CLINICAL ASPECTS OF DENTIN

PRESENTED BY: MADHURA SHEKATKAR

MDS PART II
DEPT. OF ORAL PATHOLOGY
GUIDED BY: Dr. SUPRIYA KHEUR
 CONTENT
• Introduction
• Inherited/ Developmental Dentin defects
Dentinogenesis Imperfecta
Dentin Dysplasia
Dentin Hypocalcification
Rickets
• Acquired Dentin defects
Tetracycline staining
Dentinal Caries
Eburnation of Dentin
Effects of restorative materials
Regressive alterations
 INTRODUCTION
 Dentin is formed through specialized cellular and biochemical
pathways.

 These highly complex mechanisms are controlled by genes and

influenced by epigenetic and environmental factors.

 Abnormalities of the developmental pathways may result in reduced

quantity of tissue produced and/or poor quality of mineralization,
(WK Seow 2014).
Non-collagenous proteins - initiation and control of the mineralization -
associated -collagen molecules-growth of the hydroxyapatite crystals.

Proteins-- mineralization --dentine and bone --phosphoprotein family.

Mutations-genes coding-- type 1 collagen or extracellular matrix -

mineralization -dentine abnormalities.

 Proteins involved - common to both dentine and bone such as type 1

collagen, both skeletal and dentine defects observed.

However, if the proteins are specific to dentine, such as the dentine

sialoproteins, the defects will be limited to dentine only.
 INHERITED DENTIN DEFECTS
• Inherited defects of dentine may be grouped into:
Dentine tissues only
Bone involvement together with the dentine defect.

• Shield’s classification of inherited dentine defects, which is based on

clinical phenotypes:
Dentinogenesis Imperfecta
Dentin Dysplasia
DENTINOGENESIS IMPERFECTA
 Most common type.
 Hereditary developmental
disturbance.
Autosomal dominant condition.
 Opalescent brown discoloration.
 Overlying enamel fractures readily.
 Rapid wear and attrition of the
teeth.
 Progressive pulp obliteration.
 ETIOLOGY
• DI associated with mutation of dentin sialo phosphoprotein
gene(DSPP).

• Gene maps to chromosome number 4.

 Dentinogenesis Imperfecta Type I
( opalescent dentin, dentinogenesis imperfecta with osteogenesis imperfecta, opalescent teeth with
osteogenesis imperfecta, shield’s type I)

• Seen with a genetic fragile bone condition, osteogenesis imperfecta.

• Osteogenesis imperfecta is caused by defects in the two genes encoding type

I collagen.

• Both dentitions are affected with an opalescent brown discoloration.

• Due to reduced support of the dentine, the overlying enamel may split
readily from the dentin when subjected to occlusal stress.
• Radiographically-- bulbous crowns, narrow roots and pulp chambers are
narrow or obliterated.

• Dentinogenesis imperfecta type I can also be seen in other conditions such

as Ehlers-Danlos and Goldblatt syndromes.
 DENTINOGENESIS IMPERFECTA TYPE II:
(dentinogenesis imperfecta without osteogenesis imperfecta, opalescent teeth without osteogenesis imperfecta, shield’s type II,
capdepont teeth)

• Autosomal dominant condition.

• Caused by a mutation in the DSPP gene.

• Entity clearly distinct from osteogenesis imperfecta with opalescent

teeth, and affects only the teeth.

• The teeth are blue-gray or amber brown and opalescent.

• On dental radiographs:
 the teeth have bulbous crowns,
 roots that are narrower than normal,
 pulp chambers and root canals are smaller than normal or completely
obliterated.

• Sauk et al (1976) noted an increase in glycosaminoglycans in EDTA

soluble dentin in the teeth from patients with this disorder as
compared to controls.
 DENTINOGENESIS IMPERFECTA TYPE III:
(shield’s type III, Brandywine type)

• The crowns of the deciduous and permanent teeth wear rapidly after
eruption and multiple pulp exposures may occur.

• The dentin is amber and smooth.

• Patients with Shields type III, or the Brandywine type, do not have stigmata of
osteogenesis imperfecta.

• Radiographically it shows great variability in the deciduous teeth, ranging

from normal to changes as in type I & II.
# Extensive studies have proven that
dentinogenesis imperfecta is clearly a
disorder distinct from osteogenesis
imperfecta hence the following revised
classification is proposed.
 DI I: ( opalescent dentin, DI without osteogenesis
imperfecta, Shields type II, capdepont teeth)

• It is caused by mutation in the DSPP gene

(gene map locus 4q21.3), encoding dentin
phosphoprotein and dentin sialoprotein.

• Clinical features:
1 in 6000-8000 children.
Teeth are blue-gray or amber brown and
opalescent.
Enamel split readily when subjected to
occlusal stress.
DI II: (Shields type III, Brandywine type of dentinogenesis imperfecta)

• This disorder was found in the Brandywine triracial isolate in southern

Maryland.

