The wasting diseases of teeth, namely attrition, abrasion and dental erosion have taken their toll in the population around the world due to the changing lifestyles, increase in the stress levels and many others factors that were persistent earlier but have suddenly increased drastically. This presentation brings to light the new factors that have attributed to this condition as well as discusses the previous ones.

1. Wasting Diseases Of
Teeth
Presented by; Guided by;
Dr. Prachee Hendre Dr. Suresh Lele
2nd MDS Prof, HOD &
Guide

2. Contents
 Introduction-tooth structure
 Definition
 Tooth wear
◦ Classification of tooth wear
◦ Prevalence and distribution of tooth wear
◦ Etiology
◦ Chemistry of demineralization
◦ Method to measure tooth wear

3.  Attrition
 Abrasion
 Abfraction
 Erosion
 Approaches to prevention of tooth wear
 Restorative management of worn dentition
 Conclusion
 References

4. Introduction- Tooth structure
 The enamel and dentine have a distinct capacity to
recognize and respond to stimuli.
 Dentition is unique in terms of mineralized tissue
biology, because Ca(PO4) is exposed to the outer
environment.
 Prism is the fundamental structural unit of enamel.
 The dentine is porous biological composite
composed of apatite crystal fillers in collagen
matrix.(Pashley 1996)
 Dentine is much softer and so exhibits much faster

5. Enamel structure
 Enamel is the most calcified and hardest tissue of
the body.
 It is produced by cells of ectodermal origin-
ameloblasts
 The prisms are composed of millions of
hydroxyapetite crystals.The boundaries of human
enamel crystals are incomplete cervically.
 The configuration of enamel crystals is related to
the organization of the ameloblasts.

6.  Chemically enamel consists of 96%inorganic
material and 4%-organic material and water.
 The inorganic material is formed of the
hydroxyapetite crystals which form the enamel
prisms.
 The organic material mainly consists of the specific
enamel proteins- amelogenins(90%) and
nonamelogenins and lipids.
 The inorganic core of the prisms are mainly made
up of Mg and CO3 hence making the core more
soluble in acids than the periphery.

7. Mineralization of enamel
matrix
 It takes place in two stages primary and secondary
stages.
 In the first stage immediate partial mineralization occurs
in the matrix segments and interprismatic substance is
laid down.
 The 2nd stage or maturation stage is characterized by
gradual completion of mineralization unlike bone and
dentin.
 This stage starts from the height of the crown and
progresses cervically.

8. Dentin structure
 Unlike enamel dentin is viscoelastic and suspetible
to slight deformation.
 It consists of 35% organic and 65%inorganic
material.
 Organic substance is collagenous fibrils embedded
in ground substance
mucopolysaccarides(proteoglycans and GAGs)
 Inorganic structure consists of hydroxyapetite
crystals with a formula of 3Ca3(PO4)2.Ca(OH)2

9. Dentin mineralization
 The mineralization sequence is,
1) Hydroxyapetite crystal deposition on surface of
collagen fibrils and ground substance.
2) Crystals are arranged in orderly fashion with the long
axes parallel to the fibril long axes.
3) In the islands of mineralization the crystals deposit
radially- spherulite form- which act as centre of
mineralization, these are the first sites of
mineralization.
 General calcification process is gradual, but the
peripheral region becomes highly mineralized at
a very early stage.

10. Tooth wear

11. Definition
 Wasting is defined as any gradual loss of tooth
substance, characterized by the formation of smooth
polished surfaces without regard to the possible
mechanism of this loss.
Carranza's Clinical Periodontology 10th ed; Clinical Diagnosis;540-
60
 Tooth wear is a common problem with a prevalence of
97%, out of which 7% exhibit pathological degrees of
wear that require treatment.(Smith and Robb 1996)
 The forms of wasting are, erosion abrasion, attrition
and abfraction.

12. Classification
Wasting
diseases of
teeth
Chemical
causes
Physical causes
Attrition
Abrasio
n
Abfraction Erosion

13. Prevalence
 Sognnaes et al 1972, published first study on
prevalence. They examined 10,000 extracted teeth,
1700 teeth (18%) showed erosive lesions with
incisors most frequently affected.
 Another study showed 30 out of 151 skulls (19.9%)
with tooth wearing.
Robb et al 1991

14.  Another study in asthamatics in India showed a
prevalence of 76.5% and 66.7% nonasthmatic
adults.
Jain M et al, Rev Clín Pesq Odontol. 2009 set/dez;5(3):247-254
 Recent study on Indian population in 2013 showed
a prevalence of 8.9% for dental erosions in school
children.
Kumar S et al, Journal of Oral Science, Vol. 55, No. 4, 329-336,
2013

15. Etiology
 It is a result of a pathologic, chronic or localized
loss of dental hard tissue surface by forces, acids
and/or chelation without bacterial involvement.
Ten Cate and Imfeld 1996
 The causes are intrinsic and extrinsic

16. Etiology
ExtrinsicIntrinsic
 Recurrent vomiting
 Medical conditions
 Side-effects of drugs
 Psychogenic vomiting
syndrome
 Eating disorders
 Chronic alcoholism
 Pregnancy induced
vomiting
 Regurgitation
 Occupational factors
 Diet
 Medicaments
 Behavioral factors
 Habits

