ENDODONTIC DISEASES

1. ENDODONTIC DISEASES
Dr Ambalika Raj,
1st Year PGT,
Department of Endodontics

2. Contents
1. Introduction to endodontic diseases
2. Etiology
3. Classification of endodontic disease
4. Pathogenesis
5. Pulpal disease
6. Sequlae of pulpal disease/ Periradicular lesions
7. Non-microbial endodontic diseases

3. Endodontics -
The branch of dentistry concerned with the morphology, physiology and pathology of the human
dental pulp and periradicular tissues. Its study and practice encompass the basic and clinical
sciences including the biology of the normal pulp and the etiology, diagnosis, prevention and
treatment of diseases and injuries of the pulp and associated periradicular conditions.(AAE)

4. INTRODUCTION
• Dental Pulp is the formative organ of tooth and the vitality of a tooth depends on the pulp.
Therefore it is important to recognize the pathosis associated with it for its successful
elimination.
• Endodontic disorders are generally diseases or injuries that affect the pulp present in the
crown as well as in the root canal and the tissues surrounding the roots.[ Periradicular tissue
]
• Depending upon severity and duration of insult and host response , pulpal response can
range from transient inflammation to total necrosis.
• Infection from the pulp may spread to the periradicular tissues resulting in lesions in these
areas which can even lead to losening of the teeth.

5. ETIOLOGY
• Irritants
1. Microbial Irritants - Streptococcus mutans, lactobacilli, and Actinomyces ,etc.
2. Mechanical Irritants - Deep cavity preparations, removal of tooth structure without proper cooling,
impact trauma,occlusal trauma, deep periodontal curettage, and orthodontic movement of teeth. in
addition, lack of an apical stop after cleaning and shaping can cause overextension of filling materials
into the periapex, resulting in physical and chemical damage.
3. Chemical Irritants - dentin cleansing, sterilizing, and desensitizing substances,
temporary and permanent filling materials,cavity liner,
Antibacterial agents such as silver nitrate, phenol with and without camphor,
and eugenol.
cavity cleansers such as alcohol, chloroform, hydrogen peroxide, and various acids,
chemicals present in desensitizers, cavity liners and bases, as well as temporary
and permanent filling materials.
Antibacterial irrigants used during cleaning and shaping of root canals, intracanal
medications, and some compounds present in obturating materials.

6. CLASSIFICATION OF PULPAL DISEASES
• No correlation between histologic findings and symptoms.
• Clinical classification : Signs & symptoms
• Helps : appropriate treatment , prognosis , restorative needs
• Indistinct demarcation between the classes.
Garfunkel et al :direct correlation -49 percent,partial correlation - 46percent

7. GROSSMAN'S Classification
1.Pulpitis ( inflammatory disease ) 2. Pulp degeneration
i. Reversible i. Calcific
a.Acute ( symptomatic ) ii. Others
b.Chronic ( asymptomatic )
ii. Irreversible 3. Pulp necrosis
a. Acute
i. Abnormally responsive to cold
ii.Abnormally responsive to heat
b. Chronic
i.Asymptomatic with pulp exposure
ii.Hyperplastic pulpitis
iii.Internal resorption

8. BAUME -
• Symptomless vital pulp - Deep caries -
pulp capping done
• History of pain - Amenable to
pharmacotherapy & restorative
rehabilitation.
• Infected pulps - Extirpation & immediate
RCT
• Infected & necrosed pulps -Intracanal
serous drainage - medicament prior to RCT

9. SELTZER & BENDER -
(A) Treatable without pulp extirpation and (B) Untreatable without pulp extirpation
RCT : and RCT :
• Intact, uniflamed pulp Chronic partial pulpitis with necrosis
• Transitional stage Chronic total pulpitis
• Atrophic pulp Total pulp necrosis
• Acute pulpitis
• Chronic partial pulpitis without
necrosis

10. American Board of Endodontics (ABE ) - 2007
• Normal pulp
• Reversible pulpitis
• Irreversible pulpitis
- Symptomatic
- Aymptomatic
• Pulp necrosis
• Previously initiated therapy