• Clinical features:
 Crown of primary and permanent teeth wear rapidly after eruption and
multiple pulp exposures occur.

 Dentin is amber and smooth.

 The enamel frequently separates easily from the underlying defective dentin.
• Radiographic features:
Primary teeth: large pulp chamber and root canal.
Permanent teeth: pulp spaces smaller than normal or completely obliterated.
Appearance of shell teeth.
 HISTOLOGIC FEATURES
• It is a mesodermal disturbance.

• The dentin, is composed of irregular tubules, often with large areas of uncalcified
matrix.

• The tubules tend to be larger in diameter and thus less numerous than normal in
a given volume of dentin.

• In some areas there may be complete absence of tubules.

• The pulp chamber is usually almost obliterated by the continued deposition of

dentin.
ELECTRON MICROSCOPE
 DENTIN DYSPLASIA

• Also called as ROOTLESS TEETH.

• DD is a rare disturbance of dentin formation characterized by normal

enamel but atypical dentin formation with abnormal pulpal
morphology.

• It is hereditary disease transmitted by autosomal dominant

characteristic.
 CLASSIFICATION
• Shields classification:
1. Type I: Dentin dysplasia
2. Type II: anomalous dysplasia of dentin

• Witkop classification:
1. Type I: Radicular DD
2. Type II: coronal DD
 CLINICAL FEATURES
• Type I (radicular):

 Both dentitions are affected.

 Although the teeth appear clinically normal in morphologic appearance and color.

 Occasionally there may be a slight amber translucency.

 The teeth generally exhibit a normal eruption pattern, although delayed eruption has been
reported in a few cases.

 The teeth characteristically exhibit extreme mobility and are commonly exfoliated
prematurely or after only minor trauma as a result of their abnormally short roots.
• Type II (coronal):

 Both dentitions are affected.

The deciduous teeth have the same yellow, brown, or bluish-gray opalescent
appearance as seen in dentinogenesis imperfecta.

The clinical appearance of the permanent dentition is normal.

RADIOGRAPHIC FEATURES
• Type I (radicular):

 The roots are short, blunt, conical, or similarly malformed.

 Deciduous teeth, the pulp chambers and root canals are usually completely
obliterated.

Permanent dentition, a crescent-shaped pulpal remnant may still be seen in the pulp
chamber.

Periapical radiolucencies representing granulomas, cysts, or abscesses involving

apparently otherwise intact teeth.
• Type II (coronal):

 The pulp chambers of the deciduous teeth become obliterated as in type I

and in dentinogenesis imperfecta.

The permanent teeth, exhibit an abnormally large pulp chamber in the

coronal portion of the tooth, ‘thistle-tube’ in shape.

In such areas radiopaque foci resembling pulp stones may be found.

 Periapical radiolucencies do not occur unless for an obvious reason.

 HISTOLOGIC FEATURES

• Type I (radicular):

 Areas of calcified tubular dentin, osteodentin, and fused denticles are seen.

Normal dentinal tubule formation appears to have been blocked.

New dentin forms around obstacles and takes on the characteristic appearance described
as ‘lava flowing around boulders’.

Electron microscopic studies by Sauk and his coworkers have suggested that this pattern
of ‘cascades of dentin’ results from repetitive attempts to form root structure.
• Type II (coronal):

 The deciduous teeth exhibit amorphous and atubular dentin in the radicular
portion.

 In permanent teeth the pulp has multiple pulp stones or denticles.

 DENTIN HYPOCALCIFICATION

• Due to failure of union of globules (deposition of calcium salts in

organic matrix) leaving interglobular areas of uncalcified matrix.

• No alteration in clinical appearance.

• Easily detected in ground section and decalcified histologic

sections.

• Parathyroid deficiency or rickets can produce hypocalcification.

 Rickets
• The most well-known condition that shows developmental dentine defects
is familial hypophosphatemia.

• Also known as ‘vitamin D-resistant rickets’ which displays cardinal features

of X-linked dominant inheritance and renal phosphate wasting.

• The condition is associated with reduced reabsorption of phosphate in the

renal tubules and characteristic rachitic bone deformities.

• A fibroblast growth factor (FGF) with endocrine properties, FGF23, that

appears to mediate many of the hypophosphatemia conditions has been
found to have a major role in this disorder.
Histological examination
• The teeth involved in familial hypophosphatemia often reveals poorly
mineralized globular dentine.

• Tubular defects extending close to the dentino-enamel junction.

• These defects predispose the pulp to exposures and infection as soon

as the enamel is removed, either from minimal caries or attrition.
 TETRACYCLINE STAINING
• Antibiotic tetracycline taken either by
pregnant women, an infant or a child can
become incorporated in developing dentin.

• Clinically staining is generalized in deciduous

teeth, depending upon dose of drug,
ranging in colors, from yellow to gray brown.

