REGRESSIVE ALTERATIONS! REGRESSIVE ALTERATIONS! References: shafer, Allen, Max n Stern, Internet!

1. G D
M -----------------------RNING
!
By: Dr. Ram Thiramdas

2. TRY TO GUESS THE TOPIC?

3. REGRESSIVE
ALTERATIONS
OF TEETH
(RAOT)

4. • Results inResults in wear and tearwear and tear – Mostly n few– Mostly n few
exceptions.exceptions.
• Impaired structures Impaired function.Impaired structures Impaired function.
• A variety of alterations in . . . . . . (E, D, P & C)
• There are not developmental abnormalities
or inflammatory lesions.

5. Complete loss/defect in enamel leads to dentinal hypersensitivity!
RAOT- Changes seen
in the teeth structure.

6. THERE IS NO BACTERIAL INVOLVEMENT IN RAOT!

7. • These regressive changes results fromThese regressive changes results from
-General-General ageing process.ageing process.

8. - Chronic injury- Chronic injury to the tissues.to the tissues.

9.  Enamel
 Attrition
 Abrasion
 Erosion
 Abfraction
 Dentin
 Dentinal sclerosis
 Dead tracts
 Secondary dentine
 Pulp
 Reticular atrophy of pulp
 Pulp calcifications
 Resorption of teeth
 External
 Internal
 Cementum
 Hypercementosis
 Cementicles
REGRESSIVE
ALTERATIONS OF TEETH

10.  Physiologic wearing away of a tooth as a result of tooth to
tooth contact as in mastication and occlusion.
 Term- Latin verb ATTRITUM refers to the action of
rubbing against another surface.

11. The older a person gets, the
more attrition he exhibits.
“The older a person gets, the
more RAOT SEEN”

12. •Up to some degree it is physiological, when the
amount of tooth loss is extensive and begin to affect
the esthetic appearance and function ,the process is
considered as pathologic.

13. AETIOLOGY
•AGEING OF AN INDIVIDUAL.
•HABITS SUCH AS CHEWING TOBACCO OR
GUM.
• ABNORMAL TEETH ARRANGEMENT
CAUSING TRAUMATIC OCCLUSION.

14. •PYSCOLOGICAL DISORDER PATIENTS.
•COARSENESS OF THE DIET.
•BRUXISM.

15. FACTORS:
a) Poor quality or absent enamel –
eg: Fluorosis
Enamel hypoplasia
Dentinogenesis imperfecta
a
A.
B.
c.
b
c

16. b) Premature contacts - Edge-to- edge
occlusion.
c) Intraoral abrasives, erosion, grinding
habits.

17. CLINICAL FEATURES:
 Abnormalities in occlusion and chewing pattern .
 Occlusal , incisal, proximal surface.
 Primary & permanent dentition.
 Primary dentition : Amelogenesis and Dentinogenesis
imperfecta.

18.  M > F.
 Habits.
 According to Robinson there is also shortening of
dental arch due to proximal attrition.

19. APPEARANCE:
 As a small polished facet on the cusp tip or ridges or slight
flattening of an incisal edge.

20.  Advanced Conditions: when enamel is
completely worn it appear as yellow or brown
staining of the exposed dentine. Thus there is
formation of secondary dentin to protect pulp.

21.  Correction of abnormalities in teeth
structure.
 Correction of parafunctional habits.

22. Protection of tooth by metal or metal
ceramic crowns, where structural defects
exists.
Construction of occlusal guards in bruxism
habit if persists.

23. DEF : Abrasion is a pathological wearing away of
tooth by some abnormal mechanical process.
•The term – Latin verb – ABRASIUM –means
to scrape off and implies wear or partial
removal through a mechanical process.
•Mainly on exposed root surfaces.

24. • Different foreign substances produce different patterns
of tooth abrasion .
• Though the etiology is varied , the pathogenesis under
these different conditions is essentially identical .
a. Tooth brush abrasion
b. Habitual abrasion
c. occupational abrasion
d. prosthetic abrasion
e. Ritual abrasion

25. RIGHT HAND BRUSHING LEFT HAND BRUSHING

26. • Most common type .
• Horizontal direction .
• Horizontal cervical notches on buccal surfaces of exposed
radicular cementum and dentin at the CEJ in the teeth with
some gingival recession .

27. Foregin body
abrasion

28. So, change your tooth brush
before it turns into a sun flower.

30. • Pipe smokers, Tooth picks / Dental floss

31. •Prosthetic abrasion.
•Ritual abrasion.

