Endodontics and periodontics inter relationship

1. ENDODONTIC-PERIODONTIC
INTERRELATIONSHIP
PRESENTED BY:
PRABLEEN ARORA
MDS STUDENT 1

2. INTRODUCTION
o In 1964, Simring and Goldeberg - first described the
relationship between endodontics and periodontics.
• ENDODONTIC LESION is used to denote an
inflammatory process in the periodontal tissues
resulting from noxious agents present in the root canal
system of the tooth, usually a root canal infection.
• PERIODONTAL LESION is used to denote an
inflammatory process in the periodontal tissues
resulting from accumulation of dental plaque on the
external tooth surfaces.
2

3. • Embryonic
• Anatomic
• Functional
Pulp &
periodontium
interrelation
• 1st described effect of periodontal disease on
pulp
Turner & Drew
(1919)
• 1st described relationship between periodontal
& pulpal disease
Simring &
Goldberg (1964)
3

4. HISTORY
• Cahn (1927) was one of the first investigator to state that periodontal
disease had an influence on the pulpal tissue. This influence to the close
proximity of these structures in the region of the apical foramen.
• Bender (1936), in a study reported that a large number of extracted teeth
had lateral and accessory canals. He presented evidence that pulpal
inflammation and degeneration could result from periodontal disease.
• Chacker (1974) in his studies, described vascular anastomoses through
lateral and accessory canals. He also commented on the potential for
communication through exposed dentinal tubules. 4

5. • Torabinejad (1985) studied 25 teeth from a single patient
and could not establish any interrelationships between
periodontal and pulpal diseases.
• Hiatt (1977) and Hemington (1979) stated that there is no
apparent relationship between periodontal and pulpal
disease.
5

6. CLASSIFICATION OF PULPAL DISEASES
6

7. CLASSIFICATION OF PERIRADICULAR DISEASES
Periradicular
State
Symptom Pulpal Status
Percussion
Response
Palpation
Response
periapical
radiolucency
Sinus Tract
Normal
periapex
None Varies None None Not present Not present
Acute
periradicular
periodontitis
Painful Inflamed Painful Varies Not present Not present
Chronic
periradicular
periodontitis
None Nonvital None None Present Not present
Acute
periradicular
abscess
Painful Inflamed Painful Painful Varies Not present
Chronic
periradicular
abscess
None Nonvital None None Present Present
Condensing
osteitis
None/pain Inflamed None None Radiopaque Not present
7

8. PERIODONTAL-ENDODONTIC
CLASSIFICATIONS
Based on etiology by Simon, Glick and Frank 1972
Type 1
Primary endodontic
lesions
Type 2
Primary endodontic
lesions with secondary
periodontal involvement.
Type 3
Primary periodontal
lesions
Type 4
Primary periodontal
lesions with secondary
endodontic involvement.
Type 5
True combined
lesions.
8

9. 9

10. Weine in 1982 classified endo-perio lesions into 4
types (Based on ETIOLOGY of the disease)
Class 1
Tooth in which symptoms
clinically and radiographically
simulate periodontal disease
but are in fact due to pulpal
inflammation and/or necrosis
Class 2
Tooth that has both pulpal or
periapical disease and
periodontal disease
concomitantly.
Class 3
Tooth that has no pulpal
problem but requires
endodontic therapy plus root
amputation to gain
periodontal healing.
Class 4
Tooth that clinically and
radiographically simulates
pulpal or periapical diseases
but in fact has periodontal
disease. 10

11. Torabinejad and Trope classification (1996)
(Based on the origin of the periodontal pocket)
i)endodontic origin
ii)periodontal
origin
iii)combined endo-
perio lesion
iv)separate
endodontic and
periodontal
lesions
v)lesions with
communication,
vi)lesions with no
communication,
11

12. AAP 1999 CLASSIFICATION
Periodontitis Associated with
Endodontic Disease
(i)endodontic-
periodontal
lesion
(ii)periodontal-
endodontic
lesion
(iii)combined
lesion.
12

13. ETIOPATHOGENESIS
13

14. Anatomic Considerations of Pulpal and Periodontal
Continuum
Apical foramen
Furcation canals
Lateral canals,
Accessory canals
14

