The document provides a comprehensive overview of pulp and periapical diseases, including their etiology, classifications, clinical features, treatment options, and histopathological aspects. It covers various conditions such as reversible and irreversible pulpitis, chronic pulpitis, apical periodontitis, and osteomyelitis, detailing their causes and symptoms. Additionally, it discusses diagnostic features like radiographic and histological findings, and outlines treatment protocols for these dental pathologies.

1. PULP & PERIAPICAL DISEASES
Dr NONITHA S

2. CONTENTS
• INTRODUCTION
• ETIOLOGY OF PULP DISEASE
• CLASSIFICATION OF PULP DISEASE
• REVERSIBLE PULPITIS
• ACUTE PULPITIS & CHRONIC PULPITIS
• CHRONIC HYPERPLASTIC PULPITIS
• GANGRENOUS NECROSIS OF PULP
• DISEASES OF PERIAPICAL TISSUE
• ACUTE APICAL PERIODONTITIS
• CHRONIC APICAL PERIODONTITIS
• PERIAPICAL ABSCESS
• OSTEOMYELITIS

3. INTRODUCTION
PULP
• Dental pulp is a delicate connective tissue consisting of
-Tiny blood vessels
- Lymphatics
- Myelinated and
- Unmyelinated nerves
- Undifferentiated connective tissue cells
• provides the tooth’s nutrients.
• Pulpitis is the inflammation of dental pulp tissue

4. ETIOLOGY OF PULP DISEASE
• Physical: - Mechanical
- Thermal
- Electrical
• Chemical
• Bacterial

5. 1. PHYSICAL
A. Mechanical
1) Trauma- a) Accidental b) Iatrogenic dental
procedures
2) Pathologic wear
3) Crack through the body of the tooth
4) Barometric changes

6. B. Thermal
1) Heat during cavity preparation
2) Exothermic heat during setting of cement
3) Conduction of heat and cold through deep
restoration with out a protective base
4) Frictional heat during the polishing of
restoration c)
C. Electrical - Galvanic shock

7. 2. CHEMICAL :
A) Phosphoric acid, acrylic monomer
B) Erosion
3. BACTERIAL
A) Toxins associated with caries
B) Direct invasion of pulp from caries or trauma
C) Anachoresis: Transportation of microbes
through the blood or lymph to an area of
inflammation without pulp exposure.

8. CLASSIFICATION OF PULP DISEASE
PULPITIS: inflammation of the dental pulp,
which can be acute or chronic.
1) Acute
• Reversible
• Irreversible
2) Chronic
• Chronic hyperplastic pulpitis
• internal Resorption

9. 3) Pulp degeneration
calcification
4) Necrosis

10. AERODONTALGIA
• Toothache occurring at low atmospheric
pressure experienced either during flight or
during a test run in a decompression chamber
• Observed in higher altitudes over 5000 feet
• Tooth with chronic pulpitis can be
symptomless at ground level, but it may cause
pain at high altitudes because of reduced
pressure
• Treatment: Lining the cavity with a varnish or
a base of zinc phosphate cement with a sub
base of ZOE cement in deep cavities

11. ACUTE REVERSIBLE PULPITIS
(PULP HYPEREMIA)
• Mild to moderate inflammatory condition of the pulp caused
by noxious stimuli in which the pulp is capable of returning to
the un-inflammed state following removal of the stimuli.
Etiology:
• Trauma
• Thermal changes in large metallic fillings
• Excessive dehydration of the cavity
• Galvanism
• Dental caries

12. Clinical features
• Pain: mild to moderate
• The etiological factor is obvious
Histopathological features
• – Pulp hyperemia (dilation of blood vessels)
• – Exudation
• – Inflammatory cell infiltration (neutrophils)
• – Reactions usually remain localized adjacent to
the cause
Treatment: remove the cause

13. Dilatation of blood vessels
Dentin
Inflammatory cell infiltrate

14. ACUTE IRREVERSIBLE PULPITIS
Etiology
• Acute dental caries
• Pulp exposure
• Severe irritation
Clinical features
• Pain: severe, spontaneous and continuous
• Little response to simple analgesics
• Pain increases when patient lies down

