Regressive alterations of teeth

Regressive alterations of teeth

1. Dr Amitha
Dept of oral and maxillofacial pathology

2. CONTENTS
◦Attrition
◦Abrasion
◦Erosion
◦Abfraction
◦Fractures
◦Localized Nonhereditory Enamel
Hypoplasia
◦Localized Non Hereditary
Enamel Hypocalcification
◦Localized Non Hereditary Dentin
Hypoplasia
◦ Localized Non Hereditary Dentin
Hypocalcification
◦Discoloration
◦Malformation
◦Amelogenesis Imperfecta
◦Dentinogenesis Imperfecta

3. ATTRITION
•Attrition is mechanical wear of the incisal or occlusal
surface as a result of functional or parafunctional
movements of mandible ( tooth- to- tooth contact .
•Is a continuous, age dependentprocess, which is
usually physiologic.
•Seen in both deciduous and permanent dentition.(rare
in decidous not retained for a longer period of time).
•Seen in children those who have Dentinogenesis and
Amelogenesis imperfecta.
•Men exhibit more severe attrition than women.

4. 2 TYPES
a) Proximal surface attrition
b) Occluding surface attrition
Proximal surface attrition :
◦Widening of proximal contact areas.
◦Decreased mesio-distal width of teeth.
◦Interproximal space will be decreased in
dimension.
Occluding surface attrition :
◦Loss, flattening, faceting and /or reverse cusping
of occluding elements.
◦Loss of vertical dimension of tooth.
◦Cheek biting and gingival irritation occurs.

5. .
Predisposing factors;
◦coarseness of diet ,chewing tobacco or bruxism,
occupation –person exposed to an atmosphere of
abrasive dust.
Clinical manifestation
◦Appearance of small polished facet on a cusp tip or
ridge or a slight flattening of incisal edge.
◦Gradual reduction of cusp height & flattening of
occlusal inclined plane with aging.
◦Tooth sesitivity
◦TMJ problem elicited especially in the overclosure
situation.

6. ◦In some older patients, the enamel of the cusp tips or
incisal edges is worn off, resulting in cupped-out
areas because the exposed, softer dentin wears
faster than surrounding enamel.
◦Sometimes these areas are an annoyance because
of food retention or the presence of peripheral,
ragged, sharp enamel edges.
◦Advanced attrition – enamel may worn away results
in an extrinsic yellow or brown staining of exposed
dentin from food or tobacco.
◦May progress to complete loss of cuspal
interdigitation.

10. ABRASION
• Abrasion is an abnormal tooth surface loss resulting from
direct friction forces between the teeth and external objects or
from frictional forces between contacting teeth components in
the presence of an abrasive medium.
•It is the pathologic wearing away of tooth substance
through some abnormal mechanical process .
Mainly due to :
Tooth brushing
Abnormal habits
•

11. Causes
◦Improper brushing technique
◦Abrasive dentrifices & Hard tooth brush
◦Habits such as holding a pipe stem by the teeth,
opening of bobby pins with the teeth (resulting
notching of incisal edges of maxillary CI )
◦In carpenters, tailors, shoe makers who holds nail,
tacks and pins between the teeth
◦Improper use of tooth picks and dental floss
◦Pipe smokers, Chewing tobacco

12. Clinical features
◦Tooth brush abrasion is more common, occuring
cervically.
◦Usually occurs on exposed root surfaces of teeth and
in sometimes incisal and occlusal surfaces.
◦Abrasion caused by dentrifices appears as “v” shaped
or wedge shaped ditch on the root side of CEJ in
teeth with gingival recession.It also involving cervical
enamel and dentin.
◦Abrasion more common on left side of mouth in right
handed people.
◦Canines and premolars are most affected.
◦Exhibit sharp margins and sharp internal angles.
◦Exposed surface appears smooth and polished.
◦ Sometimes the surface may show scratches.