11. Walton & Torabinejad
• Normal
• Reversible pulpitis
• irreversible pulpitis
• Hyperplastic pulpitis
• Necrosis

12. Torabinejad & Shabahang -
• Normal pulp
• Reversible pulpitis
• Irreversible pulpitis
• Hyperplastic pulpitis
• Necosis
• Previously treated pulp

13. Tronstad -
• Healthy pulp
• Aymptomatic pulpitis
• Symptomatic pulpitis
• Necrotic pulp
Ingle & Beveridge
• Incipient acute pulpalgia
• Moderate & advanced acute pulpalgia
• Chronic pulpalgia
• Hyperplastic pulposis
• Necrosis

14. Castelucci -
• Healthy pulp
• Hyperemia
• Pulpitis
• Necrosis
Abbott -
A. Clinically normal pulp
B. Reversible pulpitis
Types - Acute Chronic, Necrobiosis
C. Pulp necrosis
types - Necrosis without infection , Necrosis
with infection
D. Pulpless canals
types - Pulpless and no sign of infection
Pulpless and infected
E. Degenerative changes
types - Atrophy,
Pulp canal obliteration - partial or total
Hyperplasia
Internal resorption - Inflammatory & replacement

15. • G. Previous Root Canal Treatment
types : Satisfactory - no signs of infection
- infected
Technically inadequate
- no signs of infection
- infected
• H. Endodontic - Periodontic lesions
Classification based on the origin of the periodontal defect
- Lesions of endodontic origin
- Lesions of periodontal origin
- Combined endo-perio lesion
Types : Separate endo & perio lesions that do NOT communicate
Endoodontic & Periodontal lesion that DO communicate

16. Application of the International Classificat of Diseases to Dentistry and
Stomatology (3rd ed ), World Health Organization (WHO) , Geneva , 1995
KO4 DISEASES OF PULP AND PERIAPICAL TISSUES
• K04.0 Pulpitis
• K04.00 Initial ( hyperaemia )
• K04.01 Acute
• K04.02 Suppurative ( pulpal abscess )
• K04.03 Chronic
• K04.04 Chronic , ulcerative
• K04.05 Chronic , hyperplastic (pulp polyp )
• K04.08 Other specified pulpitis
• K04.09 Pulpitis , unspecified
• K04.1 Necrosis of pulp
Pulp gangrene
• K04.2 Pulp degeneration - Denticles , Pulp calcification , Pulpal stones
• K04.3 Abnormal hard tissue in pulp
• K04.3X Secondary or irregular dentine ; Excludes Pulpal calcification & Pulp stones

17. Pathogenesis of pulp disease
• Bacteria are responsible for most pulpal diseases.
• The pulp responds to these agents in the form of inflammation.
• Both acute and chronic inflammatory response however one type may blend into the other as
presented on histological examination.
• The pulp's inflammatory response is to the toxins rather than the bacteria themselves.
• toxins - Lipoteichoic acid (LTA) and Lipopolysaccharide (LPS)
↓ ↓
Gram +ve bacteria Gram -ve bacteria

18. IN CASE OF DENTAL CARIES - MOST COMMON ETIOLOGY
Cariogenic bacteria in dental plaque
produces acids and enzymes
dissolves minerals of enamel, dentin;
digests organic matrix
more permeable enamel
first bacterial toxins , later on bacteria themselves
travel via the dentinal tubules
reach pulp and elicit an inflammatory and immunological response

19. • Pulpal pathology consists of inflammatory response characterized by :-
1. Histological changes
2. Hemodynamic changes
3. Neural changes
• All these changes occur simultaneously inside the pulp.
• Immune response in dental pulp is the same basic process that occurs elsewhere but IN A
UNIQUE ENVIRONMENT.
• The pulpal tissue is within a low-compliance chamber. If the tissue is presented with a new
antigen, the innate immune response is initiated and followed a few days later by the
specific response.
• If the tissue is presented with an antigen it has met before, the specific response will be
initiated immediately.

20. •
It is the innate immunity which allows the host to survive the initial steps of infection , while
the acquired immunity allows the host to eliminate the invading pathogens.