15. Apical foramina
• Major connections between periodontal
and pulpal tissues.
• Direct route of communication between
pulp and periodontium.
• Bacteria and inflammatory byproducts
may exit readily through the apical
foramen to cause periapical pathosis.
• The apex is also a portal of entry of
inflammatory byproducts from deep
periodontal pockets to the pulp.
• Hangeland et al (1974) reported that
the total histological disintegration of
pulp occurs only when Apical foramen
are infected.
Lateral / accesory canals
•Found along length of root canals.
•Varying frequencies depending on their
location.
•59.5% of maxillary second premolars.
•78.2% of those located in apical regions of
root canals
•28.4% of permanent molars in furcation
regions,
•Can lead to chronic periradicular periodontitis
resulting from chronic pulpal diseases
• Usually heal after successful completion of
endodontic therapy.
15

16. • Kirkham reported that out of 100 permanent
human teeth extracted as result of severe
periodontal disease, only 2 teeth possessed
accessory canals within periodontal pockets.
• Thus, likelihood that primary periodontal
infections will reach dental pulp through
accessory canals is rare.
16

17. Advanced
pulpitis
Pulp necrosis
Inflammatory
bone
resorption at
root apex
Apical
periodontitis or
an apical
abscess.
Known as
retrograde
periodontitis
• Because it
represents
periodontal
tissue breakdown
from apical to
cervical direction
Identified as a
periapical
radiolucency
(PARL)
17

18. Dentinal Tubules
Maintain a tapered
structure along length
from pulpodentinal
complex (PDC) to DEJ
Diameter of 2.5 μm at PDC
and 0.9 μm at DEJ.
Permeable structure
Permeability Changes at
different locations along
root surface according to
size & density of dentinal
tubules.
Bacterial colonization
in tubules from
infected root canals.
Dentinal tubules may allow
pulpal irritation from chronic
periodontal infections.
Presence of patent dentinal tubules, especially when cementum layer is denuded,
favors the spread of microorganisms between the pulp and periodontal tissues.18

19. Dentin permeability
↓ By root planing
Result in formation
of smear layer that
is acid-labile.
↑ On removal of
smear layer
Resulting in tubular
penetration of oral
pathogens pulpal
irritation.
19

20. CONTRIBUTING FACTORS
Root perforation
Vertical root fractureRCT procedures
Posts
20

21. ETIOLOGICAL FACTORS
LIVE PATHOGENS
• Encountered in a diseased pulp and in periradicular tissues may include
bacteria, fungi and viruses.
BACTERIA
• Bacteria. Bacteria play a crucial role in the formation and progression of
both endodontic and periodontal diseases . The periradicular tissues
become involved when bacteria invade the pulp, causing either partial or
total necrosis.
• Kakehashi et al. (92), in a classic study, demonstrated the relationship
between the presence of bacteria and diseases in pulp and periradicular
tissues.
• In their study, pulps of normal rats were exposed and left open to the oral
environment. Consequently, pulp necrosis ensued, followed by
inflammation of periradicular tissue and lesion formation.
• However, when the same procedure was performed on germ-free rats, not
only did the pulps remain vital and relatively noninflamed, the exposure
sites showed evidence of dentin repair. 21

22. • Moller et al. confirmed these findings in monkeys and reported
that noninfected necrotic pulp tissue did not induce periradicular
lesions or inflammatory reactions.
• Nonetheless, once the pulp became infected, periradicular lesions
and inflammation occurred in the apical tissues.
• Proteolytic bacteria predominate in the root-canal flora, which
changes, over time, to a more anaerobic microbiota.
• Rupf et al. (167) studied the profiles of periodontal pathogens in
pulpal and periodontal diseases associated with the same tooth.
• Specific PCR methods were used to detect Aggregatibacter
actinomycetemcomitans, Tannerella forsythia, Eikenella corrodens,
Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella
intermedia and Treponema denticola.
• These pathogens were found in all endodontic samples and also in
teeth with chronic apical periodontitis and chronic adult
periodontitis.
• It therefore appears that periodontal pathogens.
22

23. Fungi (Yeasts)
• Presence and Prevalence of fungi associated with endodontic
disease is well documented.
• Fungal colonization associated with radicular pathosis has
been demonstrated in untreated root caries, dentinal tubules,
failing root-canal treatments , apices of teeth wit
asymptomatic apical periodontitis and periradicular tissues.
• Majority of the recovered fungi were candida albicans.
• Fungi colonization - Immune compromising diseases such as
cancer
- Certain intra canal mediaments,
- Local and systemic antibiotics and
- Previous unsuccessful endodontic therapy. 23

