3. HYPOMINERALISATION
• A reduced quality of enamel is termed as
hypomineralisation
• Normal thickness , Partial mineralisation
• Appear opaque, creamy white / yellow brown discoloration
4. AETIOLOGY?
Can be Localised :
Trauma
Radiation
Infection to primary teeth
Can be generalised :
• Systemic: Childhood oncology, coeliac disease,
Hypocalcaemia
• Environmental : Fluorosis , Molar Incisal Hypo
mineralisation
• Genetic:Amelogenesis Imperfecta
5. HYPOPLASIA:
• A reduced quantity of enamel (with irregularly shaped teeth )
is termed as Hypoplasia
• Thin, pitted small size of teeth
6. AETIOLOGY
Can be Localised :
Trauma
Radiation
Infection to primary teeth
Can be generalised :
• Systemic:Vit D deficiency ,Renal disease
7. CHARACTERISTICS HYPOPLASIA HYPOMINERALISATION
PITTED ENAMEL Yes No
WHITEYELLOW OPACITIES No Yes
HARD ENAMEL Yes No
SOFT PORUS ENAMEL No Yes
POORQUALITY ENAMEL No Yes
REDUCEDAMOUNT OF ENAMEL Yes No
BONDINGAFFECTED No Yes
10. AMELOGENESIS IMPERFECTA
• Group of hereditary conditions that affect structure and
appearance of dental enamel.
• Autosomal dominant, recessive or X-linked
• CHARACTERISTICS:
Hypo mineralisation /Hypoplasia
Discoloration
Sensitivity
Enamel fragility
11. RESTORATIVE CHALLENGES?
• Sensitivity
• Dental Caries
• Asymmetrical Gingival contour
• Compromised periodontal health
• Discoloration/aesthetics
• Compromised resin bonding to enamel
• Accelerated tooth wear – loss of OVD and I/O space
• Un erupted and ectopic teeth
• Increased reliance on dentin bonding agent if enamel is lost
12. CLASSIFICATION:
TYPE-1 HYPOPLASTIC TYPE (61%)
Reduced enamel thickness with rough surface
Normal enamel radio-opacity to dentin
1A - Hypoplastic, Pitted autosomal dominant.
1B - Hypoplastic, Local autosomal dominant.
1C - Hypoplastic, Local autosomal recessive.
1D - Hypoplastic, Smooth autosomal dominant.
1E - Hypoplastic, Smooth X-linked dominant.
1F - Hypoplastic, Rough autosomal dominant.
1G - Enamel agenesis, Autosomal recessive.
13. TYPE-2 HYPOMATURATION TYPE (32%)
Normal thickness, softer consistency, mottled discoloured
appearance, easily be chipped away
Enamel radioopacity similar to dentin
IIA – Hypomaturation, Pigmented autosomal recessive.
IIB – Hypomaturation, X-linked recessive.
IID – Snow-capped teeth, Autosomal dominant.
18. 2. CONTROL PHASE
• Prophylaxis
• Fluoride varnish application
• Extraction of primary canine
• Restoration of anterior teeth to normalWidth/Length ratio
with Resin Composite
• Fissure sealant on intact occlusal surfaces
• Posterior teeth: Composite to correct occluso-gingival heights
19. 3. DEFINITIVE PHASE:
• Orthodontic treatment (Fixed)
(correct malocclusion, extrude permanent canines, midline
diastema, provide inter radicular space for future restorative
work)
Oral hygiene Instructions
20. MOLAR INCISAL HYPOMINERALISATION
• MIH is hypomineralisation of one or more of the first
permanent molar and often but not necessarily involving
incisor teeth
• Disruption in the amelogenesis process most probably
occurring in the early maturation stage or even earlier at the
late secretory phase
22. DIFFERENTIAL DIAGNOSIS:
• FLOUROSIS (It affects teeth in a symmetrical, bilateral pattern unlike MIH
which is asymmetrical.
Teeth affected by fluorosis are caries-resistant while in MIH they are caries-
prone.)
• ENAMEL HYPOPLASIA (The borders are mostly regular and smooth,
indicating developmental and pre-eruptive lack of enamel.
The margins in MIH with post-eruptive enamel breakdown are sharp and
irregular due to post-eruptive shearing of weakened enamel.
• AMELOGENESIS IMPERFECTA (Familial history)
• WHITE SPOT LESION (Occur in areas of plaque stagnation)
• TRAUMATIC HYPOMINERALISATION (history of dental trauma to the
primary predecessor tooth )
23. MANAGEMENT:
MOLARS:
Enhanced prevention, remineralisation and sensitivity management
Toothpaste 1450 ppm F
Dietary advice
CPP-ACP
EnamelonTreatment Gel
Fissure seal MIH molars (Resin Vs GIC )
• Problems of LA
2% lidocaine HCL and 4% articaine HCL are possibly the most frequently used LA
agents
• Resin Infiltration: ICON System
• Restoration: GIC and RMGIC
• Full/ Partial coverage crowns
• Extraction
27. DENTINOGENESIS IMPERFECTA:
• An inherited disorder of dentine formation.
