This document provides an overview of periradicular diseases, including the normal periradicular tissues of cementum, periodontal ligament, and alveolar process. It describes various periradicular pathologies such as acute apical periodontitis, periapical abscess, chronic apical periodontitis, and periapical cyst. Acute apical periodontitis presents as pain and swelling, while chronic apical periodontitis often causes no symptoms. A periapical abscess forms when an acute infection leads to suppuration, and a periapical cyst is a localized pathological sac formation in the periapical region. The document discusses the histopathology, clinical features, diagnosis, and treatment of these

1. Presented by R.Senthil Kumar
PERIRADICULAR DISEASES

2. INTRODUCTION
 Periradicular diseases are the diseases affecting the Periradicular
tissues which comprises of cementum, periodontal ligament &
alveolar process.
 Because of inter-relationship between pulp and Periradicular
tissues, pulpal inflammation can cause inflammatory changes in
periodontal ligament even before the pulp becomes totally necrotic.

3. NORMAL PERIRADICULAR TISSUES
Cementum
Periodontal ligament
Alveolar process

4. CEMENTUM
 Bone like calcified tissue that covers the roots of teeth.
 Derived from mesenchymal cells of dental follicle that differentiate
into cementoblasts. Cementoblasts deposit a matrix – CEMENTOID
that is incrementally calcified and produces two types of cementum
1. acellular cementum
2. cellular cementum

5. ACELLULAR CEMENTUM CELLULAR CEMENTUM
AC
cementocytes

6. Acellular cementum is deposited first against the dentin
forming the cementodentinal junction, it covers the cervical
and middle thirds of the root.
The cellular cementum is usually deposited on the acellular
cementum in the apical third of the root and alternates with
layers of acellular cementum.
The cellular cementum is deposited at a greater rate thereby
entraps cementoblasts in the matrix. These entrapped cells are
called CEMENTOCYTES.
These cementocytes lie in crypts called lacunae, they
communicate to adjacent lacunae through canaliculi, that
serve as pathways of nutrients.
Because cementum is avascular, its nutrients come from the
PDL, as incremental layers of cementum are deposited, the
PDL may be further displaced, and some cementocytes may
die as a result and may leave empty lacunae.

7. Thickness of cementum
at CEJ – 20 to 50 micrometer
at Apical third – 20 to 150 micrometer
Greater thickness at apex is due to continuous deposition of
cementum during eruptive life of tooth to preserve its height
in the occlusal plane.
This continuous deposition also forms the mature apical
foramen and an average deviation of the apical foramen of 0.2
to 0.5mm from the center of the root apex.
The fibers of periodontal ligament occur between
Cementoblasts embedded into the cementum called
SHARPEY’s FIBRES.

8. FUNCTIONS OF CEMENTUM
 Preserve height of tooth in the occlusal plane
 Repair of root fractures & resorption
 Closing of immature roots by apexification procedure
 Protective function – more resistant to resorption than bone
due to its avascular nature
 Sealing of accessory and lateral canals after RCT.

9. PERIODONTAL LIGAMENT
The periodontal ligament is a dense, fibrous connective tissue that
occupies the space between the cementum and the alveolar bone.
COMPOSITION
 Fiber bundles
 Cells
 Ground substance
 Interstitial tissue
 Blood &lymph vessels
 Nerves

10. PRINCIPAL FIBER GROUPS
 A. Trans-septal group
 B. Alveolar crest group
 C. Horizontal group
 D. Oblique group
 E. Apical group
 F. Inter-radicular group
Periodontal fibers are the principal structural components of the
PDL.

11. ACTIVE CELLS OF PERIODONTAL LIGAMENT
1. Fibroblast
2. Cementoblasts
3. Osteoblast
4. Osteoclast
5.Cementoclasts.
OTHER CELLS
6. undifferentiated mesenchymal cells
7. epithelial rests of Malassez
8. mast cells
9. macrophages

12. FUNCTIONS OF PERIODONTAL
LIGAMENT
 Attach the tooth to its alveolar socket
 To suspend the tooth in its socket
 To protect tooth & alveolar socket from masticatory injuries
 To transform vertical masticatory stresses into tension on the
alveolar bone
 Proprioception – which gives information on movement and
position in space. It triggers protective reflex mechanism &
localization of areas of inflammation in the periodontal ligament.

