The document discusses various diseases that can affect the dental pulp and periapical tissues. It begins with an introduction to pulp anatomy and functions. Key topics covered include the etiology and classification of pulpal and periradicular diseases. Specific conditions discussed in detail include reversible and irreversible pulpitis, pulp necrosis, hyperplastic pulpitis, internal inflammatory and external inflammatory resorption, and calcific, atrophic and fibrous changes that can occur in the pulp as a sequelae to injury or irritation. The document provides descriptions of the clinical, histopathological and radiographic features of each condition.

1. 1

2. 2
Dr Meenal Atharkar
MDS
DEPT OF CONSERVATIVE
DENTISTRY AND
ENDODONTICS

3.  Introduction
 Etiology of periradicular diseases
 Classification of periradicular diseases
 Theories of cyst formation
 Description of various diseases of periapical
tissues
 Diseases of periradicular tissues of
nonendodontic origin
3

4.  Conclusion
 References
4

5.  Introduction
 Important features of pulp
 Pathways
 Etiology of pulpal diseases
 Classification of pulpal diseases
 Sequelae of pulpal disease
 Progression of pulpal diseases
 Description of various diseases of pulp
 Summary
5

6.  PULP is a formative organ
of tooth.
 It builds-1. dentin during
development of tooth
-2. secondary
dentin after tooth
eruption
-3. reparative
dentin in
response to
stimulation
6

7.  Cells of pulp:
 Fibroblasts
 Undifferentiated mesenchymal cells
 Odontoblasts
 Defense cells
 Pulpal stem cells
Orbans 13th edition 7

8.  Zones of pulp:




Orbans 13th edition
8

9.  Functions of pulp:
 Inductive
 Formative
 Nutritive
 Protective
 Defensive
Orbans 13th
edition
9

10.  Pulp consist of vascular connective tissue
contained within the rigid dentin walls.
 Accurate pulpal diagnosis is the key to all
endodontic treatments.
10

11.  Located deep within the tooth.
 Radiographically- radiolucent line
 Normal pulp- coherent soft tissue, dependent on its
normal hard dentin shell for protection.
 Pulp totally surrounded by the dentinal wall.
 Total lack of collateral circulation
 Presence of cells
 Responses are unpredictable
 Correlation of clinical signs and symptoms with
corresponding specific histological picture is often
difficult.
Nisha garg
3rd edition
11

12.  Anomalous Crown
Morphology, Fractures, and
Cracks
 Periodontal disease
 Blood Stream (Anachoresis/
retrograde infection)
 Dentinal tubules
 Ingle 6th edition
12

13. 13

14.  Seltzer et al. in 1963.
 The description is very much hypothetical.
 This description was obtained largely by
examining paraffin embedded sections stained
with hematoxylin and eosin under the light
microscope.
14

15.  Cariogenic bacteria in the dental plaque
produce a mixture of acids and enzymes that
dissolve the mineral elements of enamel and
dentin and then digest the organic matrix.
 The initial removal of mineral makes the
enamel more permeable and the bacterial
toxins will diffuse well ahead of cavitation.
 Once the dentin is reached, the toxins and,
much later, the bacteria themselves will travel
along the dentinal tubules
15

16.  In vital teeth, this movement will be opposed
by the outward flow of dentinal fluid.
 Brannstrom and Linde looked at a large
number of extracted teeth and found that in
approximately 50% of teeth with white spot
lesions and no cavitation, there was histologic
evidence of inflammation in the underlying
pulp
16

17.  If the body has been exposed to the antigen
on a previous occasion, then the record of
that exposure will have been maintained by
the memory T cells.
 The production of lymphocytes
synthesizing specific antibodies will begin
very quickly
17

18.  If the antigen has not been encountered before,
new clonal lines of lymphocytes will be
developed, which takes several days.
 In either case, the production of specific
lymphocytes will take place in the lymph
nodes.
 A local interaction between antigen-presenting
cells and resident T lymphocytes.
Ingle
6th edition
18