32. •Pipe smokers

33. OCCUPATIONAL ABRASION
Develops when objects / instruments are habitually
held between the teeth by people during work .
• Carpenters
• Shoe makers

34. TAILORING

35. CLINICAL FEATURES:
• Appear as V shaped or wedge ditch on the root side of the
CEJ in the tooth with some gingival recession.
• Lesions are more wide than deep.
• Premolar and cuspids are more commonly affected.

36. • Exposure of dentinal tubules.
• Consequent irritation to odontoblast
process.
• Secondary dentine formation.

37. • Avoidance of abnormal brushing habits.
• Restorative treatment.
• Patient education.

38. DEF:
 Irreversible loss of hard dental tissues by a chemical processes
not involving bacterial action.
GERD

39. ETIOLOGY
EXTRINSIC- ACIDIC BEVERAGES ,
CITRIC FRUITS,
MEDICATIONS,
CARBONATED DRINKS,
FRUITS, DRINKS.
-SEEN ON LABIAL AND BUCCAL REGIONS.

40. INTRINSIC:
•GASTROEOSOPHAGEAL REFLEX DISEASE
(GERD) & VOMITING.
•SEEN ON LINGUAL AND PALATAL SURFACES.

41. SALIVA AS A MODIFYING FACTOR FOR EROSION
1) Salivary PH
2) Buffering capacity
3) Flow rate of saliva
NEUTRALISES
ACIDS
IN THE
ORAL CAVITY
•MINERAL IONS IN THE SALIVA HELPS IN THE
REMINERALIZATION PROCESS.

42. CLINICAL FEATURES
Broad concavities with in the smooth surface enamel.
Cupping of occlusal surface (incisal grooving) with dentine
exposure.
Increased incisal translucency.

43.  Wear on non occluding surface.
 Raised amalgam restorations.
 Hypersensitivity- trigger to secondary dentin formation.
 Pulp exposure in deciduous teeth.

44. PERIMOLYSIS:
Erosion of dental structures due to
exposure to gastric secretions is
termed as perimolysis

45. EROSION

46. TREATMENT
•Identification of the etiology is the first step in
the management of erosion.
•Gerd- general physician.
•Salivary hypofunction- sugarless
chewing gums.

47. -Use of straw for cool drinks.
- Acidic drinks should be drunk quickly rather
than sipped.
- A patient with alcholism should be treated in
rehabiltation program.

48.  Grippo – 1991
 It is pathologic loss of enamel and dentine caused by
biomechanical loading force.
 Loss of tooth surface at the cervical areas of teeth
caused by tensile and compressive forces during tooth
flexure.
 Studies need to prove the hypothetical phenomenon.

49. Crack on a wall
Yet to be proved!

50. ETIOLOGY
•FORCES PRODUCES DURING SWALLOWING,
TONGUE THRUSTING AND CLENCHING OF THE
TEETH .
•FORCES PRODUCES DURING CHEWING.
•INDIVIDUALS WITH
OPEN BITE
DEEP BITE

52.  Deep narrow V – shaped notch.
 Affects the buccal / cervical areas of teeth.
 Often affects a single tooth with adjacent
tooth unaffected.
 Most commonly affects bicuspids and
molars.
CLINICAL FEATURES

54. •Identification and correction of
aetiological agent.
•Restoration helps to keep the tooth
surface intact and prevents furthur tooth
wear.
TREATMENT

55.  Characterized by calcification of dentinal tubules.
Cause: Results due to injury to the dentinal tubules.
 DC.
 Abrasion.
 Aging process.

56. Appearance:
Translucent zone in transmitted light
(refractive index)
Seen in
- Apical third of root
- In crown midway between DEJ & surface of
pulp.
- Dentine underlying the cavity.

57. -The exact mechanism of dentinal sclerosis or
the deposition of calcium salts in the tubules is
not understood.
- Sclerotic dentin is more calcified than
reperative dentin.

58. Sclerosed dentin (1)
Dead tracts (2)
secondary dentin (3)
TRANSLUCENT DENTIN (1)
More mineralised

59. Source of Ca salts:
Dental lymph
saliva
Result:
Decreased conductivity of odontoblastic
process.
Slows the advancing carious process.
 Dye cant penetrate through the sclerotic
dentine.

60.  Dead tracts are empty dentinal tubules filled with air. These
appear dark in ground section of dentin under transmitted
light and white under reflected light.
 The dead tracts are formed due to degeneration of
odontoblastic process in the dentinal tubules. This occurs
due to exposure of dentin following attrition, abrasion or
erosion.
 Dead tracts develop in the region of cusp or incisal edge due
to death of odontoblasts as a result of overcrowding.