13. ◦Many teeth are affected.Usually on the facial
surfaces of maxillary left canine to molar region in
right handed person and vice versa
◦Modern dentrifices are not sufficiently abrasive to
damage intact enamel severely, can cause wear
cementum & dentin,particularly in horizontal
direction rather than vertical direction .
◦Pipesmoking “depression abrasion” which is an
abraded depression on the occluding surfaces of
teeth at a latero-anterior of arch coinciding with
intraoral location of pipestem.
◦Results from intrusion and abrasion of the tooth.
◦Chewing tobacco cause generalized occlusal
surface abrasion.
◦Pica-syndrome, which is due to the habit chewing
clay(mud) has a specific occlusal abrasion.
◦Iatrogenic tooth abasion.

17. PATHOGENESIS SIMILAR TO
ATTRITION.

18. EROSION
◦Erosion is the wear or loss of tooth surface by
chemicomechanical action.
◦It is the irreversible loss of dental hard
tissue that does not involves bacteria.
◦Dissolution of mineralised tooth structures
occurs upon contact with acids that are
introduced in to oral cavity from intrinsic
(eg , gastroesophageal reflux ,vomiting ) or
extrinsic sources (eg,acidic beverages ,
citrus fruits)

19. ◦Topographically, the extent of erosive lesion
can range from a fine unnoticeable line at
CEJ to substancial tooth substance loss
making an hour-glass shape out ofa tooth.

21. CAUSES

23. Saliva as a modifying factor
Netrualisation of acid

24. Clinical features:
•Erosion lesion generally present as broad, shallow,
saucer- shaped defects involving enamel and
dentin.
•No sharp line angles and the margins of the
defects are not well defined.
•Surface appears smooth and polished
•Occurs on facial or lingual surfaces.But usually on
the lingual surfaces of maxillary anteriors.
•Exogeneous agents such as lemon juice (by
lemon sucking) , cause crescent or dished defects
( rounded as opposed to angular) on the surfaces
of exposed teeth.
•Endogenous agents cause generalized erosion on
the lingual, incisal and occlusal surfaces.

25. Erosive lesion is pathognoic in following situations
:
◦No demarcation between lesion & adjacent tooth
surface..
◦Erosion usually does not affect occluding surface,
except in advanced situations.
◦Erosion rate is similar for enamel, dentin, cemetum
& sometimes for restorative materials.
◦Adacent periodontium and gingiva are sound and
healthy.
◦Tooth sensitivity to physical, chemical &
mechanical stimuli .
◦No carious lesion present.
Rate of erosion in active lesion was esteemed to
be 1micron per day.
◦Affects upper teeth especially on the facial aspect
of cuspids & premolas.

27. Preservation of enamel at gingival crevice B

28. ABFRACTION
◦Abfraction is the pathological loss of tooth
substance due to biomechanical loading forces
that result in flexure and ultimate fatigue of
enamel and dentin at a location away from
loading.
◦It has been proposed that the predominant
causative factor of some cervical, wedge- shaped
is a strong(heavy) eccentric occlusal force
resulting in microfractures or abfractures.
◦Such microfractures occurs as the cervical areas
of the tooth flexes under such loads.
◦This defect is termed idiopathic erosion or
abfraction.
◦Mainly confined to gingival third of clinical crown
was thought to the result of tooth brush abrasion.

29. ◦With each bite , occlusal forces causes teeth to
flex.
◦Constant flexing ; enamel to break from the crown
usually on the buccal surface.
◦Parafunctional habits such as bruxism and
clenching is also a cause of abfraction.
◦Forces could be static ,such as produced by
swallowing & clenching or cyclic as those
generated during chewing action.
◦Abrasive lesions were caused by flexure & ultimate
material fatigue of susceptible teeth at locations
away from the point of loading. The breakdown
was dependent on the magnitude , duration
,direction , frequency & location of the forces.
◦Having sharp margins , even be seen in a single
tooth.

30. Clinical features :
◦Appears as wedge-shaped defects on the facial
aspects.
◦With sharp margins and internal line angles.
◦In the initial stages the enamel surface is rough and
shows striations or grooves.
◦Later stages the defects progresses deeper in dentin
two or more grooves may be visible on the surface.

32. FRACTURES
a)Incomplete Fracture Not Directly Involving Vital
Pulp
◦Also called Greenstick fracture.
◦This condition is very sensitive, yet the patient can
specify only which side of the mouth rather than
the specific tooth.
a)Complete Fracture Not Involving (Not into) Vital
Pulp
◦Not associated with pain, unless the gingival
border of the fractured segment is still held by
periodontal tissue
◦Restorative treatment is indicated.

