Oral Pathology: Dr. Tasnim Hamdan Graduated From University of Valencia
Oral Pathology: Dr. Tasnim Hamdan Graduated From University of Valencia
Oral Pathology: Dr. Tasnim Hamdan Graduated From University of Valencia
Pathology
1. PMNs
2. Macrophages
3. Lymphocytes
4. Plasma cells
5. Mast cells
6. Basophils
7. Eosinophils
The reaction of the periradicular
tissues to noxious products of
tissue necrosis, bacterial products,
and antigenic agents from the root
canal has been described by FISH.
4 well-defined zones of reaction
Zone of stimulation
Zone of irritation
Zone of contamination
Zone of infection
ZONE OF NECROSIS/ INFECTION
Infection Is Present in the centre of the lesion
Micro-organisms are found in this zone
Characterised by polymorphonuclear leukocytes.
ZONE OF CONTAMINATION
Characterized by round cell infiltration.
Cellular destruction from the toxins discharged from central
zone is observed.
Bone cells are dead & might go under autolysis which results
in empty appearance of lacunae.
ZONE OF IRRITATION:
It is characterized by macrophages and osteoclasts.
Small round cells, normal bone cells can be seen.
Collagen framework is digested by phagocytic cells, i,e the
macrophages, while osteoclasts attack the bone tissue
ZONE OF STIMULATION:
Characterized by fibroblasts and osteoblasts.
At the periphery , toxin is mild enough to be a stimulant
Response to this stimulation, collagen fibres get laid down by
fibroblasts, which acts both as a wall of defence around the
zone of irritation and as a scaffolding on which the osteoblasts
built new bone.
According to his concept, periapical lesion is not an infection
by itself but the reaction of body to infection in the canal.
Clinical periapical tests
1.Percussion: indicates
inflammation of the
peridontium.
4.Periodontal Examination
Probing- determines the
level of connective tissue
attachment.
Mobility- determines the
status of PDL.
5. Radiographic Examination
Loss of lamina dura apically
Radiolucency at apex regardless of cone angle and usually
resembles a hanging drop.
Cause of pulp necrosis is usually evident.
CLASSIFICATION OF
PERIRADICULAR
TISSUES
WHO classification of periradicular tissues
CODE NUMBER CATEGORY
K04.4 Acute apical periodontitis
K04.5 Chronic apical periodontitis (apical granuloma)
K04.6 Periapical abscess with sinus (dentoalveolar abscess with
sinus, periodontal abscess of pulpal origin)
K04.60 Periapical abscess with sinus to maxillary antrum
K04.61 Periapical abscess with sinus to nasal cavity
K04.62 Periapical abscess with sinus to oral cavity
K04.63 Periapical abscess with sinus to skin
K04.7 Periapical abscess with out sinus
K04.8 Radicular cyst(apical periodontal cyst, periapical cyst)
K04.80 Apical & Lateral cyst
K04.81 Residual cyst
K04.82 Inflammatory Paradental cyst
GROSSMAN’S CLASSIFICATION
Localized collection of
pus in the alveolar bone
at the root apex of a
tooth following death of
pulp with extension of
infection through apical
foramen into
periradicular tissue.
From its origin in the pulp, the inflammatory process extends into
the periapical tissues, where it may present as a granuloma or cyst
(if chronic) or an abscess (if acute). Acute exacerbation of a chronic
lesion may also be seen.
2.1 Etiology
Trauma
Chemical & mechanical irritation
Bacterial invasion of dead pulp
tissue
Necrotic pulpal tissue debris, inflammatory cells, and bacteria,
particularly anaerobes and facultative anaerobes, all serve to
stimulate and sustain the periapical inflammatory process.
2.1 Clinical Features
Mand ant: swelling may involve the lower lip and chin
Influx of bacteria/necrotic
products of high virulence
and antigenicity
Lowering of host
defenses
Establishment of drainage.
Once symptoms subside, complete root
canal treatment.
4.Chronic apical periodontitis / asymptomatic
apical periodontitis / periapical granuloma
Symptomless sequelae of acute
apical periodontitis.
May develop and enlarge
insidiously without any subjective
signs or symptoms.
Necrotic pulp gradually releases
noxious agents with low grade
pathogenecity or in low
concentration.
Develops after inadequate root
canal treatment.
4.1 Etiology
Death of the pulp followed by mild irritation of periapical
tissue that stimulates a productive cellular reaction.
Some cases preceded by chronic alveolar abscess.
4.2 Clinical Features
Asymptomatic, discovered on routine radiographic examination.
