1. INTERRELATIONSHIP
BETWEEN PERIODONTICS
AND ENDODONTICS.
JOSHUA Gideon.
Periodontology-Sem8.
18th May 2012.

2. Overview.
 Introduction
 Influence of pathological conditions in the
pulp on the periodontium.
 Impact of disease condition in the vital pulp.
 Impact of pulp necrosis.
 Manifestation of endodontic lesions in the marginal
periodontium from lateral canals.
 Impact of endodontic treatment measures
on the periodontium.

3. Overview.
 Root perforations
 Vertical root fracture
 Influence of periodontal disease on the
condition of the pulp
 Influence of the periodontal treatment
measures on the pulp.
 Differential diagnostic considerations.
 Treatment strategies for combined
endodontic and periodontal lesions.
 Conclusion.
 References.

4. Introduction.
The fact that the periodontium is
anatomically interrelated with the dental pulp
by virtual of apical foramina and lateral canals
creates pathway for exchange of noxious
agents between the two tissue compartments
when either or both of the tissues are
diseased. Consequently, under certain clinical
conditions, diseases in one of the tissue
compartments may result in pathological
condition in the other.

5. .
INFLUENCE OF PATHOLOGIC
CONDITIONS IN THE PULP ON
THE PERIODONTIUM.

6. Impact of disease conditions in the
vital pulp.
 Disease process in the dental pulp frequently
involve inflammatory changes.
 Caries, restorative procedures and traumatic
injuries are the most common causes.
 Any loss of hard tissue integrity, exposing
dentin or the pulp directly, may allow bacteria
and bacterial products elements present in the
oral environment to affect the normal condition
of the pulp.

7. Cont.
 The resulting inflammatory lesion will be
confined and directed towards the source of
irritation for as long as the inflammatory
defense doesn’t collapse and convert into a
destructive breakdown of the pulpal tissue.
 Occasionally, disruption of the apical lamina
dura or widening of the periodontal ligament
space may be seen in the perodontium.

8. Cont.
 In such instances, typical clinical signs of
pulpitis, eg spontaneous pain, thermal
sensitivity or tenderness to percussion may or
may not be present.
 It is important to realize that as long as the
pulp maintains vitality, although inflamed or
scarred, it is unlikely to produce irritants that
are sufficient to cause pronounced marginal
breakdown of the periodontium.

9. Cont.
 Consequently no benefit will be gained from
extirpation (pulpectomy) as an adjunct to the
treatment of teeth for periodontal diseases.

10. Impact of pulpal necrosis.
 Contrary to disease conditions in the vital pulp,
pulp necrosis is frequently associated with
inflammatory involvement of the periodontal
tissue.
 The lesions are most often located at the apex
of the tooth.
 They may also occur at any site where lateral
canals exit into the periodontium.

11. Cont..
 Inflammatory processes in the periodontium
associated with necrotic dental pulps have,
similar to periodontal disease, an infectious
etiology.
 The essential difference between the two
disease entities is their respective source of
infection.
 While periodontal disease is maintained by
bacterial accumulation in the dento-gingival
region, endodontic lesions are directed
towards infectious elements released from the

12. Cont..
 Rarely will established endodontic lesions
involve the marginal periodontium, unless they
are developing close to the bone margin.
 A potential pathway for infectious elements in
root canal in such instances may be lateral
canals.

13. Manifestations of endodontic
lesions in the marginal
periodontium from lateral canals.
 Inflammatory lesions may develop from a root
canal infection at the lateral aspect of the root
and in furcation regions of multrooted teeth.
 The lesions may be induced and maintained
by bacterial products, which reach the
periodontium through lateral canals.
 Lesions appear to be rare and do not seem to
emerge at a rate that corresponds to the
frequency with which lateral canals occur in
teeth.

14. Manifestations of acute
endodontic lesions in the
marginal periodontium.
 Endodontic lesions either do not have overt
clinical signs or may present with various
acute manifestations of root canal infection.
 The asymptomatic lesions usually assume a
limited extension around the apex, while rapid
and extensive destruction that may extend
marginally along the attachment apparatus
may follow acute exacerbations.

15. Cont..
 Exudation and pus formed in the process may
drain off in different directions;
 pathways along the periodontal ligament space or
 following penetration of the alveolar bone at the
apical region with drainage in or near the gingival
sulcus/pocket warrant particular attention from a
differential diagnostic point of view.
 In addition to deep pocket probing depths, the
accompanying bone lesion may mimic that of
periodontitis.

