1. Periapical Pathology & Biology
B. Retamozo DDS, MSD

2. Pulpitis = Inflammation of the Pulp
Irritant
Chemical irritation
Fillings
Erosion
Bleaching
Thermal changes
Uninsulated large fillings
Drilling
Mechanical damage
Trauma
Bruxism
Attrition
Abrasion
Direct irritation
Bacterial irritation from caries
Cracked tooth
Root fractures
Immune response
Chemical mediators that initiate inflammation

3. Microbial Irritant Microbes produce toxins
Initially pulp is infiltrated by chronic inflammatory cells
Macrophages, lymphocytes & plasma cells
Secondarily PMNs infiltrate
Area of liquefaction necrosis

4. The Infectious Process
Sites of established infection
Main pulp canal space and walls
Accessory canals and apical delta
Dentinal tubules
Cementum surface
Extraradicular colonizations
Relative importance? – few data, but the root canal infection is of course paramount
Brynolf 1966, Langeland et al. 1977

5. The Infectious Process
Apical periodontitis
Spread to apex
Canal infection
Pulpitis
Necrosis
Increasing infectious load; increasingly difficult to treat
Time

6. The Inflammartory Process
Mast cells
Histamine release
Kinins
responsible symptoms of acute inflammation
Cellular damage releases Phospholipase A2
Prostaglandins, thrombaxanes & leukotrienes
Neuropeptides: SP & CGRP
Recruit inflammatory cells

7. Inflammation => Necrosis
Pulp can impede spread of infection
Factors
Virulence of bacteria
Ability of pulp to release inflammatory factors to prevent increase in intrapulpal pressure
Host resistance
Lymph drainage
Necrosis: coronal => apical

8. More about inflammation..
vascular response
Increased vascular permeabiltiy
Infiltrate of leukocytes
Decreased lymphatic drainage
Increased local pressure
Edema =>

9. So whats really going on?
Pulp is enclosed within calcified walls
Low compliance system
Circulation slows due to compression of venous return
Odontoblasts are altered or destroyed
Increase in tissue pressure
Compression of venules in area of injury
Progresses coronal => Apex

10. The sum total of the inflammatory response may cause more damage that the initial irritants alone!

12. Time-Course of Apical Peridontitis
Dynamics of pulpal infection
Bacterial succession and variations in virulence and pathogenicity
Host factors modulating inflammation and spread of the infection
Ultimate consequences of root canal infection

13. Microbes Type: Primary infection: Secondary infection:
Baumgartner
Type:
Dependent on the environment, nutrients, and competition
Primary infection:
Obligate anaerobes and Gram Negative bacteria.
Secondary infection:
Facultative and Gram Positive bacteria. Including E. Faecalis and candida.

14. Natural Course of the Disease Vs. Pain
Varies in intensity and severity
Pain sometimes accompanies pulpitis and apical periodontitis
Unpredictable if untreated
Pulpitis and acute apical periodontitis dominate as sources for acute dental pain in children and adults (Zeng et al 1994, Lygidakis et at 1998)
which may be debilitating to the patient and lead to absence from work and involvement of costly health services. (Ørstavik, 2009)

15. Inflammation of the periapical region
Relationship between pulpal and periapical pathosis
Periapical pathology follows pulp pathology
Periapical disease meets a more effective resistance that pulpal disease
Repair is more often achieved

16. From Pulpal to Periapical Pathosis
Resorption of bone
Separate irritants from bone
Prevents osteomyelitis

17. Periapical Pathosis
Bacterial endotoxins & inflammatory mediators trigger surrounding immune cells
Defense cells
Prevent spread of infection into bone
Cytokines: interleukins and TNF
activate surrounding osteoclasts to destroy bone

18. Periapical Pathosis
Bone is replaced by highly vascularized inflammatory tissue which can much better eliminate invading microbes than the original bone tissue could have.

19. Periradicular lesions of pulpal origin
Symptomatic apical periodontitis
Asymptomatic apical periodontitis
Apical abscess
Apical Abcess
Symptomatic
Apical Periodontitis

20. Periapical Inflammation
Abscess
Apical
Periodontitis
Cellulitis
Osteitis
Osteomyelitis
Cavernous sinus thrombosis
Periapical cyst

21. Symptomatic Apical Periodontitis
Clinical features
Localized
Frequently spontaneous
Intense throbbing pain
Painful to touch
None to minimal swelling

22. Symptomatic Apical Periodontitis
Histology
Inflammation of the PDL with acute and chronic inflammatory cells
X-ray exam
no change to slight thickening of periodontal membrane
Treatment
RCT or extraction

23. Asymptomatic Apical Periodontitis
Clinical features
Represents a “stand-off” between local resistance and noxious stimuli
Indicative of pulpal necrosis
Common
Painless
Slow growing
May transform into a cyst or granuloma

24. Asymptomatic Apical Periodontitis
Histology
Proliferation of fibroblasts and endothelial cells
Lymphocytes, plasma cells and phagocytes
Foam cells and cholesterol clefts
Epithelial rest of Malassez
X-ray
Large radiolucency up to 1cm
Treatment => RCTx or extraction