61. DEAD TRACTS

62. -Formed in response to normal or abnormal stimulus after
complete formation of tooth.
a) Physiological secondary dentin :
•Formed after root completion and eruption of teeth.
•It is regular, uniform layer of dentin around the pulp
chamber which is laid down throughout the life.
• This type of secondary dentin is produced more slowly
than primary dentin.
•Physiological secondary dentin is similar to primary
dentin and is seperated by deep stained resting line.

63. Primary dentin Secondary dentin
Contour line

64. b) Reparative secondary dentin/ Tertiary dentin /
reactive dentin
•Result of irritation, abrasion, erosion or operative
procedures.
•These processes cause degeneration of a large number of
odontoblasts. But, few odontoblasts survive and form dentin.
•The degenerated cells are replaced by the undifferentiated
cells of cell rich zone of the pulp.

65. CLINICAL FEATURES:
 No significant clinical features are there
to identify the secondary dentin
formation.
 There is decrease in the sensitivity due to
secondary dentin formation.
 THIS TYPE OF DENTIN FORMS
ADDITIONAL INSULATING LAYER
IN TOOTH.

66. Change in the direction of
the dentinal tubules as they
pass from primary (b) to
secondary ( a) dentin

67. R/F:
 Seen in in pulp horn areas as well as on the proximal
wall of teeth with proximal caries.
 Seen on routine radiographic investigations.
H/P
 Secondary dentine is rapidly formed at a rapid rate and
odontoblasts may become entrapped producing a
superficial resemblance to bone – osteodentine.
 Some times, irregular dentine and mixed dentine are seen.

68. REGRESSIVE CHANGES OR
DEGENERATIVE CHANGES OF PULP
 Reticular atrophy of pulp
 Pulp calcification
DEPOSITION OF CALCIFIED MASSES WITHIN THE
PULP FOR NO APPARENT REASON S IS CALLED PULP
CALCIFICATIONS.

69.  Characterized by presence of large vacuolated spaces in the pulp,
with a reduction in the number of cellular elements.
 Associated with degeneration and disappearance of the
odontoblasts.
 It is seen in elderly people, as the age changes. There is no clinical
significance
 It can be produced by improper fixation of the tooth and pulp after
extraction followed by histological sectioning.
 Most investigators feel it as artifact but not degenerative
change.

70. CLASSIFICATION
-DENTICLES
-PULP STONES
-DIFFUSE CALCIFICATION.
DENTICLES
•Denticles are small masses of tubular dentin formed
within the pulp near the furcation area of the tooth.
•They are believed to form as a result of epithelio-
mesenchymal interaction within the developing pulp.

71. PULP STONES
TRUE PULP STONES:
•Localized mass of calcified tissue that resemble dentine
because of their tubular structure.
•Resemble secondary dentine, because of few dentinal tubules
and irregular arrangement.
•Site : More common in pulp chambers than root canals.

72. True denticles -- Depending on attachment 2 types
 Attached denticles– attach to the dentinal wall.
 Free denticles- Not attached to the dentinal wall.
False denticles:
 Don’t exhibit dentinal tubules
 They are larger than true denticles
 Nodules appear to be made up of concentric layers or
lamellae deposited around the nidus
 Free
 Attached type
o Interstitial denticle

73. Free PULP STONE
Attached PULPSTONES
Embedded PULP STONES
PULP STONES

74. DIFFUSE DENTICLES / CALCIFIC
DEGENERATION:
 Seen in Root canals.
 Pattern of calcification is in amorphous, unrecognized
linear strands or columnar paralleling the blood vessel
and nerves of the pulp.

75. CONDITIOS WHERE PULP STONES ARE SEEN ARE
-DENTIGEROUS IMPERFECTA
-DENTIN DYSPLASIA
-REGIONAL ODONTODYSPLASIA

76.  ETIOLOGY
Local metabolic dysfunction
Trauma
Hyalinization of injured cells
Vascular damage
Fibrosis
Mineralization (Nidus formation)
Growth with time
Pulp stone

77. Types: External resorption
Internal resorption
INTERNAL RESORPTION:
(Chronic perforating hyperplasia of pulp, Internal granuloma,
Odontoclastoma, Pink tooth of mummery.)
Characteristic feature:
 Unusual form of tooth resorption that begins centrally with in the
tooth associated with peculiar inflammatory hyperplasia of pulp.
 Cause pulpal inflammation / unknown.
Two main patterns
 Inflammatory resorption
 Replacement or metaplastic resorption.

