Transcript Asymptomatic Apical Periodontitis

B. Retamozo DDS, MSD
Pulpitis = Inflammation of the Pulp
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Irritant
– Direct irritation
– Chemical irritation
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Fillings
Erosion
Bleaching
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– Thermal changes
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Uninsulated large
fillings
Drilling
– Mechanical damage
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Trauma
Bruxism
Attrition
Abrasion
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Bacterial irritation from
caries
Cracked tooth
Root fractures
Immune response
– Chemical mediators that
initiate inflammation
Microbial Irritant
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Microbes produce toxins
Initially pulp is infiltrated by chronic
inflammatory cells
– Macrophages, lymphocytes & plasma cells
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Secondarily PMNs infiltrate
– Area of liquefaction necrosis
The Infectious Process
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Sites of established infection
– Main pulp canal space and walls
– Accessory canals and apical delta
– Dentinal tubules
– Cementum surface
– Extraradicular colonizations
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Relative importance? – few data, but
the root canal infection is of course paramount
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Brynolf 1966, Langeland et al. 1977
Apical
periodontitis
The Infectious Process
Pulpitis
Necrosis
Canal
infection
Spread to
apex
Increasing infectious load;
increasingly difficult to treat
Time
The Inflammartory Process
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Mast cells
– Histamine release
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Kinins
– responsible symptoms of acute inflammation
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Cellular damage releases Phospholipase A2
– Prostaglandins, thrombaxanes & leukotrienes
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Neuropeptides: SP & CGRP
– Recruit inflammatory cells
Inflammation => Necrosis
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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
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Necrosis: coronal => apical
More about inflammation..
Inflammation => vascular response
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Increased vascular permeabiltiy
Infiltrate of leukocytes
Decreased lymphatic drainage
Edema =>
Increased local pressure
So whats really going on?
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Pulp is enclosed within calcified walls
– Low compliance system
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Circulation slows due to compression of
venous return
– Odontoblasts are altered or destroyed
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Increase in tissue pressure
– Compression of venules in area of injury
– Progresses coronal => Apex
The sum total of the
inflammatory response may
cause more damage that the
initial irritants alone!
Time-Course of Apical Peridontitis
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Dynamics of pulpal infection
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Bacterial succession and variations in
virulence and pathogenicity
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Host factors modulating inflammation
and spread of the infection
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Ultimate consequences of root canal
infection
Baumgartner
Microbes
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Type:
– Dependent on the environment, nutrients, and
competition
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Primary infection:
– Obligate anaerobes and Gram Negative bacteria.
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Secondary infection:
– Facultative and Gram Positive bacteria. Including E.
Faecalis and candida.
Natural Course of the Disease Vs. Pain
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Varies in intensity and severity
– Pain sometimes accompanies pulpitis and apical
periodontitis
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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)
Inflammation of the periapical region
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Relationship between pulpal and periapical
pathosis
– Periapical pathology follows pulp pathology
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Periapical disease meets a more effective
resistance that pulpal disease
– Repair is more often achieved
From Pulpal to Periapical Pathosis
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Resorption of bone
– Separate irritants from bone
– Prevents osteomyelitis
Periapical Pathosis
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Bacterial endotoxins & inflammatory
mediators trigger surrounding immune cells
Defense cells
– Prevent spread of infection into bone
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Cytokines: interleukins and TNF
– activate surrounding osteoclasts to destroy bone
Periapical Pathosis
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Bone is replaced by highly vascularized
inflammatory tissue which can much better
eliminate invading microbes than the original
bone tissue could have.
