Diseases Of Pulp &

Periapical Tissues
Diseases
Of
Dental
Pulp
 Etiology: FACTORS

PHYSICAL INJURY CHEMICAL INJURY MICROBIAL FACTORS

Acute Injury Bacterial invasion by:

Medicaments or
Injury on tooth
materials applied to
Cavity preparation without Dental caries
dentin diffuses
water spray through dentinal Fractured tooth where
Vigorous polishing tubules. exposed pulp
Root planning in PDL therapy Anachoretic infection
Restoration improper due to presence of
insulation bacteria in circulating
blood stream.
Chronic Injury
Attrition -abrasive food & bruxism
Abrasion -abnormal tooth brushing
 Classification Of Pulpitis
1. Acute & Chronic
2. Based on extend
- Partial pulpitis (confined a portion of pulp)
- Subtotal pulpitis

3. i. If inflammatory process confined within a portion:

- Focal /Partial pulpitis
ii. If most of pulp diseased:-Total /Generalized pulpitis

4. Another classification of acute & chronic based on

presence or absence of direct communication between
pulp & oral environment:
- Open pulpitis (pulpitis aperta) communicated exist.
- Closed pulpitis (pulpitis clausa) no communication exist.
 Focal Reversible Pulpitis (Pulp Hyperemia)
Mild, transient, localized inflammatory response.

CLINICAL FEATURES:
Tooth is sensitive to thermal changes, especially cold.
Pain - short duration, disappears on withdrawal of thermal
irritant.
Affected tooth responds to stimulation of electric pulp tester at
lower level of current indicating low pain threshold.
Teeth usually show deep caries, metallic restoration with
defective margins.
HISTOLOGICAL FEATURES:
Dilation of pulp blood vessels.
Edema fluid collection due to damage of vessel wall & allowing
extravasations of RBC or diapedesis of WBC.
Slowing of blood flow & hemoconcentration due to
transudation can cause thrombosis.
Reparative or reactionary dentin in adjacent dentinal wall.
TREATMENT & PROGNOSIS:
Carious lesion should be excised & restored or defective filling
is replaced.
If primary cause is not corrected, extensive pulpitis may result
in death of pulp.
 Dentin

