Essentials-of-Oral-Pathology-3rd-Edition by purkait

378 Essentials of Oral Pathology

DIET FACTOR Both of these mechanisms result in a signi-
ficant reduction of caries.
Physical Nature of Diet
The immune-mediated prevention of caries is
If the diet contains sufficient amount of fibrous mostly associated with the reduction in the
foods that help to keep the teeth clean as well as number of S. mutans organisms in plaque. The
stimulates the salivary flow, the chances of caries humoral and cell-mediated immune systems
formation will be less. Whereas more and more gain access into the oral cavity either via the
intake of soft and sticky foods increases the gingival cervicular fluid or via the saliva.
possibility of caries development. • The salivary immune mechanism probably

Composition of the Diet acts through secretory IgA, which prevents
S. mutans from adhering to the tooth surface.
• Presence of phosphates in the diet (either • The gingival crevicular immune mechanism
organically bound or inorganic) can reduce the involves both humoral and cell-mediated
incidence of caries. immune systems and therefore, exerts a strong
immunologic response.
• Traces of molybdenum and vanadium in the • In crevicular immune system, the immuno-
diet may reduce the incidence of caries. globulins (IgG, IgM and IgA), complements,
neutrophil leukocytes, sensitized lymphocytes
• The diet that contains adequate amounts of and macrophages, etc. are secreted through
vegetables, vitamin (A, D, K and B-complex) the gingival crevicular fluid and reach the
and minerals, etc. is often associated with a tooth surfaces.
low caries incidence. • The IgG antibodies act as opsonins, they
facilitate phagocytosis and cause death of the
• Increase in the proportion of fat in the diet S. mutans by neutrophil leukocytes and
may cause reduction in the cariogenic effect macrophages.
of sugar. • Experimental evidences suggest that
immune activity exerted by gingival
SYSTEMIC FACTOR crevicular system is much stronger than the
response obtained through the salivary
Some people hereditarily have an increased immune system.
tendency to develop caries while other people
show just the reverse tendency. CLINICAL ASPECTS OF DENTAL CARIES

IMMUNITY CLINICAL TYPES

Immune mechanism plays an important role in Pit and Fissure Caries (Fig. 9.1A)
the prevention of caries in humans. It is asso-
ciated with the formation of serum and salivary • This type of lesion occurs in the
antibodies as well as initiation of some degrees developmental pits and fissures of the teeth
of cell-mediated immune response. It is (especially if these areas are deep, narrow and
important to mention that most of the immune- retentive in nature).
mediated protective activities are specifically
directed against the S. mutans organisms, which • The teeth and their specific areas or surfaces
are considered as the most important bacterio- affected by the pit and fissure caries include
logic agents for the causation of dental caries. occlusal surfaces of molars and premolars,
buccal and lingual surfaces of molars and
Experimental immunization of rats and lingual surfaces of maxillary incisors.
monkeys with S. mutans using both live and dead
organisms as well as cell wall preparations, has • The lesions usually appear brown or black,
shown to produce the following: with little softening and opaqueness of the
• IgG, IgA and IgM clones of antibodies in the surface. When the lesion is examined by a fine

serum.
• It induces some cell-mediated immune

response.

Dental Caries 379

Fig. 9.1A: Pit and fissure caries Fig. 9.1B: Smooth surface caries

explorer tip, a “catch point” is often felt, where • Incipient caries can be prevented by topical
the explorer tip catches the area. fluorides, which help to maintain the integrity
• The lesions are smaller in the beginning but of enamel undermined by dentinal caries.
become wider as they spread towards the
dentin due to the typical orientation of the Smooth Surface Caries (Fig. 9.1B)
enamel rods.
• When the lesions reach the dentinoenamel • This type of carious lesion occurs in relation
junction (DEJ), they spread laterally to cause to the smooth surfaces of teeth, e.g. proximal
undermining of the enamel. surfaces or gingival areas of the buccal and
• The enamel directly bordering the pit or lingual aspect of tooth.
fissure may appear opaque and bluish-white
as it becomes undermined. • Smooth surface caries most commonly occurs
in the proximal surface of the teeth just below
Incipient Caries the contact point.

Definition • The lesion beings as a well-demarcated,
Initial carious lesion limited to the enamel is chalky-white opacity of enamel with no loss
called incipient caries and is characterized by a of continuity of the surface.
virtually intact surface but a porous subsurface.
• This type of carious lesions are characterized • The white spot lesion becomes pigmented
yellow or brown and it often extends buccally
by the presence of an intact enamel surface, and lingually.
but there is destruction of the enamel below
the surface layer which is called “subsurface • The surrounding enamel becomes bluish
demineralization”. white as the lesion continues to progress.
• Clinically, incipient caries presents a “chalky-
white” appearance of the tooth surface and it • The surface of the affected enamel becomes
is only found when the surface of the tooth is rough and later on, there is formation of a cavity.
dry and the typical chalky-white condition
disappears if the surface of the tooth becomes Rampant Caries (Fig. 9.1C)
wet.
• The incipient caries is a reversible process and This is an acute fulminating type of carious
the lesion can be cured due to remineralization process, which is characterized by simultaneous
by salivary mineral ions. involvement of multiple number of teeth (may
be all teeth) in multiple surfaces.
• Rapid coronal destruction occurs within a

short span of time, causing early involvement
of the pulp.

380 Essentials of Oral Pathology

• Nursing bottle caries commonly occurs in the
upper anterior teeth (as these are constantly
coming in contact with the sweetened milk);
while the lower teeth are not usually affected
as they remain under the cover of the tongue.

• Both the nursing bottle caries and rampant
caries cause early pulp involvement because
they spread at a very rapid pace and as a
result, the pulp hardly gets any time to protect

itself by forming reparative dentin.

Fig. 9.1C: Rampant caries Chronic Caries

This type of caries progresses at a slower pace
and it rarely causes pulp involvement (unless the
tooth is left untreated for many years) because
the pulp gets sufficient time to produce
secondary dentin or reactionary dentin to protect
itself.

Fig. 9.1D: Nursing bottle caries Arrested Caries (Fig. 9.1E)

• The common age of occurrence of rampant Arrested caries is a lesion whose progression is
caries is about 4 to 8 years for the deciduous ceased after the initial development. It can occur
teeth and 11 to 19 years for the permanent teeth. both in enamel and in dentin.

• Interestingly, the rampant caries can occur in Arrested caries of enamel
persons with no previous history of dental
caries and in those persons who maintain a Arrested caries in enamel may occur when the
good level of oral hygiene regularly. carious process stops before cavity formation. It
occurs when the adjacent carious tooth (from
• Moreover, rampant caries attacks those which the disease has actually spread to this new
surfaces of teeth, which are otherwise tooth) is lost or is extracted, so that the carious
considered immune to the disease. lesion in the new tooth becomes easily accessible
for cleaning and plaque control measures. It is
commonly seen in smooth surfaces of tooth.
Remineralization occurs from saliva or due to
topical fluride applications.

Nursing Bottle Caries (Fig. 9.1D) Fig. 9.1E: Arrested caries

• This is also another type of acute carious
lesion, which occurs among those children
who take milk or fruit juices by the nursing
bottle, for a considerably longer duration of
time, preferably during sleep.

• As the child takes large amounts of easily
fermentable sugars along with the milk, the
sugar facilitates the cariogenic bacteria to
produce caries at a rapid pace by fermenting
those sugars.

Dental Caries 381

Arrested caries of dentin

The arrested caries of dentin usually occurs when
a carious cavity becomes wide open; so that it
gets exposed to the cleaning measures like tooth
brushing, salivary secretions and mastication, etc.
The arrested caries presents a hard, black or
brown-colored dentinal surface at its base
(eburnated dentin). Its surface is highly
mineralized due to remineralization from oral
fluids and has increased fluoride content.

Recurrent Caries Fig. 9.1F: Root caries

Recurrent caries refers to a carious lesion that • The dentin is progressively destroyed by a
begins around the margins or at the base of a combination of both demineralization and
pre-existing defective restoration. proteolysis.

Forward Caries • Involvement of pulp occurs within a few days
(mostly because of the softer nature of the
When a carious lesion progresses unidirec- cementum and dentin).
tionally from enamel into the dentin and pulp, it
is called a forward caries. • Clinically, these lesions are extensive, shallow
and saucer-shaped, with ill-defined margins.
Backward Caries
• The actinomycotic groups of organisms are
These lesions also initially progress from enamel mostly responsible for the causation of root caries.
into the dentin, where they spread laterally and However, S. mutans and Lactobacillus acidophilus,
involve a wide area. Later on, these lesions etc. may also be associated with this disease.
proceed in a backward direction from dentin
back to enamel and affect the enamel once again • Microradiograph reveals subsurface demine-
at a different location. ralization of the root, which extend to the
dentin. Surface remineralization is also seen
Root Caries in some areas.

These are carious lesions, which involve the • The lesions often have soft surfaces with
cemental wall of the exposed root surfaces of brownish discoloration of the affected area.
teeth.
• There may be formation of sclerotic dentin as
Important features of root caries (Fig. 9.1F) the caries progresses into the dentin from
cementum.
• The development of such lesions is preceded
by exposure of the roots of the affected teeth • Sometimes, the carious lesion may encircle the
in the oral environment either due to aging or entire root of the affected tooth.
due to gingival recession.
Radiation Caries
• Because of the roughness of the cemental wall,
plaque accumulates readily in the absence of Patients receiving large doses of radiation for the
adequate oral hygiene measures and once the treatment of malignant lesions in the head and
root caries begin’s it progresses very fast. neck region, often develop a specific type of large
“caries-like lesions” in the cervical areas of the
• Cementum is invaded along the direction of teeth. These lesions begin a few weeks to few
‘Sharpey’s fibers’ and microorganisms spread months after radiotherapy. They often surround
along the incremental lines. the entire crowns of the affected teeth, gradually
weaken them and even sometimes can cause
• Cementum is destroyed beneath the plaque amputations of tooth.
over a wide area.
The exact cause of radiation caries is not
known, but it may be due to the reduced salivary
secretions, secondary to the radiotherapy.

382 Essentials of Oral Pathology

RADIOLOGICAL FEATURES OF Fig. 9.2: Photomicrograph of enamel caries
DENTAL CARIES
• Accentuation of the incremental striae of
Radiographs are often (not always) helpful in the Retzius often occurs.
detection of dental caries and usually the intra-
oral periapical (IOPA), panoramic and bitewing HISTOLOGIC FEATURES OF ADVANCED
radiographs are advised for this purpose. ENAMEL CARIES

The bitewing radiographs are especially Advance enamel caries microscopically presents
indicated for the detection of proximal caries. several zones in the tissue, which are as follows:
Usually, the pit and fissure caries radiographi-
cally appears as a “triangle-shaped” radiolucent Zone I: Translucent Zone
area, with its base located towards the
dentinoenamel junction. On the other hand, the • It is the deepest zone in the carious enamel
smooth surface caries also produces a triangle and is the first recognizable histological
shaped radiolucent area, but its base is located change at the advancing front of the lesion.
towards the surface of the tooth.
• This zone is slightly more porous than the
In these lesions if the enamel radiolucency is normal sound enamel and contains 1% by
extending up to the DEJ, it is considered that the volume of spaces (the pore volume), which is
tooth will have a cavity and there is definite 0.1% in sound normal enamel.
involvement of the underlying dentin. Whereas
if the enamel radiolucency does not extend to the • The pores are larger than the usual smaller
DEJ, there should be no clinically detectable pores seen in normal enamel. Dissolution of
cavity in the tooth. mineral occurs mainly at the junction of
prismitic and interprismitic enamel.
The root caries on the radiograph usually
produces a U-shaped radiolucent area with Zone II: Dark Zone
irregular margin.
The dark zone is located just superficial to the
HISTOPATHOLOGICAL ASPECT OF translucent zone and its dark appearance is due
DENTAL CARIES to the excessive demineralization of the enamel
due to caries.
ENAMEL CARIES • This zone is narrower in rapidly advancing

For the microscopic examination of enamel caries, caries and it is wider in slowly advancing
ground section preparations are used because the lesions.
decalcified sections of enamel become useless • This zone contains 2 to 4% pore volume.
owing to the very high concentration minerals in • Some pores are larger but other pores are
this tissue. The ground section preparation is smaller than those of the translucent zone.
examined by transmitted or polarized lights.

HISTOLOGIC FEATURES OF EARLY
ENAMEL CARIES (FIG. 9.2)

• There will be loss of interprismatic or inter-
rod substances with increase in the promi-
nence of the enamel rods.

• Appearance of transverse striations of the ena-
mel rods due to segmental demineralization.

• Dark lines often appear at right angles to the
enamel rods, suggesting segments.

Dental Caries 383

• This zone also reveals some degrees of HISTOLOGY OF DENTINAL CARIES
remineralization of the carious enamel. (CARIES IN DENTIN)

Zone III: Body of the Lesion The dentinal caries histologically presents five
zones in the tissue, which are as follows:
This zone is situated between the dark zone and
the surface layer of enamel, and it represents the Zone I (Normal Dentin)
area of greatest demineralization.
• It has a pore volume of between 5 to 25%. • This zone represents the innermost layer of
• This zone contains apatite crystals larger than the carious dentin and here the dentinal
tubules appear normal.
those of the normal enamel.
• Large crystals result from reprecipitation of • There is evidence of fatty degeneration of the
Tomes processes.
minerals dissolved from deeper zones.
• With continuing acid attacks on the enamel, • No crystals in the lumen of the tubules.
• No bacteria in the tubules.
there may be further dissolution of minerals • Intertubular dentin has normal cross-banded
both from the periphery of the apatite crystals
and their cores. collagen and normal dense apatite crystals.
• The lost minerals in the enamel are often repla-
ced by unbound H2O and organic matters. Zone II (Sub-transparent Dentin)
• This zone shows increased prominence of the
striae of Retzius. • This is the zone of dentinal sclerosis and it is
characterized by the deposition of very fine
Zone IV: Surface Zone crystal structures within the dentinal tubules
at the advancing front.
Initially, the surface zone of a carious enamel
remains comparatively unaffected despite • Superficial layer shows areas of deminerali-
subsurface demineralization and also to the zation and damage of the odontoblastic
surface remineralization. processes.
• It is about 40 μm thick.
• However, in untreated cases the surface • No bacteria in the tubules.
• This dentin is capable of remineralization.
enamel often gets destroyed and a cavity is
formed. Zone III (Transparent Dentin)
• Surface remineralization results from active
precipitation of mineral ions derived from • This zone appears transparent and this is
both plaque and the saliva. because of the demineralization of dentin due
to caries.
Ultrastructural studies (of enamel caries): Ultra-
structural studies suggest that the initial • It is softer than normal dentin.
dissolution of enamel begins along prism • Further loss of mineral ions from intertubular
boundaries and later on there is demineralization
occuring both within and between the prisms, dentin.
which results in an increase in the inter- • Large crystals within the lumen of the dentinal
crystalline gap.
tubules.
Along with dissolution there is also • No bacteria in tubules.
remineralization of enamel and change in • Cross-banded intertubular collagen still intact.
enamel crystal structures due to the combined • This zone is capable of self-repair and
effects of demineralization and reminera-
lization of enamel. remineralization.