13. ALVEOLAR PROCESS
Alveolar bone proper
bundle bone – SHARPEY’s FIBERS are embedded in it
lamellated bone
Supporting alveolar bone

14. ALVEOLAR BONE PROPER
The alveolar bone proper is the bone that lines the alveolus or the bony
sockets that house the roots of the teeth.
Because the peripheral sharpey’s fibers may be calcified, and because
lamellae are almost indistinct, this bone is thick and has a more
radiopaque appearance in radiographs than cancellous bone or PDL
spaces – called LAMINA DURA.

15. The alveolar bone proper can also be referred to as CRIBRIFORM PLATE.

16. LESIONS OF ENDODONTIC
ORIGIN
 Microbial
• Dental caries
 Trauma
• Accidental
• Instrumentation
• Traumatic occlusion
 Chemical irritation
ETIOLOGY
LESIONS OF
NONENDODONTIC ORIGIN
 Periapical cemental dysplasia
 Cementoblastoma
 Odontogenic cysts
 Central giant cell granuloma

17. PERIAPICAL CYST

18. ACUTE APICAL PERIODONTITIS
Incipient exudative and mild symptomatic inflammatory
reactions
It may be primary or initial if it starts in a healthy
periodontium
It may be secondary or exacerbating response in a
preexisting chronic lesion. This form is also referred to as
periapical flare-up, or phoenix abscess or recrudescent abscess.

19. Clinical features: intense short lived host response such as
• Pain on chewing
• Tooth elevated from socket
• Tenderness to pressure
Radiographic features:
widening of periodontal ligament space
caused by edema with accumulation of
inflammatory exudate in the connective
tissue of apical periodontal ligament

20. HISTOPATHOLOGY CHANGES
Hyperemia, vascular congestion, edema of PDL
Extravasation of neutrophils
chemotaxis
bacterial products(LPS)
complement factor C5a
repair
Radiographical changes: undetectable, since the integrity of
hard tissues has not been disturbed
If some non infectious but irritating agents have induced
inflammation, the lesion may subside and healing occurs.

21. IN CASE OF INFECTION
Hyperemia, vascular congestion, edema of PDL
Extravasation of neutrophils
chemotaxis
bacterial products(LPS)
complement factor C5a
Phagocytosis and release of leulotrienes and prostaglandins
Osteoclast activation

22. When infection is involved, the neutrophils not only kill
the microorganisms but also release leukotrienes &
prostaglandins. LTB4 attracts more neutrophils and
macrophages , and activates osteoclasts and bone
resorption occurs. Neutrophils die in great numbers and
releases enzymes from their “suicide bags”, causing
destruction of extracellular matrices & cells in the “battle
zone” preventing the spread of infection and the battle
becomes a protracted war.
Radiographically periapical widening of
periodontal ligament space is detectable
now.

23. DIAGNOSIS & TREATMENT
 Pain on percussion is classical diagnostic feature
 Pulp may be vital or nonvital
 Radiographic findings
 Treatment consist of determining the cause and releiving symptoms
 In case of nonvital tooth, root canal treatment.

24. PERIAPICAL ABSCESS
 The periapical abscess is an acute or chronic suppurative
process of periapical region
 Acute periapical abscess is an advanced exudative and
severely symptomatic inflammatory response of the periapical
tissues.
 It is caused by steady increase of inflammatory
exudate(edema), leukocyte infiltration, and suppuration.

25. ACUTE APICAL ABSCESS

26. CLINICAL FEATURES
 Tenderness on percussion, extrusion of tooth from socket
 Tooth might be slightly mobile
 Swelling of alveolar mucosa
 Loss of sleep due to pain
 Slight rise in temperature (99 – 100 degree F) in mild cases
 Severe cases it may reach (102 – 103 degree F)

27. DIAGNOSIS
 Clinical features
 Tooth does not respond to EPT , cold test
TREATMENT
 Root canal treatment
 if swelling is extensive , incision and drainage

28. CHRONIC PERIAPICAL ABSCESS
 Longstanding low-grade inflammatory reaction of periapical
connective tissues to pulp irritants
 Characterized by the formation of parulis (gumboil) and an active
pus formation draining through the stoma of a sinus tract.
 It may be sequela of an acute abscess or
may arise from a periapical granuloma.
 The sinus tract is usually lined with
granulomatous tissue but may be lined
with stratified squamous epithelium

29. HISTOPATHOLOGY
 Vascular congestion results in regional anoxia and cell
breakdown(autolysis).
 Neutrophils increase in number , releasing their proteolytic
ferments to form the pus core.
 Intensity of pain increases as pus formation adds to periapical
pressure and the pus seeks a pathway of least resistance through
trabecular spaces.