16. Impact of endodontic treatment
measures on the periodontium.
 When breakdown of periodontal tissue is
associated with a root-filled tooth, endodontic
etiology should be taken into account,
particularly if the root filling is of poor quality.
 Unfilled spaces in endodontically treated root
canals can sustain bacterial growth, and
infectious products from these may reach the
periodontium along the very same pathways
as in an untreated tooth with infected pulp.

17. Cont..
 Endodontic re-treatment may be considered as
an adjunct to periodontal therapy when a root
canal filling is of poor quality and/or displays
signs of periapical inflammation because of
the potential that bacterial elements may
become disseminated to the periodontium
along dentinal tubules exposed by periodontal
instrumentation.

18. Cont..
 Periodontal inflammatory lesions may also
result from mechanical as well as chemical
irritation initiated by root canal treatment.
 However, medicaments for irrigation and
disinfection as well as materials for filling used
in modern endodontics are comparatively well
tolerated by connective tissues of the
periodontium, even if, during treatment, they
are forced into the periodontal ligament.

19. Root perforations.
 During endodontic treatment, instrumentation
can accidentally result in perforation of the root
and wounding of the periodontal ligament.
 Perforations can be made through the lateral
walls of the root or through the pulpal floor in
multi-rooted teeth.

20. Root perforation.

21. Diagram.

22. Cont..
 The clinical course from then depends largely
on the extent the wound site becomes
infected.
 If the perforation is more apical along the root,
a wound site infection process may first lead to
an acute pain condition, including abscess
formation and drainage of pus, followed by
further loss of fibrous attachment and
periodontal pocketing.

23. Cont..
 If an iatrogenic root perforation occurs during
instrumentation of root canals, filling of the
artificial canal to the periodontium should be
carried out without delay to prevent
granulation tissue formation and wound site
infection.

24. Cont..
 Outcome of treatment depends on how well
the wound site can be sealed.
 The closer the perforation is to the marginal
gingiva, the greater the likelihood of
proliferation of sulcular epithelium to the
perforation site.

25. Vertical root fractures.
 Clinical symptoms that are typical of tooth
associated infections such as endondontic
lesions and plaque-induced periodontitis may
also appear at teeth with vertical root fractures.

26. Cont..
 A vertical root fracture is defined as a fracture
of a root that is longitudinally oriented at a
more or less oblique angle relative to the long
axis of the tooth.
 A vertical root fracture can extend the entire
length of a root and then involve the gingival
sulcus/pocket area.
 It may also be incomplete and confined to
either coronal or apical ends.

27. Cont..

28. Clinical expression.
 Clinical signs and symptoms associated with
vertical root fractures vary hugely.
 there may be pronounced pain symptoms and
abscess formation because of active bacterial
growth in the fracture space.
 In other instances, clinical symptoms may be
limited to tenderness on mastication, mild
pain, and dull discomfort.

29. Cont..
 A strong indication of a vertical root fracture is
sinus tracts occurring at both buccal and
lingual/palatal sites.
 In other instances,
a narrow, local deepening of a periodontal
pocket in an area not typical for periodontal
disease may be the only clinical finding.

31. Cont..
 The diagnosis of a vertical root fracture is often
difficult to ascertain because the fracture is
usually not readily detectable by clinical
inspection unless there is a clear separation of
the root fragments.
 To give a radiographic appearance of the
fracture in the absence of separation, the
central X-ray beam has to be parallel to the
fracture plane.

32.  A variety of diagnostic procedures should
therefore be considered.
 clinical examination should include measures
to make fracture lines visible by application of
disclosing solutions, the use of fiber-optic light,
inspection by a surgical microscope or
endoscope, or by raising a surgical flap.

33. Treatment consideration.
 Vertical root fractures that involve the gingival
sulcus/pocket area usually have a hopeless
prognosis due to continuous bacterial invasion
of the fracture space from the oral
environment.
 While there are reports of successful
management of fractured teeth by re-attaching
the fragments with bonding resin or laser
fusing after extraction followed by re-
implantation, fractured teeth are normally
candidates for extraction.

34. External root resorption
 external root resorptions, usually progress
without producing clinical symptoms and may
therefore go undetected unless observed
radiographically.
 In advanced stages, the surface defect may
interfere with the gingival sulcus and thereby
initiate an infectious process.

35. Mechanisms.
 Two mechanisms are involved in resorption of
a hard tissue:
(1) a trigger mechanism and
(2) a reason for the resorption to continue.
Thus, treatment of active root resorption
should be directed to eliminate the cause for
its continuance.