19. 19

20.  According to Grossman:
20

21. 1. MECHANICAL:
TRAUMA PATHOLOGIC WEAR
21
fracture
avulsion

22. CRACKS BARODONTALGIA
22(Rauch)

23. 2. THERMAL:
CAVITY
23
Setting of cements
Deep fillings
polishing

24. 3. ELECTRIC
24

25. 25

26. CARIES MICROLEAKAGE
26

27.  According to Wein(1891):
27

28. BACTERIAL
• Caries
• Accidental
exposure
• Fracture
• Percolation
around
restoration
• Extension of
infection from
gingival
sulcus
• Periodontal
pocket and
abscess
• anachoresis
TRAUMATIC
• acute
• chronic
IATROGENI
C
• Cutting
procedures
• Orthodontic
movement
• Periodontal
curettage
• Periapical
curettage
• chemicals
IDIOPATHIC
• Aging
• resorption
28

29. 29

30. 30

31. 31

32. Treatable without pulp extirpation and
endodontic treatment
Untreatable without pulp extirpation and
endodontic treatment
32

33. 33

34. INFLAMMATORY RETROGRESSIVE
 Hyperactive pulpalgia
 Acute pulpalgia
 Chronic pulpalgia
 Hyperplastic pupalgia
 Pulp necrosis
 Atrophic papulosis
 Calcific papulosis
34

35.  Clinically normal pulp
 Reversible pulpitis
 Irreversible pulpitis
 Pulp necrosis
 Pulpless canals
 Degenerative changes
 Previous root canal treatment
 Endodontic periodontal lesions
(A clinical classification of the status of the pulp and
the root canal systemPV Abbott, C Yu)
35

36. 36

37. 37

38. 38

39.  Strangulation theory
 Current theory
Nisha Garg
3rd edition
39

40.  Irritation
 Local inflammation of pulp
 Vasodilation, increased capillary pressure,
permeability
 Increased filtration
 Increased tissue pressure
 Thin vessel walls compressed
 Decreased blood flow and increased venous
pressure
 Increased capillary pressure
 Strangulation of blood vessels
 Ischaemia
 necrosis
40

41.  Injury to coronal pulp cause local inflammation
 If injury is severe- complete stasis of blood
vessels occur
 Net absorption of fluid into capillaries in
adjacent uninflammed area
 Increased lymphatic drainage
 Keeping pulpal volume constant.
41

42. 42

43. 43

44.  Definition:
 mild-to-moderate inflammatory condition
of the pulp caused by noxious stimuli in
which the pulp is capable of returning to the
uninflammed state following removal of the
stimuli.
44

45.  Cause-
 Trauma
 Thermal shock
 Excessive dehydration of cavity
 Placement of fresh amalgam filling
 Chemical stimulus
45

46. TYPES:
ACUTE CHRONIC
 Pain- short time
 (few hours or days)
 Pain present every time
stimulus is applied
 Pain is sharp but mild
 Radiograph- normal
 Pain- long time
 (months)
 Occasionally sensitive
to heat, cold
 pain is sharp but mild
 Radiograph- normal
46

47.  Clinical features:
 Sharp short pain lasting for a moment
 The term lingering is often a confusing term to
some, but it is used on an individual basis. If
the patient response is equal in duration on all
teeth, it would be nonlingering.
47

48.  Commonly related to recent restorations, root
scaling, traumatic brushing techniques,
incipient caries, and small infractions in the
tooth crown
 Symptoms related to sweets
 Stopping the irritation typically allows the pulp
to return to normal.
48

49.  Histopathology:
 Reparative dentin
 Disruption of odontoblasts
 Dilated blood vessels
 Extravasation of edema fluid, RBCs.
 Slowing of blood flow
 Self strangulation of pulp due to increased
arterial pressure occluding the vein at the apical
foramen.
 Chronic inflammatory cells
49

