PULP &

PERIAPICAL
DISEASES
 INTRODUCTION
 Dental pulp is the soft connective tissue
located in the central portion of each tooth.
 It has a crown & root portion .
 Pulp is a delicate specialized connective
tissue containing thin walled blood vessels,
nerve & nerve ending enclosed within dentin.
 Development of dental
pulp
 Formation starts in 8th week of IU life in
region of incisor
 1st there is proliferation & and
condensation of mesenchymal element
known as dental papilla
 The epithelial elements proliferate rapidly
& assume a bell shape & enclose future
pulp tissue
1, 3, 4 - enamel organ
1 - internal cells of the enamel organ
(these cells will be ameloblsats)
2 - dental papilla
3 - external cells of the enamel organ
4 - cells forming the main bulk of
the enamel organ (stellate reticulum)
5 - dental follicle
6 - epithelium of oral cavity
Cells of the dental papilla are fibroblast & blood vessel
& appear to be in a delicate reticulum .

The vessel bring nutrition to the rapidly growing organ

Cellular changes result in formation of a hard shell

around the central papilla .

As this occurs the papilla becomes known as dental

pulp .
1 - ameloblasts (former
external cells of the
enamel organ)
2 – enamel
3 - dentine (predentine)
4 - odontoblasts (cells
which covered the top of
dental papilla
5 - dental pulp (former
dental papilla
Dental pulp - functions

 Inductive
 Formation
 Nutritive
 Protective
 Reparative
 In forensic
STRUCTURE OF PULP
 Odontoblast

Defence
Cells cell
Histiocytes
Fibroblast Undifferentiated
mesenchymal
cells
Collagenous

Pulp Fibers
Precollagenous

Vessels

Nerve fibres
Intercellular
substance
Ground
substance
 Dental pulp is loose CT & made up of
combination of cells in extracellular
matrix of fibers in semi-fluid gel
 Contains 75% by wt of water & 25%
organic material
 Matrix made up of polysaccharides &
proteins
 Collagen is predominant extracellular
matrix component comprising 25-32% of
dry weight
 Pulp has a central zone & a
peripheral zone ,which are observed
in both the coronal & radicular pulp .
 Starting at periphery pulp divided into
Odontoblastic zone, central to it Cell-
free zone, cell-rich zone & central
zone
 Central zone contains large arteries,
veins & nerve trunk that enter the
pulp from the apical foramen &
proceed to the coronal pulp chamber
ODONTOBLASTIC
ZONE
 Odontoblasts -
 They are principal cells of pulp
 At the end of histogenesis & morphogenesis
of odontoblast , a clearly defined layer of cells
is present at periphery of dental pulp
 They are tall columnar in crown, become
cuboidal in middle of root & flat spindal shape
near the apex of root
 Nuclei are placed at different levels &
therefore cells appear to be stratified
 Odontoblast is postmitotic cell & cannot
divide; insult or injury will result in the
death of cell
 However subodontoblastic cells can
divide & lay down protective barrier of
tertiary dentin
 Odontoblast layer provides controlled
barrier between pulp & dentine
 Fully differentiated
odontoblast is a polarised
columnar cell with single
long process that extends
into predentin & dentin
within a dentinal tubule
 Cell body approximately
50μm long & 5-10μm in
width
 Nucleus is usually in the
basal half of the cell with
other organelles involved
in dentine synthesis
CELL-FREE ZONE

 Also called zone of Weil, located centrally

to odontoblastic zone
 Although called cell-free zone, it contains
some fibroblasts,mesenchymal cell &
macrophages
 Main constituents is plexus of Raschkow
CELL-RICH ZONE
 Fibroblast
 Greatest in coronal pulp,
abundant in cell-rich zone.
 Produce & maintain the
collagen & ground substance
of pulp.
 Also phagocytose and digest
collagen. Responsible for
collagen turnover in the pulp.
 Synthesize type I & III
collagen.
Undifferentiated (reserve) cells :
 Represent the cell pool from which
connective tissue cells of the pulp are
derived.
 Found in cell rich zone.
 1st cells to divide after injury.
Macrophage :
 Monocytes in the tissue.
 Active in endocytosis & phagocytosis.
 Act as scavengers.
 Process antigen & present it to memory T
cells.
Dendritic cell:
 Accessory cells of the immune
system. Called as antigen presenting
cells.
 Widely distributed in the pulp.
 Central role in the induction of T cell-
dependent immunity
Lymphocyte :
 T8 (suppressor) lymphocytes are
predominant in pulp.
 B lymphocytes are scanty in normal
pulp.
Mast cell :
 Seldom found in normal pulp tissue.
 Routinely found in chronically inflamed
pulps.
fibers
 Principal fibers is Type-1 collagen
 Arranged irregularly except in the
periphery where they aligned parallel to
forming predentin surface
 There is also large amount of Type-3
collagen
 Type-1 contains α1& α2 molecular chains
Type3 contains only α1 chains
 About 56% of pulpal collagen is Type-1
while 41% Type-3
 Collagen forms 3-5% of weight of pulp
 Non-fibrous matrix
 It falls mainly into 2 groups -
1.glycosaminoglycans
2.proteoglycans
 Glycosaminoglycans- All 4 CT GAGs found in dental
pulp ie CS, HS, Darmatan S, Hyaluronan
 CS & DS in small amount 12% & 20% respectively
 This molecule swell when hydrated, which contribute
to high fluid pressure of pulp & this provides
mechanical support but also easy movement of water
soluble molecules & cells
 Hyaluronan is only in unbond to protein & prevents cell
migration
 proteoglycans
Proteogycans
identified in the dental Possible role
pulp

Decorin Binds to type I collagen & transforming growth factor

β

Bigiycan Regulatory effect on collagen fibrinogenesis

Versican Participation in large hydrated proteoglycan

aggregates

Syndecan Attaches cell surface to fibrous collagens & other

matrix protins; binds fibroblast growth factor

Tenascin Can promote or inhibit cell adhesion, guides cell

movements

Fibronectin Cell adhesion to matrix

CENTRAL ZONE
CIRCULATION OF THE PULP
Vascular supply:
 1 or 2 afferent vessels enter the canal
via each apical foramen.
 Branches of inferior alveolar, superior
posterior alveolar, infraorbital artery.
 Metarterioles & precapillaries.
 Extensive branching-
subodontoblastic layer, coronal pulp.
 Extensive shunting system
composed of AV or VV
anastomoses.
 Active after pulp injury &
repair.
 Venules constitute the
efferent side.
 Drains into max vein via
pterygoid Plexus or
anteriorly into facial vein.
 Venules are not innervated;
thus are passive & non
constrictive
 Microvasculature of dental pulp-