Zone IV (Turbid Dentin)

• This zone is called the “turbid dentin” and is
marked by the widening and distortion of
the dentinal tubules, which are packed with
microorganisms. There is very little amount

384 Essentials of Oral Pathology

of mineral present in the dentin and
moreover denaturation of collagen fibers also
takes place.
• This zone cannot undergo self-repair or
remineralization.
• Must be removed before restorative treatment.

Zone V (Infected Dentin) Fig. 9.3: Photomicrograph of dentinal caries showing
bacterial invasion within the dentinal tubules
• This is the outermost zone of the carious
dentin and is characterized by complete TUBULAR SCLEROSIS
destruction of the dentinal tubules (as a result
of their severe expansion due to accumulation Peritubular dentin reduces the size of the indi-
of a large number of microorganisms and their vidual dentinal tubules and thus prevents the
by-products). bacterial penetration.

• The expanded tubules cause compression and REGULAR REACTIONARY DENTIN
bending of the adjacent tubules and eventually
destroy them. Reactionary dentin develops on regular basis as
a result of localized, nonspecific mild irritation
• In this zone, the areas of decomposition of to the odontoblast cells. However, this dentin
dentin, which occur along the direction of the seems to develop mostly during caries attack in
dentinal tubules, are called the liquefaction a tooth.
foci of Miller.
In regular reactionary dentin a layer of dentin
• In some areas, the cariogenic microorganisms forms at the surface of the pulp chamber deep to
spread laterally and large bacteria-filled clefts the progressive front of dentin caries and it
develop at right angles to the direction of the contains normal tubular structures.
tubules due to decomposition of dentin. These
clefts are called the transverse clefts. It is often hypermineralized as compared to
the primary dentin and it delays the pulp
• The mechanism of formation of transverse exposure by increasing the depth of the tissue
clefts is not clearly known, they may follow between carious dentin and the pulp.
the course of incremental lines, or result from
the coalescence of liquefaction of adjacent IRREGULAR REACTIONARY DENTIN
tubules.
This type of dentin forms under moderate to
• Transverse clefts may also arise by extensive severe insult by caries and this irregular
proteolytic activity along the interconnecting reactionary dentin contains only few irregularly
lateral branches of odontoblastic processes. shaped and tortuous tubules. Sometimes, the
dentinal tubules can be even absent.
• In zone V, bacteria may no longer remain
confined within the dentinal tubules and they DEAD TRACTS
invade and destroy the peri- and intertubular
dentin. In the process, the entire dentinal The dead tracts form when the odontoblast cells
structure becomes destroyed (Fig. 9.3). die and their tubules become sealed off. They
often prevent the further progression of caries
PROTECTIVE RESPONSES OF DENTIN in dentin towards the pulp.
AND PULP AGAINST CARIES

Hectic odontoblastic activity takes place in the
dentin-pulp complex in order to protect the tooth
from the invasion of caries.

Following are the protective responses from
the pulp-dentin complex:

Dental Caries 385

CARIES ACTIVITY TESTS indicates the caries “conduciveness“ of the
patient.
A number of caries activity tests have been
evolved to help detect the presence of oral Results
conditions associated with increased risk of
caries. However, no single test can be relied Changes of color Caries conduciveness
upon to predict the caries susceptibility of a Nonconducive
person with a high degree of confidence. No change in color Slightly conducive
Caries activity tests are more useful than in 15 minutes Moderately conducive
clinical examinations since these can predict Highly conducive
the need for preventive treatment before the Color changes from blue
caries has actually started. to orchid in 15 minutes Extremely conducive

SNYDER TEST Color changes from blue
to red in 15 minutes
Snyder test is the qualitative determination of
acidogenic organisms in the mouth; it measures Color changes from blue
the ability of salivary microorganisms to produce to red immediately
organic acids from a carbohydrate medium. on mixing
Glucose-agar media containing an indicator dye
(bromocresol green) is used for this test. The Color changes from
indicator dye changes from green to yellow in blue to colorless
the range of pH from 5.4 to 3.8. in 15 minutes

Paraffin-stimulated saliva (0.2 ml) is added SALIVARY BUFFERING CAPACITY TEST
into the medium, change of the medium from
green to yellow is indicative of the degrees of Salivary buffering capacity test is a chair side test
caries activity. to measure the buffering capacity of the saliva.
A special kit called “dento buff“ is used for this
Results test, which contains a small vial of weak HCl and
a color indicator chart.
If the color of the medium changes from green
to yellow within 24 hours, caries susceptibility If one milliliter saliva is put into the acid
of the patient should be considered very high. solution, its pH will rise gradually depending
upon the buffering capacity of the saliva, and this
If the similar color change occurs within change of pH is measured by the accompanying
48 hours, the patient is considered to have a color chart.
definite caries susceptibility.
Results
If the color change occurs in 72 hours, a limited
caries susceptibility is indicated. If the buffering capacity of saliva is normal, the
final pH of the solution will rise up to 5 to 7, and
Finally, if the color change does not occur in if the buffering capacity is low, the pH will rise
72 hours, the patient should be considered caries up to 4 only.
immune.
However, it is understood that more is the
SALIVARY REDUCTASE TEST buffering capacity of saliva, less will be the acid
demineralization of the tooth due to caries.
Salivary reductase test measures the activity of
reductase enzyme present in salivary bacteria. MICROBIOLOGICAL TEST
Paraffin-stimulated saliva is collected in a plastic
container and an indicator dye “diazoresorcinol” Microbiological test helps to measure the number
is added to it, which colors the saliva blue. of Streptococcus mutans and Lactobacillus
acidophilus per microliter of saliva.
The reductase enzyme liberated by the
cariogenic bacteria causes color changes in the Two samples of paraffin-stimulated saliva
medium from blue to other colors, which (1 ml each) are collected from the patient, these
are diluted 10 times and each is cultivated in two
different special media: (i) Rogosa’s SL agar
medium for Lactobacillus, and (ii) Mitis salivarius
agar medium for Streptococcus mutans.

386 Essentials of Oral Pathology

After incubation, the number of colonies METHODS OF CARIES PREVENTION
that developed in two separate media are
counted and then are multiplied by 10 (dilution The dental caries can be prevented by the
factor) to estimate the number of bacteria in 1 following methods:
ml of saliva. Limit substrate
• Eliminate sucrose from the diet or reduce its
Result
amount.
If the count is more than 10,00,000 S. mutans and • Eliminate sucrose from the “in-between”
more than 1,00,000 L. acidophilus, the caries
susceptibility of the individual should be meals and snacks.
considered very high. Modify oral microflora
• Bactericidal mouth-rinse by chlorhexidine
If the count is less than 1,00,000 S. mutans and • Topical fluoride treatments
less than 1,000 L. acidophilus, the individual is • Antibiotic treatment by vancomycin and
considered less susceptible to caries.
tetracyclines
S. MUTANS DIP-SLIDE METHOD Plaque disruption—by brushing and floosing,
etc.
This test measures the number of S. mutans Modify tooth
colonies in modified MSA; the saliva is collected • Systemic fluorides
for 5 minutes and is poured over the agar-coated • Topical fluorides
slide. Slides are then dried and bacitracin disks • Maintain a smooth surface of the tooth
are placed in the middle of the inoculated agar Stimulate salivary flow
about 1 cm from each other. The slide is then • Eat noncariogenic fibrous foods that require
incubated in a tube containing CO2 for 48 hours.
A zone of inhibition 10 to 20 mm in diameter is lots of chewing.
formed around each bacitracin disk. S. mutans • Use sugarless chewing gums.
presents small blue colonies with the zone of • Administer sialogogues
inhibition. Restore tooth surface
• Restore all cavitated lesions
Result • Seal pits and fissures at caries risk
• Correct all defects, e.g. marginal crevice,
The colony density is compared with a model
chart and classified as 0 (negligible), 1 (less than proximal overhangs.
100,000), 2 (100,000-1000, 000) and 3 (more than
1000,000) S. mutans colony forming units/ml of CARIES VACCINE
saliva.
Dental caries fulfills the criteria of an infectious
ENAMEL SOLUBILITY TEST disease and the possibility of preventing it by
vaccination has been persuaded over a long
Popularly known as ‘Fosdick calcium dissolution period of time. The rationale is that immuni-
test’; in this test patient’s saliva is mixed with zation with Streptococcus mutans should induce
glucose and thereafter measured amount of (in an immune response, which might prevent the
milligram) powdered enamel is mixed with it dental caries in the following ways:
and kept for 4 hours. • It will prevent the ability of the micro-

Acid which is produced due to fermentation organisms to colonize on to the tooth surface.
of glucose by the cariogenic bacteria present in • It can alter the pattern of polysaccharide
the saliva cause is dissolution of powdered
enamel. The test measures the amount of metabolism by the bacteria and thereby
enamel powder dissolved during the 4-hour reduce their adhering capacity on to the tooth
period. surface.
• It can reduce ability of microorganisms to
produce acids also.
• It can reduce caries by helping in the process
of killing the cariogenic microorganisms.

Dental Caries 387

The caries vaccines are usually given at the 7. Bowden GH, Hardie JM, Slack GL. Microbial variations
age of about 6 months, before the eruption of the in approximal dental plaque. Caries Research
deciduous teeth. Oral administration or sub- 1975;9:253-77.
cutaneous injection of killed Streptococcus mutans
can induce the formation of specific IgA, IgG and 8. Bowen WH, Genco RN, O'Brien TC. Immunologic
IgM in the blood. aspects of dental caries special supplement to
immunology abstracts Washington, DC, Information
Passive immunization against caries can also Retrieval Inc, 1976.
be done by injecting specific IgG class of antibody
against the S. mutans. 9. Bowen WH. Nature of plaque. Oral Sci Rev, 1976;9:3.
10. Brannston M, Lind PO. Pulpal response to early
Although the caries vaccine is theoretically
very convincing, it has failed to gain a wide range dentinal caries. J Dent Res 1965;44:1045-50.
of acceptance because these vaccines produce 11. Brooks JD, Mertz-Fairhurst EJ, Della-Giustiana VE,
some cardiotoxicity in humans by cross-reacting
with the heart tissue. Williams JE, Fairhurst CW. A comparative study of two
pit and fissure sealants: three-year results in Augusta,
The enzyme glucosyl transferase converts Georgia. J Am Dent Assoc 1979;99:42.
sucrose into glucans, which are important for 12. Brunelle JA, Carlos JP. Changes in the prevalence of
accumulation of S. mutans on the tooth surfaces. dental caries in US school children, 1961-1980. J Dent
Antibodies against glucosyl transferase enzyme Res, 1982;61:1346.
have been tested in experimental animals and it 13. Carlesson J, Grahnen H, Jonsson G. Lactobacilli and
has been observed that these antibodies can streptococci in the mouths of children. Caries Research
reduce the accumulation of plaque and the 1975;9:333-9.
incidences of caries. 14. Chen WC, Noncillis GH. The kinetics of dissolution of
tooth enamel-a constant composition study. Journal of
However, this mechanism is more effective in Dental Research 1986;65:663-8.
rodents and it has got little effect on primates. 15. Cohen S, Burns RC. Pathways of the pulp. St Louis,
CV Mosby, 1984.
Experimental Caries in Animals 16. Darling AI. The pathology and prevention of caries,
British Dental Journal 1959;107: 287-302.
Dogs have been used as experimental 17. Dawes C. The nature of dental plaque, films and
animals for producing experimental caries; calcarious deposits. Ann NY Acad Sci 1968;153:102-19.
however, no caries could be produced in this way 18. DePaola PF, Soparkar PM, Tavares M, Allukian M Jr,
probably because dogs are naturally immune to Peterson H. A dental survey of Massachusetts school
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19. Douglass CW, Gammon MD. The epidemiology of
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PULPAL DISEASES sensory fibers of the trigeminal (fifth cranial)
nerve and sympathetic branches from the
Dental pain is probably one of the most common superior cervical ganglion. Each bundle contains
sufferings as experienced by patients with both myelinated and non-myelinated axons.
various dental diseases. Large numbers of
patients take refuse to the dentist only when they The myelinated fibers are of two types namely
are cornered by the misery of pain in the tooth. the Aα fibers and Aβ fibers, whereas the non–
myelinated fibers are designated as C-fibers.
Dental pulp has the unique importance in this Physiologically the Aα fibers are responsible for
regard, as it is the main component part of tooth, transmitting the sharp localized pain in the pulp
and the Aβ fibers are responsible for transmitting
where the pain actually begins form. Pulp is the the mechanical, thermal and tactile sensations.
soft delicate connective tissue that occupies the The C-fibers are associated with the transmission
central portion of the tooth and it has got two of dull, diffuse pain in the dental pulp.
parts namely the pulp chamber (the coronal
portion) and the root canals (the radicular DENTIN-PULP COMPLEX
portion).
Dentin is the vital and cellular hard tissue,
The cellular constituents of pulp include the ultimately and inseparably related to the ground
odontoblasts cells (which form dentin) the substance to the dental pulp. It is important to
fibroblasts (which form and maintain the pulp note that the dentin and the pulp together act as
matrix) and undifferentiated mesenchymal cells a unit called the “Dentin-Pulp complex”, while
(from which the connective tissue cells of the responding to the injurious stimuli of various
pulp are derived) besides this, dental pulp also nature in the tooth.

contains macrophages and lymphocytes. The ETIOLOGY OF PULPAL DISEASES
macrophages remove bacteria from pulp and
interact with other inflammatory cells during A large number of factors causing injuries to the
inflammation. The lymphocytes (mainly–T dentin-pulp complex have been identified, which
lymphocytes) in the dental pulp are associated may be of either acute or chronic in nature. As a
with immune defense systems. The extracellular general rule, the response to the injurious stimuli,
component of pulp or the pulp matrix consists which can cause damage or necrosis to cells
of collagen fibers and ground substance. The varies with the stimulus intensity and with the
fibers found in the pulp are mainly the type I defense capacity of the body.
and type III collagen in about 55:45 ratio. The
ground substance in pulp is composed of glyco- The dentin-pulp complex responses to injuries
saminoglycans, hyaluronic acid, chondroitin or stimuli in similar ways to other vital tissues
elsewhere in the body but some aspects of its
sulfate, glycoproteins and water. The function of responses are the consequences of its unique
ground substance is to support the pulpal cells structure. As the pulpal tissue is lying within the
and to act as the medium of transport for solid confinement of dentinal walls and because
nutrients and metabolites. Beside the afferent and its entire blood supply depends upon the smaller
efferent blood vessel, the pulp is richly inner- blood vessels passing through the tiny apical
vated by numerous nerve fibers, which enter the foramina, (often it makes the pulpal tissue a little
pulp through the apical foramina. The nerve
bundle entering the pulp consists mainly of