No pain on percussion.
Associated tooth has a necrotic pulp therefore should not respond
to the electrical or thermal stimuli.
4.3 Histologic Features
Periradicular granuloma or cyst. The only accurate way to
distinguish these two entities is by histologic examination.
4.4 PERIAPICAL GRANULOMA
A growth of granulomatous
tissue continuous with the
periodontal ligament
resulting from death of the
pulp and the diffusion of
bacteria and bacterial toxins
from the root canal into the
surrounding periradicular
tissues through the apical
and lateral foramina.
4.4.1 Histologic Features
The periradicular granuloma consists predominantly of
granulation inflammatory tissue with many small capillaries,
fibroblasts, numerous connective tissue fibers, inflammatory
infiltrate, and usually a connective tissue capsule
Occasionally, needle-like spaces (the remnants of cholesterol crystals),
foam cells, and multinucleated foreign body giant cells are seen in these
lesions
4.4.2 Zones of well established granuloma
4.4.3 Treatment
Root canal treatment is recommended.
Removal of cause of inflammation is usually followed by
resorption of Granulomatous tissue and repair with
trabeculated bone.
4.5 Periapical Cyst / Radicular cyst
Pathological cavity containing fluid, semi fluid or gaseous material,
frequently but not always lined by epithelium
Direct sequelae of chronic apical periodontitis, not every lesion
develops into cyst
According to the studies 6-55% lesions are cyst.
Hypothesis related wid this growth
Abscess Theory
An abscess cavity is formed within the connective
tissue and is then surrounded with proliferating
epithelial tissue, thereby producing a cyst.
4.5.1 Etiology
Cyst develops from dormant epithelial cell rests that proliferate
probably under the influence of inflammatory cytokines & growth
factors released by various cells residing in the lesion.
When proliferation occurs within the body of the granuloma, it
plugs the body of the AF which limits the egress of the bacteria.
Sometimes, epithelial plugs protrude out of the apical foramen
resulting in a pouch connected to the root & continuous with the
root canal.
There are 2 distinct
categories of radicular cyst
4.5.2 Periapical pocket cyst
Characterized by
cavities that are
completely enclosed
in epithelial lining
and are totally
independent of the
root canal of the
affected tooth.
4.5.4 Clinical features
No symptoms associated with
development of a cyst except
incidental to necrosis of the
pulp.
May become large enough,
however, to become obvious
as a swelling.
Pressure of the cyst may be
sufficient to cause movement
of the teeth, owing to
accumulation of cystic fluid.
If left untreated, may
continue to grow at the
expense of the max or mand.
Age incidence: peak in 3 rd , 4 th and 5 th decade
Sex incidence: Slightly more males.
Frequency: Commonest cystic lesion of jaws.
Primarily symptom less.
Discovered accidentally during routine dental X ray exam.
Diagnostic criteria – associated teeth are non vital
Rare in deciduous teeth.
4.5.5 Histologic Features
Cavity is lined by
stratified squamous
epithelium.
Surrounded by connective
tissue that is infiltrated by
lymphocytes, plasma cells,
and polymorphonuclear
neutrophils.
Contains debris and
eosinophilic material.
Cholestrol clefts,
macrophages, giant cells .
4.5.6 Radiological features
Cyst
5.Chronic alveolar abscess/ chronic suppurative
apical periodontitis/ asyptomatic apical abscess
Characterized by
presence of an abscess
draining through a sinus
tract.
5.1 Etiology
Source of infection is in
the root canal.
It is a natural sequelae of
death of the pulp with
extension of the infective
process periapically, or
may result from a
preexisting acute abscess.
5.2 Clinical Features
Tooth is asymptomatic or mildly painful.
Detected only during radiographic examination or because of the
presence of a fistulous tract, which can be either intraoral or
extraoral.
Exudate can also drain through the gingival sulcus of the
involved tooth mimicking a periodontal lesion with a pocket.
Vitality test is negative.
5.3 Radiographical Examination
With involvement of the parapharyngeal space, the swelling tracks down the
neck and oedema can quickly spread to the glottis.
Swallowing and opening the mouth become difficult and the tongue may be
pushed up against the soft palate.
7.1 Etiology
Anatomical complexity
Apical biofilms
Cholestrol clefts
Foreign body reaction to
gp
Cellulose granuloma
Periapical scar tissue
7.2 Bacteriology
EXTERNAL
External surface
resorption
External inflammatory
root resorption
External replacement
resorption or ankylosis
INTERNAL
10.2 Etiology
Trauma
Excessive forces
Granuloma
Cyst
Central jaw tumors
Impaction of teeth
Bleaching
Systemic diseases
If no cause is evident, the
disorder is called as
idiopathic resorption.