Below are the parts of the dental

pulp.
 Subodontoblastic capillaries (SC)
 Terminal arterioles (TA)
 Precapillary sphincters (PC)
 Postcapillary venules (PCV)
 Arteriovenous anastomosis (AVA)
 Lymphatic channels (LC)
 Vascular physiology
Normal :
 Dental pulp is highly vascularised tissue.
 Capillary blood flow in coronal region twice
than in radicular.
 Blood supply regulated by local factors
and sensory & sympathetic nerves.
 Smooth muscles on vessels have alpha &
beta adrenergic receptors.
 Pulpal blood flow greater in peripheral
layer than in central layer.
 Pathologic
 Pulpal injury evokes a biphasic vascular response.
 Initial vasoconstriction followed by vasodilatation
& increased vascular permeability.
 Localized edema associated with leakage from
primary venules occur & local tissue pressure
raises.
 Reduction in regional blood flow & lymph
drainage.
 To compensate, redirection of blood in AV shunts
and the efferent pulp vessels.
 If severe injury, compensation cannot
occur.
 Local ischemia & progressive tissue
destruction results.
 Painful stimuli release substance P &
calcitonin gene related peptide, they
increase vascular permeability and
edema.
NATURE OF INFLAMMATORY RESPONSE IN PULP
Both humoral & cellular responses occurs in the pulp.
Release of chemical mediators
initiate inflammation
Vascular response
Increase in permeability of vessels nearest the site of injury.
Extravasation of fluid in connective tissue spaces ( edema)
elevation in local pressure.
Result of inflammatory process—infiltration of leucocytes
around the dilated vessels.
 mild histologic pulp changes
mild increased in cellularity

Moderate histologic pulp

changes
--increased cellularity
--disruption of odontoblastic
layer
--increased vascularity
Severe type of histologic pulp changes
--Marked cellular infiltration & necrosis
--Odontoblast layer also destroyed
--Predentin missing
Factors that causes Localized blood
flow, odontoblast degeneration, formation
of dead tract dentin
Inflammation
vasodilatation and increased
subodontoblatic capillary
permeability
reduce blood flow and
increase the leakage of
albumin into the tissue
degeneration of localized
odontoblasts and formation of
dead tract dentin
 Results of capillary permeability
An increase in capillary permeability
and filtration results in edema and
increased Thp.

Localized areas of inflammatory

changes with an elevation in Thp in
the low compliant pulp chamber
would collapse adjacent low
pressure venules.

The net effect is reduced blood flow,

producing ischemia, cellular acidosis
and degeneration of the
metabolically active odontoblasts.
Research has documented that
healthy dental pulp can
respond to a localized
inflammation without "self
strangulation" .

 Protective mechanisms
include:
a) increased absorption of
the fluid and albumin by the
non-inflamed
microvasculature,
b) lymphatic channels and
c) redistribution of blood flow
through AVA shunts.
Lymphatics
 Arise as small thin walled vessels in
the coronal region.
 Removal of inflammatory exudates &
transudates as well as cellular debris.
 All drain into regional lymph glands
(submental, submandibular, cervical)
 Differentiated from small venules by-
- presence of discontinuities in vessel
wall.
- absence of RBC in the lumen.
INNERVATION

 Nerve supply follows distribution of

the blood vessels.
 Majority are nonmyelinated & in close
association with blood vessels .
 Many are sympathetic in nature.
 Terminals are on the muscle cells of
larger vessels and function in
vasoconstriction.
 Large myelinated fibers mediate the
sensation of pain.
 Parietal layer of nerves has plexus of
Rashkow.
 Nerve axons from the parietal layer
either terminate at the pulp-predentine
border or in the dentinal tubules.
 Sensory response in the pulp cannot
differentiate between heat, touch,
pressure or chemicals.
 Neuroanatomy
 Sensory nerves supplying the pulp are
mixed.
 Myelinated axons are classified according
to diameter & conduction velocity:
- A δ- 1 to 6 µm, slow conducting myelinated,
numerous.
- A β- 6 to 12 µm , faster conducting
myelinated.
 Stimulation of these fibers result in fast,
sharp pain, localized.
 Nonmyelinated Nociceptive axons or C
fibers most numerous.
 Chiefly in the pulp core.
 Stimulation produces slow, Dull &
diffuse pain.
Pulp testing

 Electric pulp tester delivers a current

sufficient to overcome enamel &
dentine resistance & stimulate
sensory A fibers at the pulp-dentine
border zone.
 Tests activate hydrodynamic forces
which excite intradental A fibers.
 C fibers are not activated.
DISEASES OF PULP
Factors that makes the pulp unique (in inflammatory
process):-
1) Almost totally surrounded by hard tissue (dentin)—
limits the area for expansion.
2) Total lack of collateral circulation- limit its ability to
cope up with bacteria, necrotic tissue& inflammation.
3) Posses –unique cell- odontoblast, & cells that
differentiate into hard tissue secreting cells—form
dentin to protect pulp from injury.
4) Biopsy & direct medication is impossible without
causing necrosis of entire pulp.
5) Pain & sensitivity are the only sign that determine
severity of pulp inflammation.
Etiology of pulpal diseases
Accor. To Grossman’s

 Mechanical
 Thermal
 Electrical
 Chemical
 Bacterial
Classification of Pulp diseases

Main basis of pulp classification can be

 According to duration & inflammation
 Whether it involve total or partial pulp
 According to direct communication with oral
cavity
 Whether it is infected or sterile
 Clinical classification based on symptoms
 Whether it is treatable or untreatable
According to Grossman
1.Pulpitis (inflammation) 2.Pulp degeneration-
1.Reversible Pulpitis a.calcification
a. Symptomatic (acute) b. others
b. Asymptomatic ( chronic) 3.Necrosis
2.Irreversible pulpitis
Acute
a. abnormally responsive to cold
b. abnormally responsive to heat
Chronic
a. asymptomatic with pulp exposure
b. hyperplastic pulpitis
c. internal resorption
ACCORDING TO INGLE
1. INFLAMMATORY CHANGES/
HYPERACTIVE PULPALGIA
a.Hypersensitivity b. Hyperemia-
acute- decreased flow blood
chronic-decreased drainage of venous blood
2.ACUTE PULPALGIA-
a. incipient
b. moderate
c. advanced
3. CHRONIC PULPALGIA-
a. Hyperplastc pulpitis
b. Necrosis of pulp
4. DEGENERATIVE CHANGES-
a. Atrophic changes
b. Calcific pulposis
HISTOLOGIC CLASSIFICATION BY
SELTZER