24. • Reduction in the numbers of specific strains of bacteria in the
root canal during endodontic treatment may allow fungal
overgrowth in the remaining low nutrient environment.
• Another possibility is that fungi may gain access to the root
canal from the oral cavity as a result of poor asepsis during
endodontic treatment or post-preparation procedures.
• In addition, it has been demonstrated that the presence of
fungi in root canals is directly associated with their presence
in saliva and oral tissues .
• These findings further stress the importance of using aseptic
endodontic and periodontal techniques, maintaining the
integrity of dental hard tissues and covering the tooth crown
as soon as practical with a well-sealed permanent restoration
in order to prevent reinfection.
24

25. Viruses
• There is increasing evidence to suggest that viruses plays an
important role in both endo-perio disease.
• Herpes simplex virus is frequently detected in Gingival
crevicular fluid and periodontal lesions
• Cytomegalovirus was found in about 55% of periodontal
pocket (Hutter 1991).
• Epstein-Bair Virus type 1 was detected in more than 40% of
pocket (Slots et al ).
• Sabet et al suggested that human cytomegalovirus and E-B
virus play a role in the pathogenesis of symptomatic periapical
lesions.
25

26. Non-living etiologic agents
A. Extrinsic agents
Foreign Bodies
 Dentin and cementum chips, amalgam, root canal filling
materials, cellulose fibers from absorbent paper points,
gingival retraction cords, leguminous food and calculus like
deposits.
 Response to foreign body – acute or chronic reaction –
symptomatic or asymptomatic conditions.
 Mechanical or surgical removal of the foreign body is the
treatment of choice.
26

27. Intrinsic agents.
Cholesterol
• Present in apical periodontitis ( Histopathologic
finding) - induce a typical foreign body reaction.
• Cholesterol released by disintegrating erythrocytes of
stagnant blood vessels within periapical lesion,
lymphocytes, plasma cells which die in great numbers
and disintegrate in chronic periapical lesions or by the
circulating plasma lipids.
• Accumulation of cholesterol crystals in inflamed
periapical tissues - causes of failure of Endo therapy
27

28. Russell Bodies
• Found in most inflamed tissues, accumulations of an
Eosinophilic substance.
• Caused by the synthesis of excessive amounts of
normal secretary protein in certain plasma cells
engaged in active synthesis of immunoglobulins.
Rushton hyaline bodies
• Unique feature of some odontogenic cysts.
• They are keratinous in nature, of hematogenous
origin, a specialized secretory product of odontogenic
epithelium.
28

29. Biologic Effects of Pulpal Infection on
Periodontal Tissues
Early inflammatory changes in pulp very little effect on
periodontium
Local invasion of cariogenic bacteria or shift in bacterial content of
biofilm can lead to inflammatory changes in dental pulp
This happens in absence of caries extension into pulp chamber
Bacterial by-products relevant to pulpitis include lactic acid,
ammonia, urea, lipopolysaccharide (LPS), and lipoteichoic acid (LTA)
Dental pulp capable of managing numerous microbial insults
because of extensive intrapulpal lymphatic system. 29

30. Pulpal inflammatory response induced through
various mechanisms by various microbial challenges.
LPS and LTA bind
toll-like receptors
(TLRs).
present on surface of some
immune cells in pulp, and
induce release of
inflammatory mediators
such as prostaglandins,
cytokines, and
chemokines.
TNF-α, IL-1, IL-8,
IL-12, and
chemokines CCL2
and CXCL2
role in pulpitis.
IL-1 released from
macrophages after
stimulation with
LPS
responsible for bone
resorption leading to apical
periodontitis.
30

31. Progression of the pulpal and periradicular pathosis
Normal tooth-
richly vascularized
and innervated
Microbial
challenges- local
inflammation
Pulpal
inflammation
Chronic inflammation
of periradicular
tissues and abscess
formation.
31

32. BIOLOGICAL EFFECTS OF PERIODONTAL
INFECTION ON THE DENTAL PULP
• Langeland et al 1974 indicated then when
pathologic changes do occur in the pulp of the
tooth as a result of advanced periodontal disease
pulp does not usually undergo degenerative changes
as long as the main canal has not been involved.
If the vasculature of the pulp remains vital, no
inflammatory reaction occurs and there is no
symptom of pulp pathosis 32