390 Essentials of Oral Pathology

more extravulnerable) moderate degree of injury RESPONSE OF DENTIN AND PULP TO
to pulp often elicits an exaggerated amount of INJURIOUS STIMULI
damage.
Being a vital and cellular tissue, dentin always
Factors causing injury to the pulp plays a major role in protecting the dental pulp
from various injurious stimuli. The dentinal
A. Physical Factors activity that helps to safeguard the pulp from
Acute Injury noxious stimuli is as follows:
• Accidental blow to the tooth.
• Heating due to grinding. I. Indirect pulpal response through dentinal
• Cavity preparation without water spray. changes.
• Vigorous polishing with rotary instruments.
• Root planning in periodontal therapy. II. Direct pulpal response.
• Large metallic restoration with inadequate
INDIRECT PULPAL RESPONSE THROUGH
insulation. DENTINAL CHANGES
Chronic Injury
• Attrition due to abrasive foods or bruxism. It is achieved through two processes:
• Abrasion due to abnormal tooth brushing. A. Dentinal sclerosis
B. Chemical Factors B. Formation of reparative dentin.
Medicaments or materials applied to dentin surface
may cause damage to the pulp by diffusion through A. Dentinal Sclerosis (Transparent Dentin)
the dentinal tubules. • It is produced by the rapid laying down of
C. Microbial Factors
• Dental caries with bacterial invasion of dentin peritubular dentin.
• Dentinal sclerosis reduces dentin permeability
and pulp.
• Bacterial invasion into the pulp from a fractured and thereby minimizes the risk of pulpal
damage from chemical or bacterial agents.
tooth, where the dental pulp is exposed to the • Crystals of calcium phosphate may also be
oral environment. deposited within the dentinal tubules as a
• “Anachoretic infection” of the pulp occurs, when response to slowly progressing caries.
bacteria present in the circulating bloodstream • Dentinal sclerosis can also occur as a normal
tend to accumulate in the pulp and cause aging process.
infection.
B. Reparative Dentin
CLASSIFICATION OF THE PULPAL • Reparative dentin is produced only by those
DISEASES
odontoblast cells, which are directly affected
Inflammatory Diseases by the injurious stimuli, and not by the entire
odontoblast cells of the dental pulp.
• Focal reversible pulpitis. • If the intensity of the injurious stimulus is
• Acute pulpitis. high, the reparative dentin is deposited
• Chronic pulpitis. rapidly and exhibits sparse, irregular tubular
• Chronic hyperplastic pulpitis. pattern with frequent cellular inclusions.
• When the stimulus is less active, reparative
Other Miscellaneous Conditions of dentin is deposited less rapidly with regular
the Pulp tubular pattern and minimum cellular inclu-
sions.
• Aerodontalgia • In most of the areas, there is no continuity
• Necrosis between dentinal tubules of reparative dentin
• Reticular atrophy and the overlying primary or secondary
• Calcifications dentine. This minimizes dentin permeability
• Pulpal metaplasia. and provides more protection to the pulp.

Diseases of Dentin-Pulp Complex and Periapical Tissues 391

DIRECT PULPAL RESPONSE TO • Young people develop focal reversible pul-
INJURIOUS STIMULI pitis more often than the older individuals
because of the more reparative capacity of the
• The pulpal tissue tries to eliminate or pulp tissue among the former group.
neutralize the damaging factors and initiate
tissue repair. • Pulpal stimuli, which cause reversible pulpitis
in young people often causes irreversible
• Cellular damage to the pulpal tissue results pulpitis to the older individuals because of the
in the release of vasoactive and chemotactic less pulpal tissue viability.
mediators in the area.
• The affected tooth responds to stimulation by
• Vasoactive mediators produce vasodilatation electric pulp tester at a lower level of current
and the chemotactic agents attract specific (including a lower pain threshold) when
inflammatory cells to the injured tissue. compared with an adjacent normal tooth.

• Pulpal tissue also produces immunoglo- • The involved tooth often has large carious
bulines, e.g. IgG, IgM, IgA and complement lesions or restoration with improper insulation.
C3 and C4 in response to the bacterial antigens
of dental caries. HISTOPATHOLOGY

FOCAL REVERSIBLE PULPITIS Histologically, focal reversible pulpitis presents
the following features (Fig. 10.1):
Focal reversible pulpitis or pulp hyperemia is a • Acute inflammatory reaction in the pulp
mild, transient, localized inflammatory reaction
in the pulp, which can be treated by conservative limited to the odontoblastic or subodonto-
means, without involving any form of direct pulp blastic regions, adjacent to the irritated
therapy. dentinal tubules.
• Dilatation of pulpal blood vessels with
Etiology of focal reversible pulpitis increased vascular permeability.
• Edema in the pulp with infiltration by the
• Slowly progressing chronic carious lesion. polymorphonuclear leukocytes in the area.
• Stimuli of short duration, e.g. cutting dentin • Odontoblast cell nuclei may be displaced into
the dentinal tubules due to either increased
while cavity preparation. local tissue pressure or due to abnormal
• Metallic restoration without proper thermal dentinal fluid movements during injury.
• Few odontoblast cells could be damaged in
insulation. the localized area of injury.
• Chemical irritation to the pulp (e.g. acid etching • Thrombosis of pulpal blood vessels may occur
in some cases.
in cervical margin of tooth).
• Excessive pressure by orthodontic appliances.f.

Severe attrition or abrasion of tooth with
minimal dentin thickness.

CLINICAL FEATURES Fig. 10.1: Photomicrograph of focal reversible pulpitis

• The tooth with focal reversible pulpitis is
sensitive to thermal changes, especially to
cold.

• Pain often results while drinking cold fluids
or when ice or cold air is applied to the tooth.

• The pain is of very short duration and it
disappears as soon as the thermal irritant is
withdrawned.

• Pain also results when the tooth is exposed to
extremely high temperatures.

392 Essentials of Oral Pathology

• Repair takes place by redifferentiation of odon- CLINICAL FEATURES
toblast cells, which are damaged and some-
times with deposition of reparative dentin. Acute pulpitis is often considered as one of the
most dreaded disease of tooth because of the
TREATMENT horrific nature of pain involved in it. The disease
usually presents the following features:
Treatment of focal reversible pulpitis is mostly • The tooth is extremely sensitive to hot and
directed towards elimination of the primary
irritating factors and restoration of tooth cold stimuli; however the pain in acute
wherever necessary. pulpitis can start spontaneously in the absence
of any stimulus.
Reversible pulpitis due to dental caries is • A short and severe “lancinating” type of pain
usually treated by the following means: is often elicited from the affected tooth.
• Effective dietary change. • Application of hot or cold stimuli causes an
• Sealing of the exposed dentinal surface. increase in the intensity of pain and such type
• Excavation of carious dentin followed by of pain persists for a longer duration even after
the stimuli are removed.
placement of a suitable dressing material (e.g. • As the dental pulp is located within the solid
zinc oxide–engenol). confinement of dentinal walls, intra-pulpal
pressure builds-up quickly and so is the pain,
ACUTE PULPITIS since there is lack of escape route of
inflammatory exudates during pulpal
Acute pulpitis is an irreversible condition inflammations.
characterized by acute, intense inflammatory • In the initial stages of acute irreversible
reaction in the pulpal tissue. pulpitis the pain can be localized or rather the
patient can identify the offending tooth,
MODE OF DEVELOPMENT however in the more severe later stages the
pain becomes regional and the patient is
Acute pulpitis can occur in the following unable to identify the offending tooth.
pathways: • The intensity of pain increases during sleep
• As an extension of the focal reversible pulpitis. because there is an increase in the local blood
• As a de novo condition, where the inflam- pressure in head and neck region in supine
position, which results in increased flow of
mation is acute from the beginning. blood in the pulp chamber. More flow of blood
• As an acute exacerbation of the chronic in the pulp chamber causes more compression
of the nerves resulting in more pain.
pulpitis. If the entrance to the pulp opening is not wide,
acute pulpitis not only causes an excruciating
Etiology of acute pulpitis pain but also helps in quickly spreading the
inflammation throughout the pulp with
• Caries progressing beyond the dentinal barrier subsequent necrosis.
and reaching the pulp. • Acute pulpitis is often associated with micro-
abscess formation in the pulp along with
• Pulp exposure due to faulty cavity preparation. liquefaction degeneration.
• Blow to tooth with subsequent damage to pulp. •. When drainage is established, small amount
• Excessive heating of tooth during cavity of pus exudes from the opening, which has a
noxious odor.
preparation without water spray. • The affected tooth responds to a lower level
• Chemical irritation to the pulp. of current, if electric pulp tester is used.
• Cracked tooth syndrome.
• Tooth or teeth coming in the line of fracture

when the jaw is traumatized.
• Anachoretic infection to the pulp.
• Recurrent caries around a pre-exiting restoration.
• Metallic restoration in a tooth without proper

thermal insulation.

Diseases of Dentin-Pulp Complex and Periapical Tissues 393

• Pain subsides when the drainage is Fig. 10.3: Photomicrograph of pulp abscess
established or when the pulp undergoes
complete necrosis. TREATMENT
As acute-pulpitis is an irreversible condition no
• The tooth is neither mobile and nor tendered treatment can be accomplished without an active
to percussion; unless the pulpal inflammation and surgical pulp therapy, which could range
has spread beyond the root apex into the from partial to complete removal of pulp.
periapical region.
The treatment modalities are as follows:
• Patients with acute pulpitis are often appre- • Drainage of exudate or pus from the pulp
hensive and moderately ill.
chamber.
• When intrapulpal pressure becomes very high • Direct pulp capping.
during acute inflammation, it can cause • Root canal treatment (RCT).
collapse of the apical blood vessel. This pheno- • Extraction of tooth.
menon is known as “pulp-strangulation”.
CHRONIC PULPITIS
HISTOPATHOLOGY
Chronic pulpitis is a condition characterized by
Acute pulpitis presents the following histopatho- a low grade, often persistent inflammatory
logical features (Fig. 10.2): reaction in the pulpal tissue with little or no
• Severe edema in the pulp with vasodilatation. constitutional symptoms.
• Moderate to dense infiltration of polymorpho-
ETIOLOGY
nuclear leukocytes. Etiology for chronic pulpitis is same as that of
• Focal or complete destruction of the odonto- the acute pulpitis but here the irritants are of low
virulence.
blast cells at the pulp dentin border.
• Many micro-abscess formations, charac-

terized by areas of liquefaction degeneration
in the pulp being surrounded by dense band
of neutrophils and microorganisms (Fig. 10.3).
• In severe cases, there may be complete
liquefaction and necrosis of the pulp with
total destruction of the odontoblastic cell
layer. This phenomenon is known as acute
suppurative pulpitis.
• Death of the pulp may also be accompanied
by tissue dehydration. This condition is
known as “dry gangrene of the pulp”.

MODE OF DEVELOPMENT

• Chronic pulpitis mostly occurs as a chronic
inflammatory reaction in the pulp from the
very beginning.

• Occasionally, it may be present as a quiescent
phase of the pre-existing acute pulpitis.

Fig. 10.2: Photomicrograph of acute pulpitis CLINICAL FEATURES
Generally in chronic pulpitis the signs and
symptoms are much milder in comparison to the
acute pulpitis.

394 Essentials of Oral Pathology

• The tooth with chronic pulpitis may be PATHOGENESIS
asymptomatic for quiet some time.
Pulp polyp exhibits an intense proliferation of
• In other cases there may be an intermittent the pulpal connective tissue and this type of
dull and throbbing pain in the tooth. hyperplastic tissue growth depends on several
factors, which are as follows:
• The tooth is less sensitive to hot and cold
stimuli. Contributing factors for pulp polyp

• The tooth usually responds to a higher level • Persistence of balance between injurious agents
of current when electric pulp tester is used. It and tissue resistance.
happens due to degeneration of most of the
nerve fibers in the chronically inflamed pulp. • Presence of a low grade sustained inflammation.

• Even if the pulp is exposed to the oral • Pulp tissue should be well-vascularized with
environment through a large open cavity in excellent tissue reactivity.
the tooth, still a very little pain is felt.
• The carious cavity should be wide open.
• Manipulation of the chronically inflamed pulp
by small instruments often elicits bleeding but • The patients must be young with good body
the maneuver causes little pain. resistance.

HISTOPATHOLOGY • The apical foramen of the affected tooth must
be wide so that pulpal strangulation and
• The chronic inflammatory response in the complete necrosis due to inflammation does
pulp is characterized by cellular infiltration not occur.
by lymphocytes, plasma cell and If all these factors are favorably present, a tooth
macrophages, etc. with chronic pulpitis many progress further into
chronic hyperplastic pulpitis. However, the
• The chronic nature of the inflammation may incidence rate is quite low.
continue for a long-time with occasional
periods of acute exacerbations. CLINICAL FEATURES

• Blood capillaries are prominent and few • Pulp polyp clinically appears as a small,
microorganisms are also found in the pulpal pinkish-red, lobulated mass, which
tissue. protrudes from the pulp chamber and often
fills up the carious cavity.
• Prolonged chronic inflammation may
encourage fibroblastic activity in the pulp with • The teeth in which pulp polyp commonly
formation of collagen bundles. develops are often the deciduous molars and
first permanent molars.
• Persisting chronic pulpitis may cause diffuse
or solitary areas of calcification in the pulp. • The condition is obviously seen in either
children or young adults.
• Chronic inflammation in the pulp in some
cases may result in internal resorption of the • The affected tooth always has a large open
tooth. carious cavity, which is present for a long
duration.
TREATMENT
• The lesion bleeds profusely upon provocation.
• Root canal treatment or • If traumatized, the pulp polyp becomes
• Extraction of tooth.
ulcerated and appears as a dark red, fleshy
PULP POLYP (CHRONIC HYPERPLASTIC mass with fibrinous exudate on the surface.
PULPITIS) • The involved tooth is usually painless but it
may be sensitive to thermal stimuli.
Pulp polyp is an unusual type of hyperplastic • Although pulp polyp is a purely connective
granulation tissue response in the pulp, which tissue growth, it may be sometimes super-
is characterized by an overgrowth of the tissue ficially epithelized.
outside the boundary of the pulp chamber as a
protruding mass.

Diseases of Dentin-Pulp Complex and Periapical Tissues 395

• The epithelized surface of the pulp polyp may
sometimes show even well-formed retes peg-
formation.