A.INFLAMMATORY CHANGE
1. Intact pulp with scattered chronic
inflammatory cells
2. Acute pulpitis
3. Chronic total pulpitis with partial necrosis
4.Chronic partial pulpitis( hyperplastic)
5. Pulp necrosis
B.DEGENARATIVE CHANGES
1. Atrophic pulp
 According to Shafer
Pulpitis (inflammation)
 Focal reversible Pulpitis

 Acute Pulpitis or Chronic Pulpitis

a. partial b. subtotal c. total
According to communication with oral cavity
a. open b. closed

 Chronic hyperplastic Pulpitis

 Gangrenous necrosis of pulp

Reversible pulpitis

Pulp hyperemia –
 It is mild to moderate inflammatory condition of
pulp caused by a noxious stimuli in which the pulp
is capable of returning to uninflammed state
following removal of stimuli.
 Symptoms
 Sharp ,shooting ,lancinating pain caused by cold
stimuli, lasting for only moments.
Pain occurs spontaneously .
Pain disappears on removal of stimulus.
Tooth responds to stimulation by electric pulp tester at
lower level of current than that of adjacent normal teeth
Teeth exists usually deep carious lesions or restorations
with defective margins
H/p
 The lesion show predominantly acute
inflammatory cell infiltration & inflammation is
localized at base of involved tubules.
Dilation of pulpal blood vessels with increase in
vascular permeability.
Edema of tissues.
Acute inflammatory cell
infiltration.
 Reparative dentin
formation
 Diagnosis
Pain—sharp—brief duration ceasing when irritant
is removed.
Visual examination-may show caries/traumatic
occlusion & undetected fracture.
Radiographs- normal Pdl and lamina dura depth of
caries or cavity penetration may be evident.
Vitality test- responds to cold.
 Electric pulp test – less current to cause pain

 Prognosis- favorable if irritant is removed early

 Irreversible pulpitis
 It is persistent inflammatory condition of pulp,
symptomatic or asymptomatic caused by noxious stimuli.

 It has both acute and chronic stages in pulp.

 In acute phase usually caused by hot or cold stimulus or

pain occurs spontaneously.

 Pain persist for several min. to hours ,lingering after

removal of stimulus .
Symptoms
 Early stage pain is spontaneous ,sharp ,piercing or shooting.
 Rapid onset of pain which lingers after removal of stimuli.
 Pain exacerbates on lying down or bending due to change in
intrapulpal pressure.
 Pain is often continuous ,Referred pain.
 Later stages pain is severe ,boring, throbbing which increases with
hot stimulus.
 Patient often kept awake at night due to pain.
 Pain is increased by heat & relieved by cold, although continued
cold may intensify the pain.
 Histopathology
 Acute Pulpitis
 The dilated and
engorged capillaries
surrounded by many
neutrophils are classic
microscopic features of
acute inflammation;
therefore, this is acute
pulpitis.
 Acute Pulpitis

 Early in the course of

disease, PMNLs are
confined to localised area &
the remenders of the pulp
tissue appears relatively
normal even at this period,
there may be localised
destruction of pulp tissue &
formation of small abscess
 When such abscesses are
seen on microscopic
examination they are known
as "microabscesses.“
 Chronic Pulpitis
 This section reveals a
"mixed" inflammatory
reaction. The dilated
capillaries and
neutrophils suggest
"acute inflammation,"
while lymphocytes and
fibroblasts suggest
"chronic inflammation."
The lesion is changing
from acute to chronic
inflammation.
 Diagnosis
Visual examination and history
Radiographs
shows extent of caries
periapical area may be normal .
Percussion – tender ( increased intrapulpal pressure)
Vitality test
Thermal test – Responds more readily to cold.
But, inflammation progresses heat intensifies
the response (expansible effect on blood
vessels).

Electric pulp test- Initial stages– less current required.

As tissue becomes necrotic more current
required.
 DIFFERENTIAL DIAGNOSIS OF REVERSIBLE AND
IRREVERSIBLE PULPITIS:

FEATURES REVERSIBLE IRREVERSIBLE

PULPITIS PULPITIS

1) Pain type Sharp and fleeting Intense, continous and

pain, ceases after prolonged
stimulus is removed
2) Stimulus External stimulus No external stimulus

3) Pain at night/ No Yes

postural
4) Referred pain Not usually found Common finding
5) History Any history of recent History of caries,
dental procedures. trauma, extensive
restoration.
6) Percussion/ If due to occlusion If PDL involved
Occlusion percussion test percussion test
positive positive otherwise
normal.
7) Pulp tests
a) EPT Normal response Normal to elevated
response
b) Cold Exaggerated Pain relieved by cold
response occasionally
c) Heat
Normal exaggerated Acute pain
response
8) Color change No Yes
9) Radiograph Caries, defective or Caries, defective
unbased restoration. restorations PDL space
enlargement

10)Treatment Removal of decay, Pulpectomy,

repair of defect, pulpotomy, occlusal
restoration, ZOE adjustment.
dressing, occlusal
adjustment.
 Treatment
 Pulpectomy
 Pulpotomy for posterior tooth as an
emergency procedure
 Extraction of unrestorable tooth

 Prognosis- favorable if pulp is removed

and proper endodontic therapy and
restoration
 PULP ABSCESS (Cornual abscess )

 If the carious process continues to advance towards

the pulp ,local destruction will probably increase in
the pulp.
 When the injury is sufficient great , cause death of
the large number of leukocyte ,pus is formed.
 If the tissue response & vascular supply are good
abscess is walled off locally, by the formation of
fibrous barrier, to form a local pulpal abscess known
as cornual abscess .
 Patient may complaint of pain .
(Slight or intermittent)
 Tooth is hypersensitive to thermal stimuli.
 Respond normally to vitality test.
 mostly seen in pulp horn.
 H/P - It shows a zone of tissue necrosis & dead
leukocyte lying in contact with the tubules involved
by caries .
 This zone is usually roughly hemispherical in form .
 It is surrounded by a zone of heavily infiltrated
tissue showing edema & necrosis .
 Outside the zone is an area of less damage, in
which vessel are dilated ,granulation tissue &
fibrous tissue formation may be found attempting to
wall off the lesion .
 Chronic hyperplastic pulpitis \ pulp polyp
 Definition
 It is a productive pulpal inflammation due to an extensive
carious exposure of young pulp .
 There is a development of granulation tissue, covered by
epithelium and resulting from long standing ,low grade
irritation.
 Nature of pulp response depends on,
- Strength & duration of irritants
- Resistance of pulp
- Extent of tissue affected
 Etiology
Slow, progressive, carious exposure of pulp.
Mechanical irritation and bacterial infection.
For its development a large open cavity, young resistant
pulp, chronic low grade stimulus is necessary.
 Symptoms
 Asymptomatic ,except during mastication when
pressure of food bolus may cause discomfort.
 Bleeds easily on probing, common in deciduous teeth.
 Histopathology
 pulp polyp is a complex of new
capillaries, proliferating growth
of inflammed connective
tissue, fibroblasts &
inflammatory cells
 Sensory nerve elements
almost totally absent near the
surface
 As tissue expands it may
acquire cover of stratified
squamous epithelium
 The tissue in the pulp chamber
transformed in to granulation
tissue.
 Diagnosis
 Seen in children and young adults.
 Pain usually absent.
 Fleshy ,reddish pulpal mass fills most of the pulp chamber or
cavity or extends beyond confines of tooth.
Bleeds easily on probing.
 Vitality tests: The tooth may respond feebly/ not
at all to thermal tests.
 Electric Pulp tests: More current than normal is
required .
 Differential diagnosis-proliferating gingival
tissue
Treatment
complete removal of pulp followed by restoration
 Internal resorption /pink tooth