50.  Diagnosis:
 Pain
 Visual exam
 History
 Radiographs
 Percussion test –negative
 Vitality test- responds to cold
50

51.  Differential diagnosis:
 Irreversible pulpitis
 Treatment:
 Prevention- best
 Sedative dressing
 Early insertion of restoration
51

52.  Definition:
 persistent inflammatory condition of the
pulp, symptomatic or asymptomatic, caused
by a noxious stimulus.
 It is defined as the point where an inflamed
pulp is no longer capable of healing and
returning to normal. (Ingle 7th
edition)
52

53.  Cause:
 Bacterial involvement
 Chemical, thermal, mechanical injuries
 Reversible pulpitis-untreated
53

54.  Types:
 Description:
 Clinical
Features:
 Pain on percussion
 Radiograph:
 Treatment:
54

55.  Clinical features:
 Pain- (early)-sharp, piercing or shooting and it
is generally severe, intermittent or continuous.
 - (late)- severe, boring, gnawing,
throbbing, nocturnal pain
 Pain increased by heat and relieved by cold.
55

56.  Histopathology:
 Chronic inflammatory response
 PMNLS, lysosomal enzymes
 Capillaries are prominent
 Fibroblastic activity evident
 If the carious process continues to advance
and penetrates the pulp, areas of ulceration
seen.
56

57.  Diagnosis:
 Pain
 Deep cavity
 Probing
 Radiograph
 Thermal test
 Pulp testing-positive
57

58.  Differential diagnosis:
 Reversible pulpitis
 Treatment:
 Pulpectomy
 Pulpotomy
 Surgical removal
58

59.  Definition-
 productive pulpal inflammation due to an
extensive carious exposure of a young pulp.
 This disorder is characterized by the
development of granulation tissue, covered at
times with epithelium and resulting from long-
standing, low-grade irritation.
59

60.  Cause:
 Bacterial involvement
 Chemical, thermal, mechanical injuries
 Reversible pulpitis-untreated
60

61.  Clinical features:
 growth of pulp tissue from the pulp chamber
that is usually covered with epithelium.
 younger population
 can be found in both primary and permanent
dentition.
 Symptomless
61

62.  Histopathology:
 the surface-stratified squamous epithelium-
The pulp polyps of deciduous teeth.
 The grafted epithelial cells are desquamated
cells- saliva
 Plasma cells and lypmhocytes infiltration
 Such epithelium may be derived from the
gingiva or from freshly desquamated
epithelial cells of the mucosa or tongue.
62

63.  The tissue in the pulp chamber is often
transformed into granulation tissue, which
projects from the pulp into the carious lesion.
 The granulation tissue is young, vascular
connective tissue containing
polymorphonuclear neutrophils, lymphocytes,
and plasma cells.
 The pulp tissue is chronically inflamed.
 Nerve fibers may be found in the epithelial
layer.
63

64.  Diagnosis:
 Reddish mass
 Less sensitive
 Bleeds easily
 Radiographs
 Thermal test
 Pulp testing –
delayed response
64

65.  Differential diagnosis:
 Proliferating gingival tissue
 Treatment:
 Elimination of polypoid tissue
 Extirpation of pulp
 Endotherapy
65

66.  pulp plays an important role in 2 types of
resorption:
 Internal inflammatory
 External inflammatory
66

67.  an idiopathic slow or fast progressive
resorptive process occurring in the dentin of
the pulp chamber or root canals of teeth.
67

68.  Cause- may be trauma
68

69.  Pathogenesis of internal root resorption
69
Internal Resorption: A Review Dr. Vikas Swami

70.  Clinical features:
 oval-shaped enlargement of the root canal
space
 asymptomatic and is first recognized clinically
through routine radiographs.
 Pain may be a presenting symptom if
perforation of the crown occurs and the
metaplastic tissue is exposed to the oral fluids.
70

71.  For internal resorption to be active, at least
part of the pulp must be vital, so that a positive
response to pulp sensitivity testing is expected.
 Pink tooth
71

