Information about Periradicular diseas...

2. CONTENTS
INTRODUCTION
ETIOLOGY
DIAGNOSIS
CLASSIFICATION:
REFERNCES
MCQs

3. INTRODUCTION
• Pulpal disease is only one of the several cause of disease
of periredicular tissues because of the inter-relationship
between the pulp and periredicular tissues.
• Pulpal inflammation causes inflammatory changes in the
periodontal ligament even before the pulp becomes totally
necrotic.

4. ETIOLOGY
=Most common microorganisms:
• streptococcus
• peptostreptococcus
• provotella
=Black pigmented microorganisms:
• enterococcus
• fusobacterium
• porphyromonas
• eubacterium

5. DIAGNOSIS
Extra oral examination:
• skintone
• facial asymmetry
• swelling
• extra oral sinus
• sinus tract
• tender or enlarged cervical lymphnodes

6. Intra oral examination :
• soft tissue and teeth to look for discoloration, abrasion,
restoration, etc………

7. CLINICAL PERIAPICAL TESTS
• Percussion
Indicates inflammation of periodontium.
• Palpation
Determines how far the inflammatory process has extended
periapically.
• Pulp vitality
Thermal tests which can be heat or cold.
Electrical pulp testing.

8. • Periodontal examination
a) probing
Determines the level of connective tissue attachment.
b) mobility
Determine the status of periodontal ligament .

9. • Radiographic examination:
Pulpal origin have four characteristic_
-Loss of lamina dura apically.
- Radiolucency at apex regardless of cone angle.
- Radiolucency resembles a hanging drop.
-Cause of pulp necrosis is usually evident.

10. _CLASSIFICATION_
1.Acute periradicular disease:
a) acute apical periodontitis:
- vital.
- nonvital.
b) Acute alveolar abscess.
c) Phoenix abscess.

11. 2.Chronic periredicular disease with areas of
rarefaction:
a) Chronic apical periodontitis:
- Chronic alveolar abscess.
- periapical granuloma.
- cystic apical periodontitisradicular cyst.
b) persistant apical periodontitis.

12. 3.Condensing osteitis.
4.External root resorption.
5.Disease of the preiredicular tissues of nonendodontic
origin.

13. _ACUTE APICAL PERIODONTITIS_
• It is defined as painful inflammation of the periodontium as a
result of trauma, irritation or infection of the periodontium as a
result of trauma, regardless of whether the pulp is vital or
nonvital.

14. ETIOLOGY:-
• In vital tooth,
-Occlusal trauma
-high points in restoration
-wedging or farcing object between teeth.
• In non vital tooth,
-it is associated with sequelae to pulpal

15. Diseases.
• Tooth is tender on percussion.
• Dull, throbbing and constant pain.
• Pain occurs over short period of time.
• Negative or delayed vitality test.
• No swelling.
• Pain on biting.
• Cold may relieve pain or no reaction.
• Heat may exacerbate pain or no reaction.
• No radiographic sign.

16. inflammatory reaction occur in apicalperiodontal ligament
↓
Dilatation of blood vessels
↓
Initiation of inflammatory response of polymorphonuclear leukocytes and round
cells
↓
Accumulation of serous exudate
↓
Distention of periodontal ligament and extrusion of tooth, slight tenderness
↓
If irritation continues
↓
Loss of alveolar bone

17. Endodontic therapy should be initiated on the affected tooth at the
earliest.
To control postoperative pain following initial endodontic therapy,
analgesics are prescribed.
Use of antibiotics, either alone or in conjunction with root canal
therapy is not recommended.
If tooth is in hyperocclusion, relieve the occlusion.
For some patients and in certain situations, extraction is an
alternative to endodontic therapy.

18. _ACUTE APICAL ABSCESS_
• It is a localized collection of pus in the alveolar bone at the root
apex of the tooth, following the death of pulp with extension
of the infection through the apical foramen into periradicular
tissue.

19. ETIOLOGY:-
• Invasion of bacteria from necrotic pulp tissue.
• Trauma chemical or mechanical injury.
• Irritation by chemical or mechanical treatment during RCT.

20. SIGNS AND SYMTOMS:-
• Tooth is nonvital.
• Rapid pain.
• Slight tenderness.
• Palpable fluctuant swelling.
• Mobility.
• Tooth may be in hyperocclusion.
• Increased WBC count.

