The document discusses pulp and periapical diseases. It begins by describing the pathobiology of the periapex and classifying pulpoperipaical pathoses. It then discusses the classifications of Franklin Weine and the WHO for pulpoperipaical lesions. Key lesions discussed include acute and chronic apical periodontitis, periapical granuloma, periapical cyst, condensing osteitis, and Ludwig's angina. Differential diagnoses and clinical signs and symptoms are also covered.

1. PULP AND PERIAPICAL
DISEASES
 Submitted by
Hina bhatia
(521)

2. Contents
 Introduction
 Pathobiology of periapex
 Acute and chronic
 Inflammation Vs Immunology
 Classifications of pulpoperipaical pathoses
 Clinical signs and symptoms

3.  Healing mechanisms
 Differential diagnosis
 Ludwig’s angina , Cellulitis
 Osteomyelitis , Periapical actinomycosis
 Foreign body reactions
 Conclusion
Contents

4. Introduction

5. Apical Pulp tissue
 less cellular
 more fibrous
 whitish in colour
 large conc of glycogen →anaerobic environment
 higher conc of sulfated glycosaminoglycans
 fibrous tissue ~ PDL

6. Apical dentin
 Less tubular , more amorphous , irregular
 Sclerotic dentin increases with age
 Odontoblasts of the pulp are absent/flattened/cuboidal
 Optically transparent
 Less permeable

7. Pathways of infection
Opening in dental hard tissue wall
caries
clinical procedures
trauma induced fractures
microcracks
Bacteria from the gingival sulcus/ P.pocket
Endodontic reinfection
Anachoresis

8. HOST ALLERGEN

9. HOST ALLERGEN
Inflammation
Phagocyte system
Lymphatic system / T & B cells
Immune/complement system
Neural mechanism
chemotaxis
Endotoxins
Exotoxins
Enzymes
PUS / tissue damage
Stimulation of
clast cells

10. Exudate (inflam edema)- pain
Acute (exudative)
Chronic (proliferative)

11. Classification by Franklin.s.weine
Perapical pathosis of pulpal origin:
1.Painful pulpoperiapical pathoses
a. Incipient acute apical periodontitis
b. Advanced ’’ ’’ ’’
(i) acute periapical abscess
(ii) recrudescent / phoenix abscess
(iii) subacute peiapical abscess
2. Non painful periapical pathoses
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst

12. Hirsch et al (1979) – surgically excised pulpoperiaical lesions
I. Periapical granuloma
II. Epithelial granuloma
III. Radicular cyst with modern (chronic inflammation)
IV. Radicular cyst with strong ( acute or subacute )
inflammation and epithelial necrosis
V. Radicular cyst without inflammation (chronic or acute)

13. WHO(1995) CLASSIFICATION
Code
number
CATEGORY
K04.4
K04.5
K04.6
K04.60
K04.61
K04.62
K04.63
K04.7
K04.8
K04.80
K04.81
K04.82
Acute apical periodontitis
Chronic ’’ ’’ (periapicalgranuloma)
Periapical abscess with sinus
Periapical abscess wth sinus to maxillary antrum
’’ ’’ ’’ to nasal cavity
’’ ’’ ’’ to oral cavity
’’ ’’ ’’ to skin
Periapical abscess without sinus
Radicular cyst(apical periodontal cyst, periapical cyst)
Apical and lateral cyst
Residual cyst
Inflammatory paradental cyst

14. Classification by Franklin.s.weine
Perapical pathosis of pulpal origin:
1.Painful pulpoperiapical pathoses
a. Incipient acute apical periodontitis
b. Advanced ’’ ’’ ’’
(i) acute periapical abscess
(ii) recrudescent / phoenix abscess
(iii) subacute peiapical abscess

15. Painful pulpoperiapical pathoses
Early apical changeHealthy tooth
a. Incipient acute apical periodontitis
b. Advanced ’’ ’’ ’’
(i) acute periapical abscess
(ii) recrudescent / phoenix abscess
(iii) subacute periapical abscess

16. Abscess
Healthy tooth Early apical change

17. Abscess
Tooth becomes extremely tender
Vascular congestion
Regional anoxia
Cell breakdown(autolysis)
Neutrophils increase in number
Release osteolytic fragments
Pus core

18. Gumboil (parulis)
Breach the cortical bone (sinus
opening)
“STOMA”
ACUTE
CHRONIC

19. parulis / gum boil
(acute/chronic)
stoma
(chronic)

20. Apical periodontitis

21. A draining sinus is evident on the labial aspect of the upper left lateral incisor.
(A) A gutta percha (GP) point has been placed into the draining sinus in order to trace its
origin.
(B) The radiograph taken with the GP point in the sinus shows that it tracks from the
periapical region of the upper left central incisor, which has a chronic apical abscess.
The lateral incisor has chronic apical periodontitis but this tooth is not associated with
the draining sinus.

