINOGENESIS
• Differentiation of ameloblasts from IEE
• Induction of DP to form odontoblast by
ameloblast
• Formation of odontoblast&sub odontoblast
• Formation of predentin
• Formation of odontoblastic process
• Formation of mantle&circumpulpal dentin
• Formation of radicular dentin

124. Primary physiologic
dentin
Secondary physiologic
dentin
Tertiary dentin or
reparative dentin or
reactionary dentin or
irregular secondary dentin
Mantle
dentin
Circumpulpal
dentin

125. • Primary dentin,
most prominent
dentin in the tooth,
lies between the
enamel and the
pulp chamber
• The outer layer
closest to enamel
is known as mantle
dentin
approximately 150
micrometers wide
• Primary dentin,
most prominent
dentin in the tooth,
lies between the
enamel and the
pulp chamber
• The outer layer
closest to enamel
is known as mantle
dentin
approximately 150
micrometers wide

126. DIFFERENCE BTW M.D,C.D
•MD is the
peripheral part of
primary dentin & is
20microns thick
•Collagen fibres are
large.
•Phosphoryn is
absent
•Matrix vesicles
seen which serve as
nidi
•Mineralisation is
less
•Interglobular dentin
•It forms the bulk of
tooth & major part
of primary dentin.
•Collagen fibres are
fine & closely
packed
•Phosphoryn is
unique to CD
•Matrix vesicles
absent
•More than MD
•Interglobular dentin
is seen in CD

127. SECONDARY DENTIN
• Narrow band bordering pulp
• Dentin formed after root completion
• Few tubules
• Forms slowly
• Not uniform, appears in greater amounts on roof
and floor of coronal pulp chamber
• Bend at primary-secondary tubules interface

128. Primary dentin
Secondary dentin

129. TERTIARY DENTIN

130. Tertiary dentin

131. INTERGLOBULAR
DENTIN
• Mineralization begins in
small globular areas,
fail to coalesce
• Hypomineralized zone
between globules –
interglobular dentin
• Defect of mineralization
and not of matrix
formation
• Dry sections – lost,
appears black in
• Mineralization begins in
small globular areas,
fail to coalesce
• Hypomineralized zone
between globules –
interglobular dentin
• Defect of mineralization
and not of matrix
formation
• Dry sections – lost,
appears black in
Interglobular dentin
EnamelDEJ
Dentinal tubules

132. Interglobular dentin
Enamel
DEJ
Dentinal tubules

133. GRANULAR LAYER
Adjacent to Cementum
Increase from CEJ to apex
Results from coalescing and looping of terminal
portions of dentinal tubules

134. TOMES GRANULAR LAYER
Cementum
Hyaline layer
Tomes granular layer

135. INCREMENTAL LINES
LinesofRetzius
LinesofOwen

136. NEONATAL LINES IN DENTIN

137. INTRATUBULAR NERVES
Nerve endings in pre-dentin and inner dentin
– 100 to 150um from pulp
In close association with tubule
Small vesicles - neurotransmitters

138. Dentin sensitivity

139. THERMAL STIMULI
Movement of fluid in dentinal tubules
Fluid movement across cell membrane of odontoblasts
activate mechanical /pressure /chemical /voltage gated receptors
Opening of ion channels leading to increase in sodium influx
generating membrane potential
Depolarization of nerve
Sensation of pain

140. DEAD TRACTS
Odontoblasts degenerate,
tubules filled with air
Black in transmitted and
white in reflected light
Decrease sensitivity
Odontoblasts degenerate,
tubules filled with air
Black in transmitted and
white in reflected light
Decrease sensitivity
Dead
tracts
Dead
tracts