33. c)Fracture Involving (into) Vital Pulp
•Always result in pulpal infection and severe pain.
•If tooth is restorabe, immediate root canal therapy is indicated, otherwise it must be
extracted.

34. •Ellis classification :
•Class 1 : Fracture of enamel, involving little or no dentin.
•Class 2 : Fracture of enamel and dentin, but no pulp.
•Class 3 : Fracture of enamel, dentin and pulp.
•Class 4 : Tooth becomes non-vital with or without loss of crown.
•Class 5 : Traumatically avulsed tooth.
•Class 6 : Frature of root wit or withot crown fracture.
•Class 7 : Displacement of tooth without fracture of crown or root.
•Class 8 : Cervical crown fracture
•Class 9 : Fracture of deciduous teeth

38. NON HEREDITORY ENAMEL
HYPOPLASIA
•Occurs when ameloblasts are injured during
enamel formation, resulting in defective enamel
formation (diminished form or calcification or both
).
•Usually seen on anterior teeth and first molars in
the form of opaque white or light brown areas with
smooth, intact, hard surface or of pitted or
grooved enamel, which is usually hard &
discoloured.
Causes :
•Nutritional deficiencies (vit.A,C & D)
•Exanthematous diseases (Measels,chicken
pox,Scarlet fever)
•Congenital syphilis

39. ◦Hypocalcaemia
◦Fluorides
◦Birth injury,prematurity, Rh hemolytic disease
◦Local infection or trauma
◦Idiopathic
Clinical features :
◦In mild condition, few small grooves, pits,or fissures
on the enamel surface.
◦In severe condition, rows of deep pits arranged
horizontally across the surface of tooth.
◦Enamel hypoplasia due to congenital syphilis is not
of pitting variety, instead almost pathognomic
appearance.It involves maxillary & mandibular
permanent incisors and first molars.

40. ◦The anterior teeth affected are called “Hutchisons
teeth”& molar are called “Mulberry Molars” (Moon’s
molars,Fournier’s molars).
◦Enamel Hypoplasia due to local infection or truama
seen in single tooth, commonly permanent max.
incisors or max. or mand. Premolars called Turner’s
teeth and the condition is called Turner’s Hypoplasia.
◦Occurs as mild brownish discolouration of the enamel
to a sever pitting and irregularity of the crown.
◦Due fluoride ingestion during the time of tooth formation
result in mottled enamel.

42. •Depending upon the level of fluoride in the water supply,
1)Questionable changes charecterizd by white flecking or spotting of enamel.
2)Mild changes manifested by white opaque areas involving more of tooth surface
area.
3) Moderate & severe changes showing pitting and brownish staining of the surface
4) Corroded appearance of the teeth
Moderately or severly affected teeth may show wear & even fracture of the enamel

43. Non Hereditary Enamel
Hypocalcification
◦Destruction of ameloblast interfere the formation of
enamel.
◦Also interfere with mineralization of matrix.
◦Clinical features :
◦Affected area will not be defective.
◦Chalky and soft to indendation and will be stainable.
◦If extensive it changed to attrition & abrasion.
◦Enamel can be chipped if the lesion involves the entire
surface.

44. Non Hereditary Dentin
Hypoplasia◦Odntoblast are disturbed by
enironmental irritation.
◦Result in defective dentin deposition.

45. Non Hereditary Dentin
Hypocalcification
◦Have same cases as Hypoplasia.
◦Dentin is softer, more penetrable, and less resilient. Eg.
Interglobular dentin
◦Mostly the lesion is unnoticed.

47. Discolouration
Classified as
◦Extrinsic : Surface staining due calculus.
◦Intrinsic : Changes in one or more of tooth
tissues
◦1)Discolouration in enamel –Hypoplasia &
Hypocalcification
◦2) Discolouration in dentin – Due to non vitality
resulting in disintegration of dentinal tubules or
from pigmentation or staining.
◦3) Tetracycline discolouration
◦4) Discolouration in pulp

49. Malformation
◦Either in micro or macro forms.
◦Usually hereditary in origin.
◦Most common type is one or two teeth
become smaller called peg teeth.
◦Commonly upper laterals are involved