TREATMENT
Treatment is done either by root canal treatment
or by extraction of the affected tooth.

Fig. 10.4: Photomicrograph of pulp polyp AERODONTALGIA

HISTOPATHOLOGY Aerodontalgia is an unusual type of dental pain,
which occurs as an effect of change in the
Pulp polyp histologically presents the following altitude.
features (Fig. 10.4):
• The hyperplastic pulpal tissue lesion presents CLINICAL FEATURES

the features of a granulation tissue mass, con- • Aerodontalgia affects some persons who,
sisting of numerous proliferating fibroblasts experience pain in the tooth during high
and young blood capillaries. altitude flight or during deep sea diving.
• There may be edema and hyperemia of the
pulpal tissue. Moreover, focal areas of pulp • At ground levels the tooth is completely
necrosis, which are surrounded by area of asymptomatic.
fibrosis, are often seen.
• Inflammatory cell infiltration chiefly by the •. In some cases the pain may not start readily
lymphocytes, plasma cells and sometimes during flight or during diving, instead it may
polymorphonuclear neutrophils in the tissue occur few hours or days later.
are common.
• Reparative secondary dentin may be formed • The condition may be related to subclinical
adjacent to the dentinal wall of the affected pulpitis.
tooth.
• Stratified squamous type epithelial lining is • Sometimes, similar problem may happen in
often observed on the surface of the pulp an endodontically treated tooth with improper
polyp, which resembles oral epithelium. obturation of the canals.
• The epithelial cells on the surface of the polyp
are believed to be the desquamated epithelial • The entrapped air in the improperly obturated
cells, which came either from the buccal root canals may expand during flight or during
mucosa, gingiva or from the salivary gland diving (due to alteration in the atmospheric
ducts. pressure), which creates pressure in the
• These cells are carried via saliva and are periapical nerve bundles and produce pain.
transplanted on to the surface of the pulp
polyp. PULP NECROSIS
• When the pulp polyp is present for a long-
time, persistent rubbing of the buccal mucosa Pulp necrosis may occur either due to pulpitis or
against the lesion may help in the grafting of due to injury and subsequent occlusion of the
epithelial cells on its surface. apical blood vessel.
• A coagulative type of necrosis of the pulp

occurs due to ischemia.
• When the necrosis follows pulpitis, the

breakdown of inflammatory cells may lead to
liquifactive degeneration in the pulp.
• The necrosed pulp may become secondarily
infected by putrefactive bacteria from caries.
• The gangrenous necrosis of pulp is usually
associated with a foul odor, when the pulp
chamber is opened for endodontic therapy.

396 Essentials of Oral Pathology

• In sickle cell anemia, blockage of the pulpal
vessel by sickled or defective RBCs may result
in pulp necrosis.

DIAGNOSIS OF PULPAL DISEASES

Several clinical tests are performed for the eva-
luation of pulpal disease, which are as follows:

History Fig. 10.5: Photomicrograph of necrotic pulp

• Pulpitis history often reveals the state of the Bacteriology of pulpal infections: The commonly
disease. History of intense pain in the tooth, encountered microorganisms in the dental
which continues even after the removal of pulp during acute or chronic pulpitis are as
stimulus, indicates an irreversible pulpal folows:
damage.
(I) ANAEROBIC ORGANISMS
• If the pain or sensitivity comes down as soon Gram-negative rods
as the stimulus is withdrawned, the condition
is probably a reversible pulpitis. Bacteroides buccae
Bacteroides denticola
• A tooth having dull pain of late but has passed Bacteroides endodontalis
through previous bouts of sharp acute pain, Bacteroides gingivalis
indicates either chronic pulpitis or pulp Fusobacterium nucleatum
necrosis. Wolinela recta
Selenomonous sputigena
Clinical Examination
Gram-negative cocci
Clinical examination of tooth either visually or Veillonella parvula
with hand instruments may help in establishing
the diagnosis of the pulpal diseases. Gram-positive rods
• Carious exposure in a tooth can be easily Actinomyces israelii
Actinomyces odontolyticus
detected by clinical examination. Eubacterium alactolyticum
• Similarly a fractured tooth with pulp damage Eubacterium brachy
Eubacterium lentum
can also be detected by this method. Eubacterium nodatum
• Change in the color of the tooth can spell-out Lactobacillus catenaforme
Lactobailus minutus
if the pulp is vital or not.
Gram-positive cocci
Radiographic Examination Streptococcus constellatus
Streptococcus intermedius
Intraoral periapical radiographs or bitewing Streptococcus morbillorum
radiographs, etc. can help in establishing a Peptostreptococcus anaerobius
diagnosis in pulpal disease (Fig. 10.5). Although Peptostreptococcus magnus
these findings are not always perfect, Peptostreptococcus prevotii.
radiographs can often indicate if the carious
infection has reached to the pulp or if the pulpal
inflammation has already progressed beyond the
apical foramen into the periapical tissue.

Clinical Test for Evaluation of Pulp
Response (pulp vitality tests)

If the dental pulp is not in a healthy state it will
generate abnormal responses to different stimuli
and this can help in making a diagnosis of the
pulpal disease.

Diseases of Dentin-Pulp Complex and Periapical Tissues 397

Pulp vitality tests

• Heat test: Sensitivity to heat may be tested by application of hot water or heated gutta-percha stick on
the suspected tooth. A tooth having pulpitis will respond to a lower level of heat as compared to a
normal tooth. Therefore, it is always important that the response gathered from a suspected tooth
should always be compared with a normal tooth from the some arch or the opposing arch.

• Cold test: Selective application of cold water or water ice or dry ice can help in assessing the pulpal
health. This is by far the most reliable method of pulp testing.

• Percussion: Sensitivity to percussion indicates periapical inflammation in a tooth, this can happen in
pulpitis only when the inflammatory process has extended beyond the tooth apex into the periapical
area. Percussion sensitivity should be carried out both in vertical and in horizontal direction.

• Palpation: Palpation of the apical tissues may elicit tenderness or it may reveal soft or hard tissue swelling,
which are indicative of periapical inflammations.

• Pressure: Gentle pressure on the tooth often helps to diagnose fracture or cracked tooth syndrome. It
can also give indication regarding the presence of periapical inflammation.

• Electrical pulp test: The electric pulp testing reveals the varying degrees of sensory reply in the pulp,
which alters in different inflammatory states. In reversible pulpitis the pulp gets stimulated at a lower
level of current as compared to that of a normal pulp (because of lower pain threshold). In irreversible
pulpitis the threshold level is further lowered and the pulp responds to an even lower level of current. In
chronic pulpitis the pulp responds to a higher level of current (as compared to normal pulp) and it
happens due to the decreased number of sensory nerve fibers in the pulp as a result of necrosis.

• Laser Doppler flowmetry: It can be used as an advanced diagnostic aid for accurate diagnosis of pulpal
pathology.

(II) AEROBIC AND FACULTATIVE Gram-positive rods
ANAEROBIC ORGANISMS Actinomyces naeslundii
Actinomyces viscosus
Gram-negative rods
Capnocytophaga ochracea Gram-positive cocci
Eikenella corrodens Streptococcus mutans
Campylobactor sputorum Streptococcus milleri
Streptococcus mitior
Streptococcus sanguis

Factors causing retarded healing of the pulp tissue following injury

There are many factors both physiological and pathological which reduce the healing capacity of the pulpal
tissue. And because of this pulp becomes less able to withstand mechanical chemical or inflammatory insults.

The factors are as follows:
• Decrease in the vascularity and cellularity of pulp in advanced age.
• Fibrosis and calcification in the pulp.
• Decrease in the volume of pulp tissue due to continuous dentin deposition
• Obliteration of the pulp canal due to injury causes decrease in the blood supply to pulp and the residual

pulp tissue eventually dies.
• Chronic periodontal disease can cause more and more deposition of reparative dentin and therefore

reduce the size of the pulp chamber and diameter of root canal.
• Gross calcification in the pulp tissue due to hereditary disorders, e.g. dentinogenesis imperfecta may

reduce the ability of pulp to survive injury.
• Developmental anomalies of tooth, e.g. dens-invaginatus, may provide an easy access for progression of

dental caries towards the pulp.
• Systemic diseases, e.g. diabetes, anemia and nutritional deficiency, etc. cause a general reduction in the

host defence mechanism and therefore have an obvious effect on pulp as well.
• Radiotherapy in the jawbones with subsequent effect on the tooth pulp.

398 Essentials of Oral Pathology

DISEASES OF THE PERIAPICAL Possible complications:
TISSUES • Periapical abscess formation
• Regional lymphadenopathy
PRIMARY ACUTE APICAL • Cellulitis
PERIODONTITIS • Development of periapical granuloma.

Primary acute apical periodontitis mostly occurs TREATMENT
as a result of extension of the pulpal inflam- Extraction or endodontic treatment of the
mation into the periapical tissues. The lesion may diseased tooth.
also occur as a result of occlusal trauma and in
such cases the pulp is vital. PERIAPICAL GRANULOMA
(CHRONIC APICAL PERIODONTITIS)
CLINICAL FEATURES
DEFINITION
• Moderate pain and sensitivity in the tooth. Periapical granuloma is a localized mass of
• Slight extrusion of the tooth due to escape of granulation tissue around the root apex of a non-
vital tooth, which develops in response to a low
inflammatory exudates into the apical grade infection or inflammation.
periodontal ligament.
• The most important and determining feature Etiological factors in periapical granuloma
is the severe pain on slight pressure during
mastication. It happens because normal • Extension of the pulpal inflammation or infection
chewing pressure becomes too heavy for the beyond the root apex.
tooth as it is extruded or raised occlusally due
to apical inflammation. • Occlusal trauma.
• There is discomfort in the tooth initially and • Orthodontic tooth movements with excessive
gradually it becomes more and more
tendered, even to mere touch. uncontrolled force.
• Thermal changes (hot and cold) do not • Acute trauma due to blow on the tooth.
aggravate the pain. • Perforation to the root apex during endodontic
• As the disease progresses, the inflammation
becomes more and more severe with forma- therapy.
tion of pus in the apical region, at this stage • Spread of periodontal infection into the root
the pain is very intense and is throbbing in
nature. apex.
• The gingiva overlying the affected root may • Chemical irritation.
be red and tendered.
• Acute apical periodontitis due to pulpal PATHOGENESIS
infection is not reversible and mostly turns
into chronic apical periodontitis or periapical Most of the periapical granulomas develop due
granuloma. to the spread of pulpal infections beyond the root
• Sometimes the exudates may penetrate the apex. The root canal of a non-vital tooth is an
overlying bone and periosteum and cause soft ideal environment for bacterial growth because
tissue swelling and even cellulitis. it protects the organisms from normal body
• Intrestingly once the facial swelling develops defenses, as well as it provides them with good
the pain in the offending tooth becomes less nutrition. In case of periapical granuloma a
due to relief of pressure in the periapical balance between the pathogenicity of bacteria
region of the tooth. within the canal and the defense capacity of the
• The regional lymph nodes are often enlarged periapical tissue is established.
and tendered.
Inflammation in the periapical region causes
destruction of the apical periodontal ligaments,
adjoining alveolar bone and cementum, etc.

Diseases of Dentin-Pulp Complex and Periapical Tissues 399

Later on, these tissues are replaced by a mass of HISTOPATHOLOGY
“granulation tissue”. The granuloma increases Histologically, periapical granuloma presents the
in size due to the gradual resorption of the following features (Fig. 10.6):
surrounding bone by chemical mediators like— • The lesion appears as a granulation tissue
osteoclast activating factor (OAF) and collage-
nase, etc. which are released by the chronic mass consisting of proliferating fibroblasts,
inflammatory cells. endothelial cells and numerous immature
blood capillaries.
CLINICAL FEATURES • Chronic inflammatory cells, e.g. macrophages,
lymphocytes and plasma cells, etc. are often
• The offending tooth produces sensitivity to present in the lesion.
percussion, which occurs due to edema, • Some lesions show the presence of epithelial
hyperemia and inflammation of the apical islands, cholesterol clefts and foam cells.
periodontal ligaments. • Giant cells are also found on rare occasions.
• The plasma cells often produce immuno-
• There can be mild pain and discomfort in the globulin (IgG, IgM, IgA and the IgE, etc.).
tooth during chewing solid foods. Besides this, there is also presence of T
lymphocytes in the lesion.
• Patient may give a previous history of pain in • Although periapical granuloma is a “sterile”
the tooth (earlier when pulpitis was present), lesion, it is often observed that few bacteria
which had subsided thereafter. (e.g. Actinomyces israelii, Actinomyces naeslundii
and Arachnida proprionica) are almost always
• The involved tooth is always non-vital and it present in the lesion and they are not affected
does not responds to thermal or electric pulp by the cellular immune mechanism.
testers. • The epithelial cell rests of Malassez, a natural
component of the periodontal ligament, pro-
• The tooth may be slightly elongated from its liferate in response to chronic inflammation
socket and is tendered to the chewing and these proliferating cells later on may
pressure. undergo cystification to produce radicular
cyst.
• In many cases, periapical granuloma may be • The bony tissue at the periphery of the lesion
asymptomatic throughout its course. is usually lined by osteoclast cells with areas
of bone resorptions.
• There may be severe pain and sensitivity in • Resorption of cementum and dentin often
the tooth during acute exacerbations of the occurs as a result of the chronic inflammation
disease.
Fig. 10.6: Photomicrograph of periapical granuloma
RADIOLOGICAL FEATURES

• Most of the lesions are detected incidentally
during routine radiographic examinations.

• In the initial stages, periapical granuloma
radiographically shows widening of the
periodontal ligament space of the tooth.

• Fully developed lesions usually produce a well-
defined, radiolucent area of varying size, which
appears to be in continuity with the root apex.

• Sometimes, the radiolucent lesion is well-
demarcated from the surrounding normal
bone by a thin sclerotic margin.

• In other cases, the radiolucency blends
gradually with the surrounding tissue.

• Long-standing periapical granuloma may
show varying degrees of root resorption and
loss of apical lamina dura.