72.  Histopathology:
 Osteoclastic activity
 Lacunae present
 Multinuclear giant cells/ dentinoclasts present
 Metaplasia of pulp
72

73.  Diagnosis:
 Crown or root or
both affected
 1-2years
 Maxillary anterior
teeth-common
 Pink spot
 Radiograph
 Pulp test-
delayed/negative
73

74.  Differential diagnosis:
 Perforation of root
 External resorption
 Treatment:
 Extirpation of pulp
 Endotherapy
 Perforation repair
74

75.  Characterised by necrotic infected pulp tissue
that provide stimulus for periodontal
inflammation.
 Etiology- cemental damage
75

76.  Clinical features:
 2 types:
 Apical with apical periodontitis due to root
canal infection
 Lateral due to cemental damage
76

77. 77

78. 78

79.  Older people teeth
 May be result of persistent, mild irritation in
teeth of younger people.
 Early stage- no definite clinical symptoms
 Tooth not discolored, pulp may react normally.
 3 forms: calcific, atrophic and fibrous
79

80.  1. Calcific:
 Replaced by calcific material
 Within pulp chamber or root canal
 Calcified material has laminated structure
80

81.  Classified as:
 1. position:
 Free
 Attached
 Embedded
 2. structure:
 True
 False
81

82.  Degeneration of complete pulp space may
occur as a sequelae to a traumatic injury
 Characterised by rapid deposition of hard
tissue
 Tooth- asymptomatic, discoloration
 Obliteration is evident radiographically.
82

83.  2. atrophic:
 In pulps of older people
 Fewer stellate cells
 Intercellular fluid is increased
 Pulp tissue is less sensitive
83

84.  3. fibrous:
 Replacement of cellular elements by fibrous
connective tissue
 Leathery fiber
 No distinguishing clinical symptoms to aid in
diagnosis.
84

85.  Mechanism- direct local extension from the
jaw.
 Rare
 chondromyxosarcoma of the mandible.
 Oral Squamous cell carcinoma
85

86.  Death of pulp
 Sequel to inflammation or following a
traumatic injury to which pulp is destroyed
before an inflammatory reaction takes place.
 Ischemic infarction develops which lead to
formation of dry gangrenous necrotic pulp.
86

87.  Cause:
 Necrosis of the pulp can be caused by any
noxious insult injurious to the pulp, such as
bacteria, trauma, and chemical irritation.
87

88.  Types:
88
Coagulation
necrosis
•Soluble
portion of
tissue is
precipitated
Caseation
•Cheesy
mass
Liquefaction
necrosis
•Proteolytic
enzymes
convert the
tissue into
softened
mass, a
liquid or
amorphous
debris.

89.  Clinical features:
 discoloration of the tooth
 the tooth may have a definite grayish or
brownish discoloration
 Teeth with partial necrosis can respond to
thermal changes
89

90.  Histopathology:
 Necrotic pulp tissue, cellular debris, and
microorganisms may be seen in the pulp
cavity.
 The periapical tissue may be normal, or slight
evidence of inflammation of the apical
periodontal ligament may be present.
90

91.  Diagnosis:
 Pain- absent in total necrosis
 History- trauma, history of severe pain
 Radiograph- large cavity/ restoration
 Vitality test- nonresponding
 Treatment:
 Preparation and obturation of canals
91

92.  A tooth with necrobiosis has both inflamed and
necrotic (usually infected) pulp tissue.
 Partial necrosis
 the key factor to the spread of the disease
process is the presence of bacteria within the
necrotic part of the pulp
 The necrotic tissue may be in the coronal
portion of the pulp (e.g., pulp chamber) with
the inflamed tissue apically.
92

93.  mixture of the signs and symptoms of both
pulpitis and necrosis with infection.
 Teeth with necrobiosis may also have apical
periodontitis with radiographic evidence of a
widened periodontal ligament space, which
may be unexpected because the patient has
reported sensitivity to hot and/or cold stimuli.
93