Periradicular lesions of pulpal origin
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Symptomatic apical periodontitis
Asymptomatic apical periodontitis
Apical abscess
Symptomatic
Apical Periodontitis
Apical Abcess
Periapical Inflammation
Periapical
Abscess
Apical
Periodontitis
Cellulitis
Osteitis
Osteomyelitis
Cavernous sinus
thrombosis
Periapical cyst
Symptomatic Apical Periodontitis
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Clinical features
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Localized
Frequently spontaneous
Intense throbbing pain
Painful to touch
None to minimal swelling
Symptomatic Apical Periodontitis
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Histology
– Inflammation of the PDL with acute and
chronic inflammatory cells
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X-ray exam
– no change to slight thickening of
periodontal membrane
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Treatment
– RCT or extraction
Asymptomatic Apical Periodontitis
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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
Asymptomatic Apical Periodontitis
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Histology
– Proliferation of fibroblasts and endothelial
cells
– Lymphocytes, plasma cells and phagocytes
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Foam cells and cholesterol clefts
– Epithelial rest of Malassez
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X-ray
– Large radiolucency up to 1cm
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Treatment => RCTx or extraction
Asymptomatic Apical Periodontitis
Periapical Abscess
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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
Periapical Abscess
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Clinical features
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Rapid onset of extreme pain
Painful to percussion
Not localized – adjacent teeth can be painful
SWELLING present
Sinus tract can form
Potentially life threatening
Periapical Abscess
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Histology
– Resembles and acute apical periodontitis
– Involvement of the adjacent bone and soft tissue
– Pus and tissue necrosis
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X-ray
– Widened PDL to large alveolar radiolucency
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Treatment
– Rx for antibiotics
– Establish drainage
Untreated Apical Abscess
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Cellulitis
– Infection travels through the facial planes of least resistance
– Fever
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Osteomyelitis
– Infection within bone through the medullary spaces
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Parulis = “gum boil”
Ludwig’s angina
– Swelling in floor of mouth elevates tongue and blocks
airway
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Cavernous sinus thrombosis
– Infection from MX premolars and molars extends into the
cranial vault
End-Points of Root Canal Infections
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Immediate abscess and sinus tract formation: incidence?
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Chronic, stable encapsulation
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Chronic cyst formation
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Exacerbation of chronic lesion: incidence (5% per year?)
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Sinus tract formation: incidence?
20 – 70%
– Any available surface, sinus, nose, mucosa, skin
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Spreading oral infection: incidence?
– Submandibular, sublingual, local fascies
– Eyes, brain, mediastinum
Spread of infection…
The path of least resistance
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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
Apical Periodontal Cyst / Granuloma
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Clinical features
– The most common cyst of the jaws
– May be asymptomatic of become
symptomatic
– Slow continuous enlargement
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X-ray
– Well-circumscribed radiolucency
– Associated with apices of teeth
– May cause resorption of teeth and bone
Apical Periodontal Cyst
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Histology
– Inflammatory cells
– Prominent epithelial lining without keratin
– Body of cyst filled with semifluid material
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Treatment => Usually require apical
surgery if persistant
Periapical Granuloma
Initial
Post RCT
Post Apicoectomy
2 Year Post Op
Apical Cyst vs. Granuloma
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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
Natural Course of the Disease:
Conclusions
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Unpredictable if untreated
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It does not heal
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Potentially very painful
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Serious complications/sequelae are rare
Filling therapy
Endodontics
Extraction
Pulpitis ->Necrosis->Apical Perio->Acute phases->Local spread->Systemic spread
condensing osteitis
aka periapical osteosclerosis
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Bone sclerosis around apices of tooth with pulpitis
Occurs when there is high tissue resistance to low
grade infection
Clinical features
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Adolescents and young adults
Most common in mandibular first molars
Tooth usually has large carious lesion
No symptoms
Condensing Osteitis
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Histology
– Dense bony trabeculation
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X-ray
– Area of radiopaque sclerotic bone with no
radiolucent border
– Entire root outline is visible
– 85% disappear after extraction
Condensing Osteitis
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Treatment
– None
– RCTx
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Bone Scar
– The residual area of condensing osteitis that remains
after resolution of inflammation
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Differential diagnosis
– Idiopathic osteosclerosis
– Periapical cemental dysplasia
Condensing osteitis
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.
Tooth for Competency II
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Plastic Maxillary Premolar
Before the exam
– Mount tooth
– Place your box number in the acrylic of the tooth
– Take 2 initial x-rays
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Get nail polish and start check
Access
Clean, shape and obturate one canal
Tooth for Competency II
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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
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Place tooth in ziplock bag with paperwork
and x-rays marked with your box # to your
instructor
Final words
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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
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Clinic privileges
– Any molar
Mounted in Endo typodont on the manikin
 Access, clean, shape and obturate all canals
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Dental Humor