400 Essentials of Oral Pathology

but in some areas along the root, cemento- PERIAPICAL ABSCESS
blastic activity may predominate leading to (DENTOALVEOLAR ABSCESS)
hypercementosis like reaction.
DEFINITION
TREATMENT
Periapical abscess can be defined as a localized,
The lesion is treated either by extracting the tooth acute or chronic suppurative infection in the
or by performing root canal treatment in the tooth periapical region of a non-vital tooth.
with apicoectomy or apical curettage.
Etiological factors of periapical abscess
SEQUELAE
• Extension of pulpal infection into the periapical
Sequelae of periapical granuloma: tissue.
• If the granuloma continues to enlarge, resorp-
• Fracture of tooth with pulp exposure.
tions of root apex or apical bone may occur. • Accidental perforation of the apical foramen
• Acute exacerbation may produce (acute apical
during root canal treatment, which results in
periodontous) with severe pain, discomfort entry of pulpal microorganisms into the
and tenderness to percussion. periapical area.
• Suppuration in the periapical granuloma may • Extension of periodontal infection into the
lead to acute periapical abscess formation. periapical tissues.
• Proliferation of epithelial cell rest of malassez • Secondary bacterial invasion into the pre-existing
may lead to development of radicular cyst. periapical granuloma or cyst or scar.
• Low-grade infection from periapical granu- • Anachoretic infection of the periapical tissues.
loma may cause osteosclerosis (bone
apposition) in the apical region of tooth. PATHOGENESIS
• Similar low-grade infections may cause
hypercementosis in the affected tooth as well. Periapical abscess often results from a mixed
bacterial infection caused by strict anaerobes, e.g.
ACUTE EXACERBATION OF Prevotella and Porphyromonas, etc. Anaerobic
CHRONIC PERIAPICAL GRANULOMA streptococci and staphylococci also play major
(PHOENIX ABSCESS) roles in causing the disease.

• Most of the periapical granulomas clinically CLINICAL FEATURES
remain quite as long as the balance between the
bacteria contained within the root canal and • Periapical abscess is a common odontogenic
body’s defense in the granuloma is maintained. infection and constitutes about 2 percent of
all apical radiolucencies.
• If this balance is lost somehow, an explosive
type of acute exacerbation occurs in the pre- • Acute abscess produces severe pain in the
existing chronic lesion, which is known as affected tooth.
“phoenix abscess”.
• There will be localized swelling and an ery-
• Clinically phoenix abscess presents severe thematous change in the overlying mucosa.
pain, local swelling, extreme tenderness in the
tooth upon pressure and sometimes facial • The pain aggravates during percussion or
cellulitis, etc. when pressure is applied with the opposing
tooth.
• The intense pain in phoenix abscess may result
from excessive accumulation of purulent • Pressure from purulent exudates and
exudates. inflammatory infiltrates in the periapical area
often causes extrusion of the tooth from its
• Treatment is done by drainage either via the socket.
root canal or by an incision over the localized
swelling. Antibiotics are always given to • The associated tooth is non-vital and
control the infection. sometimes it can be mobile also.

• The affected area of the jaw may be tendered
on palpation.

Diseases of Dentin-Pulp Complex and Periapical Tissues 401

• Elevated body temperature and localized • The lesion appears as a zone of liquefaction
lymphadenitis are common findings in necrosis, which is made up of proteinaceous
periapical abscess. exudates, necrotic tissue and a large number
of viable or dead neutrophils (pus).
• Application of heat on the tooth intensifies
pain, whereas application of cold relieves the • The adjacent tissues surrounding the
pain temporarily. liquefaction zone have many dilated blood
capillaries and infiltration with neutrophils.
• If prompt treatment is not given, the abscess
penetrates the cortical plate of bone (mostly • Inflammatory change is also observed in the
buccal) and invades into the adjacent soft periodontal ligament and adjoining bone–
tissues, thereby causing cellulitis. marrow.

• Pus discharging sinus often develops on the • Bony trabeculae in the periapical region may
alveolar mucosa over the affected root apex show empty lacunae, which results from the
and sometimes on the skin overlying the death of the osteocytes.
jawbone.
• In chronic periapical abscess the inflammatory
• If the host resistance is high or the virulence cell pattern is different and in these lesions
of the organisms involved in periapical often exhibit infiltration by lymphocytes,
abscess is low, a chronic stage of the abscess plasma cells and macrophages, etc.
sets in, which mostly remains asymptomatic.
• Areas of bone destruction are also accom-
• Unlike the acute lesions, chronic periapical panied by areas of fibrosis as well as bone
abscess usually produces mild, dull pain and regeneration in chronic lesions.
it also produces intraoral or extraoral pus vii. Pus discharging sinus in chronic abscess
discharging sinuses. is often lined either by a granulation tissue or
by a squamous epithelial lining.
• Infections from the acute periapical abscess
often spread to the facial spaces, leading to TREATMENT
space infections.
For the treatment of acute periapical abscess
• Infection of the facial spaces may be further standard principles of management of acute
complicated by the development of septi- inflammation are as follows:
cemia, Ludwig’s angina and cavernous sinus • Drainage is established either through an
thrombosis, etc.
opening in the tooth or by an incision over
• In periapical abscess, spread of periapical the soft tissue swelling at the apex region.
infections into the medullary spaces of bone • Antibiotics are administered against the
may produce osteomyelitis in some patients. offending microorganisms.
• Once the acute phase of the disease is
RADIOLOGICAL FEATURES brought under control, the affected tooth is
treated either by root canal therapy or by
As the acute periapical abscess develops quite extraction.
rapidly, there is little time for the lesion to cause
any significant amount of bone resorption that OSTEOMYELITIS
could be detected radiographically. Therefore,
radiographic changes in acute abscess are DEFINITION
minimum and are limited to only slight
thickening of the periodontal ligament space in Osteomyelitis can be defined as the
apex region of the involved tooth. inflammation of bone and bone marrow along
with the surrounding periosteum. The
However, in chronic periapical abscess, inflammatory condition involves all the
radiographs often reveal small radiolucent areas structures of bone, e.g. the bone marrow,
at the root apex with poorly defined margins. haversian systems, periosteum, blood vessels,
nerves and epiphyses, etc.
HISTOPATHOLOGY

Histologically, periapical abscess presents the
following features:

402 Essentials of Oral Pathology

Classification of osteomyelitis • Spread of infection following removal of tooth
without proper asepsis and antibiotic
There are various types of osteomyelitic lesions coverage.

occurring in the jawbones, which can be broadly • Compound fracture of the jawbone with
divided into two groups—acute osteomyelitis and exposure of bone outside the skin or
chronic osteomyelitis. According to the specificity mucosa.
of the causative microorganisms, osteomyelitis may
• Gunshot injuries in the jaw with soft tissue
be of two types—specific osteomyelitis and non- laceration and exposure of bone.
specific osteomyelitis.
Acute osteomyelitis • Spread of microorganisms from overlying soft
tissue (skin or mucosa) infections.
Most commonly encountered (Nonspecific)
• Post-radiation secondary infection.
lesions in this category include:
• Acute suppurative osteomyelitis Predisposing factors of osteomyelitis
• Acute subperiosteal osteomyelitis
• Acute periosteitis Local Factors
• Anatomical site of the disease: The mandibular
Chronic osteomyelitis
Nonspecific type bone has poor blood supply in comparison to
• Chronic intramedullary osteomyelitis that of the maxilla, besides this it has more
• Chronic focal sclerosing osteomyelitis compact bony pattern due to which, osteomye-
litis occurs far more commonly in mandible than
• Chronic diffuse sclerosing osteomyelitis maxilla.
• Chronic osteomyelitis with proliferative • Pre-existing bone disease: Long standing bony
disease like Paget’s disease of bone, fibrous
periosteitis dysplasia, cystic lesions, osteopetrosis, etc. many
• Chronic subperiosteal osteomyelitis render the jaw bones more susceptible to
osteomyelitis, when infections occur in the
• Chronic periosteitis. tissue.
Specific type • Radiation injury: Radiotherapy to the head and
• Tuberculous osteomyelitis. neck area often produces obliterative endarte-
• Syphilitic osteomyelitis. ritis, which results in impaired blood supply to
the jawbones. Therefore in such conditions
• Actinomycotic osteomyelitis. possibility of osteomyelitis is increased once the
Radiation induced osteomyelitis infection in the bone sets in.
Systemic Factors
Idiopathic osteomyelitis Predisposing factors (systemic) in osteomyelitis
favor the development of the disease by lowering
ETIOLOGY OF OSTEOMYELITIS the body resistance to infections. These factors
include the following:
Numerous etiologic factors have been identified, • Malnutrition and chronic alcoholism
which can cause osteomyelitis and these factors • Drug addiction
are as follows: • Anemia, especially sickle cell anemia
• Direct spread of infection from dental pulp • Diabetes (poorly controlled)
• Acute leukemia
into the jawbone. • Agranulocytosis
• Spread of infection into the bone from the pre- • Syphilis
• Measles and typhoid fever.
existing suppurative odontogenic infections, • HIV infection and AIDS.
e.g. • Extremes of age
– Periapical abscess. • Urinary tract infection.
– Periodontal pocket involved in a fractured

jaw bone.
– Infected periapical granuloma
– Infected periapical cyst.
– Acute necrotizing ulcerative gingivitis
– Periodontal abscess.
– Pericoronitis
– Infected and fractured tooth/retained root

tip.

Diseases of Dentin-Pulp Complex and Periapical Tissues 403

• Infection to the pre-existing bony diseases, e.g. • Due to thrombosis of the nutrient vessels and
Paget’s disease of bone, fibrous dysplasia and excessive pressure from the inflammatory
osteopetrosis, etc. exudates against the rigid and confined space
in the bone, the nutrition supply to the bone
• Phosphorus poisoning cells is completely disturbed resulting in death
• Anachoretic infections of cancellous bony trabeculae with formation
• Idiopathic factors. of ‘sequestrum’.

Being an inflammatory disease, development • The infection then spreads via the Volkmann’s
of osteomyelitis depends mainly upon the canals in the cortical plates and reaches to the
balance between the virulence and number of external surface of bone below the periosteum,
microorganisms present in the bone and the local inflammation at this area results in periosteitis.
or systemic defense capacity of the patient’s body
to infection. • Accumulation of more and more exudates and
pus cause separation between the cortical
However, besides these two main factors there plates of bone and the periosteum.
are several other predisposing factors which play
determining role in the pathogenesis of • Further extension of the inflammation may
osteomyelitis. lead to single or multiple sinus tracts forma-
tion, which communicate between the bone
MICROORGANISMS INVOLVED IN and the external surface of the skin and
OSTEOMYELITIS mucous membrane.

Osteomyelitis due to specific bacterial infections • As the cortical plates of the bone get the blood
like tuberculous, syphilitic and actinomycotic supply from the overlying periosteum,
group of organisms occurs in the jawbones quite separation between the cortical plates and
often. Osteomyelitis of the jaws due to non- the periosteum results in necrosis of the
specific bacterial infections is far more common cortical bone.
as compared to the specific types and micro-
organisms responsible for this type of infections • Although the periosteum is infected and
are as follows: elevated from the cortical bone, a few bone-
• Aerobic organisms forming cells still survive in it and when the
acute phase of the disease subsides, a new
Staphylococcus aureus layer of bone may form over the sequestrum
Hemolytic Streptococcus which completely surrounds it, the enclosed
• Anaerobic organisms sequestrum is now called the ‘involucrum’.

Bacteroids • Pus discharges from the involucrum through
Anaerobic Streptococcus. sinuses called cloacae and bathe the surface
of the sequestra.
PATHOGENESIS OF OSTEOMYELITIS The above mentioned pathogenic mechanisms

In osteomyelitis inflammation and destruction apply largely to suppurative osteomyelitis.
of bone take place by the following mechanisms: However, there can be several cases of osteo-
• Infection from the periapical lesions or infec- myelitis, which are characterized by simul-
taneous bone destruction and bone formation
ted pulp or other foci enters into bone marrow (e.g. non-suppurative osteomyelitis and Garre’s
first and from there it extends into the osteomyelitis, etc.). In these lesions, a balance
cancellous bony spaces. always exists between the virulence of the
• As the infection is established, the lumina of pathogenic organism and the host’s local and
the nutrient vessels of the living bone are systemic defense mechanism.
occluded by the formation of thrombus. (The
thrombus consists of dead or viable ACUTE SUPPURATIVE
neutrophils, microorganisms and necrotic OSTEOMYELITIS
tissue debris, etc.)
Acute suppurative osteomyelitis is a serious
type of diffusely spreading acute inflammation

404 Essentials of Oral Pathology Fig. 10.8: Osteomyelitis-II

of the bone, characterized by extensive tissue Fig. 10.9: Acute osteomyelitis causing
necrosis. formation of extraoral sinus

CLINICAL FEATURES

Age: Acute osteomyelitis usually occurs after
30 years of age as there is more probability of
systemic diseases from this age and onwards and
moreover there is also decreased bony resistance
to infection (due to reduced vascularity).

Sex: Incidence is more among males than
females.

Site: The mandible is involved more often than
the maxilla as it has a limited blood supply and
it is a dense bone with thicker cortical plates.
The mandibular lesions are usually diffuse in
nature, while the maxillary lesions are mostly
well-localized. Moreover the maxillary lesions
are rare and are seen in infants or neonates
following birth injuries or severe otitis media,
etc.

Bacteriology: Staphylococci and Streptococci are
the organisms, which predominantly cause acute
suppurative osteomyelitis of the jaw. However,
Actinomyces israelii, Prevotella, Porphyromonous
and Bacteroids can also cause the disease.

CLINICAL FEATURES (FIGS 10.7 TO 10.10)

• Acute suppurative osteomyelitis often causes
severe throbbing, deep seated pain and diffuse
large swelling of the jaw along with the related
soft tissues.

• Often there is loosening and soreness of the
regional teeth with difficulty in taking food.

Fig. 10.7: Osteomyelitis-I Fig. 10.10: Intraoral view of the same patient showing large
area of soft tissue necrosis in mandibular molar region

• The overlying gingiva is often red, swollen
and tendered to palpation.

• Excessive muscle edema may cause difficulty
in mouth opening and swallowing.

• Patients often complain of excessive salivation
and bad breath, etc.

Diseases of Dentin-Pulp Complex and Periapical Tissues 405

• Multiple intraoral or extraoral pus discharging RADIOLOGICAL FEATURES (FIGS 10.12
sinuses often develop and moreover discharge
AND 10.13)
of pus can also be seen from the gingival
crevice of the affected teeth or from the socket • In the initial stage of the disease, when bone
destruction is yet to occur, no noticeable
(Figs 10.9 and 10.10). radiographic change is observed in the jaw.
• Regional lymph nodes are enlarged and
• At this stage of the disease, a radionuclide scan
tendered in most cases. may be helpful in documenting the subtle
• Paresthesia or anesthesia of the lip (either on bony changes occurring in the jaw.

the affected side or the entire lip) is a common • Radiographic changes become more apparent
and characteristic phenomenon. in about ten days time since the onset of the
disease and these radiographic changes are
• Reddening of the overlying skin or mucosa is characterized by large areas of radiolucencies
often seen in advanced stages of the disease. in the jaw bone, with ill-defined, moth-eaten
margins (Fig. 10.12).
• In acute suppurative osteomyelitis, patients
are slightly febrile and the general symptoms • Sequestra are frequently seen as multiple
radiopaque foci of diminished radiodensity
include fever, malaise, anorexia and vomiting, within the lesion.
etc.
• The sequestra become more sharply defined
• In the absence of adequate therapy, metastatic as they are gradually separated from the
spread of infection to different body systems normal bone.

may become inevitable and it can lead to • Peripheral bone reaction at the margin of the
cellulitis, bacteremia or septicemia, etc. lesion is not evident in case of early acute lesions,
however, in the chronic stages of the disease,
• Distension of the periosteum occurs due to sub-periosteal new bone formation may be seen
accumulation of pus and later on whenever in the jaw (especially in young patients).

sub-periosteal new bone formation occurs, the • In case of subperiosteal new bone formation,
bony swelling becomes firm or hard. the radiograph reveals thin, curved strip of
radiopacity on the outer surface of the bony
• Necrotic bone fragment or sequestrum may cortex.
exfoliate spontaneously from the bony
• The involucrum radiographically appears as
wound (Fig. 10.11). a gray shadow on the outer surface of the
• Once the acute phase of the disease is over, cortical plate.

a chronic phase often sets in, which usually
presents much milder clinical symptoms.