141. SCLEROTIC / TRANSPARENT
DENTIN
Collagen fibers and
hydroxyapatite
appear in tubules
Tubule lumen
obliterated with
mineral appear like
peritubular dentin,
same refractive index
so transparent dentin
Light in transmitted and
dark in reflected light
Collagen fibers and
hydroxyapatite
appear in tubules
Tubule lumen
obliterated with
mineral appear like
peritubular dentin,
same refractive index
so transparent dentin
Light in transmitted and
dark in reflected light
Sclerotic dentin
Dental
caries

142. TERTIARY DENTIN
•Reactionary - tertiary dentin formed by
surviving primary odontoblasts following a mild
stimulus such as attrition
•Reparative - formed by a new generation of
odontoblasts , often irregular in structure
•Point to note : Odontoblasts retain ability to form dentin in vital
teeth throughout life of tooth, and, if they are destroyed,
mesenchymal precursor cells differentiate into new, odontoblast
like cells
•Reactionary - tertiary dentin formed by
surviving primary odontoblasts following a mild
stimulus such as attrition
•Reparative - formed by a new generation of
odontoblasts , often irregular in structure
•Point to note : Odontoblasts retain ability to form dentin in vital
teeth throughout life of tooth, and, if they are destroyed,
mesenchymal precursor cells differentiate into new, odontoblast
like cells

143. WHAT TO NOTE……….
1.187 mm2 of
reactionary dentin
for every 1mm of
RDT

144. BARRIER EFFECT
• Tubules are more irregular, the dentin is less
mineralized, higher content of organic material
than primary dentin
• Interface between the dentin formed by primary
odontoblasts and that formed by odontoblast-
like cells - tubules in the two dentins do not
directly communicate
• “Barrier effect” – A defensive mechanism

145. Physiological dentin
Tertiary dentin
Pulp

146. CLINICAL IMPLICATIONS
• DENTINOGENESIS IMPERFECTA
TYPE I – DI associated with osteogenesis
imperfecta
TYPE II -- DI associated without
osteogenesis imperfecta
TYPE III - DI of “brandywine type”
Translucent opalscent teeth Precocious obliteration of pulp chamber
&canal
Blue sclera

147. PULP

148. • Pulp is unique
• Soft mesenchymal origin with specialized
cells ie. Odontoblasts arranged peripherally in
direct contact with dentin matrix
• Situated in low compliance environment that
limit its ability to increase volume during
episodes of vasodilation and increased tissue
pressure
Careful regulation of blood flow is
critical

149. A CONNECTIVE
TISSUE…………..

150. Loose connective tissue
Rich source of stem cells
Houses no. of tissue elements
52 pulp horns
Total volume of pulp = 0.38 cc
Mean volume of single pulp = 0.02 cc

151. STRUCTURAL ORGANIZATION
•Cells
•Principle cells:
Fibroblasts
•Special stem cells:
Undiffentiated
mesenchymal cells
•Blood derived defense
cells:
Macrophages, Plasma
cells
•Extra-cellular
components
•Fibers
Collagen, Elastin
•Ground substance
Proteoglycans = protein
core + gycosaminoglycans
•Adhesive glycoproteins
Fibronectin

152. PULP – WHY TO WORRY????????PULP – WHY TO WORRY????????
Low compliance environment
Dentin permeability
Sensory innervations
Micro-circulation system

153. BACTERIA ENTERING THROUGH DENTINAL
TUBULES

154. NEUTROPHILLS
PASSING THROUGH
DENTINAL TUBULES

155. MICROCIRCULATIONMICROCIRCULATION
Microcirculatory system
Largest vascular components are arterioles
and venules
No true arteries or veins enter or leave pulp
Lacks collateral supply, dependent upon
few arterioles
Microcirculatory system
Largest vascular components are arterioles
and venules
No true arteries or veins enter or leave pulp
Lacks collateral supply, dependent upon
few arterioles

156. PULP ZONES
Cell-rich zone
Odontoblastic zone
Cell-free zone
Cell-rich zone

157. ODONTOBLASTIC ZONEODONTOBLASTIC ZONE
• Odontoblasts
• Terminal capillary network
• Terminal axons from plexus of Raschkow
• Class II MHC molecule- expressing dendritic cells
• Collagen fibers, proteoglycans, fibronectin
• Korff fibers