33. • Kobayashi et al 1990 compared the microflora from
root canal and periodontal pockets of caries free
teeth (necrotic and non-vital).
• Concluded that there were far fewer bacteria in
root canal but both areas showed similar bacteria
strains which suggested that the periodontal pocket
may be the source of bacteria found in infection
within the root canal system.
33

34. • Protection and preservation of the cementum and
dentin surrounding the tooth also play important
role in preserving the health of the pulp and
preventing the ingress of periodontal pathogens.
• Dentin thickness also contributes to the protection
of the pulp.
• Stanley 1968 stated that if a 2-mm thickness of
dentin remains between the pulp and irritating
stimulus, there is little chance of pulpal damage.
34

35. Periodontal Procedures
• Pulpal changes seen in periodontal disease were closely related to
periodontal treatment .
• Vigorous scaling and root planning removes cementum –
- expose dentinal tubules
- transport irritants
- pulpal inflammation
- necrosis of the dental pulp
• Presence of an intact cementum layer - protection of the pulp from
plaque and other periodontal pathogens that migrate along the root
surface during the development of advanced periodontal disease.
35

36. Precautions during periodontal therapy
• Avoid use of irritating chemicals
• Minimise use of ultrasonics & rotary scaling
instruments when < 2 mm of dentin thickness
remaining
• Allow minor irritation to subside before
adding insult to injury
36

37. Diagnosis
SIGNS & SYMPTOMS ENDODONTIC ORIGIN PERIODONTAL ORIGIN
PAIN SHARP DULL, MORE EVEN PAIN
DIFFICULT TO LOCALIZE EASY TO LOCALIZE
DRAINS BY A FISTULA
THROUGH THE ALVEOLAR
MUCOSA OR GINGIVA
DRAINS THROUGH THE
SULCUS/ PERIODONTAL
POCKET
Pulpal pain : exacerbated by certain stimuli.
•Acute pain to thermal stimuli subsides after several days as pulp becomes necrotic.
•Bacteria and bacterial products migrate down the complex canal system.
•As the infection extends to and then past the apical foramen, tooth becomes
particularly sensitive to bite pressure and percussion
REVERSIBLE
PULPITIS
IRREVERSIBLE
PULPITIS
37

38. • Necrotic tooth periradicular abscess elevation
of tooth.
Patient with irreversible pulpitis or chronic pulpal
infection may be completely asymptomatic.
38

39. PERIRADICULAR ABSCESS PERIODONTAL ABSCESS
EXTREME pain to pressure , bite percussion and,
at times, to palpation if the infection has
penetrated the cortical bony plate.
Periodontal abscesses are thought to cause
less pain because there is little or no
elevation of the periosteum.
A periradicular abscess is usually more sensitive
to palpation around the tooth apex if the
infection has penetrated through the bony
cortical plate.
The swelling and edema with a periodontal
abscess is generally confined to the cervical
portion of the tooth.
redness can be detected more apically if a pulpal
abscess has started to swell and elevate the
surrounding tissues.
Redness and a smooth appearance of the
marginal gingival tissues are more common
with abscesses of periodontal origin
usually probe normally but may also display
increased mobility, depending on the amount of
bone loss.
bleeding on probing, suppuration, increased
pocket depth, increased tooth mobility, and
occasionally, lymphadenopathy.
The most prevalent site is a sinus tract
that develops when the area of swelling breaks
through the mucoperiosteum and exits the
mucosal tissue, either near or at some distance
from the site of the infection. along the
periodontal ligament and the infection may
dissect the ligament along the surface of the root
and exit the tooth at the height of the epithelial
attachment
Periodontal abscesses are associated with
severe periodontal destruction.
39

40. OR
The path of least resistance may be along
the periodontal ligament and the
infection may dissect the ligament along
the surface of the root and exit the tooth
at the height of the epithelial attachment
This results in a periodontal defect that
probes along a narrow path to the apex
of the root. Both the sinus tract and
narrow sulcular lesions can usually be
traced to the infected tooth or offending
root using a gutta percha point.
40

41. Periodontal infection Endodontic infection
Coronal Integrity Intact crown structure and
absence of coronal defects
loss of coronal integrity, such as
occurs with caries, failing
restorations,
extensive restorations and the
existence of cracks or fractures
that extend to the pulpal tissues
•this does not mean that all periodontal infections are devoid of coronal defects nor
that all endodontic lesions exhibit loss of coronal integrity.
•When pulp tissue is severed by laxation or avulsion, for example, one would expect to
find a necrotic pulp in the absence of coronal defects.
• If left untreated, such lesions originating from primary pulpal infection will lead to
the breakdown of the periodontium as in CPP or CPA.
• primary periodontal lesions can develop in teeth with coronal defects.
•true combined lesions (so-called “endo-perio” lesions) would present with
periodontal infection with extensive coronal destruction.
41