22.  Toxic components from pulp irritants / necrosis
 Occlusal disharmony – persistant periapical tissue
compression
 Related to root canal procedures
ETIOLOGY of Painful pulpoperiapical pathoses

23. Etiologic factors related to rot canal procedures
Note the space between the
gutta-percha filling and the root
canal walls clearly visible
JOSE´ F. SIQUEIRA

24. Common problems that may cause post-treatment disease
at least seven problems
1. Inadequate RCT without iatrogenically altered root canal morphology
2. Inadequate RCT with iatrogenically altered root canal morphology
3. Infection remaining in inaccessible areas in the apical portion of the root
4. Extraradicular infection including extruded dentin debris with bacteria present in
the dentinal tubules
5. True radicular cysts and tumors
6. Foreign body reaction to cholesterol crystals or extruded materials such as talc-
contaminated guttapercha, particles of paper points, and particles of sealer
7. Vertical root fractures

25. The quality of the root canal obturation as visualized on a buccal–lingual radiograph is in no
way indicative that the root canal was well sealed, particularly when canals are oval or
ribbon-shaped in transverse section. Note the discrepancy of the image taken in a
buccal–lingual direction as compared to that taken in a mesio-distal direction.
Endodontic Topics 2005, 10, 123–147

26. Diagnosis
 Slight tenderness to intense continuous throbbing
pain
 Sense of fullness
 Readily localised – tenderness on percussion
 Palpable fluctuant swelling
 Vitality test (if viable Cfibers )
 Radiographs

27. 2 . Non-Painful pulpoperiapical pathoses
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst

28. 2 . Non-Painful pulpoperiapical pathoses
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst

29. Pulpoperiapical osteosclerosis (Condensing osteitis)
Occur most frequently in the mandible, around teeth with a
periapical granuloma or radicular cyst, RCT,or restorations.
exudate from the pulp (low toxicity and long standing) the resulting mild irritation
circumscribed proliferation of the periapical bone.
“condensing osteitis or focal sclerosing osteomyelitis”

30. Incipient Chronic apical periodontitis
Initially chronic periapical connective response to pulpal irritants
characterized by :
 slightly widened apical periodontal space (containing dilated blood
vessels, a mild inflammatory exudate)
 a dense accumulation of chronic inflammatory cells(plasma cells and
lymphocytes)
If the pulpal contaminants are not removed the response will
intensify to one of the acute or chronic forms

31. a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst

32. Periapical granuloma
This is advanced form of chronic apical periodontitis; characterized by
growth of granulation tissue and the presence of chronic inflammatory
cells (granulomatous) in response to continued pulpal irritation.

33. Zones of periapical granuloma
Exudative
Granulomatous
Granulofibrotic
Fibrotic granulomas O3 OR,Endo 1996:81:93-102

34. Periapical cyst
“A periapical cyst is chronic inflammatory response of the periapex
that develops from chronic lesions with preexisting granulomatous
tissue.”
characterized by:
Central fluid filled epithelium lined cavity surrounded by
granulomatous tissue and peripheral fibrous encapsulation.

35. Periapical / Radicular cyst
 Direct sequel to chronic AP
 Incidence: 6-55%
 Two types : true and pocket
 Typical radiographic appearance-round/pear shaped
radiolucent unilocular lesion less than 1cm in diameter
 Process of formation
Dormant cell rests of malassez proliferate
Epithelium lined cavity comes into existence
Cyst grows in size

36. Do periapical cysts heal ?

37. Differential diagnosis

38. Granuloma vs Cyst vs Abscess
Chronic
non painful
Definite outline
Smaller in size
Chronic
non painful
Sclerotic opaque
border
Bigger in size
Contain more
protein and
albumins
Acute /Chronic
Pain/non painful
Swelling/parulis
Sinus opening(chronic)
Diffuse outline
Mobility of the tooth
history
Conformative  histology