94.  Evaluation of a new means of pulpal
diagnosis through a prospective study of 133
cases
Walid Lejri, Nabiha Douki, Ines Kallel
94

95. 95

96. 96

97.  Periapical tissue consist of surrounding
alveolar bone, periodontal ligament and
cementum.
97

98.  The alveolar process is defined as the part of
maxilla and mandible that forms and supports
the sockets of teeth.
 Functions
 Structure
 Age changes
98

99.  It is a fibrous connective tissue that is
noticeably cellular.
 Functions
 Cells
 Fibers
 Unique features
99

100.  Mineralised dental tissue covering the
anatomic roots of human teeth.
 1st described microscopically by 2 pupils of
Purkinje in 1835.
 Thinnest at CEJ
 Thickest- apex
 Functions
 Cells and
cementoid tissue
Orban’s 13th edition 100

101.  In contrast to pulp, periradicular tissues have
an :
 Unlimited source of undifferentiated cells
 Rich collateral blood supply
 Lymph drainage system
101

102.  In normal periapical tissues, the tooth is not
tender to percussion or pressure
 There is not any tenderness to palpation of
the mucosa overlying the periapical region.
102

103.  Radiographically, the lamina dura is intact and
the periodontal ligament space has a normal
and consistent width along the entire root.
103

104. 104

105.  EXOGENOUS
FACTORS
 •Microbes
 •Chemical agents
 •Mechanical irritation
 •Foreign bodies
 •Trauma
 ENDOGENOUS
FACTORS
 •Host metabolic
byproducts
 •Cytokines and other
inflammatory mediators
 Ingle 7th
edition
105

106. 

Shafer’s 6th edition 106

107.  1.Ingle:
 Normal periradicular tissues
 Asymptomatic apical periodontitis
 Symptomatic apical periodontitis
 Acute apical abscess
 Chronic apical abscess
 Condensing osteitis
107

108.  2. WHO:
108

109.  3. Wein:
109

110.  4. Grossman:
110

111.  Symptomatic Apical Periodontitis
 Asymptomatic Apical Periodontitis
1. Apical Granuloma
2. Chronic Apical Periodontitis
 Asymptomatic Apical Periodontits With Cyst
Formation
1. Radicular Cyst
2. Chronic Apical Periodontitis With Cyst
Formation
 Asymptomatic Apical Periodontitis With Reactive
Bone Form
1. Condensing Ostietis Or Chronic Focal
Sclerosing Osteomyelitits
111

112. 1.ACUTE APICAL PERIODONTITIS
 Primary
 Secondary
2.CHRONIC APICAL PERIODONTITIS
3. APICAL ABSCESS
 Acute
 Chronic
4. PERIAPICAL CYST
 True
 Pocket
P.N.R. Nair. Pathogenesis of apical periodontitis
and the causes of endodontic failures.
112

113. 113

114.  Acute apical periodontitis
 DEFINITION- painful inflammation of the
periodontium as a result of trauma,
irritation, or infection through the root
canal, regardless of whether the pulp is vital
or nonvital.
 Characterised by acute inflammation in PDL
114

115.  Causes:
 1.Vital tooth-
 occlusal trauma,
 high points in restoration
 Biting suddenly on hard objects
 2.Nonvital tooth-
 sequelae to pulpal disease
(necrosis)
 iatrogenic (over instrumentation,
root canal medication irritation)
115

116.  Clinical features:
 Pain- 3 reasons
 tenderness present.
 Tooth- slightly sore, extruded
 Pain on mastication and closure
 Pain-intense, pounding and localized
 Tooth grown out or pushed out of alveolus
 Delayed vitality test
 Sometime periodontal widening
Ingle 7th edition
116

117.  If the insult was short in nature, such as with
trauma induced by a file passing through a
sterile, noninfected pulp tissue, the symptoms
will usually soon subside and healing will take
place.
117

118.  On the other hand, if the insult is continuous
and persistent, such as the permanent
communication between bacteria growing in
the root canal and the host response in the
apical periodontium, events may take one of
two other routes.
 Ingle
6th edition
118