42. Radiographic Appearance
• Periradicular lesions originating
from primary pulpal infection will
lead to a retrograde periodontitis,
which migrates from the root
apex in a cervical direction.
• integrity of the lamina dura, which
almost always is violated in the periapical
or lateral radiolucency .
• Periodontal infections will lead
to the loss of crestal bone from
the cervical apical direction.
42

43. Thermal testing is usually the most reliable way of determining pulpal health or
disease.
periodontal infection periradicular
infection and a
periodontal abscess
VITALITY vital to thermal testing unless
the acute condition is a true
combined lesion in which both
endodontic and periodontal
compartments
have become diseased.
Nonvital
Patients with an irreversible pulpitis often report a lingering painful response to a thermal
stimulus.
In later stages of pulpitis, heat exacerbates the symptom more than the cold, and the application
of cold may even cause short-term pain relief.
Although thermal testing can be informative as to the status of the pulp, a patient’s response to
thermal stimuli may be confused with hypersensitivity resulting from exposed dentin and patent
dentinal tubules without pulpitis.
Therefore, thermal testing must be combined with other diagnostic criteria, as discussed
previously, to distinguish between the lesions originating from pulpal or periodontal infection.43

44. Primary Endodontic lesions
Causes:
• Deep caries.
• Large restorations.
• Traumatic injuries.
• H/o pulp capping or pulpotomy.
• Poor RCT.
Characteristics/C/F:
• Tooth mobility.
• Narrow pocket.
• Swelling in mucobuccal fold.
• Tenderness to percussion.
• Severe pain
• Sinus tract
• Localized bone loss 44

45. Diagnosis:
Radiographs
Pulpal test: -ve.
Rapid onset.
Tracing of Sinus tract.
Periodontal probing.
• Treatment:
Complete resolution- after
conventional endodontic therapy.
• Prognosis- Excellent
Necrotic pulp. (A) Abscess on the buccal aspect of the tooth is traced
with a gutta-percha cone.
(B) Periapical radiograph showing radiolucency associated with the
mesial and distal roots, as well as the furcation area. (C) Radiograph
taken 4 months after root-canal therapy showing active bony healing.
(D) Clinically, the buccal periodontal defect has healed and probing is
normal.
45

46. Primary Endodontic lesions with
secondary periodontal involvement
• Causes:
• Untreated primary endodontic lesion.
• Plaque/calculus
• Restoration of crown where pins and
posts are misplaced
• Root perforation
• Characteristics/C/F:
– Long standing pulpal pathoses.
– Superimposition of plaque/calculus.
– Generalized periodontal disease.
• Diagnosis:
– Pulpal test: -ve.
– Significant periodontal inflammation.
– Radiographic evidence of angular defects
– At the initial site of the endo involvement.
– Periodontal probing
46

47. Treatment
• Endodontic treatment
• Periodontic treatment
• With endodontic therapy only part of the lesion can be expected to heal.
• According to Ingle and Beveridge prognosis of primary periodontal lesions
is not as favorable as primary endodontic lesions.
• It has been seen bone loss due to endodontic lesion is reversible but
irreversible due to periodontal lesion.
Prognosis
• For endodontic lesion is superior
• Periodontal therapy depends on the severity of periodontal involvement.
• Must receive regular maintenance
47

48. Primary endodontic disease
with secondary periodontal involvement.
(A) Preoperative radiograph of
a symptomatic mandibular right
first molar. Pulp-sensitivity tests
were negative. Initial diagnosis of
periapical periodontitis caused by a
necrotic pulp was established. (B)
Endodontic treatment was performed;
however, a residual deep
pocket (7–9 mm) on the mesial root
remained. (C) Examination reveals a
large mucogingival defect with minimal
keratinization and absence of
attached gingiva. (D) Upon exploration,
severe bone loss and abundant
calculus on the mesial root
were observed. (E) The root surface
was then debrided and the bony
defect cleaned. (F) The bony defect
was repaired with bone graft material
and a resorbable membrane. (G)
Two-month follow-up shows active
healing of the defect.
48