• Pathologic fracture may occur sometimes due
to weakening of bone as a result of progressive

destruction.

Fig. 10.11: A piece of dead bone (sequestrum) Fig. 10.12: Acute suppurative osteomyelitis causing large
area of bone destruction on left side of mandible

406 Essentials of Oral Pathology

Fig. 10.13: Radiograph of osteomyelitis • Bacterial colonies are often seen within the
marrow tissue of the inflamed bone.
• Sometimes, “cloacae” (a hole formed during
the process of sinus development) may be seen • Some areas of the affected bone undergo
as dark shadow traversing the bony opacity. complete necrosis with degeneration of both
osteoblast cells (bordering the bony
HISTOPATHOLOGY (FIG. 10.14) trabeculae) and osteocyte cells (inside the
lacunae) and therefore results in the develop-
• In acute suppurative osteomyelitis, the bone ment of sequestrum.
marrow undergoes liquefaction and a
purulent exudates occupy the marrow space. • Sequestrum therefore is a dead or necrosed
fragment of bone, which is separated from the
• Thrombosis of the blood vessels also occurs remaining viable bone.
in the medullary spaces.
• Sequestrum gradually undergoes sponta-
• A large number of acute inflammatory cell neous resorption or it may exfoliate through
infiltrations occur in the Haversian canal and mucous membrane or skin.
the periphery of the bone, which predomi-
nantly contains polymorphonuclear neutro- • When the sequestrum becomes surrounded by
phils (PMN) with occasional presence of new vital bone, the mass of enclosed non vital
lymphocytes and plasma cells. bone is called involucrum.

• Bony trabeculae exhibit reduced osteoblastic • Sometimes the infection in the bone becomes
activity with loss of osteocytes from the walled off. This may lead to a localized abscess
lacunae along with increased osteoclastic formation (Brodie’s abscess). The abscess may
resorptions, which often produces scalloping remain within the bone as a sterile lesion or it
at the bony margins. may act as persistent source of infection.

DIFFERENTIAL DIAGNOSIS

• Metastatic tumor in the bone with secondary
infection.

• Primary intra-alveolar carcinoma.
• Primary mesenchymal malignant neoplasm.
• Primary lymphoma of bone.
• Intraosseous salivary gland neoplasm.

TREATMENT

• Incision and drainage of the inflammatory
exudates and pus.

• Antibiotic therapy.
• Removal of the sequestrum.
• Elimination of the primary source of infection,

e.g. offending tooth, etc.

Fig. 10.14: Photomicrograph of acute osteomyelitis CHRONIC SUPPURATIVE
OSTEOMYELITIS

Depending on the severity of symptoms and the
course of the disease over the time, suppurative
osteomyelitis is divided into two varieties—acute
and chronic. The disease, which is persisting for
more than a month, is called chronic suppurative
osteomyelitis.

Diseases of Dentin-Pulp Complex and Periapical Tissues 407

• Chronic suppurative osteomyelitis may be the • Within the radiolucent area multiple
sequelae of acute suppurative osteomyelitis, radiopaque foci are evident, which represent
in which proper treatment is either not done areas of “sequestrum” formations.
or inadequately done.
Radiographically chronic osteomyelitis may
• The disease may also arise primarily as a present at least four different images, which are
chronic, low-grade inflammatory reaction in as follows
the bone, without any pre-existing acute phase.
A. An ill-defined radiolucency in the bone with
• It is generally believed that lower levels of ragged borders.
virulence of the causative microorganisms, e.g.
Staphylococci, Bacteroids and Actinomyces, B. A radiolucency with multiple radiopaque foci
etc. are mostly responsible for the development within it, the later structures represent sequestra.
of chronic suppurative osteomyelitis.
C. A dense zone of radiopacity with faint radio-
ETIOLOGY lucency at the margin.

Nonspecific microorganisms like staphylococci, D. A “salt and pepper” radiographic effect in the
streptococci, Bacteroids and Actinomyces, etc. bone.
mostly cause the disease.
HISTOPATHOLOGY
CLINICAL FEATURES
Chronic suppurative osteomyelitis often presents
• The molar area of mandible is more frequently the following features (Fig. 10.15):
affected. • Chronic inflammatory reaction in the bone

• In case of chronic suppurative osteomyelitis, with accumulation of exudates and pus within
the pain is usually mild and dull vague in the medullary spaces.
nature even if the disease is very extensive. • The lymphocytes, plasma cells and macro-
phages, etc. predominate among the
• Patients often give history of dull vague pain inflammatory cells.
in the jaw for several weeks, which had • Osteoblastic and osteoclastic activity occur
started following an acute tooth abscess, tooth parallely with formation of irregular bony
fracture or extraction, etc. trabeculae having reversal lines.
• Sequestrum may develop in the later stages
• Pain is usually mild and insidious in nature, of the disease.
which does not always correspond to the real
severity of the disease. TREATMENT

• Jaw swelling is a common feature but mobility • Administration of antibiotics after bacterial
of teeth and sinus tract formations, etc. are culture and sensitivity testing.
rare.
• Surgical intervention in order to remove the
• On rare occasions sinus tracts may develop sequestrum (saucerization of the bone).
both intraorally and extraorally with intermit-
tent discharge of purulent materials.

• Anesthesia and paresthesia of the lip are very
uncommon.

• Acute exacerbations of the chronic disease
may occur from time to time.

• Sequestrum is often found, which protrudes
from the ulcerated skin or mucosal surfaces.

RADIOLOGY Fig. 10.15: Photomicrograph of chronic osteomyelitis

• Radiographically chronic suppurative
osteomyelitis mostly presents a “moth-eaten”
radiolucent area in the bone with poorly
defined margins.

408 Essentials of Oral Pathology

CHRONIC FOCAL SCLEROSING • The associated tooth is non-vital and usually
OSTEOMYELITIS (CONDENSING presents a large carious lesion, it is mostly
OSTEITIS) asymptomatic or is associated with occasional
mild pain.
DEFINITION
• The disease can also occur in relation to a non-
Chronic focal sclerosing osteomyelitis or carious tooth and in such cases, traumatic
condensing osteitis is a rare non-suppurative malocclusion is the most likely factor, which
inflammatory condition of bone characterized by is precipitating the disease.
sclerotic bone formation around the root apex
of a nonvital tooth. • When the associated tooth is removed, the
lesion may remain within the jaw for an
PATHOGENESIS indefinite to period of time without symptoms.

The condition develops as a result of chronic RADIOLOGICAL FEATURES
persistent inflammation in the bone, where
resistance of the tissue against infection is very The lesion radiographically presents the follow-
high or where the virulence of the infective ing features:
organisms is low. • Well-circumscribed radiopaque mass with

A low-grade inflammation in the jaw bone uniform radiodensity; seen around the root
causes stimulation of the osteoblast cells, which apex of a nonvital tooth.
results in the formation of dense trabecular bone • There is no radiolucent border around the
in the area and this process is known as lesion as may be seen in cemento-osseous
osteosclerosis. dysplasia.
• The affected tooth exhibits an apical inflam-
Osteosclerosis with additional bone formation matory process with widening of periodontal
may sometimes results in decreased marrow ligament space.
spaces. • The radiopacity is not separated from the root
apex and the root tips are usually identified
ETIOLOGY within the radiopaque lesion.
• A residual area of condensing osteitis that is
The disease often occurs in young individuals, seen after resolution of the inflammatory focus
having low grade sustained inflammation in the is known as ‘bone scar’.
bone. • In case the lesion is found in edentulous jaw,
there are always positive histories that an
The common conditions, which can precipi- infected tooth was earlier removed for that
tate chronic focal sclerosing osteomyelitis, area.
include the following: • The border of the lesion is usually well-
• Chronic pulpitis. defined or sometimes the border may be
• Traumatic malocclusion. ragged.
• The radiodensity of the lesion is much higher
CLINICAL FEATURES as compared to the surrounding normal bone.

• The disease fsfrequently develops in children HISTOLOGICAL FEATURES
or young adults before the age of 20 years.
• There is usually presence of a dense mass of
• Mandibular first molars are mostly involved sclerotic bone in the lesion with little or no
with this condition. However, mandibular interstitial marrow tissue.
second molars or premolars can also be
involved on rare occasions. • Wherever the bone marrow is present it is
usually fibrotic and is often infiltrated by
• The condition is mostly asymptomatic and chronic inflammatory cells.
there is no bony expansion seen.

• Majority of the lesions are discovered
incidentally during routine radiographic
examination of the jawbone.

Diseases of Dentin-Pulp Complex and Periapical Tissues 409

DIFFERENTIAL DIAGNOSIS and even sometimes all four quadrants of both
jaw could be affected at a time.
• Mature cementoma • The disease is usually asymptomatic but
• Peripheral osteoma
• Complex odontoma sometimes the patients may complain of a
• Cementoblastoma vague pain in the jaw with foul taste in the
• Osteoblastoma mouth.
• Bony exostoses
• Metastatic tumor. • Acute exacerbation may occur in the lesion,
which often produces mild pain, suppuration
TREATMENT and fistulas tract formation, etc.

• The affected tooth should be treated endo- • SAPHO syndrome—It is a special entity
dontically or it should be removed. characterized by chronic multifocal osteo-
myelitis with hyperostosis and osteitis of the
• No treatment required for the bony lesion.
• Biopsy may be necessary to rule out metastatic bone. The condition is associated with
negative bacterial culture and is non-
malignancy. responsive to antibiotic therapy.

DIFFUSE SCLEROSING OSTEOMYELITIS RADIOGRAPHIC FEATURES

DEFINITION • Radiograph shows areas of diffuse or nodular
sclerosis of the bone.
Diffuse sclerosing osteomyelitis is a different
entity form the small, isolated lesions of focal • The appearance may be similar to the “cotton-
sclerosing osteomyelitis. It is mainly confined to wool” radiopacities seen in Paget’s disease of
the mandible and it typically involves a large bone.
section of the bone.
• The border between the sclerotic bone and the
normal bone is not well-demarcated.

ETIOLOGY HISTOPATHOLOGY

Diffuse sclerosing osteomyelitis is a proliferative • Diffuse sclerosing osteomyelitis shows
reaction in response to a low grade inflammation formation of dense irregular bone within a
or infection in the jaw bone. hypocellular fibrous stroma (Fig. 10.16)

The infections in such cases are usually wide • Bony trabeculae often reveal multiple reversal
spread or diffuse in nature and are derived either and resting lines.
from the periodontal tissue or from the periapical
tissue. • Patchy distribution of chronic inflammatory
cells is often found in the marrow tissue.
These infections are usually subclinical in
nature. Investigators have identified two bacteria
in association with this disease, which are namely
the Propionibacterium acnes and Peptostreptococcus
intermedium.

CLINICAL FEATURES Fig. 10.16: Photomicrograph of
sclerosing osteomyelitis
• Diffuse sclerosing osteomyelitis is usually seen
among elderly people.

• It is mostly seen among blacks and racial
groups.

• More common among females.
• Mandible is mostly affected in diffuse sclero-

sing osteomyelitis especially in edentulous
areas. The disease can affect the maxilla as well

410 Essentials of Oral Pathology

DIFFERENTIAL DIAGNOSIS is occurring in a young person with high degree
of body resistance and excellent tissue reactivity,
Diffuse sclerosing osteomyelitis is to be may often precipitate Garre’s osteomyelitis.
distinguished from the following lesions:
• Paget’s disease of bone It is therefore understandable that the above-
• Osteopetrosis mentioned factors contribute to a strong
• Cementomas osteogenic potential of the periosteal osteoblast
• Gardner’s syndrome cells in the affected jaw bone.
• Late stage of fibrous dysplasia.
Generally in Garre’s osteomyelitis, a low-
TREATMENT grade chronic inflammation spreads through the
cortical bone of the jaw and it initiates a
No treatment is required as the disease is often proliferative reaction in the periosteum, leading
asymptomatic and is too extensive for surgical to sub-periosteal new bone formations.
removal. In case of acute exacerbations, surgical
debribement and removal of the sequestrum is It is important to note that an acute and intense
done along with antibiotic therapy. type of inflammation or infection in the jaw bone
usually does not produce Garre’s osteomyelitis,
CHRONIC OSTEOMYELITIS WITH since this type of infection does not permit
PROLIFERATIVE PERIOSTITIS sufficient time for the bone to undergo any sub-
(GARRE’S OSTEOMYELITIS) periosteal osteogenesis.

DEFINITION CLINICAL FEATURES

Garre’s osteomyelitis represents a reactive Age: Children and young adults (mean age is
periosteal osteogenesis in response to low-grade 13 years).
infection or trauma. The condition was first
authentically reported in 1893 by German Sex: There is no sex predilection.
physician C Garre and it is characterized by focal
gross thickening of the involved bone due to sub- Site: Mandible is commonly involved in Garre’s
periosteal new bone deposition (duplication of osteomyelitis in its posterior part. Maxilla can be
the cortex). affected on rare occasion.

Predisposing factors for the development of PRESENTATIONS
Garre’s osteomyelitis
• The involved jaw bone often presents a
• Chronic periapical abscess. grossly carious, nonvital tooth (mostly lower
• Chronic periapical granuloma with secondary first permanent molar tooth).

infection. • The tooth is always associated with periapical
• Infected periapical cyst. or sometimes other inflammatory foci.
• Perifollicular infection in an erupting tooth or
• There is thickening and swelling of the
impacted tooth. affected bone with little or no pain.
• Chronic parotid abscess.
• Chronic periodontal infection. • The size of the swelling may be ranging from
• Other chronic infections in the soft tissue centimeters to a lesion spanning the entire
length of the mandible.
overlying the jaw.
• Chronic trauma in the jaw bone. • The thickness of the bone may be up to 1 cm.
• Mechanical irritation in the jaw from dentures. • Occasionally slight tenderness or a vague pain

PATHOGENESIS may be felt in the affected area of bone.
• The overlying skin and oral mucosa appears
It is usually believed that a low-grade, sustained
infection or inflammation of the jaw bone, which normal.
• Garre’s osteomyelitis is generally a solitary

lesion, however multifocal lesions are also
sometimes reported.
• Slight pyrexia and moderate leukocytosis may
be present but the erythrocyte sedimentation
rate (ESR) is normal.