21. Polymorphonuclear leukocytes infiltrate and initiate inflammatory response
↓
Accumulation of inflammatory exudates in response to active infection
↓
Distention of periodontal ligament
↓
Extrution of the tooth
↓
If the process continues, separation of periodontal ligament
↓
Tooth becomes mobile
↓
Bone resorption at apex
↓
Localized lesion of liquefaction necrosis containing polymorphoneuclear
leukocytes,debries,cell remanents and purulent exudates.

22. TREATMENT:-
• Nonsurgical endodontic treatment.
• Incision and drainage.
• Extraction.
• In case of localized infection, antibiotics provide.
• In case of systemic complication, antibiotics given in addition to drainage of
tooth.
• To control postoperative pain, nonsteroidal anti-inflammatory drugs are
given.

23. _PHONIX ABSCESS_
• It is defined as an acute inflammatory reaction superimposed on an existing
chronic lesion, such as cyst or granuloma.
• Occurs due to lowering of the body defence or increasing of virulence or
due to blockage of sinus of chronic abscess by pus or debris.
• Tooth may be tender to touch.
• As inflammation progress, tooth may be elevated in the socket and may
become sensitive.
• Mucosa over the radicular area may be sensitive to palpation and may
appear red and swollen.

24. TREATMENT:-
• Establishment of drainage.
• Once symptoms subside complete RCT can be done.

25. _PERIAPICAL GRANULOMA_
• It is one of the most common sequelae of pulpitis.
• It is usually described as a mass of chronically inflamed granulation
tissue found at the apex of nonvital tooth.
• Periapical granuloma is a cell-mediated response to pulpal bacterial
products.
• Bacterial toxins cause mild irritation of periapical tissues.
• This leads to cellular proliferation and thus granuloma formation.

26. CLINICAL FEATURES:-
• Mostly asymptomatic.
• Sometimes pain and sensitivity is seen.
• Tooth is not sensitive to percussion.
• No mobility.
• No response to thermal or electric test.
• Lesions are discovered on radiographic examination.

27. RADIOGRAPHIC FEATURES:-
• Thickening of periodontal ligament at the root apex seen.
• Size may small lesion to large radiolucency exceeding more
then 2cm in diameter.
• Root resorption is also seen.

28. HISTOPATHOLOGIC FEATURES:-
• It consists of inflamed granulation tissue that is surrounded by
a fibrous connective tissue wall.
• The granulation consist of dense lymphocytic infiltrate which
further contains neutrophils, plasma cells, histiocytes and
eosinophils.

29. TREATMENT:-
• In restorable tooth-
root canal therapy is preferred.
• In non-restorable tooth-
extraction followed by curettage of all
apical soft tissue.

30. _CYSTIC APICAL PERIODONTITIS/
RADICULAR CYST_
• It is an inflammatory cyst which results because of
extension of infection from pulp into the surrounding
periapical tissue.

31. ETIOLOGY:-
• Caries.
• Irritating effect of restorative materials.
• Trauma.
• Pulpal death due to development defects.

32. It is frequently asymptomatic.
Discovered when periapical radiograph of teeth with nonvital pulp
is taken.
Males>Females.
Seen in 3rd and 4th decades of life.
Site:-Highest in maxillary anterior.
-In Mandible posteriors, separate small cysts arise from each
apex of
multirooted teeth.
Slowly enlarging swelling.
Involved tooth is usually nonvital, discolored, fractured or shows
failed root canal.

33. PATHOGENESIS:-
• Periapical granuloma are initiated and maintained by the
degradation prducts of necrotic pulp tissue.
• Cyst formation occurs as a result of epithelial proliferation.
• Sometimes. Epithelial plugs protrude out from the apical
formation resulting in a pouch connected to the root and
continuous with the root canal. This termed is “POCKET or BAY
CYST”.

34. RADIOGRAPHIC FEATURES:-
• It appears as round, pear or ovoid shaped
radiolucency.
• Endodontic treatment.
• Apicoectomy.
• Extraction.(severe bone loss).

35. _CHRONIC ALVEOLAR ABSCESS_
• It is known as suppurative apical periodontitis which is
associated with gradual egress of irritants from root canal
system into periradicular area leadinf to formation of an
exudate.

36. ETIOLOGY:-
• It is similar to acute alveolar abscess.
• It also result from necrosis.
• It is associated with chronic apical periodontitis that has
formed an abscess.
• Sinus is seen.