119.  Histopathology:
 Blood vessels:dilated,
 polymorphonuclear leukocytes are present
 These changes are localised to apical area as it
is richly vascular.
 an accumulation of serous exudate distends
the periodontal ligament and extrudes the
tooth slightly.
119

120.  If the irritation is severe and continued, osteoclasts
may become active and may break down the
periradicular bone;

Shafers 6th edition 120

121.  Diagnosis:
 Pain
 Pulp sensititvity test- no response
 Percussion test- always positive
 Palapation test- positive
 Radiograph- normal or thickened PDL space
 Differential diagnosis:
 Chronic apical periodontitis
 Acute alveolar abscess
121

122.  Treatment:
 Endotherapy
 Relieving high points
122

123.  is a long-standing periapical inflammatory
lesion with radiographically visible
periapical bone resorption but with minimal
or no clinical symptoms.
 Characterised by inflammation and
destruction of apical periradicular tissues
123

124.  Clinical features:
 The radiological appearance
of the lesion may take a
wide range of shapes and
sizes
 May develop and enlarge
insidiously
 Necrotic pulp evident and
releases noxious agents
 Develops after inadequate
root canal treatment.
124
Ingle 7th edition

125.  Tooth crown- darkened
 Presence of extensive caries or coronal
restoration
125

126.  Histopathology:
 Histologically, the radiolucent area
associated with asymptomatic apical
periodontitis will be either a granuloma or a
cyst.
 Indistinguisable radiographically
 Biopsy
126
Shafer’s 6th edition

127.  Diagnosis:
 History of severe pain
 Pulp sensitivity test- negative (pulp is
necrotic)
 Percussion test- negative
 Palpation test- negative
 Radiograph-early- thickened PDL space
 - advanced- radiolucent area
around root apex
127

128.  Differential diagnosis:
 Symptomatic apical periodontitis
 Apical abscess
 Treatment:
 Root canal treatment
 Removal of cause of inflammation is usually
followed by resorption of Granulomatous
tissue & repair with trabeculated bone.
128

129. 129

130.  Histopathology:
 Chronic inflammatory cells:
 Periphery- fibrous tissue formed
 Epithelized or non epitheliazed
 Cells form strands including PMNLS and
inflammatory cells- pecularity
130Shafer’s 6th edition

131.  Epithelium may form ramified structures that
enclose islands of granulomatous tissues
containing lymphocytes, plasma cells, rich
circulatory networks
 Most common form of apical periodontitis
131

132. 132

133.  Bhaskar- 2308 periapical lesions specimens-
 48% granuloma,
 42% cyst,
 10% other
 Nair et al- 256 ap lesions –
 50% granuloma,
 35%abscess,
 15% cysts.
 Types and incidence of human periapical
lesions obtained with extracted teeth
133

134.  Treatment:
 Endotherapy
 Removal of cause of inflammation.
 Extraction followed by curettage of apical area
soft tissue.
134

135.  Inflammatory lesion of endodontic origin
characterised by presence of cavity lined by
epithelial cells
 Lining- stratified squamous epithelial cells
 Sometimes- ciliated columnar epithelium
135

136.  Cause:
 Nair PNR, Pajarola G, Schroeder HE. Types and incidence of human
periapical lesions obtained with extracted teeth. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 1996: 81: 93–102.
 Nair PNR. Non-microbial etiology: periapical cysts sustain post-
treatment apical periodontitis. Endod Topics 2003: 6: 96–113.
136

137.  Nutritional deficient theory/ breakdown theory
 Abscess theory
 Immunological theory
 Fusion theory
Ingle 7th
edition
137

138. 138

139. 139

140.  Diagnosis:
 Pulp tests- no response
 History of pain
 Radiograph- loss of continuity of lamina dura
with rarefaction area.(round)
 Radiolucent area large and may include more
than one tooth.
 Differential diagnosis:
 Globulomaxillary cyst
 Traumatic bone cyst
 Lateral periodontal cyst
Grossman 13th edition
140