Diseases of Dentin-Pulp Complex and Periapical Tissues 411

RADIOGRAPHIC APPEARANCE DIFFERENTIAL DIAGNOSIS

• Garre’s osteomyelitis radiographically • Ossifying fibroma
presents a central jaw lesion with a mottled, • Immature fibrous dysplasia
predominantly radiolucent appearance, the • Ewing’s sarcoma
lesion often has few radiopaque foci. • Osteoblastic osteosarcoma
• Osteoma
• The affected periosteum forms several layers • Fracture callus
of reactive vital bone and as a result the expan- • Metastatic tumor of the jaw bone
ded cortex of bone radiographically exhibits • Pulse granuloma.
many concentric or parallel opaque layers,
which often produce a typical “onion skin” TREATMENT
appearance.
• Elimination of the causative agent.
• These concentric bone laminations may be as • Extraction of the offending tooth and antibiotic
many as 12 in numbers, these are roughly
parallel to each other and the underlying therapy.
cortical surface of bone. • The cortical swelling undergoes spontaneous

• The standard occlusal radiograph reveals a physiologic remodelling and does not
smooth, convex, bony overgrowth on the required any additional surgical intervention.
outer cortex of the jaw. This is often called
‘duplication’ of the cortex. GIANT CELL PERIOSTITIS WITH
HYALINE CHANGE (PULSE
• Few newly formed bony trabeculae are often GRANULOMA)
oriented perpendicular to the “onion skin”
layers. DEFINITION

Common diseases associated with periosteal A large variety of foreign materials can be
implanted into the oral tissues, some which can
new bone formation in the jaw initiate a granulomatous reaction. Such reactions
are characterized by chronic inflammation and
• Osteomyelitis subsequent formation of a ring-shaped hyaline
eosinophilic structure in the tissue and few giant
• Trauma cells.

• Cyst The term “pulse granuloma” has been coined
since vegetable materials especially pulses are
• Malignancy, e.g. osteosarcoma believed to cause these disease more often than
others. The disease occurs when the vegetable
• Fracture of bone. material is introduced into the oral tissue via
extraction socket or surgical flaps or open root
HISTOPATHOLOGY canals, or through ulceration in the oral mucosa.

• The lesion histologically presents areas of CLINICAL FEATURES
newly formed bone, consisting of multiple
osteoids and primitive bony tissues in the sub- • Clinically the lesion is either dome-shaped or
periosteal region. multinodular and it is usually soft or firm in
consistency.
• Parallel rows of highly cellular and reactive
woven bones are seen. • Mucobuccal fold is the most common site for
the development of pulse granuloma and
• Osteoblastic activity dominates the outer often there is thickening of the periosteum due
surface of bone while both osteoblastic as well to proliferative periostitis.
as osteoclastic activities can be observed in the
central part of bone. • Pain is not a prominent feature unless there is
suppuration.
• The marrow spaces contain fibrous tissue
showing patchy areas of chronic inflammatory
cell infiltration.

• On rare occasions there may be presence of
small sequestra.

412 Essentials of Oral Pathology

Classification of endodontic-periodontic lesions

According to Simon, the endodontic-periodontic lesions are classified into four types:
• Primary endodontic lesions: Here the infection originates in the pulp, which later on extends via the

accessory canals or apical canals into the periodontium and produce a resultant inflammation there.
Clinically and radiographically the disease simulates periodontal defects. Endodontic treatment alone
usually solves the problem.
• Primary endodontic lesions with secondary periodontal involvement: If prompt endodontic therapy is
not done in a situation, where the pulpal infection has already spread into the periodontium, then
periodontal tissue breakdown will occur. Treatment in such cases will involve both endodontic as well as
the periodontal therapy.
• Primary periodontal lesion with secondary endodontic involvement: If an accessory root canal comes in
the path of a progressive periodontal infection, then the pathogenic organisms from the periodontium
may take entry into the pulp via such canals and results in secondary pulpal infections and necrosis.
Moreover infection along the root may also reach to the apex and cause retrograde infection of the
dental pulp via the apical foramen. Treatment will be both periodontal and endodontic in such cases.
• True combined lesion: Periodontal and endodontic lesions may arise independently in a tooth and at
some stage both these lesions may coalesce together to establish a true combined endodontic-periodontic
disease. Dual therapy for both lesions required but prognosis is mostly poor.

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An infective process involving the tooth and its FACTORS RELATING TO THE HOST
supporting structures is known as odontogenic
infections. If the host or the patient has a high degree of
body resistance, the distant spread of infection
In the oral cavity, a large number of such from the oral cavity is less likely to occur and
odontogenic infective lesions are often encoun- vice versa.
tered, which originate either from the gingival
tissue or from the periapical sites. FACTORS RELATING TO THE SITE OF
INFECTION
Infections from the gingival tissue often
involve the deeper periodontal ligaments and the The site of initial involvement of the odontogenic
supporting alveolar bone and they may infection also determines whether it will remain
eventually progress to the periapical region of localized or will make a distant spread.
tooth.
The thinner cortical plates of bone or loose
In most instances of periapical infections, the tissue spaces around the wound may offer little
microorganisms are derived from the necrosed resistance to the spread of infection, therefore,
dental pulp as a sequel of dental caries. infections from such areas may often spread
diffusely.
The common odontogenic infections which
are often encountered in the oral cavity include However, thicker cortical plates of bone and
pericoronitis, periodontal abscess, periapical tough tissue sites (e.g. areas of muscle attachments)
abscess, subperiosteal abscess and the osteo- may actually prevent the spread of distant spread
myelitis of various types. of infection.

Once the odontogenic infections reach the SPACE INFECTIONS
bone or muscle or mucosa or lymph nodes, etc.
they may either resolve spontaneously or spread Odontogenic infections often spread through
to the local or the distant sites. natural pathways into potential tissue spaces
situated between different planes of fascia.
Factors determining spread of oral
Infections into the various tissue spaces are
infections to distant sites known as the ‘space infections’. Such infections
in the vicinity of the jaw bones can be divided into
• Virulence of the microorganisms. two broad groups, namely, those related to the
maxilla and those related to the mandible.
• Immunity of the host.
SPACE INFECTIONS RELATED TO
• Anatomical site of the initial infection. MAXILLA

FACTORS RELATING TO ORGANISMS CANINE FOSSA INFECTION
Source of infection: Maxillary canine tooth.
Some organisms producing odontogenic infec-
tions are more virulent than others, moreover, a
few organisms, e.g. Streptococcus aureus can
produce enzymes like hyaluronidase and
fibrinolysins, etc. which help in the spread of
infection into distant areas by breaking tissue
barriers.

Spread of the Oral Infection 415

Clinical Features Clinical Features
• Pain and tenderness over infraorbital region. • Trismus and pain
• Elevated body temperature • Swelling of the eyelids when postzygomatic
• Submandibular lymphadenopathy.
fossa is involved.
Treatment • Dysphagia due to involvement of pharynx.
• Extraction or endodontic treatment of the • Swelling in the preauricular region, which may

involved canine tooth. extend up to the cheek.
• Antibiotic therapy.
Treatment
PALATAL SPACE INFECTION • Surgical drainage
• Antibiotic therapy
Source of Infection • Extraction or endodontic treatment of the
Maxillary lateral incisors and infection via palatal
roots of maxillary molars. offending tooth.

Clinical Features PTERYGOMANDIBULAR SPACE INFECTION
Pain and an extremely tendered swelling over the Pterygomandibular space is the inferior portion
palate. of the infratemporal space.

Treatment Boundary: The space lies between the internal
• Antibiotic therapy pterygoid muscle and the ramus of the mandible.
• Extraction or endodontic treatment of the
Sources of Infection
involved tooth. • Pericoronitis of mandibular third molar tooth.
• Infected needles or injection into the space.

INFRATEMPORAL SPACE INFECTION Clinical Features

Boundary Infratemporal space is bordered by • Severe trismus
the following structures: • Radiating pain
Anteriorly Maxillary tuberosity • Swelling of the lateral-posterior region of soft
Posteriorly Lateral pterygoid muscle, condyle
Laterally of the mandible, temporalis muscle. palate may be seen.
Tendon of the temporalis muscle,
Medially coronoid process of mandible Treatment
Lateral pterygoid plate, inferior belly
of the lateral pterygoid muscle. • Drainage
• Antibiotic treatment
Contents of Infratemporal Space • Treatment of the offending third molar

• Pterygoid plexus tooth.
• Internal maxillary artery
• Mandibular nerve, myelohyoid nerve TEMPORAL POUCH INFECTION
• Lingual nerve, buccinator nerve and chorda
Source of Infection
tympani nerves
• External pterygoid muscle. Secondary infections from the submasseteric,
pterygopalatine and infratemporal spaces.
Source of infection: Infected maxillary molar
teeth. Maxillary molars are the common offending
teeth.
Infected needles or solution used for injection
of the maxillary tuberosity. Clinical Features
• Pain and trismus
• Swelling may be an occasional feature.

416 Essentials of Oral Pathology

Treatment maxillary space and inferiorly by the myelohyoid
• Surgical drainage muscle.
• Antibiotic therapy.
Source of Infection
PAROTID SPACE INFECTION Mandibular anterior teeth.
Parotid space is a compartment formed by split-
ting of the investing layer of deep cervical fascia. Clinical Features
• Painful swelling in the submental area.
Contents • Occasionally dyspnea and dysphagia.
• Parotid glands
• Extra- and intraglandular lymph nodes Treatment
• Facial nerve, auriculotemporal nerve • Antibiotic therapy
• Posterior facial vein • Extraction or endodontic therapy to the
• External carotid, internal maxillary and
offending tooth.
superficial temporal arteries.
SUBMANDIBULAR SPACE INFECTION
Source of Infection Boundary: Submandibular or submaxillary space
Secondary infections from lateral pharyngeal and is bordered by the following structures:
submasseteric spaces. Medially—Hyoglossus and digastric muscles.
Laterally—Superficial fascia and skin.
Clinical Features Superiorly—Posterior portion of hyoglossus
• A smooth, painful swelling in front and below muscle.

the external ear. Contents: Submandibular salivary gland and
• Fever, chills, etc. lymph nodes.
• Sometimes, the entire side of the face may be
Source of infection: Infected mandibular molars.
swollen.
Clinical Features
Treatment • Submandibular space infection is the most
• Surgical drainage
• Antibiotic therapy. common of all space infections in the orofacial
region (Figs 11.1 to 11.3).
SPACE INFECTIONS RELATED TO
MANDIBLE

MENTAL SPACE INFECTIONS

Source of Infection
Mandibular anterior teeth.

Clinical Features
• A tense painful swelling in the chin region.
• This kind of swelling can also occur in the

localized nonodontogenic infections.

Treatment
• Surgical drainage
• Antibiotic therapy
• Treatment of the offending tooth.

SUBMENTAL SPACE INFECTION Fig. 11.1: Submandibular space infection resulting in
extraoral sinus formation
Boundary: Anteriorly the midline of mandible,
posteriorly the anterior border of the sub-

Spread of the Oral Infection 417

Treatment

• Surgical drainage
• Antibiotic therapy
• Treatment of the offending tooth
• Tracheotomy may be required in cases of

airway obstruction.

Fig. 11.2: Intraoral view of the same patient SUBLINGUAL SPACE INFECTION

Boundary: Sublingual space is situated above the
submandibular space and it is bordered by the
following structures:
Superiorly—Mucosa of the floor of the mouth.
Inferiorly—Mylohyoid muscle.
Antero-laterally—Body of the mandible.
Posteriorly—Hyoid bone.
Medially—Median raphae of the tongue.

Source of Infection

• Mandibular teeth except second and third
molars.

• Sublingual infections may be transported from
the submandibular space.

Clinical Features

• Swelling of the floor of the mouth
• Airway obstructions in severe cases
• Dysphagia
• Infections can spread to involve the tongue.

Fig. 11.3: X-ray reveals periapical radiolucency in Treatment
mandibular molar region • Drainage
• Antibiotic therapy
• Fever, chill and anorexia. • Elimination of the source of infection.
• Pain with swelling near the angle of the
LATERAL PHARYNGEAL SPACE INFECTION
mandible. Lateral pharyngeal or parapharyngeal space is
• Submandibular space infection often results in situated deep in the neck and infection of this
space often terminates fatally.
lymph adenitis in the submandibular lymph
node and sialadenitis in the submandibular Boundary
salivary gland. Anteriorly—Buccopharyngeal aponeurosis,
• Infections from the submandibular space may parotid gland and pterygoid muscles.
extend to the sublingual and submental spaces, Posteriorly—Prevertebral fascia.
and rarely to the lateral pharyngeal spaces. Laterally—Carotid sheath.
• Involvement of the pharynx and the larynx may Medially—Lateral wall of the pharynx.
cause dyspnea and dysphagia.
• Distant spread of infection from the subman- Source of Infection
dibular space may result in infections of the • Mandibular third molar.
cranial fossa or of the mediastinum. • Infection of the palatine tonsils, mastoid air

cells and parotid glands.

418 Essentials of Oral Pathology

• Infection may also come from the retro- Inferiorly—The fascia attaches on the inferior
mandibular space. border of mandible and then covers its body from
both buccal and lingual side.
Clinical Features
Superiorly—It becomes continuous with the
• Pain, trismus with fever and chill. alveolar periosteum and muscles of the facial
• Dysphagia and dyspnea due to involvement expression having attachment to the mandible.

of the pharynx and larynx. Contents
• Infection from lateral pharyngeal space may
• Body of mandible excluding the ramus, along
spread to the mediastinum via the prevertebral with the covering periosteum.
fascia.
• Fascia and muscle attachments.
Complications • Teeth and periodontium.

• Septicemia Source of Infection
• Respiratory paralysis
• Thrombosis of the internal jugular vein • Mandibular teeth.
• Erosions of the internal carotid artery. • Periodontal infection of the regional teeth.
• Blood-borne infections.
Treatment • Infection following fracture of mandible.
• Surgical drainage • Extension of infection from neighboring tissue
• Antibiotic therapy
• Elimination of the primary source of spaces.

infections Clinical Features
• Maintenance of airway patency.
• The odontogenic infections perforate either the
RETRO-PHARYNGEAL SPACE INFECTION buccal or the lingual cortical plates of mandi-
Boundary ble before they spread to the mandibular body
Anteriorly—Wall of the pharynx. space.
Posteriorly—Prevertebral fascia.
Laterally—Lateral pharyngeal space and carotid • The clinical manifestation varies and it
sheath. depends upon factors like the source of
infection, which cortical plate (buccal or
Source of Infection lingual) has been perforated and at what level
Lateral pharyngeal space. of the bone.