• Encompasses a group of autosomal dominant traits, affecting
both primary and permanent dentitions
28. AETIOLOGY:
Mis-sense mutation of genes that encode type-1 collagen
Tissues in which type 1 collagen is the main matrix protein
are affected and include bone, sclera and dentine
• Type 1 : COL1A1, COL1A2
• Type 2, 3 : DSPP (Dentin sialophospho protein)
33. RESTORTIVE CHALLENGE:
• Difficult Endo treatment (obliteration of pulp chambers, short
roots , abnormal mineralization )
• Spontaneous abcesses in absence of coronal pathology
• Unpredictable bond to enamel ( fractures away easily )
• Caries
• Aesthetics
• Accelerated tooth wear (loss of OVD )
• Short roots- Cr lengthing may be required
34. MULTI DISCIPLINARY APPROACH:
PAEDIATRIC:
OHI and Prevention
ORTHODONTICS:
Ortho input 10-12 years
Align teeth can help ease of brushing, placement of restorations,
replacement of teeth when required and interocclusal schemes
RESTORATIVE: 16-18 Years
REPLACEMENT: 21 yrs
MAXILLOFACIAL SURGEON
40. DIAGNOSIS:
CLINICALLY RADIOGRAPHICALLY
Normal Crown Cylindrical/rectangular shaped
Lack of inter radicular Enlarged pulp cavity below CEJ
area upon probing
Elongated body of tooth
High roof of pulp cavity
Lack of CEJ Constriction
Apical displacement of furcation
Thin cervical dentin
41.
42.
43. DENTINAL DYSPLASIA
• Dentine dysplasia (DD) is a rare, autosomal dominant
condition that manifests itself clinically with discoloured and
malformed teeth
• A hereditary disturbance in the formation in dentine with
subsequent alterations in pulp development.
50. DENS INVAGINATUS
• Developmental malformation in which there is infolding of
enamel into dentin.These infolds represent stagnation sites
for bacteria and can predispose to dental caries.
• The teeth most commonly affected by DI are lateral incisors
followed by maxillary central incisors, and more rarely
premolar and canine teeth
51. AETIOLOGY:
Infection, Trauma,Growth pressure on the dental arches
during odontogenesis causing infolding of the enamel5 and
rapid proliferation of the internal enamel epithelium into the
underlying dental papilla.
52. CLASSIFICATION:
• Class I: This is a partial invagination that is confined to the crown
of the tooth. These lesions involve dentine and enamel but do not
extend past the cement-enamel junction (CEJ) or involve the
pulp.
53. • Class II: This partial invagination extends beyond the crown of the
tooth and into the root, beyond the CEJ. These lesions may or
may not involve pulp, but remain within the anatomy of the root.
There is no communication with the periodontal ligament
54. Class IIIa: This complete invagination extends through the root. It
communicates with the periodontal ligament through a second foramen
on the lateral aspect of the tooth.
Class IIIb: This complete invagination extends through the root, and
communicates with the periodontal ligament at the apical foramen.
Often there is no direct involvement of the pulpal anatomy but the lesion
causes significant disruption to the dental anatomy
55.
56. CLINICAL FEATURES:
• Asymptomatic
• Abnormally shaped tooth
(wider and associated with an exaggerated talon cusp or even
conical in shape±𝑝𝑖𝑡)
• Be mindful that lateral incisors are the most commonly
affected teeth. If these teeth exhibit any clinical features of a
dens (such as a pronounced talon cusp or incisal notching),
adjunctive radiographic examination
• Symptomatic: Patients may present with symptoms of
irreversible pulpitis or apical periodontitis.
57. RADIOGRAPHIC FEATURES:
• Radiolucent pockets underneath the cingulum and incisal
edges of affected teeth. (Pockets can be surrounded by radio-
opaque enamel)
• More extensive lesions may appear as fissures, with or without
radio-opaque borders
• Communications between the invaginations and the
periodontal ligament may be evident either on the lateral
aspects of the tooth or its apex.
If such communications are present and a patient
develops pulpal pathology, a ‘butterfly’ like periapical
radiolucency
58. MANAGEMENT:
• ‘blunderbuss’ apex
• CLASS-1:
Early detection of caries
Seal with Acid etch flowable composite
Pulp necrosis
RCT (Include whole invagination into access cavity and
use of USTips and Endo microscope)
59. CLASS-2 :
If the tooth does not exhibit any signs of pulpal pathology:
The invagination should be thoroughly debrided using
ultrasonic instruments and hypochlorite. can be restored
without accessing the root canal system
If in close proximity with the pulp:
The invagination can be dressed with MTA or Calcium hydroxide
and seal with composite
If pulpal involvement:
RCT
62. DENS EVAGINATUS:
• Dens evaginatus (DE) is a developmental anomaly describing
teeth with supplemental cusps or protuberances consisting of
enamel surrounding a core of dentine, and typically with
pulpal tissue
• DE arises as a result of abnormal evagination of the internal
epithelium and ecto mesenchymal cells of the dental papilla
into the stellate reticulum of the enamel organ.
• Mandibular second premolars are most commonly affected
63. CLASSIFICATION:
Location of the tubercles
• Tubercle on the inclined plane of the lingual cusp
• Cone-like enlargement of the buccal cusp
• Tubercle on the inclined plane of the buccal cusp
• Tubercle arising from the occlusal surface obliterating the
central groove
66. • Type 1 - Talon, a well defined additional cusp that
projects palatally and extends at least half the distance
from the cementoenamel junction (CEJ) to the incisal
edge
• Type 2 - Semitalon, an additional cusp that extends less
than half the distance from the CEJ to the incisal edge
• Type 3 - Trace talon, prominent cingula
• Type-4- Occlusal DE
• Type-5- Buccal DE
• Type-6- Palatal DE/ Lingual DE