Dilation of blood vessels

Inflammatory cell infiltrate

 Acute Pulpitis
Irreversible condition characterized by acute, intense
inflammatory response in pulp.
Sequela of focal reversible pulpitis.
Acute exacerabation of chronic inflammatory
response.
CLINICAL FEATURES:
Teeth extremely sensitive to thermal changes.
Hot or cold stimuli cause increase in pain intensity &
persists.
Pain persists even after the removal of stimulus.
 Pain - poorly localized.
Intrapulpal abscess formation cause severe
pain lancinating or throbbing type. (10
15mins)
Intensity of pain can increase when patient
lies down.
Acute pulpitis with
Intrapulpal abscess
Pulp vitality test indicats increased sensitivity at low level
of current.
Pulpal pain is due to:
- pressure built up due to lack of exudate escape.
- pain producing substances from inflammation.
Pain subsides when drainage is established or when pulp
undergoes complete necrosis.
The tooth is not tendered to percussion unless the pulpal
inflammation has spread beyond the root apex into the
periapical region.
HISTOLOGIC FEATURES:
Edema in pulp with vasodilation.
Infiltration of polymorphonuclear leukocytes along
vascular channels & migrate through endothelium lined
structures.
Destruction of odontoblasts at pulp dentin border.
Rise in pressure due to inflammatory exudate local
collapse of venous part of circulation Tissue hypoxia
& anoxia Destruction of pulp & abscess formation.
Abscess consists pus, leukocytes & bacteria.
Numerous abscess formation cause pulp liquefaction &
necrosis. (acute suppurative pulpitis)
TREATMENT & PROGNOSIS:
Drainage of exudate from pulp chamber.
Pulpotomy & placing calcium hydroxide over entrance of
root canal.
Root canal treatment.
Extraction of tooth.
 Chronic Pulpitis
Persistent inflammatory reaction in pulp with little or non
constitutional symptoms.
CLINICAL FEATURES:
Pain is not prominent feature
But if it is present it may be mild, dull ache which is
intermittent.
Reaction to thermal changes is reduced in comparison to
acute counterpart because of degeneration of nerves.
Response to pulp vitality tester is reduced.
 Wide open carious lesion & with exposure of pulp
cause relatively little pain.
Manipulation with small instruments often elicits
bleeding but with little pain.
Selzer and his associates emphasized that
in chronic type the pulp is mostly
necrosed without pain.
HISTOLOGIC FEATURES:
Infiltration of mononuclear cells, chiefly lymphocytes &
plasma cells, with vigorous connective tissue reaction.
Capillaries are prominent; fibroblastic activity & collagen
fibers in bundles.
 Tissue reaction may resemble the granulation
tissue.
When this occurs on the surface of the pulp
tissue in a wide open exposure, the term
ulcerative pulpitis is used.
If pulpal reaction vacillates between an acute & chronic
phase causes pulp abscess formation, which is
surrounded by fibrous CT wall, which is called Pyogenic
Memberane
TREATMENT & PROGNOSIS:
Root canal therapy
Extraction of tooth.
The dental pulp exhibits an area of fibrosis and chronic
inflammation peripheral to the zone of abscess formation.
Chronic Hyperplastic Pulpitis (pulp polyp)
Overgrowth of pulp tissue outside the boundary of pulp
chamber as protruding mass.
CLINICAL FEATURES:
Children & young adults with high degree of tissue
resistance & reactivity & responds to proliferative lesions.
Pulp - pinkish red globule of tissue protruding from
chamber & extend beyond caries.
Most commonly affected are deciduous molar & Ist
permanent molars.
Pulp is relatively insensitive because of presence of only
few nerves.
 Lesion bleeds profusely upon provocation.
Due to excellent blood supply high tissue resistance &
reactivity in young persons leads to unusual proliferative
property of pulp.
Some cases, gingival tissue adjacent, may proliferate into
carious lesion & superficially resemble hyperplastic
pulpitis.
- So careful examination is made to determine
whether connection is with pulp or gingiva.
HISTOLOGIC FEATURES:
Hyperplastic tissue is basically granulation tissue,
consisting delicate CT fibers & young blood capillaries.
Inflammatory infiltrates lymphocytes, plasma cells &
 Stratified sq. epithelium covering
polyp

Granulation tissue

Carious tooth

Pulpal tissue
 Stratified squamous type epithelial lining resembles oral
mucosa with well formed rete pegs.
Grafted epithelial cells are believed to be desquamated
epith. Cells, which carried by saliva.
Origin of these cells is unknown. They are degenerated
superficial squames, which ve lost dividing capacity.
When pulp polyp is present for a long time, persistent
rubbing of buccal mucosa may help in grafting of epith.
cells.

TREATMENT & PROGNOSIS:

Extraction of tooth or pulp extripation.
Gangrenous Necrosis of Pulp
Untreated pulpitis results complete necrosis of
pulp.
As this is associated with bacterial infection pulp
gangrene.
It is associated with foul odor when pulp is opened for
endodontic treatment.
In sickle cell anemia, blockage of pulp vessels be defective
RBC results pulp necrosis.
Non vital pulp maintain general histology being non
purulent.
This may be due to trauma or infarct.
Necrosis of pulp
 REVERSIBLE PULPITIS
Mild moderate inflammatory
condition.
Nature of pain is mild & diffuse.
Brief duration & can be produce
cold stimuli that elicits the pain
mostly, although 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
intensity.
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.
Diseases
Of
Periapic
al
Tissues
 Pulpitis

Acute chronic

Apical periodontitis
Acute chronic

Periapical abscess Periapical granuloma

Acute chronic

Periodontal cyst

Osteomyelitis
Acute chronic

Focal Diffuse

Periosteitis

Cellulitis Abscess
Apical Periodontitis
Inflammation of PDL around apical portion of root.
Cause: spread of infection following pulp necrosis, occlusal
trauma, inadvertent endodontic procedures etc.
Types: 1.Acute Apical Periodontitis
2.Chronic Apical Periodontitis
 Acute Apical Periodontitis
CLINICAL FEATURES:
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.