141. 141

142.  Treatment:
 Endotherapy- 80-98%
 Periodic observation
 Surgical enucleation
 Extraction
142

143.  Localised collection of pus in the alveolar
bone at the root apex following death of
pulp with extension of infection through
apical foramen into periradicular tissue
143

144.  Cause:
 Trauma
 Chemical and mechanical irritaion
 Bacterial invasion
144

145. PRIMARY SECONDARY
 Pain- short time
 Swelling- rapid onset
 Pus discharge
 Pressure on tooth
 Tender to touch
 May have fever
 Radiograph- lack of
radiolucency
 Result of imbalance
between intracanal
infection and host
defense system
 Pain- short time
 Same features
 Radiograph-
radiolucency
145

146.  Clinical features:
 Tenderness
 Severe throbbing pain
 Swelling
 Pus
146

147.  Histopathology:
 Epithelial strands formed
 Types:
 Epithelised – exacerbation of granuloma
 Non epithelised- phagocytic activity
147
Shafer’s 6th edition

148. 148

149.  Diagnosis:
 Visual
 Caries
 Pulp sensitivity test- delayed
 radiograph
149

150.  Treatment:
150

151. 151

152.  Acute inflammatory reaction superimposed
on an existing chronic lesion such as a cyst
or granuloma.
 Causes:
 Influx of bacteria/necrotic products
 Mechanical irritation.
152

153.  Clinical features:
 Tender
 Tooth elevated from socket
 Mucosa- red, swollen.
 Commonly associated with initiated RCT
 Vitality test- no response
153

154.  Treatment:
 Drainage
 Symptoms subside- complete rct
154

155.  Long standing low grade
infection of periradicular
alveolar bone
 Characterized by presence
of abscess draining
through a sinus tract
 Chronic suppurative
apical periodontitis,
asymptomatic apical
abscess
155

156.  Clinical features:
 Asymptomatic
 Detected during radiograph
 Exudate can also drain through
gingival sulcus
 Vitality test-no response
 Draining sinus come and go.
 May be intraoral or extraoral
156

157. 157

158.  Diagnosis:
 Extensive caries
 Gutta percha insertion to track the path
 Pulp test- no response
 No tenderness
 Pus extruding from periapical area
158

159.  Treatment:
 Elimination of infection
 Endotherapy
 Surgical intervention
159

160.  External resorption is a lytic process occurring
in the cementum or cementum and dentin of
the roots of teeth.
 Loss of cementum and/or dentin from the
roots of the teeth originating in the PDL.
160
Seltzer and Bender 3rd edition

161.  Types:
 Surface Resorption (Repair Related)
 Infection Related (Inflammatory Root
Resorption)
 Trauma Related Replacement Resorption
(Ankylosis)
 Spontaneous Ankylotic Resorption
 External Multiple Sites Of Ankylosis (Infection
Related Resorption)
 Cervical Invasive Resorption
161

162.  Replacement inflammatory surface
162

163.  Invasive cervical
 ankylotic
163

164.  • Bacteria- cause
 • Resorption can affect all parts of root.
 • Diagnosed 2-4 weeks after injury.
 • Resorption rapidly progress – total root
resorption within few months.
 • Most common after intrusion & replantation.

Ingle 7th edition
164

165.  Pathogenesis:
 Initial resorption penetrate cementum &
expose dentinal tubules.
 • Toxins from bacteria in dentinal tubules
/infected root canal diffuse to PDL.
 • Osteoclastic process continue- bone
resorption
 • Process progress & root dentin is resorbed
until root canal is exposed.
165

166.  If bacteria eliminated from root canal &
dentinal tubules – resorptive process get
arrested
 • Resorption cavity gets filled with bone /
cementum (according to the vital tissue
available adjacent to resorptive site )
166

167.  Clinical features:
 Increased mobility
 Dull percussion tone
 Sometimes tooth extruded
 No response to sensitivity testing
 Sometimes sinus tract develop
167