23. 1. Histopathological changes
• When the foreign antigens successfully penetrate the enamel and the dentin , then the odontoblasts
encounter them , act as defense cells.
• They express chemokines , defensins and TLR ( toll like receptors ) = antigen recognition receptors.
• If injury to odontoblasts is extensive - new odontoblasts are formed - secrete tertiary dentine (
reparative dentin ).
• Inside the pulp , the antigens are encountered by PMN's and macrophage.
( first line of defense ) ( Phagocytes )
• Phagocytes cause phagocytosis of the foreign particle - free oxygen radicals are produced like OH-
Radical ,etc along with pus formation ( when the PMN's die ) - further irritate the nerve cells.
• If the process is less severe - lymphocytes and plasma cells replace the PMN's - inflammatory process
confined to the surface of the pulp.
• Such a chronic inflammatory state is localized for a long time until the microbes penetrate deeper into
the pulp and cause an acute reaction - Flare up.
• Else the chronic process continues till all of the pulp is involved ultimately leading to its death.

24. 2. Haemodynamic changes -
• 3 basic response ( Kim ,S ;1985 Journal of endodontics )
1. Vasodilatation of blood vessels in pulp
2. Increased vascular permeability
3. Vascular stasis
Inflammatory reaction elicited
initially vasodilatation of blood vessels
increased blood flow
increase in intravascular pressure

25. precipitates increase in capillary permeability (also due to inflammatory mediators
like histamine , bradykinin , prostaglandin ,etc)
macromolecules leak out of the capillaries into the interstitial tissue
This causes the fluid to move out from the capillaries to the tissues outside
this results in accumulation of fluid in the tissues
edema
increased pulpal tissue pressure

26. • Low compliance of pulp = detrimental to pulp survival (pulp is
enclosed in rigid walls , hence forms a low compliance system
wherein a small rise in tissue pressure causes passive compression
of venules and even complete collapse )
• When the tissue pressure > venule pressure , there is increased flow
rsistance in vessels because of compression of venules.
• drainage is disturbed resulting in reduction of blood flow to pulp and
congestion of venules.
• this results in slow flow of blood leading to RBC aggregation /
increased hemoconcentration.
• this causes the blood viscosity to increase along with the pCO2 and
decrease ph of blood.
VENOUS STASIS

27. • this ultimately results in
• This can lead to and
• if the removal of tissue fluid by venules and lymphatics does not match
the filtration of fluid from capillaries , then exudate is formed.
• if exudate is drained by pulpal cavity or absorbed , then necrosis is
delayed.
If not , then the exudate egress into periradicular tissues and results in
periradicular pathosis.The exudate is drained by sinus tract formation.

28. 3. Neural changes -
a. Sympathetic nerves ( control blood flow by vasoconstriction of precapillaries)
• inhibit production of proinflammatory cytokines
• stimulate the production of anti inflammatory cytokines
• recruit inflammatory cells to the affected area
• inhibit odontoclast activity
b. Afferent sensory nerve of trigeminal system
• secrete neuropeptides like substance P and CGRP which cause vasodilatation
and increased capillary permeability.
• Bradykinin activates nociceptors of pulp while prostaglandin sensitize them to
lower the firing threshold.

29. • This activation and sensitisation of primary
afferent nociceptors by inflammatory mediators
result in :-
• Allodynia
• Hyperalgesia
• Spontaneous pain
Central mechanism -
• Sufficient input from the C fibres result in
increased excitability of central neurons (
hyperexcitation ). NO , leukotrienes produced
also cause amplification of noxious and non
noxious input to the central neurons.

30. PULPAL DISEASES
• Pulpitis - a clinical and histologic term denoting inflammation of the dental pulp ;
clinically described as reversible or irreversible and histologically
described as acute , chronic or hyperplastic.( AAE )
1. REVERSIBLE PULPITIS -
• A clinical diagnosis based on subjective and objective findings indicating that the inflammation shoul
resolve and the pulp return to normal.
• Causes - trauma , from blow or from a disturbed occlusal relationship
Thermal shock ( cavity preparation ),
Excesssive dehydration of cavity or irritation of exposed dentin,
Placement of fresh amalgam filling in contact with cast restoration,
Chemical stimulus , as from sweet or sour foodstuffs or caries.