15. Histopathological features:
• Inflammation involves the whole dental pulp
• Vascular dilatation and edema
• Inflammatory (granular cells) infiltration
• Odontoblasts near to the cause are destroyed
• Formation of a minute pulp abscess
• In a few days pulp undergoes liquefaction and
necrosis
Treatment: RCT
Extraction of tooth

16. Dental pulp exhibiting acute
inflammatory infiltrate consisting
predominantly of polymorphonuclear
leukocytes.

17. CHRONIC PULPITIS
Etiology
• previous acute pulpitis
• Chronic dental caries
Clinical features
• Pain: absent or mild to moderate, dull ache
and intermittent.
• Reaction to thermal changes is reduced
compared to acute pulpitis

18. Histopathological features:
• Mononuclear cell inflammatory infiltration-
lymphocytes, plasma cells
• Evidence of fibroblastic activity
• Minute abscess- if exist it is localized by
granulation tissue
Treatment: RCT
Extraction of tooth

19. The dental pulp exhibits an area of fibrosis and chronic
inflammation peripheral to the zone of abscess formation.

20. CHRONIC HYPERPLASTIC PULPITIS PULP
POLYP
• Characterized by the development of granulation
tissue, covered at times with epithelium and resulting
from long standing low grade irritation
Etiology:
• Opened cavity
• Starts as chronic or acute
• Wide apical foramen (children)

21. Clinical features:
• Red pinkish soft nodule protruding into the
cavity
• most commonly in children and young adults
• Relatively insensitive to manipulation
• Most common in deciduous molars & first
permanent molars
• Lesion bleeds profusely upon provocation.

22. • Due to increased blood supply, tissue
resistance & reactivity in young persons leads
to unusual proliferation of pulp.
• Different from gingival polyp (adjacent gingival
tissue may proliferate into carious lesion &
superficially resemble hyperplastic pulpitis.)

23. Histopathological features:
• The polyp surface is covered with stratified squamous
epithelium.
• Epithelium may be derived from gingiva or from freshly
desquamated epithelial cell of mucosa or tongue.
• The polyp consists of granulation tissues
• It contains delicate connective tissue, fibers and blood
vessels
• Mononuclear inflammatory cell infiltration
Treatment:
• Rct or extraction of the teeth

24. Hyperplastic tissue - basically
granulation tissue, consisting
delicate CT fibers & young blood
capillaries with Inflammatory
infiltrates – lymphocytes, plasma
cells & PMNLs.

26. REVERSIBLE PULPITIS
• Mild – moderate
inflammatory condition.
• Nature of pain is mild &
diffuse.
• Brief duration & can be
produce cold stimuli that
elicits the pain mostly, hot,
sweet or sour food may also
initiate the pain.
• Once stimulus is removed,
pain is usually subsides.
• Tooth responds to electric
pulp tester at lower currents.
• Reversible pulpitis if allowed
to progress can led to
irreversible pulpitis.
IRREVERSIBLE PULPITIS
• Sharp, severe, radiating pain
of long duration & varying.
• Pain continues even after
the stimulus is removed.
• Pain may exacerbate with
bending over or lying down.
• It may progress to more
severe pain that is gnawing
or throbbing.
• Increased by stimulus, like
heat & at times relieved by
cold although the cold may
intensify the pain.
• When infection extends into
PDL - apical periodontitis.

27. DISEASES OF
PERIAPICAL TISSUES

29. DISEASES OF
PERIAPICAL TISSUES
• Apical periodontitis
– Acute
– Chronic (periapical granuloma)
• Periapical abscess
• Periapical cyst
• Osteomyelitus

30. APICAL PERIODONTITIS
• Inflammation of PDL around apical portion of root.
• Types: 1.Acute Apical Periodontitis
2.Chronic Apical Periodontitis
• Etiology:
 spread of infection following pulp necrosis,
 occlusal trauma,
 Bitting suddenly on high objects
 Inadvertent endodontic procedures
 Pushing the infected material into apical portion
 Chemical irritation from root canal medicaments

31. ACUTE APICAL PERIODONTITIS
CLINICAL FEATURES:
• Tooth is tender on percussion & pain can be
• severe making closure of the teeth
difficult.Thermal changes does not induce pain.
• Slight extrusion of tooth from socket.
• Cause tenderness on mastication due to
inflammatory edema collected in PDL.
• Due to external pressure, forcing of edema
fluid against already sensitized nerve endings
results in severe pain.