• Permanent dentition can also be affected

depending upon age at which tetracycline
was prescribed.
How does tetracycline actually cause teeth
discoloration?

• (Anthony J, 2015) If the teeth are exposed to tetracycline (whether in utero or

through oral administration) at a time of tooth mineralization or calcification,
tetracycline will bind to calcium ions (calcium orthophosphate) in the teeth.

• If this happens prior to the eruption of the teeth through the gingiva, the
tetracycline bound to calcium orthophosphate will cause an initial fluorescent
yellow discoloration.
• However, upon eruption of the teeth and exposure to light, the
tetracycline will oxidize causing the discoloration to change from
fluorescent yellow to a nonfluorescent brown over a period of months
to years.

• The location of the tooth discoloration directly correlates to the stage

of tooth development at the time of tetracycline exposure.

• Permanent teeth tend to show a less intense but more diffuse

discoloration than primary teeth.
 DENTINAL CARIES

Three changes are seen as caries spreads in dentin.

1. Weak organic acids demineralize the dentin.

2. The organic content of dentin, especially collagen undergoes
degeneration and dissolution.
3. Breakdown of the structural integrity and bacterial invasion.
Infected Affected
Dentin Soft and demineralized,
teeming with bacteria.
Dentin Demineralized dentin, not
Collagen is irreversibly yet invaded by bacteria.
denatured. Collagen cross linking
Clinically zone 4 and 5 remains.
constitute the infected
dentin.

Discoloured and softer than

normal dentin that does not
Cannot re-mineralise. flake easily.
Soft necrotic tissue followed The deeper zones 2 and zone
by dry leathery dentin which 3 are the affected dentin.
flakes away with an
instrument.
 EBURNATION OF DENTIN
• A condition observed in arrested dental
caries.
• Exposed portion of reactive sclerotic
dentin.
• Characterized by a large open cavity in
which there is lack of food retention.
• It occurs almost exclusively in caries of
occlusal surface.
• The superficially softened and decalcified
dentin is burnished and takes a brown-
stained, polished appearance and is hard.
 EFFECT OF RESTORATIVE
MATERIALS
• SILVER AMALGAM:

Silver amalgam is used as a filling material in dentistry.

It is an innocuous material, particularly in shallow cavities.

Beneath deep cavities filled with amalgam Manley found a decrease in the
number of odontoblasts, as well as mild inflammatory cell infiltration of the pulp.

Dark colored metallic components of the silver alloy turn the dentin dark gray
and tooth may appear discolored.
• GLASS IONOMER:

 Glass-ionomer cement is considered as biocompatible and is widely used as filling and lining
material and as a luting agent.

 It consists of Fluor aluminosilicate glass powder and polycarboxylic acid.

 Glass-ionomer cement bonds to the dentin by chemical and mechanical means.

 Chemical bonding --exchange of ions between carboxylic groups of the substrate and calcium
ions derived from partially dissolved apatite crystallites.

 Mechanical interlocking --demineralization of exposed dentin by polycarboxylic acid treatment.

 Collagen fibers can be exposed and an intermediate layer can be formed between glass-
ionomer material and un-demineralized dentin.
ACID ETCHING:

This process demineralizes hard tissues and

exposes the organic matrix.

In contrast to the scanty organic matrix of

enamel which is lost during the demineralization
and subsequent washing, the components of
dentin are demineralized selectively.

Peritubular dentin demineralizes quicker than

does the intertubular matrix.

 Demineralization of dentin widens the tubules,

makes them funnel shaped towards the surface.
It exposes the collagen in the wall of the
tubules and also uncovers the openings of a
large number of lateral branches.

The exposed collagen forms an interwoven

mesh of fibers in which the resin infiltrates.

This collagen mesh infiltrated by resin is

referred to as the hybrid layer.

After polymerization, the resin-impregnated

collagen, together with the resin in the dentinal
tubules and their branches, constitutes the
adhesion between the dentin and the resin.
MINERAL TRIOXIDE AGGREGATE (MTA):
(Takashi et al 2009)
The available literature suggests that the action of MTA is attributable to the
natural wound healing process of exposed pulps, although MTA can stimulate
hard-tissue-forming cells to induce matrix formation and mineralization in vitro.

MTA is a moisture friendly biocompatible material composed of refined

Portland cement and bismuth oxide.

The ability of MTA to induce reparative dentinogenesis or dentin bridge

formation has been consistently demonstrated in various studies where the
deposition of fibro-dentin, followed by reparative dentin formation, which was
characterized by the presence of polarized odontoblast-like cells and a tubular
dentin-like matrix, was seen.
 REGRESSIVE ALTERATIONS

 Attrition
 Abrasion
 Erosion
 Abfraction
 Dentinal Sclerosis
 Dead tracts
 Resorption of teeth
THANK YOU