31. • Histologically hyperaemia present.
• Symptoms - sharp pain lasting for a moment ,
brought about by cold than hot food and by cold air.
also caused by sweet , sour food.
no spontaneous pain
removal of stimuli provides immediate relief.
usually aymptomatic
• Diagnosis - Removal of stimulus ends the pain
Thermal test - cold test - elicits pain
Electric pulp test - less current than control tooth

32. 2. Irreversible pulpitis -
i) Asymptomatic irreversible pulpitis - A clinical diagnosis based on subjective and objective
findings indicating that the vital inflamed pulp is incapable of healing.
Additional descriptors : no clinical symptoms, but inflammation produced by caries, caries
excavation,trauma.
ii) Symptomatic irreversible pulpitis - A clinical diagnosis based on subjective and objective
findings indicating that the vital inflammed pulp is incapable of healing.
Additional descriptors : lingering thermal pain , spontaneous pain , referred pain
• Clinical features - Early stage - Paroxysm of pain ( temperature change , particularly cold ;
sweet or acid foodstuffs , pressure from packing food into cavity
or suction exerted by tongue),
Pain continues even on removal of stimulus,
Spontaneous Pain,
Sharp , shooting ,piercing pain ,severe
Intermittent or continous pain,
Pain increases on lying down

33. • Referred pain to adjacent teeth , temple or sinuses (upper posterior teeth) and to the ear
(lower posterior tooth )
• Later stage - Dull , gnawing pain , throbbing
Pain at night
Pain increased by heat and sometimes relieved by cold
although continued cold exposure intensify pain.
• Pain - reduced by exposure and drainage of the pulp.
• Later stages - Apical periodontitis present.
• Diagnosis - Pulp may be exposed, grayish scum like layer over exposed pulp and dentin.
This layer contains food , debris , degenerated PMN's ,microbes and blood cells.
Odour of decomposition present
THERMAL TEST - early stage-elicits pain which persists after removal of stimlus
late stage - pulp exposure -normal response but it reacts feebly
ELECTRIC PULP TEST -

34. Chronic Hyperplastic pulpitis ( Pulp polyp )
• A form of chronic pulpal inflammation usually following carious or
traumatic exposure ; characterized by proliferation of dental pulp
tissue from the exposed pulp chamber , filling the cavity with a
pedunculated or sessile ,pinkish-red, fleshy mass; usually covered
with epithelium.
• Histopathologically - Surface of pulp polyp is covered with
stratified ,squamous epithelium derived from
buccal mucosa or gingiva.
-The tissue in the pulp chamber changes to
granulation tissue - young ,vascular
connective tissue containing PMN's ,
lymphocytes and plasma cells.

35. CAUSE - Slow , progresse exposure of pulp.
a large open cavity ,
young resistant pulp,
chronic , low grade irritation
CLINICAL FEATURES - usually asymptomatic,
- Reddish cauliflower -like outgrowth from a cariously exposed occlusal surface
- Occasionally signs of IP - spontaneous pain as well as lingering pain on
hot ,cold stimuli.
- Discomfort during mastication
DIFFERENTIAL DIAGNOSIS - Gingival polyp
DIAGNOSIS - seen in children and young adults,
- appearance of polypoid tissue ( clinical characteristic ),
- Polypoid tissue less sensitive than normal pulp tissue but more than gingival
tissue,
- Bleeds easily,
- radiographically , a large open cavity with direct access to pulp
THERMAL PULP TEST - feeble or no response
ELECTRICAL PULP TEST - more current than normal required

36. Internal Resorption -
• An inflammatory process initiated within the pulp space with
loss of dentin and possible invasion of the cementum.
• Maybe caused by trauma.
• Histopathologically, the pulp is transformed into vascularized
inflammatory tissue with dentinoclastic activity.
• Presence of lacunae filled by osteoid tissue.
• Multinucleated giant cells or dentinoclasts present .
• Chronically inflamed pulp.
• CLINICAL FEATURES - Asymptomatic ,
mostly on maxillary anteriors
crown - PINK SPOT-granulation tissue
• DIAGNOSIS - radiographic defect more extensive on pulpal
wall than on the root surface.