RADIOGRAPHIC FEATURES:

Appear normal except for widening of PDL space.

HISTOLOGIC FEATURES:
PDL shows signs of inflammation -vascular dilation
-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 due to occlusal trauma.
Extraction & endodontic treatment be done to drain
 Chronic Apical Periodontitis
(Periapical Granuloma)
Most common sequelae of pulpitis or apical periodontitis.
If acute (exudative) left untreated chronic (proliferative).
Periapical granuloma is localized mass of chronic granulation
tissue formed in response to infection.
But term is not accurate since it doesnt shows true
granulomatous inflammation microscopically.
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 on solid food.
Tooth may be slightly elongated in socket.
Sensitivity is due to hyperemia, edema & inflammation of
PDL.
Fully developed granuloma seldom presents more severe
clinical symptoms.
In many cases, asymptomatic.
No perforation of bone & oral mucosa forming fistulous tract
unless undergoes acute exacerbation.
RADIOGRAPHIC FEATURES:
Thickening of PDL at root apex.
As proliferation of granulation tissue and concomitent bone
resorption continues, periapical area appears to be
 Thin radiopaque line or zone of sclerotic bone sometimes
seen outlining lesion.
Long standing lesion may show varying degrees of root
resorption.
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.
Lymphocytes produces IgG, IgA, IgM & IgE modulators
of disease activity.
 Plasma cells containing Russels body are found
extracellularly.
T lymphocytes produce cytotoxic lymphokines, collagenase &
other enzymes & destructive lymphokines, they are
responsible for destructive potential of periapical lesion.
Collection of cholesterol clefts, with multinuclear gaint cells.
Epithelial rests of Malassez may proliferate in response to
chronic inflammation & may undergo cystification.
Bacteriologic Features:
Strep. viridans, strep. Hemolyticus, non hemolytic strep,
staph. aureus, staph. Albus, E coli & pnemococci are isolated
from lesion.
TREATMENT & PROGNOSIS:
Extraction & RCT with / without apicoetomy.
Periapical Granuloma

Root Apex

Granulation Tissue
 Residual Cyst
Type of inflammatory odont. 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.
 Periapical Abscess
(Dento-Alveolar abscess, Alveolar Abscess)
Developed from acute periodontitis / periapical granuloma.
Acute exacerbation of chronic lesion Phoenix Abscess
Cause due to pulp infection, traumatic injury pulp
necrosis, irritation of periapical tissues ( endo procedures).
CLINICAL FEATURES:
Features of acute inflammation.
Tenderness of tooth, which relives after pressure
application.
Extreme painful tooth extrude from socket.
Systemic manifestations like lymphadenitis & fever may
present.
Periapical abscess
 Extension to bone marrow spaces produce osteomyelitis, but
clinically considered as Dento-Alveolar abscess swelling of
tissues.
Chronic abscess generally presents no features, since it is
mild, well circumscribed area of suppuration which spread
from local area.
RADIOGRAPHIC FEATURES:
Slight thickening of PDL space.
Radiolucent area at apex of root.
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.
 Inflammatory infiltrate, cellular
debris, necrotic materials etc..

Periapical abscess
 Marrow space show inflammatory infiltrates.
Tissue around area show suppuration containing serous
exudate.
TREATMENT & PROGNOSIS:
Drainage of abscess by opening pulp chamber or extraction.
RCT.
If untreated, causes osteomyelitis, cellulites & bacteremia &
formation of fistulous tract opening to oral mucosa.
Cavernous sinus thrombosis has been reported.
 Osteomyelitis
Inflammation of bone & marrow contents.
Secondary changes due to inflammation of soft tissue content
of bone.
Predisposing Factors:
- trauma, accidents, gunshot wounds, radiation damage,
Pagets disease & osteoporosis.
- systemic conditions like malnutrition, acute leukemia,
uncontrolled DM, sickle cell anemia & chronic alcoholism.