51. AMELOGENESIS IMPERFECTA
◦Enamel is defective in form or calcification as a
result of hereditary and has an appearance
ranging from essentially normal to extremely
unsightly.
◦Also called Hereditary enamel dysplasia or
Hereditary brown enamel or Hereditary brown
opalescent teeth.
◦3 types
◦Hypoplastic
◦Hypocalcified
◦Hypomaturation

52. ◦In radiographically, the overall shape of the teeth may
or may not be normal depending upon the amount of
enamel present on the tooth and the amount of
occlusal & incisal wear.
◦Enamel appear totally absent or when present appear
as thin layer, chiefly over the tips of cusp and on
interproximal surface.
◦No treatment except for the improvement of cosmetic.

54. DENTINOGENESIS IMPERFECTA
◦Is a hereditary condition in which only the dentin is
defective.
◦Normal enamel is weakly attached and lost early.
◦Affecting both decidous and permanent detition.
◦Affected teeth are gray to yellowish brown and have
broad crowns with constriction of cervical area resulting
a ‘tulip’shape
◦Radiographically, teeth appear solid, lacking pulp
champers and root canals.
◦Enamel is easily broken leading to exposure of dentin
that undergo accelerated attrition.

55. ◦2 types
◦Dentinogenesis imperfecta 1
◦Dentinogenesis imperfecta 2
Dentinogenesis imperfecta type 1
◦Also called Opalescent dentin or Capdepont teeth or
Den. Imperfecta with out Osteogenesis imperfecta. Or
Shields type II.
◦Affects only the teeth, no bone fractures.
◦Blue grey or amber brown or opalescent.
◦On X-rays teeth as bulbous crowns, roots

56. are narrow and pulp champers and root canals are
smaller than normal or completely obliterated.
◦Enamel split from dentin when subjected to occlusal
stress.
Dentinogenesis imperfecta 2
◦Also called Shields type III or Brandywine type
◦Crowns of the deciduos and permanent teeth wear
rapidly after eruption.
◦Multiple pulp exposure may occur.
◦X-rays of decidous teeth show large pulp Champers
and root canals & reduced in size as age advances.
◦Permanent teeth have pulpal spaces that are either
smaller than normal or completely obliterated.
◦Appearance of shell teeth.

58. CLINICAL
MANAGEMENT
OF NON-
CARIOUS
LESIONS

59. •Non-carious lesions require clinical attention if any of
the following factors exist :
1)Tooth sensitivity
2)Compromised esthetic
3)Risk of tooth fracture
4)Pulpal damage
5)Caries
6)Poor periodontal health

60. Treatment options
◦Dentin desensitization
◦Restorations
◦Endodontic therapy
◦Periodontal therapy

61. ◦1) Dentin desensitization
◦Used in situations where minimal amount of dentin is exposed (less than 1mm) &
patient experiences hypersesitivity.
◦This managed by any of the method suggested for dentin desensitization such as :
◦Fluoride varnishes or fluride iontophoresis
◦Dentin bonding agents
◦Use of desensitization tooth pastes

62. 2) Restortions
Indicated in following situations
◦Considerable loss enamel and dentin
◦Esthetic is compromised
◦Deep lesion affecting the strength of the tooth and pulpal
integrity
◦Caries beginning in the cervical lesion
◦Significant sensitivity of the exposed dentin
Choice of restorative material :
◦Class v non carious lesion with any of the permanent
restorative material presently available.
◦Of these, Amalgam, direct gold, cast gold inlays and
ceramic inlays are no longer preffered as they require
some amount of cavity preparation to make the
restoration retentive.

63. ◦Currently composite resins and glass ionomer
cements are used.Because they are adhesive and
do not require extensive cavity preparation.
◦Composite resin restorations :
Steps
a) Tooth preparation :
◦No cavity preparation is necessary for class v non
carious lesions.Shape of the defect is amendable
for filling .However enamel margin beveled to
increase the surface area for bonding & to
produce esthetic .
b) Pumice prophylaxis :
◦Clean the surface of any debris or plaque.