37. PULP DEGENERATION
• 1. Calcific degeneration - part of pulp tissue replaced by
calcific material
A. Pulp stones / denticles
B. Calcific metamorphosis
A. Pulp stones - A calcified mass occurring within the pulp or
attached to pulp space walls;
classified as true or false denticles, according to composition
and morphology,
- free, adherent or interstitial denticles, according to their
location in relation to the pulp space walls.
- aymptomatic unless they impinge on nerve or vessel.
B.Calcific metamorphosis - A pulpal response to trauma
characterized by rapid deposition of hard tissue
within the canal space;

38. - entire space may appear obliterated
radiographically due to extensive deposition,even
though some portion of the pulp space remains
in histological sections.
- Yellowish discoloration of crown .
Calcific metamorphosis occurs in response to
death and replacement of the odontoblasts.

39. 2. Others -
• Atrophic degeneration - in pulps of older people,
• Reticular Atrophy - artifact caused by delay of the fixative
agents in reaching the pulp.
• Fibrous degeneration - replacement of cellular elements
by fibrous connective tissue.
- “leathery fiber “ appearance of pulp.
• Pulp artifacts - vacoulization of odotoblasts and caused
by poor fixation of specimen tissue
PULP NECROSIS
• A clinical diagnostic category indicating death of the dental pulp.
The pulp is usually nonresponsive to pulp testing.
• Sequele of inflammation or following traumatic injury where pulp is
destryoed before inflammatory response occurs.

40. • Two types -
1. Coagulation necrosis
2. Liquefaction necrosis
• Coagulation necrosis - soluble portion of tissue converted to solid material.
• Caseation is a form of coagulation necrosis in which the tissue is converted into
cheesy mass consisting of coagulated proteins, fats and water.
• Liquefaction necrosis - Proteolytic enzymes - convert tissue- softened mass,
liquid or amorphous debris
End product of pulp necrosis -
Intermediate products -

41. • CLINICAL FEATURES - No painful symptom,
1st sign = crown discoloration,
Dull , opaque appearance of crown,
Sometimes definite grayish or
brownish discoloration.
• DIAGNOSIS - THERMAL TESTS - No response
ELECTRIC TEST - No response
TEST CAVITY - No response
• Partial necrosis - respond to thermal tests because of vital
nerves passing through adjacent inflamed tissue
• Complete necrosis - minimal response sometimes ( due to
moisture present formed by liquefaction necrosis. )
• Ultimately necrosis may extend into the periapical region
resulting in lesions.

42. SEQUELAE OF PULPAL DISEASE / PERIRADICULAR
LESIONS
• The inflammatory exudate formed as a result of necrosis in pulp follows the
path of least resistance i.e. through the apical foramen to the periradicular
tissues outside.
• These noxious products produce bone resorption and granulation tissue .
• The formation of a periapical granuloma - attempt by the system to contain the
bacteria and their toxins from reaching into deeper structures.
• Thus, periapical inflammatory lesions may be considered to be a successful
host response to bacteria and bacterial by-products in an infected root canal
system.
• The periradicular pathologic tissues contain PMN's ,lymphocytes, plasma
cells,
macrophages, and mast cells along with immunoglobulins IgG, IgA, IgM, IgE
and complement.

43. • In the presence of inflammatory cells , immunoglobulins,
and complement in the periradicular tissues , anaphylactic ,
cytotoxic ,antigen- antibody complex and delayed
hypersensitivty reactions may occur.
• Initially ,PMNs follow the gradient of - C5a ( generated by the
activation of the complement system at the site where bacteria
are present ) This gradient serves as a chemotactic signal.
• Complement may be activated directly by bacterial constituents
such as bacterial endotoxin (lipopolysaccharide, LPS). This
represents the basic, innate immune response of the host.
• Fisher defined four zones of reactions of periradicular tissues to
noxious products of necrosis-
1. Zone of infection
2. zone of contamination
3. zone of irritation
4. zone of stimulation

44. • Zone of infection - PMN, microbes (center of lesion),
bacterial toxins.
• Zone of contamination - lymphocytes, round
cells,empty lacunae
• Zone of irritation - macrophages and osteoclasts
normal bone cells, preparatory
activity for repair
• Zone of stimulation - fibroblasts , osteoblasts.