Types: 1. Acute suppurative osteomyelitis

2. Chronic suppurative osteomyelitis:
i. Chronic Focal Sclerosing Osteomyelitis
ii. Chronic Diffuse Sclerosing Osteomyelitis
 Acute osteomyelitis Chronic Osteomyelitis
Serious sequelae of Develops from
periapical infection, resultsuntreated, acute osteo.
in spread into medullary Or arise from dental
spaces with necrosis of infection without
bone. preceeding acute stage.
CLINICAL FEATURES
Acute & subacute osteo. Clinical features are similar to
involve either acute, except that Signs &
maxilla/mandible. symptoms are milder, with
less pain.
In maxilla, lesion remains well
localized whereas in mandible, Acute exacerbations may
bone involvement is diffuse. occur periodically and present
al features of acute osteo.
Some osteo. refered as
neonatal maxillitis in infants
 Infants seriously ill & may
not survive disease. Pain is less severe.

Adults - severe pain, trismus Temperature still elevated, but

& parasthesia of lips in mand. mild.
& elevated temperature with Leucocytes slightly greater
regional lymphadenopathy. than normal.
WBC count elevated. Teeth may not be loose & sore,
Teeth involved is loose and so mastication is possible even
sore, eating difficult. though jaw may not be
perfectly comfortable.
Pus exudates from gingival
margins. Suppuration may perforate
bone & overlying skin or
Until periostitis, no swelling or mucosa to form fistulous tract
no reddening on skin /mucosa. & empty on surface.
 RADIOGRAPHIC FEATURES
Progress rapidly and Evidence Single /multiple radiolucencies.
demonstrated until disease
developed for 1-2weeks. Lamina dura less apparent,
blends with surrounding
Loss of continuity of lamina granular sclerotic bone.
dura.
Trabeculae - fuzzy, indistinct
Root resorption.
& radiolucent.
Irregular margins.
Saucer shaped margins.
Moth eaten appearance.
 Acute Osteomyelitis:
Ill defined area of radiolucency
of right body of mandible.

Chronic Osteomyelitis:
Ill defined area of radiolucency
of right body of mandible on
extracton site.
 HISTOLOGIC FEATURES
Inflam. Exudate in medullary Chronic inflam. Reaction in
spaces. bone - exudate & pus
Inflam. Cells neutrophillic accumulation in medullary
PMnuclear leucocytes, occasional spaces.
lymphocytes & plasma cells. Lymphocytes, plasma cells &
Destroyed osteoblasts lining macrophages.
bony trabeculae. Osteoblastic & osteoclastic
Depending duration of process activity occur parallely with
trabeculae loss viability & irregular bony trabeculae
undergo slow resorption. formation with reversal lines.
Later stages - Sequestrum
may develop
 Acute Osteomyelitis
Nonvital bone shows absence
of osteocytes in lacunae.
Peripheral resorption,
bacterial colonisation &
inflam. Response.

Chronic Osteomyelitis
Chronic inflamation &
reactive fibrous CT
filling intertrabecular
spaces.
TREATMENT & PROGNOSIS:
Drainage, debridement & antimicrobial therapy.
When intensity of disease attenuated sequestrum seperates
from living bone .
If sequestrum is small, it gradually exfoliates through
mucosa.
If large surgical removal necessary since natural process
of bone resorption would be extremely slow.
Unless proper treatment done, Acute SO may preceed to
develop periosteitis, soft tissue abscess /cellulitis.
 Chr.Focal Sclerosing O Chr.Diffuse Sclerosing O
A reaction to mild bacterial Proliferative reaction of bone
infection entering bone to low grade infection. Entry
through carious tooth in of infection is not due to
persons having higher degree carious lesion but Due to
of tissue resistance & tissue diffuse periodontal disease.
reactivity. Tissue reacts to
Insidious in nature, presents
infection by proliferation
no clinical indications of
rather than destruction.
presence.
CLINICAL FEATURES
Commonly in children & Common in older, with
young adults & rarely old age. edentulous mandibular jaw.
Common tooth: mand Ist On exacerbation: vague pain,
molar presenting large carious unpleasant taste & mild
lesion. suppuration many times with
fistula formation opening to
No other signs & symptoms of
mucosa & drains.
 RADIOGRAPHIC FEATURES
Well circumscribes radiopaque Cotton wool appearance.
mass of sclerotic bone extending
radiopaque lesions extensives
below apex on roots.
and Sometimes bilateral.
Root outline nearly visible with
intact lamina dura. Occasional Bilateral
involvement in both maxilla &
PDL space widened & is mandible in same patient.
important to distinguish
cementoblastoma. Border between sclerosis &
normal bone is indistinct.
Lesion border: abutting normal
bone, may smooth & distinct or Pattern may actually mimic
appear to blend into surrounding Pagets disease or cemento
bone in contrast to focal cemento osseus dysplasia.
osseus dysplasia which has
radiolucent border.
Radiopacity stands out indistinct,
contrast to trabeculation of
normal bone
 Focal sclerosing osteomyelitis