30.  Unless drainage is established the exudative inflammatory response
may spread diffusely, creating peripheral areas of cellulitis.
Incisors – swelling of lip
Maxillary canines – ala of nose
Maxillary premolars – swelling of eyelid
 The soft vestibular tissues overlying root end
may become inflamed and painful to palpation.
 The more intense pain occurs as the pus
penetrates the outer plate of bone and begin
to raise the periosteum.
 Once the periosteum and mucosa are
ruptured, the pain subscides and will not
return unless the drainage is blocked.

31. DIAGNOSIS
 Discoloration of tooth
 Asymptomatic, or mildly painful
 Presence of sinus tract
 Tooth does not react to electric or thermal pulp tests
 Radiograph with Gutta – percha cone into sinus tract
TREATMENT : root canal treatment

32. PHOENIX ABSCESS
 Diagnosis is based on the acute symptoms plus radiographic
examination, which reveals a large periapical radiolucency.
 An acute periapical exacerbation that arises from a previously
existing chronic lesion as the granulomatous zone becomes infected.
 This is the painful phase of chronic periapical abscess cycle.
 When the sinus tract is blocked with coagulum or proliferating
epithelium over the stoma, drainage ceases, periapical pressure
increases, and the tooth becomes mildly tender to percussion.

33.  The inflammation may now spread to soft tissues adjacent to the
sinus tract stoma.
 The pressure causes the tissues to baloon outward – parulis develops.
 Symptoms, when present, are generally mild and of low intensity.

34. CHRONIC APICAL PERIODONTITIS
 Also known as dental or periapical granuloma.
 Localized mass of granulation tissue formed in periapical
region in response to the infection from the root canals.
 It is the most common of all sequelae of pulpitis or acute
apical periodontitis.

35. CLINICAL FEATURES
 The involved tooth is usually nonvital
 Most of the cases are asymptomatic
 Slightly tender to percussion and may produce a dull sound
 The patient may complain about mild pain on chewing of solid food
 There is usually no perforation of overlying bone and mucosa unless
the lesion undergoes an acute exacerbation (phoenix abscess)

36. Zones of well established granuloma as described by Dr.W.E.FISH
Zone I : zone of necrosis/infection
presence of necrotic pulp in root canal results in the diffusion of toxic material into
the periapex. (antigens, exotoxins, endotoxins, bacterial enzymes, chemotactic factors)
Zone II : zone of contamination or exudative inflammatory zone
the toxicity of the root canal irritants is reduced by the fluid and cellular exudative
activity in this zone. This reduction in toxicity stimulates osteoclastic resorption of
contaminated periapical bone. Radiographic widened apical periodontal space becomes
evident now.
(liquefaction necrosis, PMNs, macrophages)

37. Zone III : zone of irritation or granulomatous zone or proliferative inflammatory zone
the gap is opened in bone surrounding the lesion, will ultimately be filled with
granulomatous tissue to form this zone. Viable microorganisms are absent. (proliferating
fibroblasts, capillary budding, lymphocytes, plasma cells, macrophages, collagen)
Zone IV : zone of stimulation or secondary proliferative zone or zone of encapsulation
at the periphery of granulomatous zone the toxicity of root canal irritants become so diluted
and diminished that the irritants act as a stimulus to fibroblast and osteoblast in that area. A
wall of collagen fibers is laid to encapsulate the granulomatous tissue.

38.  Kronfeld pointed that granuloma is not an environment where bacteria live but one in
which they are destroyed .
 He compared bacteria in root canal (zone I) with an army entrenched “behind high and
inaccessible mountains”
 Apical foramen serving as “mountain passes”
 The exudative and granulomatous tissue represents a mobilized army defending the
“plains”- the periapex from the invaders.
 If only a few invaders enter the plain through the mountain pass, they are destroyed by
defenders (leucocytes)
 A mass attack of invaders results in a major battle, analogous to acute inflammation
(zone II).
 Once complete elimination of invaders is established, the defending army withdraws,
the local destruction created by the battle is repaired (zone III), and the environment
returns to its normal pattern.
K RONFE L D’ S MOUNTAIN PASS CONCE PT

39. GRANULOMATOUS TISSUE
 Healing function – by the new capillaries and young fibroblasts
 Defence function – resistance to infection augmented by presence of
• Lymphocytes
• Plasma cells – antibody synthesis, Russell bodies
• Undifferentiated cells – pluripotent cells
• Histiocytes – scavengers
 Foam cells – macrophages ingested fatty material, releases lipid
material and needles or crystals of cholesterol are found.
 Islands of epithelium may be present