46. Classification of periradicular disease
According to GROSSMAN
1.ACUTE PERIRADICULAR DISEASES
• Acute alveolar abscess
• Acute apical periodontitis
- vital
- non vital
2.CHRONIC PERIRADICULAR DISEASES WITH AREAS OF RAREFACTION
• Chronic alveolar abscess
• Granuloma
• Cyst
3.CONDENSING OSTEITIS
4. EXTERNAL ROOT RESORPTION
5. DISEASES OF PERIRADICULAR TISSUES OF NONENDODONTIC ORIGIN

47. • Ingle's classification
1. Acute apical periodontistis
2. chronic apical periodontistis
3. acute apical abscess
4. chronic apical abscess
5. Cellulitis
6. condensing osteitis
7. apical scar
Weine's Classification
PULPOPERIAPICAL DISEASE :
1.PAINFUL PULPOPERIAPICAL PATHOSES
A.Incipient acute periapical periodontitis
B.Advanced acute periapical periodontitis
i) Acute periapical abscess
ii)Recrudescent abscess
iii)Subacute periapical abscess
2.NON PAINFUL PULPOPERIAPICAL PATHOSES
A.Pulpoperiapical osteosclerosis
B.Incipient chronic periapical periodontitis
C.Advanced chronic periapical periodontitis
i)Periapical granuloma
ii)Chronic periapical absces
iii) Periapical cyst

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

49. 1. Acute Apical Periodontitis (Symptomatic Apical Periodontitis)
• Inflammation usually of the apical periodontium, producing clinical symptoms including a
painful response to biting and/or percussion or palpation. It might or might not be
associated with an apical radiolucent area.
• ETIOLOGY :-
Vital tooth - Abnormal occlusal contacts
Recently inserted restoration beyond occlusal plane
Wedging of foreign object between teeth such as toothpick
Traumatic blow to the teeth.
Nonvital tooth- sequelae of pulpal disease
iatrogenic - root canal instrumentation forcing bacteria through
apical foramen
forcing irritating irrigants or medicament orobturating
material through apex.
Perforation of root and overinstrumentation.
abnormal contacts

50. • SYMPTOMS -
- Pain and tenderness of tooth
- tooth = slightly sore
- tooth may feel extruded
- pain on closure and mastication.
• DIAGNOSIS -
- Pain on percussion
- mucosa overlying the root apex may or may not be tender to
palpation.
- radiographically - thickened PDL or a small
area of rarefaction if pulpless tooth involved,normal periradicular
structures if vital pulp involved.
• DIFFERENTIAL DIAGNOSIS - Acute alveolar abscess

51. HISTOPATHOLOGICAL FEATURES- The blood vessels are dilated, PMN's and macrophage
are present.
- Accumulation of serous exudate distends the
PDL and extrudes the tooth.
- Severe irritation - osteoclats activated - bone
breakdown
• If the insult short in nature, such as with trauma induced by a file passing through a sterile,
noninfected pulp tissue, the symptoms subside and healing takes place.
• However, if the insult is continuous and persistent, such as the permanent communication
between bacteria growing in the root canal and the host response in the apical
periodontium, events may take one of two other routes:-
• 1. It may either become more and more symptomatic, a process that may develop into an
acute apical abscess and facial cellulitis.
• 2. Alternatively ,may take a quieter route and gradually become asymptomatic apical
periodontitis, with slight or no symptoms and with typical periapical bone resorption. Factors
that dictate which route will be taken most probably involve the nature of the bacteria.

52. 2. ACUTE ALVEOLAR ABSCESS ( ACUTE APICAL ABSCESS )
• An inflammatory reaction to pulpal infection and necrosis characterized by
rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus
formation and swelling of associated tissues
• Dentoalveolar abscess , acute radicular abscess.
• It is a localized collection of pus in the alveolar bone at root apex of tooth
following death of pulp with extension of infection through the AF.
• ETIOLOGY - Trauma
Chemical irritation
mechanical irritation
bacterial invasion of dead pulp
• SYMPTOMS - 1st symptom - mere tenderness of tooth
- later on , severe, throbbing pain with attendant
swelling of the overlying soft tissue,
- Swelling more pronounced and expands beyond
original site with progression of infection