Diffuse sclerosing osteomyelitis

 HISTOLOGIC FEATURES
Dense mass of bony trabeculae
with little interstitial marrow
tissue.
Osteocytic lacunae is empty.
Trabeculae show reversal &
resting lines giving Pagetoid
appearance.
If interstitial soft tissue present
fibrotic & inflitrate of few
lymphocytes .
Osteoblastic activity ve
completely subsided.
Dense irregular trabeculae,
some borderd by active layer of
osteoblasts.
Focal areas of osteoclastic
activity seen.
Mosaic pattern, indicates
periodic resorption followed by
repair.
Soft tissue in between trabeculae
fibrous & show proliferating
fibroblast, capillaries with
lymphocytes & plasma cells.
PMN leucocytes present, if
lesion is in acute phase.
Sometimes, inflam. component
is completely burned out,
 Focal sclerosing osteomyelitis

Diffuse sclerosing osteomyelitis

 TREATMENT & PROGNOSIS
Endodontic treatment Surgical removal
Extraction If tooth is present, must
Surgical removal of sclerotic extracted.
lesion is not indicated unless Sometimes sclerosed bone will
symptomatic. remain after resolution &
remodeling is needed.
Apical Periodontal Cyst
(Radicular Cyst, Periapical Cyst, Root End Cyst)
Common odontogenic cyst encountered.
True cyst, since consits of pathological cavity lined by
epithelium &fluid filled.
Epithelium for cyst may be derived from:
-respiratory epith. (communicating with maxillary sinus)
-oral epith. from fibrous tract
-oral epith proliferating apically from PDL pocket
Etiopathogenisis
Caries, trauma, periodontal disease