168.  Diagnosis:
 Radiographs
 Differential diagnosis:
 Internal root resorption
 Incomplete root formation
168

169.  Radiograph:
 Diagnoses 2-4 weeks after injury
 Appear as progressive cavitation involving
root & adjacent alveolar bone
 Resorption progress rapidly - resulting in
total loss of root structure after only a few
months (particularly in young children)
169

170.  Treatment;
 Remove /destroy bacteria in root canal &
dentinal tubules.
 Allow healing in entire periradicular region.
 calcium hydroxide dressing
 If Ca(OH)2- used for more than 30 days –
weakening of root structure of immature teeth
causes cervical root fracture.
170

171.  Treatment:
 Mature teeth:
 Prophylactic extirpation of pulp in replanted
avulsed teeth
 Biomechanical preparation
 Ca(OH)2 intra canal medicament- 2-3
weeks
 Obturation
171

172.  Immature teeth
 (open apex):
 Ca(OH)2 (apexification)
 MTA – used as physical barrier apically
 In mature teeth – weakening does not occur.
172

173. 173

174.  Chronic focal sclerosing osteomyletis
 Condensing osteitis is the response to a low-
grade, chronic inflammation of the
periradicular area as a result of a mild irritation
through the root canal.
174

175.  It is a diffuse radiopaque lesion usually
surrounding the root apex.
 Characterised by localised reaction of bone to
low grade inflammatory stimulus regressing
from the root canal.
175
Ingle 7th edition

176.  Mostly associated with active bone formation.
 Radiopaque- localised excessive production of
bone around the root apex results in narrowing
of medullar bone spaces.
176

177.  Diagnosis:
 Condensing osteitis appears in radiographs as
a localized area of radiopacity surrounding the
affected root. It is an area of dense bone with
reduced trabecular pattern
 The mandibular posterior teeth
 vitality tests -"normal'' range.
177

178.  Treatment:
 Removal of the irritant stimulus is
recommended
 Endodontic treatment should be initiated if
signs and symptoms of irreversible pulpitis are
diagnosed.
178Ingle 7th edition

179.  Periradicular lesions may arise from the
remnants of odontogenic epithelium.
 Lesions of non endodontic origin with vital
pulps:
 Periapical cemental dysplasia/ cementoma
 Cementoblastoma
 Odontogenic cyst
 Fissural cyst
 Central giant cell granuloma
179Grossman 13th edition

180.  Early stages of periradicular cementum
dysplasia
 Early stages of monostatic fibrous dysplasia
 Ossifying fibroma
 Primordial cyst
 Lateral periodontal cyst
 Dentigerous csyt
 Traumatic bone cyst
 Myxoma
 ameloblastoma
180

181.  Squamous cell carcinoma
 Osteogenic sarcoma
 Chondrosarcoma
 Multilple myloma
181

182.  The value of pulp as an integral part of
the tooth both anatomic and functional
should be recognised and every effort
must be made to conserve it.
 A tooth affected by periapical disease
should always be treated, it cannot be
ignored.
182

183.  A vast amount of knowledge has been
accumulated on the prognosis and treatment
outcome of endodontic treatment.
 The extent of infection and the prevention of
microbial contaminant during and after
treatment are the primary clinical consideration
183

184.  Dental pulp; Seltzer and Bender; 3rd edition
 Oral Histology & Embryology; Orban 11th
edition
 Pathways of Pulp; Cohen; 10th edition
 Endodontics; Ingle; 7th edition
 Wein 6th edition
 Grossman 13th edition
 American board of Endodontics 2007
 Wikipedia
184

185.  Nair PNR, Pajarola G, Schroeder HE. Types and
incidence of human periapical lesions obtained with
extracted teeth. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 1996: 81: 93–102.
 Nair PNR. Non-microbial etiology: periapical cysts
sustain post-treatment apical periodontitis. Endod
Topics 2003: 6: 96–113.
185