53. • Tooth becomes painful ,elongated and mobile .
• If left unattended, may progress to chronic apical abscess wherein the contained
pus breaks through to form a sinus tract opening on labial or buccal mucosa.
• Further progress to osteitis , periostitis ,cellulitis or osteomyelitis.
• Swelling is seen in adjacent tissues close to affected tooth.
• Maxillary anterior teeth - swelling of upper lip may extend to eyelids
• maxillary posterior teeth - cheek swelling distorting facial fetures
• mandibular anterior teeth - swelling of lower lip and chin and even neck
• mandibular posterior teeth - swelling of cheek may extend to ear or around border
of jaw into the submaxillary region.
• The tissue at surface of swelling - taut and inflamed. (pus forms beneath it)

54. • Sinus tract formation - beginning of chronic alveolar abscess
• GENERAL SYSTEMIC REACTIONS-
1. pt. is pale, irritable and weakened from lack of sleep and absorption of
septic products.
2. Mild cases - slight rise in temperature (99-100F)
3. Severe cases - high fever (102-103F)
4. Fever with chills
5. Intestinal stasis manifested orally coated tongue and foul breath
6. Headache and malaise
• DIAGNOSIS - Clinical examination
subjective history
radiograph - periapical rarefaction ( if AAA is
exacerbation of long standing CAA), thickened PDL,
BREAKDOWN OF BONE IN ROOT APEX

55. DIFFERENTIAL DIAGNOSIS -
1. Periodontal Abscess
2. Irreversible pulpitis
HISTOLOGY:-
• localized destructive lesion of liquefaction necrosis containing numerous
disintegrating PMN leukocytes, debris, and cell remnants and an accumulation of
purulent exudate.
• Surrounding the abscess is granulomatous tissue;therefore the lesion is best
categorized as an abscess within a granuloma.
• Significantly, the abscess often does not communicate directly with the apical
foramen; thus an abscess often will not drain through an accessed tooth.
• bone resorption - Focal inflammatory immune reaction ,
localized osteoclastogenesis ( RANKL , Macrophage -CSF )
Periodontal Abscess
Acute Alveolar Abscess

56. ACUTE EXACERBATION OF CHRONIC PERIODONTITIS( PHOENIX ABSCESS)
• Acute inflammatory reaction superimposed on an existing chronic apical periodontitis.
• Noxious stimulus from diseased pulp causes acute IR in dormant lesions.
• maybe due to lowering of body defenses or irritation during root canal instrumentation.
• Tooth is tender on palpation.
• lack of response to vitality tests diagnoses a necrotic pulp.
• Differential diagnosis - Acute alveolar abscess
CHRONIC APICAL PERIODONTITIS( ASYMPTOMATIC APICAL PERIODONTITIS)
• Inflammation and destruction of apical periodontium that is of
pulpal origin, appears as an apical radiolucent area, and does not produce clinical
symptoms.
• Also known as periapical granuloma

57. CAUSE -
• Death of the pulp followed by continued mild infection of periapical tissue that
stimulate a productive cellular reaction.
DIFFERENTIAL DIAGNOSIS -
• Cannot be differentiated from other periradicular disease unless tissue is examined
microscopically.
HISTOLOGY-
• Inflammatory lesion dominated by macrophages, lymphocytes, and plasma cells.
• OUTER CAPSULE - fibrous, INNER PORTION - CT ,Blood vessels, fibroblasts
• Epithelial cell proliferation , originate from the epithelial cell rests of Mallasez.
• Foam cells , macrophages containing lipid, cholesterol.
• Cementoclastic activity or hypercementosis.

58. CHRONIC ALVEOLAR ABSCESS
• An inflammatory reaction to pulpal infection and necrosis
characterized by gradual onset, little or no discomfort and
the intermittent discharge of pus through an associated
sinus
tract.
• Source of infection - Root canal
• Clinical features - Asymptomatic , mildly painful
Sinus tract present on face
First sign of osseuos breakdown ,
discoloration of crown
• Histopathologically - Destruction of apical PDL ,
Lymphocytes , PC , fibroblasts -
periphery ; PML - center
• Sinus tracts lined by GRANULATION TISSUE
Sinus tract