64. c)Shade selection
d) Isolation
e)Acid etching & dentin bonding
f)Composite resin placement
g)Finishing & polishing
•Compomer Restoration :
•New variety introduced in 1990s
•Combines the durability of composite & fluoride
releasing ability of GIC.
•Available as a single component light curable
material in a syringe.
•Steps is same as that of composite restoration

65. ◦Indicated for class V cavities.
◦Glass Ionomer Cements :
◦Chemically cured GIC have an excellent track
record for restoring class V noncarios defects.
◦Nowadays resin-modified GIC are referred.
◦ENDONTIC THERAPY :
◦When cervical tooth loss is extensive reslting in
pulpal involvement, endodontic therapy is
necessary followed by post placement & full
coverage in the form of crown

66. ◦PERIODONTAL THERAPY :
◦Required when non-carios cervical defects are
associated with gingival recession and
mucogingival problems.
PREVENTION
◦Diet councilling
◦Use of sodium bicarbonate mouth rinse
◦Use of fluoride mouth rinse & xylitol gum
◦Psychiatric consultation
◦Correct brushing technique
◦Correct occlusal stresses
◦Provide mouth guards
◦Correct abnormal oral habits

67. Management of Attrition
◦Pulpally involved tooth should be extracted or undergo endontic therapy.
◦Para-functional activities, notably bruxism, controlled with proper discluding-protecting
occlusal splints.
◦Occlusal equilibration – by selective grinding of tooth surfaces (include rounding and
smoothening the perepheries of occlusal tables.
◦Restorative modalities- Metallic restoration in high stress concentrating areas

68. Management of Abrasion
•Remove the cause.
•Treated with fluoride solution to improve its caries
resistance.
•Lesion is exceeding 0.5mm into dentin, it should be
restored.
•Tooth is sensitive then desensitize the exposed
dentin before starting restorative treatment.
(Desensitization by 8-30% Na or Stannous fluoride
for 4 to 8 min )
•Restoration by Direct tooth coloured materials(in
anterior) & metallic restoration in posteriors.

69. Management of Erosion
◦Remove the cause.
◦If restoration is the choice of treatment, metallic
restoration is ndicated because it is resistant to
erosion.

70. Management of Fractures
◦Restoration
◦Pulp therapy
◦Prosthesis

71. Management of Enamel Hypoplasia
•Bleach the affected teeth with an agent such
as Hydrogen peroxide
•This carried out periodically,since the teeth
continue to stain.
BLEACHING
•Lightening of discolourations of teeth through
the application of chemical agents to oxidize
the organic pigmentation of teeth
•Bleaching Agents :
•Hydrogen peroxide
•Sodium perborate
•Carbamide peroxide

72. Mechansm of Action :
◦Low mol. Wt of H2O2 allows it to easily diffuse
through enamel & dentin.
◦Here it breaks down in to water and releases
perhydroxyl ions and nascent oxygen.
◦Due to its great oxidative power it breaks up
large macromolecule stains into smaller stains.
◦These reflect less light and tooth appear
lighter.The free oxygen opens the c-ring of
pigment molecules converting them into
colourless hydroxyl compound.

73. Non Hereditary Enamel
Hypocalcification
◦Mineralization of tooth enamel should be made
using fluoride application, fluoride ionophoresis .
◦Vital bleaching,laminated veneering,composite
veneering, and porcelian fused to metal and cast
ceramic crowns

74. Non heritary dentin hypoplasia and
hypocalcification
◦Intermediary bases
Calcium Hydroxide
Zinc phosphate
Polycarboxylate

75. Management of Discolouration
◦Extrinsic – Scaling & polishing
◦Intrinsic – Bleaching,laminated veneering,
composite veneering
◦Endodontic therapy

76. Management of Malformation
◦Restoration
◦Malaligned teeth is repositioned orthodontically.
◦Porcelain fusedto metal or cast ceramic veneering restoration

77. Management of Dentinogenesis
Imperfecta
◦Cast metal crown or on posterior teeth and jacket crown on anterior teeth.
◦Filling are not usually permanent because of softness of dentin.

79. CONCLUSION
◦With increasing dental awareness and improved dental care, more and more people
are retaining their teeth for a longer period of time.
◦When loss of enamel and dentin at the CEJ becomes significant, resulting in loss of
function and esthetic, restoration of these defects becomes necessary.
◦Composite resins and GIC are used extensively for restoration of non-carious cervical
defects.