 Definition
It is an idiopathic slow or fast progressive resorptive
process occurring in the dentin of the pulp chamber
or root canal of teeth.
 Etiology
 Unknown.
 history of trauma.
( either a blow or
restorative procedures.)
 Mechanism of resorption
Pulp inflammation due to infection

Alteration or loss of predentin layer and odontoblast

Undifferentiated mesenchymal cells come in contact

with mineralized dentin

Differentiate into dentinoclast

Resorption results
Symptoms:
Clinically asymptomatic.
In crown reddish area can be seen which is
called pink spot.
This reddish area represents the granulation
tissue showing through the resorbed area of
the crown.
 Histopathology
Osteoclastic activities seen in lacuna, which may be filled
in by osteoid tissue .
Granulation tissue seen.
Multinucleated giant cells or dentinoclast present—
(identical to osteoclasts).
Lost predentin & dentin are replaced by chronic
inflammatory tissue.
Metaplasia of pulp tissue by deposition of hard tissue
looks like a bone or cementum.
 Diagnosis
 Clinically – pink spot seen later.
 Radiaographic changes
radiolucent enlargement of wall of
pulp chamber and
root canal outline is distorted.

 Pulp test-positive if apical pulp is

vital.
 Treatment
 Pulp extirpation
 Root canal treatment
 If root perforation occurs then
seal it with calcium hydroxide
 Prognosis
Best before root perforation.
If root and crown perforation occurs then guarded
depending upon formation of calcific barrier or
access to perforation that permits surgical repair.
 PULP DEGENERATION:
 Degeneration is generally present in the teeth of older people
 The specific types of pulp degeneration are:

CALCIFIC DEGENERATION –in this part of the pulp tissue is

replaced by calcific material .

Types:
1. Dystrophic calcifications ( in dead & degenerated tissue)

2. Diffuse Calcifications( generally observed in root canals)

3. Denticles / Pulp stones ( usually seen in pulp chambers)

 Denticles / Pulp stones
Classification :-
According to location:
1) free
2) embedded
3) Attached
According to structure:
1) true
2) false
PULP DEGENERATION ACCORDING TO
HISTOPATHOLOGICAL DIAGNOSIS IS FOLLOWS:

 1) Atrophic Degeneration
 2) Fibrous Degeneration
 Atrophic degeneration
Seen histopathologicaly in older people.
Fewer spindle shape cells seen.
Intercellular fluid increases.
 collagen fibers/unit area increased leading to fibrosis.
Pulp is less sensitive than normal.
 Fibrous degeneration
Characterized by replacement of
cellular elements by fibrous connective
tissue.
On removal of pulp from the canal such
pulp has a characteristic appearance of
a leathery fiber.

It is asymptomatic condition.

 Pulp necrosis
 Definition
Necrosis is death of pulp. May be partial or total,
depending on extent of pulp tissue involvement.
 Types
Coagulation necrosis – the soluble portion of tissue is
precipitated or is converted into solid material.
Liquefaction necrosis — when proteolytic enzymes
convert the tissue into a softened mass ,a liquid or
amorphous debris .
 Etiology
Can be caused by any noxious insult , injury to pulp such
as bacteria, trauma or chemical irritation .

 Symptoms

Tooth might be asymptomatic.

Discoloration of tooth-- first indication of pulp death.
Dull or opaque appearance of the crown.
 Diagnosis
 Pain: absent in complete necrosis.
History of patient: Past trauma or past H/O of
severe pain lasting for few mins to few hours
followed by sudden and complete cessation of
pain.
Radiographs show large cavity or filling. an approach to
root canal .
Vitality tests ; negative.
-multirooted teeth may show mixed response.
-Teeth with liquefaction necrosis– may show positive
 Histopathology:
necrotic pulp tissues, cellular
debris, microorganisms seen
in pulp cavity.

liquefaction necrosis
(microabscess) in response to
carious exposure
Treatment
Preparation and obturation of root canal

Prognosis
Favorable with proper endodontic therapy
PERIAPICAL
DISEASES
 Diseases of the periradicular tissue
According to Grossman
 Acute periradicular diseases
Acute alveolar abscess
Acute apical periodontitis
a. vital
b. nonvital
 Chronic periradicular diseases
Chronic alveolar abscess
Chronic apical periodontitis( Granuloma)
Radicular Cyst (periapical cyst)
 Chronic periradicular disease with condensation
 Miscellaneous
External root resorption
Periradicular disease of non-odontogenic origin
Diseases of the periapical tissues (Shafer)
Acute apical periodontitis
Chronic apical periodontitis( Granuloma)
Apical periodontal cyst
Residual cyst
Periapical abscess
Osteomyelitis
Sequela of pulpitits
ACUTE APICAL
ABSCESS

ACUTE ALVEOLAR ABSCESS

ACUTE PERIAPICAL ABSCESS
ACUTE RADICULAR ABSCESS
DENTO ALVEOLAR ABSCESS
ACUTE ALVEOLAR ABSCESS

 An acute alveolar abscess is a localized collection

of pus in the alveolar bone at a root apex of the
tooth following death of the pulp .