40. Dunlap and Barker described a condition seen in occasional
periapical granulomas and described it as “giant-cell hyalin
angiopathy” – a foreign body type reaction.
This consist of collection of
• Inflammatory cell infiltration
• Collection of foreign body type giant cells
• Presence of ring like structures known as RHUSTON
BODIES, composed of an eosinophilic material
resembling hyalinized collagen.
There may also be seen fragments of foreign material, sometimes
resembling vegetable matter such as legumes, which suggested the
use of the term
“pulse granuloma”

41. RADIOGRAPHIC FEATURES
 Earliest change is thickening of periodontal ligament
at root apex
 As proliferation continues a radiolucent area is seen
attached to the apex with loss of lamina dura
 The term “periapical rarefying osteitis” is used to describe
this appearance of loss of lamina dura and periapical bone.
 The radiolucency may vary in extent. Greater than 1.5cm
in diameter is usually considered to have evolved into a cyst

42.  The periphery appears as a diffuse blending of
radiolucent area with bone – rapidly expanding
 Thin radiopaque line or zone of sclerotic bone may be
seen outlining the lesion – slow progressive one of long
standing that has probably not undergone an acute
exacerbation
 Some degree of root resorption is occasionally observed
RADIOGRAPHIC FEATURES

43. DIAGNOSIS
 Asymptomatic
 Radiographic examination
 Tooth does not respond to thermal or electric pulp tests
 Patient may give a history of pulpalgia that subsided
 Exact diagnosis can be made only by histologic examination
TREATMENT : Root canal therapy

44. PERIAPICAL CYST
 A periapical cyst is a chronic inflammatory response of the periapex that
develops from chronic lesions with pre-existing granulomatous tissue
 It is characterized by central fluid filled epithelium-lined cavity surrounded
by granulomatous tissue and peripheral fibrous encapsulation
 Generally considered as a direct sequel to chronic apical periodontitis,
But not every lesion develops into a cyst.
 Incidence of cysts among apical periodontitis lesion varies from 6%-55%.
Radicular cysts are divided into 2 categories :
• Epithelial lining completely enclosing the cavity – True cyst
• Epithelial lined cavities that are open to root canals – Bay cyst
now it is called as - periapical pocket cyst

45. The process of true cyst formation has been discussed as occuring in
3 stages:
First phase :
the dormant cell rests of malassez are beleived to proliferate,
probably under influence of growth factors released by various cells
in the lesion.
the epithelial cells undergo mitosis and proliferate in all
direction simultaneously; thus a ball of epithelial cells is formed.
Shear compares this to the MORULA STAGE in the early
embryo.
the nutrition source is enhanced by the projection of
chronically inflamed connective tissue into the ball of cells from all
directions.
CYST FORMATION

46. Second phase : the epithelium lined cavity is formed.
nutritional deficiency theory – the central cells of epithelial
have inadequate supply of nutrition and consequently undergo
necrosis and liquefaction degeneration. intercellular fluid
(edema) appears, giving the cells a sponge like characteristics.
A definite central cavity develops
containing degenerating epithelial cells,
infiltrating leukocytes attracted by the
necrotic products.
the space between the cells increase and
soon complete separation of central
epithelial cells occurs.

47. Abscess theory , postulates that the proliferating epithelium
surrounds an abscess formed by tissue necrosis and lysis
because of the inherent nature of epithelial cells to cover
exposed connective tissue surfaces
Third phase : the cyst growth occurs
The cyst wall acts as a semipermeable membrane,
protein in the dead cells in the cyst cavity increases osmotic
pressure, and attracts the fluid from surrounding granulomatous
tissue.
The cyst grows by attracting fluid into cystic lumen as
more and more epithelial cells die and contribute to continued
increase in osmotic pressure of the cystic cavity.
this growth causes pressure on capillaries in the
surrounding connective tissue , producing an ischemia, which
favors cell death and the cycle is repeated.

48. the fact that the apical pocket cyst grows eliminates
osmotic pressure as a potential factor in the development of
cyst.
Recent attention have shifted in favour of finding a
molecular basis for the cystogenesis.
Prostaglandins produced by neutrophils in cystic lumen and
IL-1-beta produced by T-lymphocytes and macrophages in the
extra epithelial areas – can activate osteoclasts , leading to bone
resorption.
the presence of effector molecules MMP-1 and MMP-2
also have been reported in human periapical cysts.