39. Condensing osteitis
Hypercementosis …. Vital , lying within intact lamina dura
and PDL space
Periapical cemental dysplasia ….lesion is seperated from
the surrounding normal bone by a
radioluscent border , vital
Osteosclerosis …. idiopathic

40. Odontogenic pain
Dentinal hypersensitivity
Reversible pulpitis
Irreversible pulpitis
Acute apical periodontitis
Acute apical abscess

41. Non odontogenic pain –musculoskeletal
Myofacial pain
TMD bruxism
Non odontogenic pain– neuropathic
Trigeminal neuralgia
Atypical odontalgia
Glossopharyng neuralgia
Non odontogenic pain– neurovascular
migraine
cluster headache
Non odontogenic pain – inflammatory
allergic rhinitis
bacterial sinusitis
Non odontogenic pain – systemic disorders
Cardiac pain
Herpes zoster
Sickle cell anaemia
Neoplastic disease

42. Ludwig’s angina
 “potentially life-threatening, rapidly expanding, diffuse inflammation
of the submandibular and sublingual spaces that occurs most often
in young adults with dental infections.”
Symptoms:
 severe neck pain
 Swelling
 Fever
 Malaise
 Dysphagia
Stridor suggests an impending airway crisis.
Causative bacteria include many gram-negative and anaerobic organisms,
streptococci and staphylococci

43. Ludwig’s angina
The submandibular space is composed of two spaces separated anteriorly by the mylohyoid
muscle: the sublingual space, which is superior, and the submaxillary space, which is inferior.
The spread of infection is halted anteriorly by the mandible and inferiorly by the mylohyoid
muscle. The infectious process expands superiorly and posteriorly, elevating the floor of the
mouth and the tongue. The hyoid bone limits the process inferiorly, and swelling spreads to the
anterior aspect of the neck, causing distortion and a "bull neck" appearance. This then evolves to

44. Cellulitis (Phlegmon)
 Cellulitis is a diffuse inflammation of the soft tissues which
is not circumscribed or confined to one area,but which,in
contradistinction to the abscess,tends to spread through
tissue spaces along facial planes.

45. Cellulitis –etiology (of face and neck)
 Dental infection as a sequelae of an abscess or
osteomyelitis,or following periodontal infection.
 Pericoronitis (operculitis)
 Infection following tooth extraction
( injection either thro an infected needle or infected area)

46. Cellulitis -pathogenesis
Microorganisms
Hyaluronidase / fibrinolysins
Breakdown or dissolve intercellular cement
substance
(hyaluronic acid and fibrin)
Streptococci are particularly potent producers of hyaluronidase
Staphylococci – less potent – also pathogenic – freq give rise to
cellulitis

47. Cellulitis – clinical features (of face and neck)
 Painful swelling of the involved soft tissues
 Skin overlying is firm and brawny,inflamed,sometimes even
purplish
(when spread is in deeper planes –normal)
 Moderatily ill-elevated temperature
 Leukocytosis
 Regional lymphadenitis
Infections arising in the maxilla – perforate the outer cortical layer of
bone above buccinator attachment –swelling of upper half of face
In mandible –below buccinatorattachment – lower half of face
Treatment – analgesics + antibiotics + removal of cause

48. Osteomyelitis
If the periapical infection and inflammation extend through the
marrow spaces of the jaw, the result is osteomyelitis.
 Odontogenic infection
 Infection thro PDL space
 Extraction wound
 Trauma-fracture
 Metastasis from remote area
of infection
In this case, you can identify the offending tooth
causing the diffuse and irregular bone destructio

49. Osteomyelitis – predisposing conditions
 Malnutrition
 Diabetes
 h/o Alchoholism
 Leukemia
 Various anaemias
 Conditions that are characterized by the formation of avascular
bone that precludes an effective defensive response
• Osteopetrosis
• Paget’s disease
• Florid osseous dysplasia
• Post-irradiation states
• Flourosis

50. Classification - Osteomyelitis
 Suppurative
> acute suppurative
> chronic suppurative
* primary
* secondary
> infantile
 Non suppurative
> diffuse sclerosing
> focal sclerosing
> proliferative periosteitis
> osteoradionecrosis

51. Acute osteomyelitis
 Develops in a matter of days
 Does not show any early radiographic changes
 Most commonly arises from a periapical abscess
 Ther is no swelling or redness until later-penetrated cortex and
involved periosteum
 WBC count and Temp
 Reflex spasm of muscles attached to the involved area of bone
 Local signs and symptoms:
severe pain,soreness of the involved teeth,which are also
loose,regional lymphadenopathy,parasthesia/anaesthesia of lip.
Radiograph – solitary/multiple small radioluscent areas
Trabeculae-decreased density,outlines become blurred or fuzzy.