49. Primary Periodontal lesions
Characteristics
• Teeth vital
• Generalized bone loss
• Calculus/plaque
• Soft tissue inflammation
• Broad based pockets
• Mobility
• Periodontal abscess during acute phase
Diagnosis
• Visual examination
• Probing
• Pulp testing- POSITIVE
• Radiographs
49

50. Treatment
• Periodontal therapy
• Root amputation
• Guided tissue regeneration
• Root canal therapy(advance cases)
Prognosis
• Depends on the outcome of periodontal therapy.
• Depends on the extent of the periodontitis and on patients ability to
comply with potential long term treatment and maintenance therapy.
50

51. Primary periodontal lesion with
secondary endodontic involvement.
Characteristics
• Deep periodontal pockets > 6-8mm
• History of extensive periodontal procedures
• Irreversible pulpal pathosis
• Large restorations
Symptoms
• Sensitivity to temperature
• Tenderness to purcussion
• Mobility
• Swelling
Diagnosis
• History of disease progression
• Probing
• Pulp testing
• Radiographic changes
51

52. Different diagnosis
• Presence of generalized periodontal disease.
• Failure of probing G.P point to reach the apex.
• Presence of pulp vitality.
• Class IV lesion will deteriorate unless periodontal treatment is instituted.
Treatment
• Periodontal therapy
• Root amputation
• Guided tissue regeneration
• Root canal therapy
Prognosis
• Depends on continuing periodontal treatment subsequent to endodontic
therapy.
52

53. Primary periodontal disease with secondary
endodontic involvement.
(A) Radiograph showing bone loss in one-third
of the root and separate periapical
radiolucency.
(B) The crown was intact but
pulp-sensitivity tests were negative.
(C) Radiograph taken immediately after root-
canal therapy showing sealer in the lateral
canal that was exposed as a result of bone loss
53

54. True combined lesions
• It arises when an endodontic disease
progressing coronally joins with an infected
periodontal pocket progressing apically.
Characteristics
• Once the pulpal and periodontal lesions
coalesce, they may be clinically
indistinguishable.
• Necrotic pulp/ failed endodontic treatment,
plaque, calculus and periodontitis will be
present in varying degrees.
Diagnosis
• Probing
• Radiographs
• Pulpal testing: negative
54

55. Treatment
• Endodontic therapy
• Periodontal therapy.
• Hemisection
• Bicuspidization
• Root amputation
Prognosis
• Depends on the each individual factor.
• Adequate root canal therapy results in resolution of the
periapical lesion
• Prognosis of the affected tooth then depends totally on the
outcome of periodontal therapy.
55

56. True combined endodontic–periodontal
disease.
(A) Radiograph showing bone loss in two-thirds
of the root
with calculus present and separate periapical
radiolucency.
(B) Clinical examination revealed coronal color
change of the tooth involved and pus exuding
from the
gingival crevis. Pulp-sensitivity tests were
negative.
56

57. True combined endodontic-
periodontal diseases
(A) Preoperative radiograph
showing periradicular
radiolucencies. Pulp sensitivity
tests were negative.
(B) Immediate postoperative
radiograph of nonsurgical
endodontic treatment.
(C) Six-month follow-up
radiograph showing no healing.
Gutta-percha cone is inserted
in the buccal gingival sulcus.
(D) Clinical photograph
showing treatment of the root
surfaces and removal of the
periradicular lesion.
(E) One-year follow-up
radiograph demonstrating
healing.
57

58. DIAGNOSIS CHARACTERSTICS CLINICAL FINDINGS TREATMENT
ENDODONTIC
LESION
•Periapical bone loss
•Drainage through
• sulcus.
•History /signs of
• extensive restorative
• treatment.
•Gingival swelling.
•Furcation bone loss
•Pulp test negative.
•Pd probing yields narrow,
• isolated pocket.
•Evidence of inadequate root
canal treatment.
•Rapid onset.
Endodontic
Treatment
ENDODONTIC
LESION WITH
PERIODONTAL
DISEASE
•Necrotic pulp.
•Generalized
• periodontitis with
• plaque & calculus.
•Pulp test negative, evidence
of inflammation/necrosis.
•Generalized increase in
pocket depth & attachment
loss.
•Radiographic evidence of
pulp & periodontal disease.
First: Endodontic
treatment,
evaluate in 2-3
months.
Then: periodontal
treatment.
PERIODONTAL
LESION
•Deep pockets.
•Extensive attachment
• loss.
•No evidence of pulpal
•H/o disease progression/
therapy.
•Deep probing.
•Pulp test positive.
Periodontal
Therapy only58