10.3 Clinical Features
Asymptomatic
On complete resorption, tooth may become mobile.
If extends into the crown, gives appearance of “pink tooth” as
seen in internal resorption.
In case of replacement resorption or ankylosis, root is
gradually replaced by bone, renders the tooth immobile, in
infraocclusion, and with a high mettalic percussion sound.
10.4 Radiographical Examination
Concave or ragged areas on the root surface or blunting of the apex.
Inflammatory root resorption caused by the pressure of a growing
granuloma, cyst or tumor adjacent to the area of radiolucency.
Areas of ankylosis have a resorbed root with no PDL space and
with bone replacing the defects.
10.5 Treatment
Asymptomatic
Incidental finding on radiographs
11.3 Radiological features
Thickening of the
cementum layer along with
blunting or rounding of
the root tip.
The biological width
between the root surface,
the alveolar bone and the
periodontal ligament is
found intact on the
radiographs.
11.4 Treatment
Asymptomatic; No treatment
Paget’s disease ; extractions become difficult
Inflamed or necrotic pulp; endodontic treatment of the
tooth is required, but it may pose great difficulty and might
necessitate surgical intervention.
12. OSTEOMYELITIS
Contiguous
focus of Hematogenous
infection spread
Direct inoculation of
microorganisms into
bone
12.4 Occurrence
Osteomyelitis in maxilla:
Rare occurrance due to
Extensive blood supply
Thin cortical plates
Abundant medullary spaces
Osteomyelitis in mandible:
An important factor in
establishment of osteomyelitis in
mandible is compromise of blood
supply
12.5 Microbiology
12.6 Acute suppurative osteomyelitis
Necrosis of bone
Necrotic tissues, dead and dying cell, pus from bacteria → fill the
marrow space
Maxilla : localized
Mandible : Diffuse and widespread
In infants: NEONATAL MAXILLITIS
Origin: Hematogenous spread or local oral infection
Seriously ill and may not survive
In adults:
Sever pain
Trismus
Parasthesia 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
12.6.4 Radiographic feature
Ill-defined area
of radiolucency
of the right body
of the mandible
12.6.5 Histologic features
Nonvital bone exhibits loss of the osteocytes from the lacunae. Peripheral resorption and
surrounding inflammatory response also can be seen
12.6.6 Treatment and prognosis
Essential measures
Bacterial sampling and culture
Drainage
Analgesics
Give specific antibiotics based
on culture and sensitivities
Debridement
Remove source of infection, if
possible
Adjunctive treatment
Sequestrectomy
Decortication if
necessary
Hyperbaric oxygen
Resection and
reconstruction for
extensive bone
destruction
UNTREATED CASES
may proceed to
development of
periostitis , soft tissue
abscess or cellulitis
12.6.7 COMPLICATIONS
12.7 CHRONIC SUPPURATIVE OSTEOMYELITIS
Swelling
Pain
Sinus formation
Purulent discharge
Sequestrum formation
Tooth loss
Pathologic fracture
12.7.2 Radiological feature
Patchy, ragged & ill defined radiolucency.
Often contains radiopaque sequestra.
12.7.3 Histology
Inflammed connective
tissue filling inter-
trabecular areas of bone.
Scattered sequestra.
Pockets of abscess.
Difficult to manage
medically :
Surgical intervention is
mandatory, depends on
spread of process.
Antibiotics are same as
in acute condition but
are given through IV in
high doses.
SMALL LESIONS
Curretage, removal of necrotic bone and
decortication are sufficient.
EXTENSIVE OSTEOMYELITIS
Decortication combined with transplantation of
cancellous bone chips.
PERSISTANT OSTEOMYELITIS
Resection of diseased bone followed by
immediate reconstruction with an autologous
graft is required.
Weakened jaw bones must be immobilized.
12.8.CHRONIC FOCAL SCLEROSING
OSTEOMYELITIS
( CONDENSING OSTEITIS)
Condensing
Osteitis
slide.118
12.9.CHRONIC DIFFUSE
SCLEROSING OSTEOMYELITIS
Clinical entity characterized by a nonsuppurative, inflammatory
process associated with recurrent swelling, trismus and pain
Common in edentulous mandible
Proliferative reaction of bone to a low grade infection.
Portal of entry is diffuse periodontal disease
12.9.1 Clinical feature
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
12.12 SCLEROTIC CEMENTAL MASSES