52. Acute suppurative osteomyelitis
The clinical manifestations in this
case are severe and debilitating.
Radiograph- Almost the entire
body of the mandible is involved
and shows diffuse mottled
resorption. The decayed first molar
is the guilty tooth.

53. Chronic osteomyelitis
 is persistent abscess of bone charact by inflammatory processes ,
including necrosis of mineralised and marrow
tissues,suppuration,resorption,sclerosis, and hyperplasia.
o Symptoms are milder,
o pain is less ,
o bone destruction is slower,
o sinus tracts develop intermittently and then cease
draining and close.

54. Chronic sclerosing osteomyelitis
Here is an extensive chronic osteomyelitis characterized
by bone formation only (chronic diffuse sclerosing
osteomyelitis).

55. Garres osteomyelitis(COPP)
 Children/young adults
 Mandibular molars-inferior border of mandible
 Hard bony nontender swelling
 Size:1-2cm;cortex becomes 2-3cm thick
 R/f: onion skin appearance-alt radioluscent,opaque layers

56. Sequestrum
In many cases of osteomyelitis there are bone
sequestra. This necrotic piece of bone is being
actively resorbed and is surrounded by intense
inflammation and granulation tissue.

57. Treatment guideline for acute or chronic osteomyelitis
 Disrupt the infectious foci.
 Debride any foreign bodies necrotic tissue, or sequestra.
 Culture and identify specific pathogens for eventual definitive
antibiotic treatment.
 Drain and irrigate the region.
 Begin empiric antibiotics based on Gram stain.
 Stabilize calcified tissue regionally.
 Consider adjunctive treatments to enhance microvascular
reperfusion (usually reserved for refractory forms only).
 Trephination
 Decortication;sequestrectomy
 Vascular flaps
 Hyperbaric oxygen therapy
 Reconstruction as necessary following resolution of the infection.

58. Extra radicular infections
Found in following situations:
1. Acute apical periodontitis lesions
2. Periapical actinomycosis
3. In ass with pieces of infected root dentin that may be displaced
into the periapex during RC instrumentation or have been cut
off from the rest of root by massive apical resorption
4. Infected periapical cysts, particularly in periapical pocket cysts
with cavities open to the root canal.

59. Actinomycosis is a chronic, granulomatous, infectious disease in humans and animals
caused by the genera Actinomyces and Propionibacterium (McGhee et al.1982).
Etiological agent :
 Actinomyces bovis- first species to be identified(Harz 1879).
 in cattle - ‘lumpy jaw’ or ‘big head disease’
 characterized by>extensive bone rarefaction,
>swelling of the jaw,
>suppuration
> fistulation.
Actinomycosis
Causative agents
 nonacid fast, non-motile, Gram-positive
‘sulphur granules’ - yellow specks in exudates.
a ‘starburst appearance’ ‘ray fungus’.

60. Actinomycosis
Human actinomycosis is clinically divided into
 Cervicofacial(60%)
 Thoracic(15%)
 Abdominal forms(20%) (Kapsimalis &Garrington 1968, Oppenheimer et al. 1978).
The most common species isolated from humans is A. israelii
which is followed by Propionibacterium propionicum
(Buchanan & Pine 1962) (Wolff & Israel
1891),
Actinomyces naeslundii (Thompson & Lovestedt 1951),
Actinomyces viscosus and
Actinomyces odontolyticus in descending order (Batty 1958)

61. Foreign body reactions
 Oral pulse granuloma
 Cellulose granuloma
 Gutta percha
 Other materials- amalgam,endo sealants,
and calcium salts derived from periapically extruded
Ca(OH)2

62. CONCLUSION
It is essential that we understand the progressive nature of
the periapical disease process as well as how and why the
various stages occur so they can be diagnosed and managed
appropriately.

63. Thank you