 It is a continuance of the disease process beginning

in the pulp and progressing to the periradicular
tissue .
 Symptom-
 First symptom may be mere tenderness of the teeth
that may be relieved by continued slight pressure
on the extruded tooth
 Later severe and throbbing pain ,with swelling of
the overlying soft tissues.
 Tooth becomes more painful ,elongated and
mobile .
 Regional lymphadenitis , fever present .
 Chronic periapical abscess
 Chronic periapical abscess present no clinical
feature , well circumscribed area of suppuration that
show little tendency to spread from the local area.
 Radiographically slight thickening of the
periodontal ligament.
 Chronic abscess shows ill defined borders.
 Because of pulp tissue is solidly enclosed ,no
drainage is possible & the infection continues to
extend in the direction of least resistance ,that is
through apical foramen & thereby involves the
periodontal ligament & periradicular bone .
 H/P –
The area of suppuration is composed of
central area of disintegrating PMN
surrounded by leukocyte ,lymphocyte ,
cellular debris ,necrotic
material and bacterial colonies.
There is dilatation of blood vessels in pdl
and marrow of the bone .
Treatment
Drainage & antibiotics
Root canal treatment
 Note the radiolucency at
the apices of the central
and lateral incisors and
that the tooth with the
root canal filling has no
periapical radiolucency.
It is the radiolucent
lesion that gave rise to
the abscess in the labial
vestibule
 Periapical Abscess
 This blood and pus-filled
lesion represents
extension of acute
periapical inflammation
onto a nearby surface.
 There is a "bump" on the
gingiva is a drainage
outlet from periapical
inflammation around this
non-vital mandibular
cuspid; it is known as a
"parulis" or "gum boil."
 ACUTE APICAL PERIODONTITIS
 Acute apical periodontitis is a painful inflammation
of the periodontium as a result of trauma ,irritation,
infection .
Causes –
 Occlusal trauma
 Over filling
 Bacterial infection
Symptom-
 Pain and tenderness of teeth .
 Slightly sore
 Extruded tooth from socket .
Bacteriology - Pulp may be sterile , if periodontitis is
due to a blow , a occlusal trauma , chemical
irritation during endodontic treatment .
Bacteria grow beyond the apical foramen may
irritate the apical periodontal tissue .
 H/P-
 An inflammatory reaction occur in the apical
periodontal ligament .
 The blood vessel are dilated ,PMN are present .
 Serous exudate distends the periodontal ligament
and extrude the tooth slightly .
 Differential diagnosis
Acute alveolar abscess.
 Treatment
 Removal of the cause.
 CHRONIC APICAL PERIODONTITIS
( PERIAPICAL GRANULOMA )
 Chronic apical periodontitis is a low grade infection &
one of the most common of all sequelae of pulpitis .

 If the acute process is left untreated ,it is incompletely

resolved & becomes chronic .

 It is essentially a localized mass of chronic granulation

tissue formed in response to the infection .
 C/F
 Involve nonvital teeth.
 Slightly tender to percussion may produces a dull
sound because of granulation tissue around root
apex .
 Patient may complain about mild pain on biting or
chewing on solid food .
 Tooth feels slightly elongated in its socket .
 Sensitivity is due to hyperemia edema, inflammation
of the apical periodontal ligament.
 Asymptomatic ,there is no perforation of overlying
bone .
 Radiographically –
- Thickening of ligament at root apex seen .
- Granuloma appear as a well circumscribed
radiolucent lesion at the root apex is seen .
 H/P –
 There is proliferation of fibroblast and endothelial
cells and formation of more tiny vascular channel,
with infiltration of chronic inflammatory cells.
 The lesion is consist of macrophages ,lymphocytes
and plasma cells .
 Many of plasma cells contain eosinophilic globules
of gamma globulin( Russell bodies) .
 Macrophages are the hallmark of granulation tissue
 Large number of phagocytes will ingest lipid
material and become collected in groups ,called as
foam cells .
 Deposits of cholesterol as well as hemosiderin
present .
 Multinucleated giant cell of foreign body type also
seen .
 Also the presence of epithelial cells seen.
 Bateriologic features-
Strepooccus viridans ,hemolyticus ,
nonhemolytic stretococci ,Staphylococcus
aureus ,albus E.coli,are seen.

 Treatment
 RCT
 Extraction of hopeless tooth.
 APICAL PERIODONTAL CYST
 RADICULAR CYST
 PERIAPICAL CYST
 ROOT END CYST
 The apical periodontal cyst is the most common
odontogenic cyst .

 It is a true cyst since the lesion consist of a

pathological cavity that is lined by epithelium and
often fluid filled.

 The epithelium lining is derived from the epithelial

rest of malassez which proliferate as a result of
inflammatory stimulus in a preexisting granuloma .
 Epithelium may be derived from –
 Respiratory epithelium of the maxillary sinus when
the periapical region communicates with the sinus
wall.
 Oral epithelium from fistula tract.
 Oral epithelium proliferating apically from a
periodontal pocket .
 Pathogenesis -
 Periodontal cyst exhibit a lumen that is lined by
stratified squamous epithelium, while the wall is
made-up of condensed connective tissue.
 Initial reaction leading to the cyst formation is a
proliferation of epithelial rest in the periapical
area involved by a granuloma .
 Proliferation of epithelium is induced by
keratinocytes growth factors elaborated by
periodontal stromal cells or inflammatory
stimulus.
 Activated T cells in the periapical granulomas
produce lymphokines that may act on the rest of
malassez causing proliferation & altered
differentiation leading to cyst formation .
 This epithelial proliferation follows an irregular
pattern of growth.
 The cyst increases in its size by osmosis local
fibrinolysis & continued epithelial proliferation.
 C/f
 Condition is asymptomatic .
 Seen between the age of 20-60 years.
 More in permanent dentition
 Involve teeth are maxillary anteriors.
 Mostly seen in non vital teeth , deep carious teeth .
 It is a lesion that represents a chronic inflammatory
process & develop over a long period of time .
 Radiographically it is identical to granuloma cyst
may be of greater size than the granuloma.
 H\p-
 Epithelial lining is stratified squamous in type .
 Epithelial thickness is uneven and show
hyperplasia .
 Actual rete peg formation sometimes occurs .
 The epithelial lining many times is discontinuous.
 Rushton body or hyaline body is present .
 These are tiny linear or arc shaped bodies in
lining epithelium that appear amorphous in
structure, eosinophilic in reaction brittle in nature.
 Their frequency of occurrence in cyst lining is 2.6 -
9.5 % cyst .
 Connective tissue composed of parallel bundle of
collagen fibers that often appear compressed .
 Variable number of fibroblasts small blood vessel
also seen.
 A characteristic feature is the almost universal
occurrence of an inflammatory infiltrate in the
connective tissue immediately adjacent to the
epithelium .(lymphocytes ,plasma cells admixed
polymorph).
 Dystrophic calcification & collection of cholesterol
slits with associated multinucleated giant cells are
seen.
 Collection of lipid filled macrophages are present .
 Content of cyst lumen are watery, straw colored,
blood tinged fluid to semisolid material ,with low
concentration of protein ,cholesterol .
 Differential diagnosis
Granuloma
 Treatment
 Curratage
 RCT
 Extraction of hopeless tooth.
 OSTEOMYELITIS