32. RADIOGRAPHIC FEATURES:
• Appear normal except for widening of PDL
space.

33. HISTOLOGIC FEATURES:
• PDL shows signs of inflammation -vascular dilation with
infiltration of PMNs
• Inflammation is transient, if caused by acute trauma.
• If irritant not removed, progress into surrounding bone
resorption.
• Abscess formation may occur if it is associated with bacterial
infection - Acute periapical abscess / Alveolar abscess.
TREATMENT & PROGNOSIS:
• Selective grinding if inflammation is due to occlusal trauma
• RCT
• Extraction & endodontic treatment be done to drain
exudate.

34. CHRONIC APICAL PERIODONTITIS
(PERIAPICAL GRANULOMA)
• Most common sequelae of pulpitis or apical periodontitis.
• If acute (exudative) left untreated turns to chronic
(proliferative).
• Periapical granuloma is localized mass of chronic
granulation tissue formed in response to infection.
• But term is not accurate since it doesn’t shows true
granulomatous inflammation microscopically.
• Presence of lateral or accessory root canals opening on
the lateral surface of the root give rise to lateral
granuloma

35. ETIOLOGY:
• Death of the pulp
• Irritation of the periapical tissue that
stimulates a productive cellular response

36. CLINICAL FEATURES:
• Tooth involved is non vital / slightly tender on
percussion.
• Percussion may produce dull sound instead metallic
due to granulation tissue at apex.
• Mild pain on chewing solid food.
• Tooth may be slightly elongated in socket.
• Sensitivity - due to hyperemia, edema &
inflammation of PDL.
• In many cases, asymptomatic.
• No perforation of bone & oral mucosa forming
fistulous tract unless undergoes acute exacerbation.

37. RADIOGRAPHIC FEATURES:
• Thickening of PDL at root apex.
• As concomoitent bone resorption &
proliferation of granulation tissue appears to
be radiolucent area.
• Thin radiopaque line or zone of sclerotic bone
sometimes seen outlining lesion.
• Long standing lesion may show varying
degrees of root resorption.

38. HISTOLOGIC FEATURES:
• Granulation tissue mass consists proliferating fibroblasts,
endothelial cells & numerous immature blood capillaries
with bone resorption.
• Capillaries lined with swollen endothelial cells.
• Its is relatively homogenous lesion composed of
macrophages, lymphocytes & plasma cells.
• Plasma cells containing Russels body are found
extracellularly.
• Collection of cholesterol clefts, with multinuclear gaint
cells.
• Epithelial rests of Malassez may proliferate in response
to chronic inflammation & may undergo cystification.

40. 1
2
4
3

41. TREATMENT:
• Extraction & RCT with / without apicoetomy.
• If untreated → apical periodontal cyst
formation.

42. RESIDUAL CYST
• Type of inflammatory odontogenic cyst in edentulous alveolar
ridge.
• Occur due to extraction of tooth, leaving periapical pathology
untreated or incomplete removal of periapical granuloma /cyst.
RADIOGRAPHIC FEATURES:
• Round /ovoid radiolucency in alveolar ridge.
• Lumen may show radiopacity - dystrophic calcification
TREATMENT & PROGNOSIS:
• Cyst should curetted & lining should be subjected to
histopathological examination.

43. PERIAPICAL ABSCESS
(DENTO-ALVEOLAR ABSCESS, ALVEOLAR ABSCESS)
• Developed from acute periodontitis /
periapical granuloma.
• Acute exacerbation of chronic lesion leads to
Phoenix Abscess
ETIOLOGY:
• traumatic injury
• pulp necrosis
• irritation of periapical

44. CLINICAL FEATURES:
• Common findings of inflammation- heat, redness,
swelling and pain.
• Tenderness of tooth, which relives after pressure
application.
• Extremely painful -tooth extrudes from socket.
• Systemic manifestations like lymphadenitis & fever may
present when confined to periapical region.
• Rapid extension to adjacent bone marrow spaces
produces acute osteomyelitis or dentoalveolar abscess.
• Chronic abscess generally presents no features, since it
is mild, well circumscribed area of suppuration which
spread from local area.