59. RADICULAR CYST ( APICAL CYST , PERIAPICAL CYST )
• An odontogenic cyst associated with a tooth with a necrotic pulp that
develops within a periradicular inflammatory lesion; derives its
epithelium from the cell rests of Malassez.
• Slow growing epithelial sac at tooth apex , lines a pathological cavity
in the alveolar bone.
• Lumen filled with proteinaceous fluid.
• Most common - Maxilla (75percent) .
• CAUSE - noxious stimuli - activate cell rests of malassez
Nutritional Deficient theory
Abscess theory
• Periapical pocket cyst - An apical inflammatory cyst containing a
sac-like, epithelium-lined cavity that is open to and continuous with
the root canal. (BAY CYST )
• Periapical true cyst - An apical inflammatory cyst with a distinct
pathologic cavity; completely enclosed in an epithelial lining so that
no communication to the root canal exists

60. • Asymptomatic , tooth may become mobile
• Radiolucency present surrounding tooth apex, larger than a
chronic apical abscess.
• Differential diagnosis - Periapical granuloma
periapical abscess
Normal bone cavity
Globulomaxillary cyst
• Cyst may or may not be infected.
• Histopathologically - Cavity lined by SSE
Immunological cells present in lining
immunoglobulins in cyst fluid.
Cyst surrounded by CT containing lymphocytes ,plasma cells and
PMN'S.
Radicular cyst radiolucency

61. PERSISTENT APICAL PERIODONTITIS
• Post treatment apical periodontitis.
• Extraradicular factors by Nair -
Apical biofilm (periapical plaque )
Actinomycosis infection
Cholesterol crystals
Foreign body reaction to gutta percha
Cellulose granuloma
Periapical scar tissue
• E.faecalis - most consistently reported.
CONDENSING OSTEITIS
• Diffuse radiopaque lesion representing a localized bony
reaction to a low-grade inflammatory stimulus, usually seen at
apex of tooth.
• Usually asymptomatic.

62. • Diagnosis is made by radiographs where localized area of
radiopacity surrounding affected tooth.
• Histopathologically ,dense bone with reduced trabecular borders
lined with osteoblats. Chronic inflammatory cells seen in bone
marrow.
EXTERNAL ROOT RESORPTION
• Resorption initiated in the periodontium and initially affecting the
external surfaces of a tooth; may be further classified as surface,
inflammatory or replacement, or by location as cervical, lateral or
apical; may or may not invade the dental pulp space.
1. External surface resorption - A physiologic process causing small
superficial defects in the cementum and
underlying dentin that undergo repair by deposition of new
cementum.
External surface resorption

63. 2. External inflammatory resorption - An internal or external
pathologic loss of tooth structure and possibly bone, resulting in a
defect; occurs as the result of microbial infection; characterized
radiographically by radiolucent areas along the root.
• infected or necrotic pulp at the apical, lateral, or cervical root
region that can be seen on a radiograph.
3. External replacement resorption (ankylosis )
- A pathologic loss of cementum, dentin and periodontal ligament
with subsequent replacement of such structures by bone,
resulting in fusion of bone and tooth.
• Occurs in cases in which severe trauma has caused
excessive damage to periodontal ligament cells.
• As a result, bone might come into direct contact with the root
surface, leading to the replacement of dental tissue with
bone tissue and ankylosis.
Inflammatory resorption
Replacement resorption

64. • Cause - Periradicular inflammation due to trauma, excessive
forces , granuloma , cyst , tumors, impaction ,systemic diseases
, idiopathic.
• Histologically , cementum resorption replaced by CT to larger
areas of resorption replaced by osseous tissue.
• Scooped out areas.
• Symptoms - ankylosed tooth - immobile - high metallic
percussion sound.
• Diagnosed by concave areas on root surface or blunting of apex.
• Differentiation between external and internal resorption may be
determined by high resolution Illuma CBCT images .
(Kamburoğlu, K., Kurşun, Ş., Yüksel, S., & Öztaş, B. (2011). Observer Ability to
Detect Ex Vivo Simulated Internal or External Cervical Root Resorption. Journal of
Endodontics, 37(2), 168–175. doi:10.1016/j.joen.2010.11.002 )
IOPA radiographs of internal cervical resorption
followed by CBCT Images of same.