 It is usually defined as inflammation of bone & bone

marrow contents ,changes in calcified tissue are
secondary to inflammation of soft tissue component
of the bone .
Classification

 According to intensity-
a. Acute
b. Subacute
c. Chronic
 According to nature of reaction-
 OSTEOMYELITIS

Acute suppurative Chronic suppurative

Radiation
Hematological Local Suppurative Focal sclerosing
Diffuse sclerosing
Florid osseous dysplasia
Sclerotic cemental masses
Garre’s osteomyelitis

Primary Secondary

Abscess

Granuloma
 Suppurative
1. acute
2. chronic- specific
3. Chronic non-specific
 Sclerosing
1. Focal
2. Diffuse
 Garre’s Osteomyelitis
 Hudson classification
a) Acute form (suppurative or non suppurative)
a) Focus contiguous factor
b) Trauma
c) Odontogenic infection
- Progressive factor
- Haematogenous
b) Chronic form
a) Recurrent multifocal Developing skeleton
b) Garre’s Osteomyelitis
c) Proliferative periostitis
d) Suppurative or Non- suppurative
c) Treatment non proper systemic compromise
- Refractive
- Diffuse Osteomyelitis
- Host parasitic compromise
Staging of Osteomyelitis
Stage I – Medullary OML – It involved medullary bone
without Compact Bone

Stage II – Superficial OML- Less than 2cm of bony defect

without involving cancellous bone

Stage III - Localized OML – Less than 2cm of bony defect

defect does not involve cortices

Stage IV -Diffuse OML - The defect is greater than 2cm

pathological fracture infection & non union of the
fracture.
 ACUTE SUPPURATIVE
OSTEOMYELITIS

 Acute suppurative osteomyelitis of the jaw

is a serious sequela of periapical infection

 That often result in a diffuse spread of

infection throughout the medullary spaces,
with subsequent necrosis of a variable
amount of bone .
 Causes –
 Dental infection.
( periapical infection , granuloma )
 Fracture or surgery.
 Polymicrobial infection .
 Tuberculosis, syphilis, actinomycosis.

 C/F-
 May involve maxilla or mandible.
 In maxilla lesion will be localized
 In mandible lesion will be diffuse.
 Seen at any age .

 Also called as neonatal maxillitis of infants and young

children.
 This osteomyelitis of infants is of hematogenous.

 Patient complaints of severe pain ,trismus parasthesia

of the lips .

 Elevation of temp with regional lymphdenopathy.

 Teeth in the area of involvement are loose sore so
that eating is difficult .
 WBC count is raised .
 Pus may exude from gingival margin.
 Until periostitis develops ,there is no swelling or
reddening of the skin or mucosa .
 Radiographically Individual trabeculae become
fuzzy & indistinct ,involved area shows ill-defined
margins with moth eaten appearance.
 Pathology –
 Infection causes acute inflammation of the marrow
tissue & the resultant inflammatory exudates
spreads through the marrow spaces .
 This lead to compression of blood vessel in the
bone ,leads to thrombosis & obstruction of the blood
flow resulting in necrosis of the bone .
 Liquefaction of the necrotic tissue ,dead & dying
inflammatory cells & bacteria form the pus ,& this
may fill the marrow spaces .
 This suppurative reaction extend through the
cortical bone to involve the periosteum
causing lifting of the periosteum, which further
leads to compromise in the blood supply to
the underlying bone resulting in further
necrosis.
 By osteolytic activity the necrozed bone
known as sequestrum, is separated from the
surrounding vital bone & exfoliate through the
sinus.
 H/P
 The medullary spaces are filled with inflammatory
exudates.
 Inflammatory cells are neutrophils ,plasma cells
,lymphocytes .
 Increased osteoclastic resorption &reduced
osteoblastic activity in bony trabeculae .
 T/t-
Antibiotics
Drainage
Sequestrectomy.
 CHRONIC SUPPURATIVE
OSTEOMYELITIS

 It may develop in inadequately treated acute

osteomyelitis or may arise from a dental infection
without a preceding acute stage .
 Rarely may occur as a complication of radiation
therapy .
 Compare to acute osteomyelitis all sign &
symptoms are milder .
 Acute exacerbations of the chronic stage may
occur periodically & these present all features of
acute suppurative osteomyelitis .

 The suppuration may perforate the bone & overlying

skin or mucosa to form a fistula tract & empty on the
surface .
 C/F –
 Mandible molar area > maxilla
 Pain with variable intensity .
 Swelling of the jaw ,loose teeth &sinus tract are
seen .
 Radiographically appear as radiolucent lesion which
show focal zones of opacification .Lesion may be
very extensive & margin are indistinct .
 H/P
 Sequestrum may be present as evidenced by both
necrotic marrow & necrotic osteocytes.
 Reversal lines reflects the waves of deposition &
resorption of the bone .
 Inflammatory cells are numerous in fibrous marrow &
osteoclastic activity are more prominent .
 CHRONIC FOCAL SCLEROSING
OSTEOMYELITIS
( CONDENSING OSTEITIS ,BONY SCAR)

 It is an focal reaction of bone to infection ;a reaction

to mild bacterial infection entering the bone through
a carious tooth in persons who have the high
degree of tissue resistance & tissue reactivity .
 The tissue react to the infection by proliferation
rather than destruction ,since the infection act as a
stimulus rather than an irritant .
 C/f –
 Most commonly seen in children & young adult .
 Most commonly involved teeth are mandibular 1st
molar ,which present a large carious lesion .
 Asymptomatic condition, Mild pain associated with
an infected pulp.
 Radiographically a well circumscribed radiopaque
mass of sclerotic bone surrounding may have
lucency at the apex of one or both roots .
 PDL space is widened.
 H/P-
- Dense mass of bony
trabeculae with little
interstitial marrow tissue .
-Osteocytic lacunae appear
empty .
-The bony trabeculae exhibit
many reversal & resting
lines giving pagetoid
appearance .
 T/t
Antibiotics
Drainage
 CHRONIC DIFFUSE SCLEROSING
OSTEOMYLITIS

 It is a condition analogous to the focal form of the

disease & represent a proliferative inflammatory
reaction of the bone to a low grade infection.
 Pathosis is grouped under three major categories-
 Diffuse sclerosing osteomyelitis
 Chronic tendoperiostitis
 SAPHO syndrome
 Diffuse sclerosing osteomyelitis

 Mostly seen in middle aged black women .