45. RADIOGRAPHIC FEATURES:
• Slight thickening of PDL space.
• Radiolucent area at apex of root.

46. HISTOLOGIC FEATURES:
• Area of suppuration composed of PMN
leukocytes, lymphocytes, cellular debris,
necrotic materials & bacterial colonies.
• Dilation of blood vessels in PDL & bone
marrow space.
• Marrow space show inflammatory infiltrates.
• Tissue around area show suppuration
containing serous exudate.

48. TREATMENT:
• Drainage of abscess by opening pulp chamber
or extraction.
• Root canal treatment.
• If untreated, causes osteomyelitis, cellulitis &
bacteremia & formation of fistulous tract
opening to oral mucosa.

49. PHOENIX ABSCESS
ACUTE EXACERBATION OF A CHRONIC LESION
• An acute inflammatory reaction superimposed on an
existing chronic lesion such as a cyst or granuloma
ETIOLOGY:
• Periradicular disease
• Bacteria released from root canals during
instrumentation may trigger acute response.
• (Most commonly associated with the initiation of
RCT)
• History of trauma

50. Clinical features:
• Common findings of inflammation- heat,
redness, swelling and pain.
• At onset, tooth is tender to touch.
• As inflammation progresses tooth may be
elevated in its socket and may become sensitive.
• Mucosa over the radicular area appears red and
swollen.
Radiographically,
• well defined periradicular lesion may be present.

51. Histopathologically,
• shows areas of liquefaction necrosis with
disintegrated polymorphonuclear leukocytes
& cellular debris surrounded by macrophages,
lymphocytes, plasma cells in periradicular
tissues.
TREATMENT:
• Drainage and debriment
• Root Canal Treatment

52. OSTEOMYELITIS
• The word “osteomyelitis” originates from the
ancient Greek words osteon (bone) and
muelinos (marrow) and literally means
infection of medullary portion of the bone.
• Inflammation process of the entire bone
including the cortex and the periosteum.

53. Predisposing factors
1. Local factors (decreased vascularity/ vitality of bone)
Trauma
Radiotherapy
Pagets disease
Osteoporosis
Major vessel disease
2. Systemic factors (impaired host defence)
Immune deficiency
chronic alcoholism
Diabetes mellitus
Malnutrition
Extremes of age

54. PATHOGENESIS
Microorganisms may infect bone through one or more
of three basic methods:
1. Hematogenous spread
2. Direct inoculation of microorganisms into bone
3. Contiguous focus of infection

55. CLASSIFICATION
Based on the duration - 2 major groups
1. Acute
2. Chronic
Suppurative osteomyelitis
3. Acute suppurative osteomyelitis
4. Chronic suppurative osteomyelitis
Non suppurative osteomyelitis
5. Chronic focal sclerosing osteomyelitis
6. Chronic diffuse sclerosing osteomyelitis
7. Garres chronic scelrosing osteomyelitis (proliferative
periostitis)

56. ACUTE SUPPURATIVE OSTEOMYELITIS
• Serious sequela of periapical infection that often results
in diffuse spread of infection throughout the medullary
spaces, with subsequent necrosis of variable amount of
bone.
Etiology:
• Poly microbial -Staphylococcus aureus, S. albus,
Porphyromonas, Prevotella, Bacteriodes
• Most common cause : Dental infection
• Other causes : Infection due to fracture of jaw, gun
shot, or hematogenous spread

57. PATHOLOGY
Acute inflammation of marrow tissues
Spread of exudate along the marrow spaces
Thrombosis of vessels due to compression
Necrosis of bone
Necrotic tissues, dead and dying cell, pus from bacteria → fill the
marrow space
Involves cortical bone → Lifting of periosteum causing further necrosis
Finally ,Osteoclastic activity >>>
Sequestrum

