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Periapical Tissues
Diseases
Of
Dental
Pulp
Etiology: FACTORS
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
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.
Acute chronic
Apical periodontitis
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:
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.
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
Pulp death
Granuloma formation
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.