25. Asymptomatic Apical Periodontitis

27. Periapical Abscess
A localized collection of pus in a cavity formed by the disintegration of tissues.
Indicative of pupal death
Type is based on the degree of exudate formation, severity of pain and the presence of symptoms
Symptomatic apical abscess
Asymptomatic apical abscess

28. Periapical Abscess Clinical features Rapid onset of extreme pain
Painful to percussion
Not localized – adjacent teeth can be painful
SWELLING present
Sinus tract can form
Potentially life threatening

29. Periapical Abscess Histology X-ray Treatment
Resembles and acute apical periodontitis
Involvement of the adjacent bone and soft tissue
Pus and tissue necrosis
X-ray
Widened PDL to large alveolar radiolucency
Treatment
Rx for antibiotics
Establish drainage

30. Untreated Apical Abscess
Cellulitis
Infection travels through the facial planes of least resistance
Fever
Osteomyelitis
Infection within bone through the medullary spaces
Parulis = “gum boil”
Ludwig’s angina
Swelling in floor of mouth elevates tongue and blocks airway
Cavernous sinus thrombosis
Infection from MX premolars and molars extends into the cranial vault

31. End-Points of Root Canal Infections
Immediate abscess and sinus tract formation: incidence?
Chronic, stable encapsulation
Chronic cyst formation
Exacerbation of chronic lesion: incidence (5% per year?)
Sinus tract formation: incidence?
Any available surface, sinus, nose, mucosa, skin
Spreading oral infection: incidence?
Submandibular, sublingual, local fascies
Eyes, brain, mediastinum
20 – 70%

32. Spread of infection… The path of least resistance
Buccal plate is the most common route due to the thin buccal bone
Outside on face
Palate
Neck below mylohyoid
PDL
Pulp canal
Maxillary sinus
Mandibular canal

39. Apical Periodontal Cyst / Granuloma
Clinical features
The most common cyst of the jaws
May be asymptomatic of become symptomatic
Slow continuous enlargement
X-ray
Well-circumscribed radiolucency
Associated with apices of teeth
May cause resorption of teeth and bone

40. Apical Periodontal Cyst
Histology
Inflammatory cells
Prominent epithelial lining without keratin
Body of cyst filled with semifluid material
Treatment => Usually require apical surgery if persistant

41. Periapical Granuloma
Initial
Post RCT
Post Apicoectomy
2 Year Post Op

42. Apical Cyst vs. Granuloma
A cyst is lined by squamous epithelium and containing necrotic material in the lumen. The cyst wall or capsule contains dense fibrous connective tissue with slight chronic inflammation and cholesterin slits surrounded by foreign body-type giant cells. There are "foam" cells in the epithelial lining.
A lesion with highly vascular tissue containing macrophages, fibroblasts, collagen, and immune cells (neutrophils, plasma cells, T and B cells, lymphocytes, eosinophils

44. Natural Course of the Disease: Conclusions
Unpredictable if untreated
It does not heal
Potentially very painful
Serious complications/sequelae are rare
Filling therapy Endodontics Extraction
Pulpitis ->Necrosis->Apical Perio->Acute phases->Local spread->Systemic spread

45. condensing osteitis aka periapical osteosclerosis
Bone sclerosis around apices of tooth with pulpitis
Occurs when there is high tissue resistance to low grade infection
Clinical features
Adolescents and young adults
Most common in mandibular first molars
Tooth usually has large carious lesion
No symptoms

46. Condensing Osteitis Histology X-ray Dense bony trabeculation
Area of radiopaque sclerotic bone with no radiolucent border
Entire root outline is visible
85% disappear after extraction

47. Condensing Osteitis Treatment Bone Scar Differential diagnosis None
RCTx
Bone Scar
The residual area of condensing osteitis that remains after resolution of inflammation
Differential diagnosis
Idiopathic osteosclerosis
Periapical cemental dysplasia

48. Condensing osteitis

49. Osteomyelitis If the periapical infection and inflammation extend
through the marrow spaces of the jaw, the result is
osteomyelitis. In this case, you can identify the offending
tooth causing the diffuse and irregular bone destruction.

50. Questions?

51. Tooth for Competency II
Plastic Maxillary Premolar
Before the exam
Mount tooth
Place your box number in the acrylic of the tooth
Take 2 initial x-rays
Get nail polish and start check
Access
Clean, shape and obturate one canal

52. Tooth for Competency II
X-rays that must be turned in with tooth
1 film for total length of root canal
1 film with largest working file to working length
1 film with master cone
2 final films
Place tooth in ziplock bag with paperwork and x-rays marked with your box # to your instructor

53. Final words
All projects must be graded before the end of the competency exam
Remediation of the competency
Must be done prior to start of break to receive satisfactory grade
Clinic privileges
Any molar
Mounted in Endo typodont on the manikin
Access, clean, shape and obturate all canals

54. Dental Humor