58. Clinical features:
• Maxilla : localized ; Mandible : Diffuse and
widespread
• Severe pain
• Trismus
• Paraesthesia of lips in case of mandibular
involvement
• Elevation of temperature
• Regional lymphadenopathy
• Loosening of teeth and exudation of pus from gingiva
• No swelling and redness till periostitis develops

59. Radiographic features:
• No Radiographic evidence until the disease
has developed for atleast one to two weeks
• Trabeculae becomes fuzzy and indistinct
Ill-defined area of radiolucency
of the right body of the mandible
Moth eaten appearance

60. HISTOLOGIC FEATURES:
• Necrotic bone- loss of osteocytes from their lacunae,
• peripheral resorption and bacterial colonization.
• Medullary space→ filled with inflammatory exudates
• The inflammatory cells are chiefly PMNs but may
show
• occasional lymphocytes and plasma cells
• Osteoblasts bordering the bony trabeculae are
destroyed
• Trabeculae may lose their viability and begin to
undergo slow resorption

61. Nonvital bone exhibits loss of the osteocytes from the lacunae.
Peripheral resorption and surrounding inflammatory response also can be
seen

62. Treatment and prognosis
1. Debridement ,
2. Drainage and
3. Drugs [Anti-microbial]
• Sequestrum >> If small, exfoliates through
mucosa
• >> If large, surgical removal
• Untreated cases may proceed to development
of periostitis , soft tissue abscess or cellulitis

63. COMPLICATIONS:
Rare but include:
• Pathological fracture Extensive bone
destruction.
• Chronic osteomyelitis Inadequate
treatment.
• Cellulitis Spread of virulent bacteria.
• Septicemia Immuno-compromised patient

64. CHRONIC OSTEOMYELITIS
• Chronic suppurative
• Chronic diffuse sclerosing
• Chronic focal sclerosing

65. CHRONIC SUPPURATIVE OSTEOMYELITIS
• Inadequately treated acute osteomyelitis
• Rarely- complication of irradiation
• Acute exacerbations of chronic stage may occur
• Fistulous tract may form which open to surface

66. CLINICAL FEATURES:
•  Swelling
•  Pain
•  Sinus formation
•  Purulent discharge
•  Sequestrum formation
•  Tooth loss
•  Pathologic fracture

67. RADIOLOGICAL FEATURE:
•  Patchy, ragged & ill defined radiolucency.
•  Often contains radiopaque sequestra.

68. • HISTOPATHOLOGY:
• Inflammed connective tissue filling inter-
trabecular areas of bone.
• Scattered sequestra.
• Pockets of abscess.
Chronically inflamed and
reactive fibrousconnective tissue
filling the intertrabecular spaces.

69. Treatment:
• Difficulty to manage medically
• Surgical intervention is mandatory
• Antibiotics are same as in acute condition but
are given through IV in high doses

70. CHRONIC FOCAL SCLEROSING OSTEOMYELITIS
( CONDENSING OSTEITIS)
• Unusual reaction of bone to infection
• Bony reaction to low grade peri-apical
infection or unusually strong host defensive
response In some instances- tissue reacts to
the infection by proliferation rather than
destruction.

71. CLINICAL FEATURES:
• Commonly affects young adults and children
• Mandibular molar is affected commonly
• Large carious lesions
• Symptoms : mild pain due to infected pulp

72. RADIOGRAPHIC FEATURES:
• Pathognomic ,well circumscribed radiopaque
mass of sclerotic bone surrounding and
extending below the apex of one or both roots
• PDL space widening.

73. HISTOPATHOLOGIC FEATURES:
• Dense bony trabeculae with little interstitial
marrow tissue.
• Many reversal and resting lines giving
pagetoid appearance.
• If interstitial soft tissue is present , it is
generally fibrotic and infiltrated with small
amount of lymphocytes.
• lacunae appears empty.

74. TREATMENT:
• Root canal treatment
• Extraction

75. CHRONIC DIFFUSE SCLEROSING
OSTEOMYELITIS
• It is the clinical entity characterized by a
nonsuppurative, inflammatory process
associated with recurrent swelling, trismus
and pain.
• Proliferative reaction of bone to a low grade
infection.
• Portal of entry is diffuse periodontal disease.