17. Chemistry of demineralization

18. Measurements of tooth wear
 Measurements in vitro
◦ Polarized light microscopy
◦ Surface profilometry
◦ Microhardness
◦ Scanning electron microscopy
◦ Microradiography
◦ Digital image analysis
◦ Iodide permeability
◦ Synthetic hydroxyapetite crystals
◦ Calcium Phosphorous dissolution

19.  Measurements in vivo
◦ Replica technique
◦ Macroscopic changes
 Measurements in situ
 Newer developments
◦ Scanning tunneling microscopes
◦ Scanning probe microscopes

20. Attrition

21.  It is defined as the physiologic wearing of the tooth
as a result of tooth-to-tooth contact, as in
mastication.
 It occurs in incisal, occlusal and proximal surfaces
of teeth.
 It is physiologic rather than a pathologic
phenomenon.
 It is associated with ageing process.

22. 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.

23. Predisposing factors;
• coarseness of diet ,chewing tobacco or bruxism,
occupation –person exposed to an atmosphere of
abrasive dust.
Clinical manifestation
• It begins as a 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 sensitivity
• TMJ problem elicited especially due to overclosure.

24.  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.

25.  The exposure of dentinal tubules and subsequent
irritation of the odontoblastic processes result in
the formation of secondary dentine.
 This aids in the protection of the pulp from further
injury.

26. Primary and secondary dentin
Primary dentin Secondary dentin
Formed before completion of teeth Formed after completion of teeth
Uniform distribution of dentinal tubules Ununiform distribution, fewer dentinal
tubules
More mineralized Less mineralized (less ca,p)

27. Abrasion

28.  It is the pathologic wearing away of the tooth
substance through some abnormal mechanical
process.
 Usually occurs in the exposed root surfaces of
teeth.
 Sometimes can be seen on incisal or proximal
surfaces.
 Robinson et al stated abrasive dentifrices as the
most common cause of abrasion.
 It manifests as a V-shaped notch or a wedge
shaped ditch on the root side of the CEJ in teeth
with gingival recession.

29. Sturdevant’s Art and Science of Operative Dentistry-A
South Asian Edition.
SIGNS & SYMPTOMS OF TOOTHBRUSH
ABRASION:
1. The lesion may be linear in outline, following the
path of brush bristles.
2. The surface of the lesion is extremely smooth and
polished, and it seldom has any plaque
accumulation or carious activity in it.
3. The surrounding walls of abrasive lesion tend to
make a v-shape .
4. Probing or stimulating (hot, cold or sweets) the
lesion can elicit pain.

30. Clinical features
 It can be seen involving cervical enamel and dentin.
 Many teeth are affected. Usually on the facial surfaces of
maxillary left canine to molar region in right handed
person and vice versa
 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.

31. • Modern dentifrices are not sufficiently abrasive to
damage intact enamel severely, can cause wear
cementum & dentin, particularly in horizontal direction
rather than vertical direction .
• Pipe smoking “depression abrasion” which is an
abraded depression on the occluding surfaces of teeth
at a latero-anterior of arch coinciding with intraoral
location of pipe stem.
• 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 abrasion.

32. Erosion

33.  It is defined as the irreversible loss of dental hard
tissue by chemical process that does not involve
the bacteria.
 Dissolution may occur on exposure to acids that
can be introduced into the oral cavity.

34. 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.

35. Abfraction

36.  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.

37.  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.

38. 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.

39. REGRESSIVE
ALTERATIONS OF TEETH
MANAGEMENT
ATTRITION Desensitizing agents such as
topical fluoride varnishes
Direct composite
restorations, Orthodontic
treatment,
Crown lengthening
procedures and Protective
splints
ABRASION AND EROSION Soft bristled tooth brush
Avoid acidic food
Composites (plastic fillings)
Glass ionomers
Fluoride varnish
ABFRACTION Occlusal adjustment
Clinical management of non-carious
lesions

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

41. Treatment options
 Dentin desensitization
 Restorations
 Endodontic therapy
 Periodontal therapy

42. 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
 Dentin bonding agents
 Use of desensitization tooth pastes

43. Restortions
Indicated in following situations
 Considerable loss enamel and dentin
 Esthetic is compromised
 Deep lesion affecting the strength of the tooth and pulpa
integrity
 Caries beginning in the cervical lesion
 Significant sensitivity of the exposed dentin.

44. ENDONTIC THERAPY
 When cervical tooth loss is extensive resulting in pulpal
involvement, endodontic therapy is necessary followed
by post placement & full coverage in the form of crown

45. PERIODONTAL THERAPY
 Required when non-carious cervical defects are
associated with gingival recession and
mucogingival problems.

46. PREVENTION
 Diet counselling
 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

47. Preventive approaches

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

49. Management of Abrasion
• Remove the cause.
• Treated with fluoride solution to improve its caries
resistance.
• Lesion exceeding 0.5mm into dentin, 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.

50. Management of Erosion
 Remove the cause.
 If restoration is the choice of treatment, metallic
restoration is indicated because it is resistant to erosion.

51. 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.

52. References
 Shafer’s Textbook of Oral Pathology, 6th ed
 Bruxism Theory & Practice, Daniel A Paesani,
Quintessence Publishing
 Tooth wear and Sensitivity, Martin Addy.
 Orban’s Oral Histology and Embryology, 12th ed