 It shows no clinical indication of its presence .
 There is an acute exacerbation of the dormant
chronic infection & results in vague pain ,unpleasant
taste & mild suppuration.
 Radiographically a diffuse patchy ,sclerosis of the
bone with ill defined margins .
 This radiopaque lesion may be extensive &
sometimes bilateral .
 H/P-
 Lesion shows dense ,irregular trabeculae of bone ,which
are bordered by an active layer of osteoblasts .
 Focal area of osteoclastic activity are seen .
 The bone show a pronounced mosaic pattern.
 The soft tissue between the individual trabeculae is fibrous
& shows proliferating fibroblast .
 Small capillary as well as small focal collection lymphocytes
& plasma cells .
 Sclerotic mass are composed of dense bone ,with reversal
line.
 T/t
 Antibiotics
 Decortication
 Low dose corticosteroid
 Hyperbaric oxygen therapy
Chronic tendoperiostitis

 It represents a reactive hyperplasia of bone that is

initiated & exacerbated by chronic overuse of the
masticatory muscle , parafunctional muscle habits .
 C/F
 Mean age -40 yr
 No sex predilection.
 Recurrent pain ,swelling of cheek ,trismus .
 Suppuration are not found .
 Cultures are negative ,with the lesions failing
to respond appropriate antibiotics .
 Sclerosis is limited to a single quadrant .
 Relatively radiolucent zones are apparent
within the areas of radiodensity ,but
histopathologic
 Examination reveals only dense bone,
formation of reactive bone ,& relatively few
signs of inflammation .
 H/p –
It shows sclerosis & remodeling of the
cortical & subcortical bone with a resultant
increase in blood volume .
T/t –
Muscular relaxation instruction
Rotation exercise
Occlusal therapy .
MR drugs.
 SAPHO syndrome
 It is a complex clinical presentation includes—
 Synovitis
 Acne
 Pustulosis
 Hyperostosis
 Osteitis
Cause is unknown.It is thought to arise in
genetically predisposed individuals who
develop an autoimmune disturbances
secondary to exposure to Dermatologic bacteria
C/F –
Seen below the age of 60 yrs.
Suffer from chronic multifocal osteomyelitis
that is typically associated with negative
microbiologic cultures& is non responsive
to antibiotic therapy
The osteolytic areas are scattered randomly
within areas of sclerotic bone .
Periosteal new bone formation is common
not related to cortical bone perforation .
 Involvement of multiple sites in anterior
chest wall, sternum, clavicles, ribs.
 In early gnathic lesions diffuse osteolytic
zones are more prominent than sclerosis
the affected bone is enlarged because of
production of periosteal new bone .
 External bone resorption & deformity of
the are characteristic in older lesion.
 H/p
 It shows active bone remodeling rather
than signs of infection ,such as abscess
formation & bone necrosis .

 T/T – Anti-inflammatory drugs

long term antibiotic therapy
Decortication.
 CHRONIC OSTEOMYELITIS WITH
PROLIFERATIVE PERIOSTITIS
 ( GARRES CHRONIC
NONSUPPURATIVE SCLEROSING
OSTEITIS ,PERIOSTITIS OSSIFICANS )
 It is a type of chronic osteomyelitis in which there is
focal thickening of the periosteum with peripheral
reactive bone formation resulting from mild irritation
or infection .

 C/f-
 It is seen in young person before age of 25 yrs .
 Most frequently involved the anterior surface of the
tibia .
 The condition in the jaw occur mainly in the
posterior mandible in the children and young adult .
 Most cases occur in the bicuspid & molar region.
 The maxilla is seldom affected & the reason for this
is not clear .
 The patient usually complaint of
 --a toothache or pain in the jaw.
 -- a bony hard swelling of the outer surface of
the jaw .
 -- with normal appearing overlying skin or
mucosa.
 The reactive periostitis may develop not as a result
of a central dental infection of jaw, that perforates
outward but as a result of an overlying soft tissue
infection or cellulitis, that subsequently involves the
deeper periosteum .
 Radiographically a carious tooth opposite the hard
bony mass .
 Focal overgrowth of bone on the outer surface of
the cortex ,which may be described as duplication
of the cortical layer of bone .
 Centrally mottled, expanded cortex with parallel
opaque layers like onion skin layers.
 H/P –
 Supracortical but subperiosteal mass is composed
of much reactive new bone & osteoid tissue with
osteoblasts bordering many of the trabeculae .
 This trabeculae are oriented perpendicular to cortex
& parallel to each other .
 The connective tissue between the bony trabeculae
is fibrous & shows a diffuse or patchy sprinkling of
lymphocyte & plasma cells.
CHRONIC
OSTEOMYELITIS Most Variable Lucent or antibiotics
infectious pain,drain mottled Sequestre
,swelling ctomy.
CHRONIC
OSTEOMYELITIS Sequela of Seen in Lucent or Tooth
with proliferative tooth lower mottled with removal
periostitis
abscess, molar concentric antibiotics
extraction (children) periosteal
opacity
Diffuse sclerosing Low grade pain,drain Opacification antibiotics
OSTEOMYELITIS
infection,pulpit ,swelling, through out
is,periodontal In jaw
diseases mandible

Focal sclerosing pulpitis asymptom Opaque treat

OSTEOMYELITIS
atic mass at root offending
apex tooth
External root
resorption
 It is a lytic process occurring in the cementum or
cementum & dentin of the roots of teeth.

 Cause – Due to the peri radicular inflammation due

to trauma ,excessive force ,cyst ,central jaw tumors,
replantation of teeth, systemic condition.
 It is a asymptomatic condition .
 When the root is completely resorbed the tooth
become mobile .
 If the external root resorption extend into the crown
it will give the appearance of pink tooth .
 Radiographically resorption appear as concave or
ragged area on root surface or blunting of the root
surface .
 Area of replacement resorption or ankylosis have a
resorb root with no Pdl space & with bone
replacing the defect .
 H/P –
 It is the result of osteoclastic activity on the root
surface of involve teeth .
 Small area of cementum resorption replaced by
connective tissue or repaired by new cementum ,to
large are of resorption replaced by osseous tissue
to scooped out area of resorption replaced by
inflammatory tissue .
 T/t-
 According to cause & amount of resorption
OTHER PERIRADICULAR DISEASES
 In addition to the commonly
encountered periapical granulomas
and cysts of the jaws, there are many
other lesions that may appear at the
apices of teeth.
 These other lesions, which range from
nonodontogenic cysts to
malignancies, must receive due
consideration in the diagnosis of
periapical disease because of their
potential impact on patient treatment
and outcome.
 In distinguishing between periapical
inflammatory disease and periapical
neoplastic disease, a definitive
diagnosis based on clinical and
radiographic parameters can never be
absolute because of the many
overlapping signs and symptoms.
 This makes differential diagnosis for a
periapical lesion as important as it is
for any other lesion of bone or soft
tissue. Unless the clinician is thinking
in broad rather than narrow terms,
serious conditions may go
undiagnosed and untreated for an
inappropriate period of time.
Periapical Diseases Classified
According to Biologic Behavior
1.Inflammatory
 Periapical Granuloma and/or scar
 Periapical cyst
 Periapical Abscess
 Actinomycosis
 scar
2.Benign
 Traumatic bone cyst
 Nasopalatine duct cyst (incisive canal
cyst)
 Langerhans cell disease
 Adenomatoid odontogenic tumor*
 Periapical cemento-osseous
dysplasia*
 Ossifying/cementifying fibroma*
 Vascular malformation
3.Benign Aggressive
 Odontogenic Keratocyst
 Central giant cell granuloma
 Myxoma
 Ameloblastoma
 Calcifying odontogenic cyst*
 Calcifying epithelial odontogenic tumor*
4.Malignant
 Metastatic disease
 Lymphoma/leukemia
 Multiple myeloma
Inflammatory periapical lesions
 A periapical or dental granuloma represents a focus of
granulation tissue and inflammatory cells that have
replaced apical bone.