36. Cont..
 The trigger mechanism in root resorption is a
root surface detached from its protective blast
cell layer.
 Detachment may follow any demage to the
cementoblastic cell layer.
 For the resorption to continue, a stimulus is
required eg. An infection or a continuous
mechanical force such as the one in
orthodontic treatment .

37. Cont..
 The treatment of root resorption should be
directed towards the cause for the continuance
of the resorption, for example removal of
infected materials in a root canal or the halt of
an orthodontic tooth movement.

38. diagrams

39. Clinical presentations.
 Root resorptions do not cause painful
symptoms.
 Unless a resorptive process is located
coronally and is undermining the enamel,
giving it a pinkish appearance, the only
way to detect and diagnose dental
resorption is by means of radiography.

40.  Only in very late stages, as the resorptive
process engages the gingival sulcus, may an
infectious process emerge with typical features
of a periodontal abscess.

41. Different forms.
 There are different forms of external root
resorption.
 The underlying mechanism is understood only
for some of them.
 A genetic link can be seen in certain cases as
external root resorptions run in families.
 There are also instances when only the
enamel of an unerupted tooth is resorbed.

42. Cont..
 External resorptions can be caused by
precipitation of oxalate crystals in the hard
tissues of patients as a result of increased
concentration of oxalates in the blood due to
kidney failure.
 Malignant tumors close to a tooth can also
cause root resorption

43. Cont..
Root resorption of known etiology are classified
as,
 Surface resorption
 Replacement resorption associated with
ankylosis
 Inflammatory resorption associated with
persistent inflammation in the periodontium
adjacent to the resorption site.

44. Subforms are:
• Peripheral inflammatory root resorption
(PIRR)
• External inflammatory root resorption
(EIRR).

45. Surface resorption.
 This type of resorption is common, self-
limiting, and
reversible.
 In a histologic study of human teeth from
individuals varying in age from 16–58 years,
only 10% of the teeth showed absence of
active resorption or signs of healed resorptions
(Henry & Weinman 1951).
 Resorptions were noted twice as often in
older than in young subjects.
 Another study demonstrated up to 88% of
teeth with active or, in most instances, healed

46. Mechanism.
 The mechanisms behind surface resorptions
are only partly understood.
 These resorptions are normally initiated in
conjunction with a localized injury to the
cementoblast cell layer, for example by
external trauma or by trauma from occlusion.
 As clast cells are attracted to the denuded root
surface, hard tissue is resorbed for as long as
the activating factors are released at the site of
injury.

47. Cont..
 The resorptive process then stops within a few
days following the disappearance of clast cells
along with the defect becoming populated with
hard tissue repairing cells leading to
cementum repair.
 The regulating factors governing this process
are virtually unknown.

48. Cont..
 Signs of active or healed surface resorptions
or both are common in the large majority of
teeth of the adult dentition.
 It is conceivable that minor traumata caused
by unintentional biting on hard objects,
bruxism, high fillings, etc., cause localized
damage to the periodontal ligament and trigger
the initiation of this type of resorption.

49. Cont..
 The process is self-limiting and self-healing
and no active treatment is required.
 During orthodontic treatment caution should
be exercised and the forces moderated so that
the risk of root foreshortening is minimized.
 When heavy forces are used the involved
teeth should be monitored radiographically.

50. Replacement resorption.
 This type of resorptive process involves
replacement of the dental hard tissues by
bone, hence the name.
 When a surface resorption stops, cells from
the periodontal ligament will proliferate and
populate the resorbed area.
 If the surface resorption defect is large, it will
take some time before periodontal ligament
cells have covered the entire surface.

51. Cont..
 In the interim period osteoblasts from the
nearby bone tissue may then arrive first and
establish themselves at the resorbed surface.
 Bone is thus being formed directly upon the
dental hard tissue.
 This results in a fusion between the bone and
the tooth substance, which is known as
ankylosis.
 Note that replacement resorption and
ankylosis are often erroneously used as
synonyms.

52. Cont..
 Clinically, ankylosis is diagnosed by absence
of tooth mobility and by a percussion tone that
is higher than in a normal tooth.
 Radiographically, a local disappearance of the
periodontal ligament contour may show an
initial stage of fusion.
 However, even in non ankylosed teeth it is not
always possible to observe the entire contour
of the periodontal ligament.