37. SYMPTOMS:-
• It is Generally asymptomatic.
• Detected by presence of a sinus in a radiograph.

38. DIAGNOSIS:-
• If patient give a history of sudden sharp pain.
• Clinical examination may show-
A large carious exposure, a restoration of
composite,acrylic,amalgam or metal.
Discoloration of crown of teeth.
• Vitality test is negative because of presence of necrotic pulp.
• Radiograph show-
Diffuse area of rarefaction.

39. TREATMENT:-
• Removal of irritant from root canal and establishing drainage
is main objective of the treatment.
• Drainage sinus is active with pus discharge surrounded by
reddish pink color mucosa.

40. _PERSISTENT APICAL
PERIODONTITIS_
• It is post treatment apical periodontitis is an endodontically
treated tooth.
• Enterococcus faecalis is found most consistently reported
organism in persistent apical periodontitis.

41. Usually it may persist because of complexity of pulp space which
can not be reached by instruments or irrigants and thus obturation
material.
Nair listed following extraradicular factors which contribute to
persistent apical periodontitis:
-Foreign body reacation to gutta percha.
-Periapical biofilms.
-Cholesterol crystals.
-Periapical scar tissue.
-Actinomyces infection.

42. _CONDENSING OSTEITIS_
• It is the response to a low grade , chronic inflammation of the
periradicular area as a result of a mild irritation through the
root canal.

43. _EXTERNAL ROOT RESORPTION_
• Resorption is a condition associated with either physiologic or a
pathologic process that result in loss of substance from a tissue like
dentin, cementum or alveolar bone.
• In external root resorption, root resorption affects the cementum or
dentin of the root.
It can be,
-Apical root resorption.
-Lateral root resorption.
-Cervical root resorption.

44. ETIOLOGY:-
• Periradicular inflammation due to,
_Infected necrotic pulp.
_Over instrumentation during root canal treatment.
_Replantation of tooth.
_Adjacent impacted tooth.

45. SYMPTOMS:-
• It is Asymptomatic during development.
• When root is completely resorbed, tooth becomes mobile.
• When external root resorption extends to crown, it gives “pink
tooth”appearance.

46. RADIOGHRAPHIC FEATURES:-
• Radiolucency at root and adjacent bone.
• Loss of lamina dura.

47. TREATMENT:-
• Removal of stimulus of underlying inflammation.
• Non surgical endodontic treatment should be tried first before
attempting surgical treatment.

48. _DISEASES OF PERIRADICULAR TISSUE OF
NONENDODONTIC ORIGIN_
• Periradicular lesions may arise from the remnants of
odontogenic epithelium.

49. Benign Lesions:-
• Early stages of periradicular cementum dysplasia.
• Early stages of monostatic fibrous dysplasia.
• Ossifying fibroma.
• Primordial cyst.
• Lateral periodontal cyst.
• Dentigerous cyst.
• Traumatic bone cyst.
• Myxoma.
• Ameloblastoma.

50. Malignant Lesions:-
• Squamous cell carcinoma.
• Ostogenic sarcoma.
• Chondrosarcoma.
• Multiple myloma.

51. MCQs
• 1. _________is defined as an acute inflammatory reaction
superimposed on an existing chronic lesion.,such as a cyst or
granuloma.
A. Periapical granuloma.
B. Phonix abscess.
C. Acute apical periodontitis.
D. Radicular cyst.

52. • 2. A 34 yr male patient come with the complain of swelling in
maxillary anterior region with the fully carious anterior tooth,
what is conclusion-
A. Radicular cyst
B. Cystic apical periodontitis.
C. None of A and B.
D. Both of A and B.

53. • 3. _____ is the malignant lesion.
A. Squamous cell carcinoma.
B. Myxoma.
C. Primordial cyst.
D. all of the above.

54. • 4. Sinus is seen in________.
A. Chronic alveolar abscess.
B. Recrudenscent abscess.
C. Chronic periodontitis.
D. Acute apical periodontitis.

55. • 5. All are periradicular pathogies except,
A. Cystic apical granuloma.
B. External root resorption.
C. Condensing osteltis.
D. non of the above.

56. ANS,
• 1.B
• 2.A n B
• 3.A
• 4.A
• 5.D

57. THANK YOU….