 Occasionally, when there is cortical perforation by the

inflammatory process, osteogenesis may not occur,
and the lesion remains as a fibrous scar even in the
presence of an adequate root canal filling.

 Also, if there is open communication between the

tooth apex and oral cavity (e.g., through a carious
lesion), the microaerophilic bacterium actinomyces,
found in the oral flora, can colonize in the inflamed
periapical tissues
 This variation of periapical granuloma can result in an
actinomycotic infection of the jaw.
  D/D done by clinical
 Periapical examinations,
Granuloma and/or radiograph & by
scar histopathological
 Periapical cyst examination, mostly
non-vital tooth
 Periapical Abscess

 Actinomycosis  In actinomycosis there

is external sinus with
sulpher granuels
 scar
 In scar pt gives previous
history of dental tt
 Benign & benign aggressive lesions
 A periapical cyst can be defined simply as a
pathologic space lined by epithelium at the
apex of a nonvital tooth.
 The epithelial proliferation can be regarded
as a defense mechanism that protects
surrounding bone from the irritants of the
necrotic dental pulp.
 It is generally agreed that once a periapical
granuloma becomes well-epithelialized,
complete bony healing is unlikely with root
canal therapy alone.
 Whether a partially epithelialized
periapical granuloma can heal following
root canal therapy is still unknown.
 Probably most of the endodontically
treated teeth in which the periapical
lesions persist (approximately 10 percent
to 20 percent of cases) will be related to
cystic change of a periapical granuloma.
 Traumatic bone cyst  Mostly teenagers,
sometimes H/o
trauma
 Nasopalatine duct cyst  Symmetrical swelling
in midpalate,
radiograph
 Mainly in children,
 Langerhans cell disease many bones are
involved, loosening
of teeth in area
affected, gingival
tissue often
inflamed,submucosal
nodule/ ulcers
  In teenager, ant. jaw, females,
 Adenomatoid
crown of impacted tooth
odontogenic tumor*
 Vital teeth, anti. mandible no
 Periapical cemento-
symptoms,middle age
osseous dysplasia*

 3-4th decay, more in mandible,

 Ossifying/cementifyin
well circumscribed,
g fibroma*
continuous growth

 Abnormal bl. Vessel

 Vascular development, poorly
malformation circumscribed, may affect
bone, may produce bruit, grow
with pt.
  May associated with
 Odontogenic
basal nevoid
Keratocyst
syndrome,
aggrasive,2-3 decay,
mand > max,
posterior
 Central giant cell  F>M, <30yr, mand >
granuloma max, anterior region

 Myxoma  10-30yrs, mand=max

 Ameloblastoma  Adult, mandi. molar
region, asymptomatic,
tooth movement or
malocclusion
 No distinctive age,
 Calcifying gender or
odontogenic cyst* location,mainly in
maxilla
 Calcifying epithelial  30-40yrs, mandibular
odontogenic tumor* posterior, peripheral
lesion,
 Malignant lesions of periradicular tissue
- Paresthesia or atypical pain;

- A lesion that appears to have no radiographic

relationship to the apical periodontal ligament
and lamina dura;

- Large lesions and lesions with ill-defined

margins; and

- A lesion-associated tooth that is intact and of

positive or equivocal vitality.
 Metastatic disease  Old age, mandibular
posterior, bone pain, loose
teeth, lip parasthesia, bone
swelling,gingival mass
 Bleeding, fatigue, in
 Lymphoma/leukemia
chronic leukemia
lymphadenopathy,
splenomegaly,boggy
gingiva

 Multiple myeloma  >30yrs,male, pain,

swelling, anemia,
bleeding, punched out
skeletal lesions
 References
 Ten Cate’s Oral Histology-6th edition
 Berkovitz 3rd edition
 Orbans oral histology
 Oral and Maxillofacial Pathology-II Edition-Neville
 Oral Pathology-Clinical Pathologic Correlation-Regezi
 Oral Pathology-Shafers
 Thoma 3rd edition
 Text book of oral &maxillofacial surgery Nilima Malik.
 Endodontic practice 11th edition Grossman
 Dentistry for child & adolescent – Mcdonald,
 How Subodontoblastic
capillary exchange
occurs
 Diffusion of O2 and CO2
between the blood and the
pulpal cells is directly
dependent upon the
concentration gradient
and inversely
proportional to the
diffusion distance.
 Fluid movement across SC
(Subodontoblastic capillaries)
is determined by the
Hydrostatic and Oncotic
pressures of blood vessels.

 The total fluid reabsorbed by

the venules and lymph
equivalent to the fluid filtered
from the blood
 The human dental pulp plays a role in both tooth
formation and maintenance.
 Pulpal inflammation can occur from microbial,
mechanical, or chemical irritants.
 The pulp may be exposed to microorganisms
suddenly due to trauma or more slowly by an
advancing carious lesion.
 The bacteria present in a carious lesion cause
pulpal effects long before they physically invade
the pulp proper.
 Bacterial byproducts, diffusing through the
dentinal tubules into the pulp, cause the local
infiltration of chronic inflammatory cells.
 As bacteria actually invade the pulp, pulpal
inflammation becomes acute with
polymorphonuclear leukocytes the dominant
inflammatory cell.
 Depending upon the severity of the pulpal insult,
the pulp may exhibit a transient inflammation
(reversible pulpitis).
 The local response of the pulpal microvasculature
allows the pulp to avoid self strangulation from the
collapse of apical vessels.
 If pulpal protective mechanisms are overwhelmed,
a irreversible pulpitis will occur which will proceed
to total necrosis. .
Pulpal pathophysiology