Pulp death

Apical bone inflammation

Granuloma formation

Stimulation, then proliferation of

epithelial cell rests of Malassez

Cystification
CLINICAL FEATURES:
Most cases are Assymptomatic
Age: commonly 20-60 yrs, involvement of decidous teeth is more
common.
Most Commonly involved tooth are maxillary anteriors.
Non vital tooth/deep caries/restoration which is painful or
sensitive on percussion.
In some cases, cyst may undergo acute exacerbation &
develop abscess that may proceed to cellulitis/ fistula.
RADIOGRAPHIC FEATURES:
Radolucency round/ ovoid with a narrow opaque margin which is
continuous with lamina dura.
In long standing cyst bone resorption of affected teeth & occasional
resorption of adj. teeth may be seen.
HISTOPATHOLOGY
Lined by non keratinized stratified sq epith.
Newly formed cyst - Epith lining thickness is uneven, due to
hyperplasia
In established cyst lining thickness is even.
Presence of Mucous secreting goblest cells in cyst lining.
Transmigration of inflam. Infiltrate through epithelium.
Supporting CT focally/diffusely infiltrated with a mixed inflam. Cell
population.
Foci of dystrophic calcification, cholestrol clefts & multinucleated
foreign body giant cell seen on cyst wall.
Rushton bodies are found in cyst lining or CT.
Russels bodies (plasma cell surrounded by immunoglobulin) seen.
 Cyst lumen consist of watery, straw colored, blood tinged fluid to semi
fluid materials, with low conc. Of protien.
TREATMENT & PROGNOSIS:
Extraction & curettage of apical zone.
RCT with apicoectomy.
Surgery
Does not recur if surgical removal is thorough.
If left untreated slowly increase in size & undergo bone resorption
but seldom there is a remarkable compensating expansion of cortical
plates.
Apical periodontal
cyst
 Sclerotic Cemental Masses
Benign fibro-osseous jaw lesions of unknown etiology, occurring
predominantly in middle-aged black females; lesions present as large
painless radiopaque masses usually involving several quadrants of the jaw
CLINICAL FEATURES:
Just same as in Diffuse sclerosing osteomyelitis present with
multiple symmetric lesion, pain, drainage & localized expansion.
RADIOGRAPHIC FEATURES:
Same as in DSO - Lesions appear as multiple sclerotic masses, located in
two or more quadrants, usually in the tooth-bearing regions.
HISTOLOGIC FEATURES:
Differences:
Cemental masses instead of sclerotic bone
Cementum large solid masses with smooth, lobulated margins, with
globular accretion pattern.
 Florid Osseus Dysplasia
Another disease similar to DSO & Sclerotic cemental masses;
described by Melrose & his associates.
characterized by lesions in upper/ lower jaw that occur when normal
bone is replaced with a mix of CT and abnormal bone. It affect middle
age Black and Asian women .
Cause obstruction of normal interstitial fluid by fibro osseus
proliferation.
RADIOGRAPHIC FEATURES:
FOD appears as well-defined mixed (radiolucent-radiopaque) or totally
radiopaque & has a radiolucent periphery & surrounding sclerosing
border similar to Periapical Cemental Dysplasia.
cotton wool appearance or large amorphous regions of calcifications.
TREATMENT:
Usually no treatment necessary.
 Chronic Osteomyelitis with Proliferative
Periosteitis
(Garres Chronic nonsuppurative sclerosing osteitis, periosteitis
ossificans)
A distinctive type of osteomyelitis with focal gross thickening of
periosteum, & peripheral reactive bone formation resulting
from mild infection or irritation.
It is essentially a periosteal osteosclerosis analogous to chronic
focal endosteal sclerosis & diffuse sclerosing osteomyelitis.
CLINICAL FEATURES:
young age <25yrs, mostly involve anterior of tibia.
Greater opportunity for infection enter maxilla & mandible,
due to peculiar anatomic arrangement of teeth.
 Cases in jaws; occurs in mandible bicuspid & molar region -
children & young adults.
Maxilla is seldom affected, reason not clear.
Toothache or jaw pain & bony hard swelling on outer surface of
jaw usually for several weeks duration.
Due to overlying soft tissue infection/ cellulitis that involves
periosteum cause reactive periosteitis.
RADIOGRAPHIC FEATURES:
Reveals a carious tooth opp: to hard bony mass.
Occlusal radiograph: focal overgrowth of bone on outer surface
of cortex, which described as duplication of cortical layer.
Mass is smooth & well calcified & may show thin but definite
cortical layer.
 CT scan of
new
proliferative
periosteitis
with onion
skin
Firm swelling laminations.
on lateral &
inferior border
of right
mandible
HISTOLOGIC FEATURES:
Supracortical but subperiosteal mass is composed of much
reactive new bone & ostoeid, with osteoblast bordering many
trabeculae.
Trabeculae orient perpendicular to cortex, with trabeculae
arranged in parellel to each other or reticular form.
CT between bony trabeculae is rather fibrous & show diffuse or
patchy sprinkling of lymphocytes & plasma cells.
Periosteal reaction infection from caries perforating cortical
plate & become attenuated, stimulating periosteum rather than
producing usual suppurative periosteitis.
TREATMENT & PROGNOSIS:
Endodontic treatment or extraction, with no surgical intervention
for periosteal lesion except for biopsy.
Periosteal bone formation /neoperiosteosis may occur in variety
of other conditions & care must be taken to exclude them from
diagonosis.
Include infantile cortical hyperosteosis (Caffeys disease),
hypervitaminosis A, syphilis, leukemia, Ewings sarcoma,
metastatic neuroblastoma & even a fracture callus.