76. Clinical features:
• it may occur at any age group , no gender
predominance.
• Common in edentulous mandible.
• Insidious in nature, no clinical indications of its
presence.
• Acute exacerbation can result in : vague pain ,
unpleasant taste , mild suppuration , many
times drainage through fistulous tract

77. Radiographic features:
• Cotton wool appearance.
• Indistinct borders because of its diffuse nature.
• Mimic Paget's disease or fibro osseous
proliferation.

78. HISTOLOGIC FEATURES:
• Dense , irregular trabeculae of bone bordered
by active layer of Osteoblasts ; focal
Osteoclastic area may be present
• Mosaic pattern appearance- indicative of
repeated periods of resorption followed by
repair
• Interstitial soft tissue is fibrotic
• Proliferating fibroblasts and occasional small
capillaries as well as small focal collection of
lymphocytes and plasma cells

79. Irregular trabeculae of bone bordered by active layer of Osteoblasts.
Proliferating fibroblasts and occasional small capillaries as well as small focal
collection of lymphocytes and plasma cells

80. Treatment and prognosis:
• Lesion is too extensive to be removed
surgically.
• Sclerotic bone is hypovascular and resistant to
antibiotics.
• Extraction of tooth as a last option utilizing a
surgical approach with removal of liberal
amounts of bone to facilitate extraction and
increase bleeding.
• Antibiotic administration during acute
exacerbation may help.

81. SAPHO syndrome
• It was first described by Chamot et al. in 1987.
• Rare and of unknown etiology.
• In 1994, Kahn et al. (1994) reported three diagnostic
criteria for SAPHO syndrome:
• 1. Multifocal osteomyelitis with or without skin
manifestations.
• 2. Sterile acute or chronic joint inflammation associated
with pustules or psoriasis on the palms and soles, acne, or
hidradenitis.
• 3. Sterile osteitis in the presence of one of the skin
manifestations.

82. CHRONIC OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS
GARRE’S OSTEOMYELITIS
• Garre’s chronic nonsuppurative sclerosing osteitis
• periostitis ossificans
• Garre’s osteomyelitis was first described by Carl
Gaffe in 1893 as
"a focal gross thickening of periosteum with peripheral
reactive bone formation resulting from infection”.
• Non -suppurating type of osteomyelitis, with a
reactive periosteal thickening due to a low-grade
irritation or infection.

83. Clinical features:
• Common : Children and young adults; Mandible
-especially in bicuspids and molars.
• Hard swelling over the jaw, producing facial
asymmetry with little or no pain.
• May develop only due to dental infection but
also from soft tissue infection or cellulitis.

84. RADIOGRAPHIC FEATURE:
• IOPA → reveals an carious tooth opposite the
hard bony mass.
• Occlusal radiograph →focal overgrowth of
bone on the outer surface of the cortex ,which
may be described as duplication of the cortical
layer of bone .

85. HISTOPATHOLOGIC FEATURES:
• Subperiosteal mass is composed of much reactive
new bone and osteoid tissue , with Osteoblasts
bordering trabeculae.
• Trabeculae is perpendicular to cortex and parallel to
each other.
• Connective tissue is fibrous and shows sprinkling of
lymphocytes and plasma cells.

86. TREATMENT:
• Extraction or endodontic treatment of the
teeth.
• No surgical intervention except biopsy to
confirm diagnosis.
• After extraction the jaws undergo remodeling
and facial symmetry is restored.
• Neoperiostitis or new periosteum formation
may occur in certain conditions.

87. CONCLUSION
• Establishment of proper diagnosis is of utmost
importance to carry out the effective clinical
procedure for the benefit of patient .
• Review after the treatment is also to be given
importance.
• 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.

88. REFERENCES
• R Rajendran, B Sivapathasundaram. Shafers textbook of oral
pathology 6th edn.
• Neville ,Damm, Allen, Bouquot. oral and maxillofacial pathology
2nd edn.
• Shear M, Cysts of the Oral and maxillofacial Regions, 4th
Edn.
• Stephane Schwartz, Garre’s osteomyelitis: a case report, The
American Academy of Pedodontics/Vol. 3, No. 3.
• Marc M. Baltensperger, Osteomyelitis of the Jaws.