53. Cont..
 Ankylosis caused by apposition of bone to a
root surface is a prerequisite for replacement
resorption.
 The condition may be seen as a form of repair
of root surface resorptions.
 No treatment is available for this condition.

54. External inflammatory
resorption.
 The term external inflammatory resorption
describes the presence of an inflammatory
lesion in the periodontal tissues adjacent to a
resorptive process.
 There are two main forms,
 peripheral inflammatory root resorption (PIRR) and
 external inflammatory root resorption (EIRR).
 Both forms are triggered by destruction of
cementoblasts and the cementoid.

55. Cont..
 In PIRR, the factor maintaining osteoclast
activation is thought to be provided by an
inflammatory lesion in the adjacent periodontal
tissue.
 EIRR, on the other hand, receives its stimulus
from an infected necrotic pulp.

56. Cont..
 Peripheral inflammatory root resorption (PIRR)
and external inflammatory root resorption
(EIRR) are two forms of progressive external
root resorption associated with persistent
inflammation in the periodontal tissues.
 While the direct cause for progression is not
well understood, infectious elements
maintaining periodontal inflammation close to
a root surface that is not covered by
periodontal ligament or epithelium appear to
drive PIRR.

57. Cont..
 To remedy the condition it is necessary to
remove all resorbing granulation tissue
surgically and fill the resorption cavity.
 In certain cases it may be possible to carry
out the treatment from the pulpal side.
 Regardless of approach, periodontal tissue
complications may ensue, including deep
pockets and suppuration from such pockets.

58. Cont..
 Treated cases should therefore be monitored
by regular clinical/radiographic follow-ups to
observe any signs of recurrence and how the
periodontal tissue copes.
 In advanced cases extraction is the only
reasonable treatment option.

59. …
INFLUENCE OF THE PERIODONTAL
DISEASE ON THE CONDITION OF
THE PULP.

60. …
 The formation of bacterial plaque on detached
root surfaces following periodontal disease
has the potential to induce pathologic changes
in the pulp along the very same pathways as
endodontic infection can affect the
periodontium in the opposite direction.

61. Cont…
 Thus, bacterial products and substances
released by the inflammatory process in the
periodontium may gain access to the pulp via,
 Exposed lateral canals and
 apical foramina as well as dentinal tubules.

62. …
 A clear cut relationship between progressive
periodontal disease and pulpal involvement ,
however, does not invariably exist.
 In fact, while inflammatory alterations as well
as localized necrosis of pulp tissue have been
observed adjacent to lateral canals in teeth
exposed by periodontal disease, a number of
clinical studies have failed to confirm a direct
correlation between periodontal disease and
pulp tissue changes .

63. …
 It seems that periodontal disease rarely
jeopardizes the vital functions of the pulp.
 Breakdown of the pulp doesn’t occur until the
periodontal disease process has reached a
terminal state ie. When bacterial plaque
involves the main apical foramina.
 As long as the blood supply through the apical
foramen remains intact, the pulp is capable of
withstanding injurious elements released by
the lesion in the periodontium.

64. Influence of periodontal
treatment measures on the pulp.
 Scaling and root planing.
 Root dentin hypersensitivity.

65. Differential diagnostic
considerations.
 Recognition of pulp vitality is essential for
differential diagnosis and for the selection of
primary measures for treatment of
inflammatory lesions in the marginal and
apical periodontium.
 Deep restorations, dental trauma, endodontic
treatment, previous pulp capping, etc, are
factors to consider when assessing the need
for endodontic Rx.

66. Cont..
 Location, form and extension of radiolucencies
as well as clinical symptoms of pain,
tenderness, abscess formation, increased
probing depth, etc, may not always distinguish
a periodontal lesion from an endodontic lesion.

67. Rx strategies for combined
endodontic and periodontal
lesions.
 Rx of combined endodontic and periodontic
lesions doesn’t differ from the treatment given
when the two disorders occur separately.

68. Treatment strategies.

69. CONCLUSION.
It should be understood that periodontal
disease may be responsible for the entire loss
of the supporting apparatus around a tooth
and may in addition be the cause of the
breakdown of the pulpal tissue.
In such cases endodontic treatment will not
contribute to periodontal healing and the
problem will have to be solved by periodontal
Rx approach.

70. …
When there is doubt as to whether a lesion
in the periodontium is of endodontic or
periodontal origin, or both, the treatment
strategy previously described may be adhered.

71. References.
 Lindhe J, Karring T, Lang NP. Clinical
periodontology and implant dentistry, 4th.
Ed. Munksgaard 2003, Copenhagen.