158. CELL FREE ZONE OF WEIL
Unmyelinated nerve fibers
Blood capillaries
Processes of fibroblasts

159. CELL RICH ZONE
• Pulp proper
• Fibroblasts
• Undifferentiated mesenchymal cells
• Defense cells
• Blood capillaries
• Nerves

160. FIBROBLASTSFIBROBLASTS
• Morphology varies
from spindle
shaped to irregular
• Cytoplasmic
processes branched
• Highly synthetic
• Rich in RER, golgi
apparatus

161. FUNCTIONSFUNCTIONS
Synthesizes collagen fibers - type I , III
Degrade and phagocytose collagen fibers
Also secrete proteoglycans and fibronectin
Source of zinc enzymes – MMPs (Collagenase, Gelatinase,
Stromelysin)
Degrade pulpal connective tissue

162. UNDIFFERENTIATED
MESENCHYMAL TISSUE
UNDIFFERENTIATED
MESENCHYMAL TISSUE
Cell rich zone near perivascular area
Stellate shaped with high nucleus to
cytoplasmic ratio
Special pluripotent cells

163. DEFENSE CELLSDEFENSE CELLS
T- lymhocytes
B- lymhocytes
Macrophages
Dendritic cells

164. PULP CIRCULATION
Extensive supply
Microcirculatory system

165. PULP INTERSTITIAL
PRESSURE
16-60 mm Hg
Pulpal pressure – highest among body tissues
P = V/ C
P = interstitial pressure
V = change in volume
C = compliance of dental pulp tissue
Tonder and kvinnsland
JDR1977

166. PULPAL BLOOD FLOWPULPAL BLOOD FLOW
Highest among oral tissues and similar to levels in brain
40-50 ml/min per 100g of pulpal tissue
Blood flow:
Arteries = 0.3-1mm per second
Venules = 0.15 mm per second
Capillaries = 0.08 mm per second

167. NEURAL REGULATION
3 types:
• Somatic efferent – carry pain impulses from A
and C fibers
• Sympathetic – terminate in walls of smooth
muscle cause vasodialation
• Parasympathetic – cause vasoconstriction

168. FUNCTIONS OF PULP
1. Inductive
2. Formative
3. Nutritive
4. Protective
5. Defensive or reparative

169. AGE CHANGES
Decreased blood vessels, nerves
Decreased cellularity
Increased thickness of collagen fibers
Increased secondary dentin
Pulp stones
Decreased blood vessels, nerves
Decreased cellularity
Increased thickness of collagen fibers
Increased secondary dentin
Pulp stones

170. PULP STONES
True – round, smooth surface, laminated
False – no shape, no lamination, rough surface
Nitzan et al – 52 impacted canines from patients of 11-
76 yrs
True stones – in all ages
False stones – younger than 25 yrs

171. WHAT WE NEED TO
UNDERSTAND……
How cavity cutting effect
dentin-pulp complex

172. BAD CAVITY PREPARATION……………..
1. Odontoblast aspiration 9. Pulp necrosis
2. Alteration in blood flow
3. Tertiary dentin formation
4. Dead tract formation
5. Separation of the dentin and pulp
6. Overheating or burning of dentin
7. Increase interstitial tissue pressure
8. Pulpitis

173. WHAT TO DO………..WHAT TO DO………..
Adequate cooling of a bur cutting at high
speed
Intermittent cutting advised
Be conservative
Use Bacteriostatic restorative materials

174. CONCLUSIO
N

175. REFERENCES
 Tencate . Oral histology
 Orbans. Oral histology and
embryology
 ORAL ANATOMY, HISTOLOGY AND
EMBRYOLOGY- BERKOVITZBERKOVITZ
 GOOGLE SEARCH

176. THANK
YOU…

177. THANK YOU