59. DIAGNOSIS CHARACTERSTICS CLINICAL FINDINGS TREATMENT
PERIODONTAL LESION
WITH ENDODONTIC LESION
•Deep pockets.
•Extensive attachment
loss.
•Increased pain.
•Evidence of pulp
disease.
•H/o disease
progression/
• therapy
•Deep probing.
•Pulp test negative.
•Pain.
•Radiographic
evidence.
First: Endodontic
treatment,
evaluate in 2- 3
mths.
Then: periodontal
treatment.
COMBINED LESION
•Etiological factors
present for both
• conditions.
•Generalized Pd
destruction that
connects to
• periapical lesion.
•Test for root
fracture.
•Pulp test negative.
o Endodontic
treatment.
o Periodontal
treatment.
59

60. ENDODONTIC PROCEDURAL COMPLICATIONS
AND THEIR EFFECTS ON PERIODONTIUM
• PERFORATION
• TOOTH FRACTURE
• SODIUM HYPOCHLORITE ACCIDENT
• RESORPTIVE DEFECTS
• DENTAL ANOMALIES
• ULTRASONIC DEVICES
60

61. PERFORATIONS
Iatrogenic perforation
Preparation of the access cavity
Instrumentation of canal space
Preparation of the tooth for post (improper post space)
Extensive gouging of a tooth with rotary instruments
during periodontal surgical procedures.
Treatment
• Minimize the time from perforation till its sealed.
• Treatment prognosis of root perforations depends on
the size, location, time of diagnosis and treatment,
degree of periodontal damage and the sealing ability
and biocompatibility of the repair material.
61

62. (a) Perforation of the pulpal floor of the mandibular first molar occurred in conjunction
with a search for root canal openings. There is also a file fragment in one of the mesial
canals. (b) The perforation was immediately sealed with guttapercha. (c) In a radiograph
taken 1 month after treatment a slight radiolucency is seen at the site of the perforation
(arrow). (d) Follow-up after 2 years showed normal periodontal conditions both clinically
and radiographically 62

63. Tooth fracture
• Crown-Root Fractures
• Horizontal Root Fractures in the Coronal Area
• Horizontal Fractures in the Midroot Area
• Horizontal Fractures in the Apical Area
• Vertical root fractures
63

64. 64

65. Sodium hypochlorite accident
• Conc. 0.5-6% (2.5% most commonly used)
• Extrusion of sodium hypochlorite into the
periradicular tissues results in rapid diffuse swelling
and extreme pain.
CAUSES
• Forcing the irrigant into surronding periradicular
tissues.
• Iatrogenic perforations
• overinstrumentation
65

66. Resorptive defects
pathological events
destruction of root canal and periradicular structural integrity
EXTERNAL RESORPTION
R/F- radicular defects
replaced with bony
trabeculation.
Causes: Trauma, damage in
cementoid layer, intracoronal
bleaching, excessive heat,
chronic inflammation of pulp
and periradicular tissues
INTERNAL RESORPTION
R/F- circular radiolucent
lesion centered within the
root canal.
Causes: chronic inflammation
of pulp and periradicular
tissues
66

67. Treatment
• Root canal treatment – complete resolution of the
resorptive process.
• combined with MTA in case of perforation repair.
• Recent studies have also assessed the potential use
of Bisphosphonates –inhibits bone resorption by
acting directly on osteoclasts.
67

68. Dental anomalies
Dens invaginatus
• Inner enamel epithelium
invaginates into the
dental papilla before
calcification.
• Increased labiolingual or
mesiodistal diameter
• Peg or conical
morphology.
• Talon cusp
• Orthograde
endodonticor surgical
treatment
Dens evaginatus
• Tubercle or protrusion of
enamel from the occlusal
tooth surface that has a
core of dentin usually
containing a thin extension
of pulpal tissue.
• Suspectible to pulpal
exposue caused by
fracture, wear, orthodontic
movement or occlusal
equilibrium.
• Prevention /prophylatic
treatment.
• Alloy or composite resin
restoration.
• Pulp capping+ MTA-PULP
EXOSED.
Lingual groove
• Distolingual surface of
the maxillary lateral
incisor.
• Infolding of inner
enamel epithelium and
hertwig’s epitheliual
root sheath.
68