78. INFLAMMATORY RESORPTION:
 Resorbed dentin is replaced by inflamed granulation
tissue.
 Site – cervical zone
 Resorption continues as long as vital pulp remains
 Coronal pulp – necrotic and apical pulp – vital
 Appear as uniform , well circumscribed symmetric
radiolucent enlargement in the pulp chamber or
canal

79.  Involvement of coronal pulp - pink tooth of mummery
as the vascular resorptive process approaches the
surface.
 When the root surface is perforated, it is impossible to
determine whether the lesion began externally or
internally.

82. REPLACEMENT INTERNAL RESORPTION:
Here portion of pulpal dentinal wall are resorbed and replaced with bone or
cementum like bone
R/F :
 Enlargement of the canal that is filled with bone or cementum like bone
will be less radiolucent than the surrounding dentin.
 So the central zone appears partially obliterated. The out line of
destruction is less defined than that seen in inflammatory resorption.

83. H/F:
 Variable degree of resorption of the inner or pulpal surface of the
dentine and proliferation of pulp tissue filling the defect.
 Lacunae shows - odontoclasts or osteoclasts so called as
odontoclastoma.
 Ch. Inflammatory cells are present.
 Lacunae like areas in the dentin or osteodentin
 Enamel is also resorbed when the internal resorption occurs in
the crown portion.

84.  Resorption begins on the external surface of teeth
ETIOLOGY:
 Periapical inflammation
 Reimplantation of teeth
 Tumors and cysts
 Excessive mechanical or occlusal forces
 Impaction of teeth
 Dental trauma
 Hormonal imbalance
 Intra coronal bleaching of pulp less teeth
 Local involvement of herpes zoster
 Paget's disease of bone
 PDL treatment

85. CHARACTERISTIC FEATURE :
Non neoplastic condition in which excessive cementum is deposited
in continuation with normal radicular cementum.
ETIOLOGY:
 Local factors
 Systemic factors
 Idiopathic factors
Conditions which favor the deposition of excessive
amount of cementum
 Accerlated elongation of tooth
 Inflammation around the tooth
 Tooth repair
 Ostitis deformans or pagets disease of bone

86. Accerlated elongation of tooth:
 Loss of antagonist hyperplasia of cementum ( to
maintain the normal width of periodontal ligament)
 Site : apex of the tooth
Inflammation at the apex of a tooth root:
 Cause – pulpal infection
 Cementum is laid down on the root surface at some distance
above the apex as the cementoblasts are induced by
inflammatory reaction
 Deposition of cementum doesn’t occur immediately adjacent
to the area of inflammation since the cementoblasts and their
precursors in this area have been lost as a result of the
inflammatory process

87. Tooth repair:
 Occlusal trauma - mild root resorption which is repaired by secondary
cementum
 Root fracture repaired by deposition of cementum between the tooth
fragments and the periphery
 Cemental tear, detachment of strip of cementum from the root due to
trauma are repaired by cementum growing in to and filling the defect
Ostitis deformans/ pagets disease:
 Generalized skeletal disease characterized by deposition of excess
amount of secondary cementum on the roots of the teeth and by apparent
disappearance of laminadura.
 Generalized hyper cementosis is suggestive of osteitis deformans

88. Spike formation:
 Characterized by the occurrence of small spikes or out growths of
cementum on the root surface.
Cause :
 Excessive occlusal trauma
 May occur due to deposition of irregular cementum in focal groups of
periodontal ligament fibers
 Exact mechanism not known
C/F:
 No significant clinical signs and symptoms
 When these teeth are extracted roots appear larger in diameter than
normal and present round apices

89. R/F:
 Thickening and apparent blunting of roots by loss in their typical
sharpened or spiked appearance.
 It is impossible to distinguish it from dentine so diagnosis is made
on shape or out line of root.

90. o Cementicles are small foci of calcified tissue which
are not true cementum but lie free in the periodontal
ligament of the lateral & apical root areas.
o These represent the areas of dystrophic
calcifications.
o Cementicles are round globules of calcium salts
which arise from focal calcifiction of connective
tissue between sharpeys bundles with no apparent
central nidus.

92. •There is small spicules of cementum torn from the root
surface known as cemental tears, if lying free in the
periodontal ligament may resemble cementicles
•Cementicals appear through calcification of thrombosed
capillaries in the pdl.
•Clusters of cemeticles at the apices of teeth may be called
CEMENTOMA
•No clinical significance.

93. Few questions to analyse,
Ready?

100. ThaNk Q
folks…