49. Histopathologically, an apical true cyst has four
major components
1. Cyst cavity
2. Epithelial wall
3. Extraepithelial tissue
4. Collagenous capsule
RADIOGRAPHICALLY – periapical raiolucency ,round
or oavl with or without sclerotic boundary will be seen
1
Fluid, necrotic tissue, cholesterol clefts, erythrocytes
Stratified squamous epithelium
Blood vessels , infiltrating cells

50. PERIAPICAL POCKET CYST
 periapical pocket cyst contain an epithelium – lined, pathologic cavity
that is open to the root canal of the affected tooth.
 Initiated by accumulation of neutrophils around apical foramen, in
response to bacteria in the apical root canal.
 Biologically, a pocket cyst constitutes as an extension of infected root
canal space into the periapex.
 an epithelial collar is formed sealing off the infected root canal and
microcystic lumen from the apical milieu and rest of the body

51. PERIAPICAL POCKET CYST
 Microorganisms at the apical foramen attract neutrophilic granulocytes
into the microlumen by chemotaxis
 However , the pouchlike lumen, biologically outside the body milieu,
acts as a “death trap” for externalized neutrophils.
 As the necrotic tissue and microbial products accumulate, the saclike
lumen enlarges to accommodate the debris.
 Periapical pocket cysts have much in common with marginal
periodontal pockets and hence the name, rather than a biologically
meaningless “bay cyst”

52. DIAGNOSIS
 Radiographic examination
 Tooth does not respond to thermal or electric pulp tests
 Previous history of pain
 Exact diagnosis can be made only by histologic examination
TREATMENT :
• resolution of the cyst following root canal therapy occurs in 80 –
98% of cases
• Surgical treatment if a lesion fails to resorb

53. CONDENSING OSTEITIS
 Productive response of periapical bone to a low – grade longstanding
pulpal irritation manifested as an increase in density of periapical bone,
due to osteoblastic hyperactivity
 The bony trabeculae increase in thickness, marrow spaces are
eliminated or reduced to small tags of fibrous tissue
 typically found in young persons around the apices
of mandibular teeth with large carious lesions and
chronically inflamed pulps.

54. RADIOGRAPHIC FEATURES
 Well – circumscribed radiopaque mass of sclerotic
bone surrounding and extending below the apex of
one or both roots.
 Intact lamina dura along entire root length
 periodontal ligament space widening
 The border of the lesion may be smooth and
distinct or appear to blend into the surrounding bone

55. APICAL SCAR
 Apical scar is not an inflammatory lesion, but rather an uncommon
pattern of healing of an apical inflammatory lesion
 It consist of dense collagenous connective tissue in bone at or near the
apex of root with a distinctive radiolucent presentation. It represents a form
of healing associated with root that has been treated surgically.
 Perforation of both facial and lingual osseous cortices is believed to result
in collagenous rather than osseous healing.
 Maxillary lateral incisors are the most frequently affected teeth
 A thorough history will help in diagnosis

56. Periradicular periodontitis
– Acute Periradicular periodontitis
– Chronic Periradicular periodontitis
Periradicular abscess
– Acute Periradicular abscess
– Chronic Periradicular abscess or
Suppurative periradicular periodontitis
COHEN
GROSSMAN
1. Acute periradicular disease
(a) Acute Periradicular periodontitis
(symptomatic apical periodontitis)
• Vital
• Nonvital
(b) Acute alveolar abscess
(c) Acute exacerbation of chronicApical
periodontitis ( phoenix abscess )
2. Chronic periradicular diseases
(a) Chronic apical periodontitis
• Chronic alveolar abscess
• Cystic apical periodontitis
(b) Persistent apical periodontitis
3. Condensing osteitis
4. External root resorption
5. Diseases of periradicular tissues of non-
endodontic origin
CLASSIFICATIN OF PERIRADICULAR DISEASES

58. PNR NAIR CLASSIFICATION

59.  Normal periapical tissues
 Symptomatic apical periodontitis
 Asymptomatic apical periodontitis
 Acute apical abscess
 Chronic apical abscess
 Cellulitis
 Condensing ostietis
 Apical scar
 Ingle’s syndrome – alveolar osteoporosis associated with bruxism
INGLE’S
CLINICAL CLASSIFICATION

60. BIBILOGRAPHY
 Endodontics – INGLE 5th & 6th edition.
 GROSSMAN’S endodontic practice – 12th edition
 Pathways of the pulp – cohen . 9th edition
 Shafer’s textbook of oral pathology. 5th edition
 Endodontic therapy – weine. 5th edition
 Principles N Practice of endodontics WALTON&TORABINEJAD. 3rd edition
 Oral radiology principles add interpretation – White & Goaz 2nd edition
 Caranza’s clinical periodontology – tenth edition