Clinical Features • If infections from incisors, cuspids and
• Pain, swelling and dysphagia, etc. bicuspids are spreading into the space by
• Retropharyngeal space infection may spread perforating the buccal cortical plate, an
induration, swelling and fluctuation of the
to the mediastinum as the prevertebral fascia labial sulcus will be observed.
extends to the posterior mediastinum.
• When infections from the same sources are
INFECTION OF THE SPACE OF BODY perforating the lingual cortical plate, swelling
OF MANDIBLE of the floor of the mouth will occur.
Boundary: A natural tissue space exists around
the body of the mandible as it is enclosed by a • Infections from mandibular molar teeth when
layer of fascia derived from the outer layer of deep perforate the buccal cortical plate above the
cervical fascia. attachment of buccinator muscle, a swelling of
the oral vestibule is seen.

• If buccal perforation takes place below the
level of attachment of buccinator muscle, a
swelling of the covering skin over mandible is
noticed.

Spread of the Oral Infection 419

• When infections of mandibular molars and CELLULITIS
premolars perforate the lingual cortical plate
of bone above the level of attachment of the DEFINITION
mylohyoid muscle, swelling of the floor of the
mouth occurs. Cellulitis is an acute edematous, purulent
inflammatory process, which spreads diffusely
• If lingual perforation occurs below the myelo- through different tissue spaces or fascial planes.
hyoid attachment, the infection spreads either
into the submandibular space or into the PATHOGENESIS
lateral pharyngeal space.
• Acute cellulitis is mostly caused by some
Treatment unusually virulent bacteria, which often
produce hyaluronidase and fibrinolysins, etc.
• Drainage
• Antibiotic therapy • Hyaluronidase and fibrinolysins cause lysis
• Treatment of the infected tooth or the other of the hyaluronic acid (universal intercellular
cement substance) and fibrin respectively, and
primary source. cause breakdown of the tissue barriers. The
enzymes, therefore, help the infective process
SUBMASSETERIC SPACE INFECTION to spread diffusely into tissue spaces.

Boundary: Submasseteric space is bordered by the • Diminished body resistance in general and
following structures: tissue resistance in particular of the host,
Medially—Lateral surface of the mandibular bacterial resistance to antibiotics, favorable
ramus. anatomic locations, etc. also help in the process
Laterally—Masseter muscle. development of cellulitis.
Anteriorly—Retromolar fossa.
Posteriorly—Parotid gland. • Microorganisms such as Streptococcus pyogenes
and anaerobes, particularly bacteroides most
Source of Infection commonly produce facial cellulitis.

• Mandibular third molars • In acute cellulitis, infection from the lower
• Infection from this tooth passes through the anterior teeth perforates the lingual cortical
plate of bone and moves into the superficial
retromolar fossa and moves into the sub- sublingual space, and from there tracks
masseteric space. backwards.

Clinical Features • Infection from lower molar teeth, after
penetrating the lingual cortical plate reaches
• Pain and swelling due to subperiosteal abscess the junction of fascial spaces at posterior border
formation. of mylohyoid muscle.

• Trismus. • From there the infection may spread forward
to reach the sublingual and submandibular
Treatment space and backwards into the parapharyngeal
spaces.
• Surgical drainage
• Antibiotic therapy Primary sources of infections for orofacial cellulitis
• Treatment of the infected third molar.
• Periapical abscess
Sequelae of odontogenic infections • Pericoronitis or pericoronal abscess
• Periodontal abscess
• Localized abscess formation • Osteomyelitis
• Acute cellulitis • Infected post-extraction wound
• Ludwig’s angina • Gunshot injuries
• Cavernous sinus thrombosis • Oral soft tissue infections
• Bacteremia, septicemia, toxemia and pyemia • Oral infection in HIV
• Bloodborne infections.

420 Essentials of Oral Pathology

CLINICAL FEATURES HISTOPATHOLOGIC FEATURES

Cellulitis clinically presents the following features: • Collection of a large amount of fibrin and serum
• Development of a large, diffuse, painful fluid in the tissue.

swelling over the face or neck with facial • Separation of periosteum and muscles from the
asymmetry (Figs 11.4 A and B). bony surface due to accumulation of fluid.
• The soft tissue swelling is usually firm and
brawny. • Acute inflammatory cell infiltration by PMN
• When cellulitis involves the superficial tissue and occasionally lymphocytes.
spaces, the overlying skin often appears
purplish. • Pus may develop in the later stages of the disease.
• However, when the infection spreads along the • Formation of sinus tracts over skin or mucosal
deeper tissue spaces, the skin appears normal.
• Fever, chill, leukocytosis, etc. are often present, surfaces.
which make the patient slightly ill.
• Regional lymphadenopathy frequently TREATMENT
develops and in untreated cases cellulitis may
spread over a wide area and sometimes involve • Bacteriological examination of the exudate or
the entire face. pus, etc
• Trismus, dyspnea and dysphagia are the
common complications. • Drainage
• Some lesions resolve completely, however, in • Antibiotic therapy
other cases pus discharging intraoral or extra- • Elimination of the primary source of infection.
oral sinuses may develop.
LUDWIG’S ANGINA

DEFINITION

Ludwig’s angina is an overwhelming diffuse,
suppurative cellulitis, which simultaneously
involves the submandibular, sublingual and
submental spaces.

Predisposing factors for Ludwig’s angina

• Diabetes mellitus
• HIV infection
• Oral transplants
• Aplastic anemia.

Figs 11.4A and B: Cellulitis CAUSATIVE MICROORGANISMS
• Hemolytic streptococci are the most frequently

encountered organisms to cause Ludwig’s
angina. However, staphylococci, bacteroides
and fusiform bacilli may also be involved.

Primary sources of infections in Ludwig’s angina

• Periapical, pericoronal or periodontal infections
from mandibular molar teeth

• Gunshot injury or stab wounds in the floor of
the mouth with secondary infection

• Infection following fracture of the mandible
• Osteomyelitis of the jawbones
• Infection of the other orofacial soft tissues
• Spread of infection from peritonsillar or

parapharyngeal abscesses
• Submandibular sialadenitis.

Spread of the Oral Infection 421

PATHOGENESIS OF LUDWIG’S ANGINA • Usually, the patient is very toxic with high fever,
chill, rapid pulse, dysphagia, sore throat,
• In Ludwig’s angina, all the three important drooling and fast respiration, etc.
spaces in the submandibular region, i.e. the
submandibular space, sublingual space and • In untreated cases, cellulitis may spread further
the submental space, are involved simulta- and cause a massive swelling in the neck above
neously. the hyoid bone; this condition is often known
as bull neck.
• Although involvement of these spaces occurs
one after the another, the spread of infection is • As the condition deteriorates further there
so rapid as if it is involving all the spaces may be development of edema glottis; which
together. is a serious condition and can result in death
due to asphyxia.
• Infection from mandibular second and third
molar teeth often perforates the lingual cortical • Other serious consequences of Ludwig’s
plate of bone (buccal cortical plate is usually angina include the development of cavernous
not perforated in the molar region as it is much sinus thrombosis, meningitis, brain abscess
harder and thicker as compared to the lingual and suppurative encephalitis, etc.
plate) below the level of attachment of the
mylohyoid muscle and spreads to the DIAGNOSIS
submandibular space.
Diagnosis is usually established by the following
• Similarly, infection from mandibular first molar methods:
teeth also perforates the buccal cortical plate • Clinical features of the disease are often very
but above the level of mylohyoid muscle
attachment, and, therefore, spreads to the specific.
sublingual space. • Leukocytosis
• Bacterial culture with identification of specific
• Submental space is usually involved by
extension of infection from the neighboring microorganisms.
spaces.
TREATMENT
• Submandibular space infections or inflam-
mations can spread to lateral pharyngeal • High dose of antibiotics.
space, from there it can spread to retropharyn- • Drainage by incision at the anterior part of the
geal space and from there it can even spread to
the mediastinum. neck.
• Emergency tracheostomy may be required in
CLINICAL FEATURES
cases of airway obstructions.
• Ludwig’s angina produces a rapidly
spreading, large, diffuse and board-like CAVERNOUS SINUS THROMBOSIS
aggressive swelling; which involves the upper (THROMBOPHLEBITIS)
part of neck and floor of the mouth bilaterally
with brawny induration. DEFINITION

• The swelling causes elevation of the tongue; Cavernous sinus thrombosis is a serious life-
which may be pushed up against the palate threatening condition characterized by formation
and the patient often has a typical open of septic thrombi within the cavernous sinus and
mouthed appearance. its numerous communicating branches.

• The enlarged tongue may protrude outside the ROUTES OF SPREAD OF INFECTIONS
mouth and the condition is called woody
tongue. External Route

• The swollen area of the neck is firm, painful, • The veins of the maxillary regions of face
nonfluctuant and does not pit upon pressure. anatomically drain into the cavernous sinus
and because of this, infections from upper lip,
• The condition is always bilateral and the face, eye and nares, etc. often reach cavernous
patient is often unable to open the mouth, speak
or swallow properly.

422 Essentials of Oral Pathology

sinus directly through facial and angular • Complete paralysis of the third, fourth and
veins. sixth cranial nerves common.
• Since facial and angular veins are quite longer
vessels and, moreover, they have no value • Pain above the eye and diminished sensation
systems in them, infections from the outer face over the forehead.
spread rapidly to the cavernous sinus via this
route. • The condition is initially unilateral but, it often
becomes bilateral within 2 to 3 days.
Internal Route
• Death may occur due to brain abscess, menin-
• Infections from internal structures (especially gitis, septicemia, toxemia or pyemia, etc.
upper and lower third molar teeth) reach
cavernous sinus via the pterygoid plexus. TREATMENT

• Spread of infection via the internal route • Maintenance of airway in cases of respiratory
usually occurs at a much slower pace, since distress
the infection has to pass through many small
and twisted venous passages of the pterygoid • High doses of antibiotic therapy
plexus. • Drainage
• Anticoagulant therapy.
Primary sources of infection in
MAXILLARY SINUSITIS
cavernous sinus thrombosis
DEFINITION
External sources
Maxillary sinusitis can be defined as the acute or
Infection from face, e.g. lip, face, nares and eye. chronic inflammations of the maxillary sinus.

Internal sources ETIOLOGY

• Periapical/Pericoronal/Periosteal abscesses • Maxillary sinusitis often occurs due to direct
extension of odontogenic infections and it
• Otitis media happens due to the typical anatomical relation
and proximity of the teeth to this sinus.
• Fracture of skull
• Usually, periapical abscess in the upper
• Meningitis premolar or molar teeth may spread to the
maxillary sinus.
• Septicemia.
• In other situations, broken root fragments of
CLINICAL FEATURES any of these teeth may be pushed into the sinus
along with some bacteria.
• Patients with cavernous sinus thrombosis are
often gravely ill and if timely intervention is • However, there are a few other causes of
not done the disease can terminate fatally. maxillary sinusitis, which are as follows:
– Common cold
• Headache, fever, vomiting, nausea and chill, – Influenza
etc. are present in the initial stages. – Exanthematous diseases
– Spread of infections from the neighboring
• Patients may also develop tachycardia, frontal or parietal sinuses
tachypnea, stiffness of the neck and irregular – Phycomycosis infection
breathing, etc. with alarming severity. – Traumatic injury to the maxillary tuberosity
followed by secondary infection.
• Occlusion of the ophthalmic veins causes
photophobia, increased lacrimation, prop- CLINICAL FEATURES
tosis, chemosis, dialatation of pupil and
edema of the eyelids, etc. • Acute maxillary sinusitis produces moderate to
severe pain in the sinus region with swelling.
• Paralysis of the external ocular muscles,
exophthalmos, fixation of the eyeball,
intraocular hemorrhage and even blindness
can occur.

• Massive swelling of the nose and forehead
areas.

Spread of the Oral Infection 423

• The pain usually increases when digital • Removal of hyperplastic epithelium by
pressure is applied over the maxilla. thorough curettage

• Patient feels pain in the teeth or in the ear • Antibiotics may be administered in acute
because the sinusitis pain is often referred to cases.
these structures.
FOCAL INFECTION
• Fever, malaise, discharge of pus into the nose
with fetid breath, etc. are the other conven- It has been observed since long time that infections
tional features of acute maxillary sinusitis. from oral cavity can spread to distant parts of the
body and produce fresh lesions over there.
• Chronic maxillary sinusitis presents little or
no pain and the disease is often discovered Orofacial tissues especially the teeth and the
during routine examinations. periodontium normally harbor numerous micro-
organisms, which are otherwise nonpathogenic
• However, sometimes there can be presence of as long as they are within the oral cavity.
vague pain, stuffy sensation in the face, mild However, once these organisms spread to the
nasal discharge with foul breath. distant organs of the body, they behave as strictly
pathogenic organisms and produce diseases.
RADIOLOGICAL FEATURES
Moreover, oral tissues are vulnerable to
• For detailed visualization of the maxillary infections caused by various microorganisms
sinus. Water’s view radiographs are speci- (e.g. bacteria, virus and fungus), which produce
fically needed. a wide variety of lesions in the oral cavity.

• Acute maxillary sinusitis radiographically Infections from these primary lesions may
does not produce any significant diagnostic spread to the distant organs to initiate secondary
findings. diseases.

• However, chronic maxillary sinusitis often DEFINITION
produces clouding of the maxillary sinus on
radiographs. Focal Infection

• This clouding of the sinus occurs due to Metastases of microorganisms or their toxins
presence of fluid and hyperplastic epithelial from a localized site of infection to any distant
tissues, which fill up the entire sinus cavity. part of the body with subsequent injury are called
“focal infections.”
HISTOLOGICAL FEATURES
Focus of Infection
• In acute maxillary sinusitis, the lining epi-
thelium of the maxillary sinus shows edema, Circumscribed area of tissue, which is infected by
occasional hemorrhage and infiltration by exogenous pathogenic organisms and is usually
acute inflammatory cells. located near the skin or mucosal surface is called
a focus of infection.
• Squamous metaplasia of the ciliated columnar
epithelium occurs in rare cases. MECHANISM OF FOCAL INFECTION

• Chronic maxillary sinusitis often produces Focal infections mostly occur by the following
marked thickening of the lining epithelium mechanisms:
with formation of numerous epithelial • Spread of “pathogenic microorganisms”
polyps.
from their primary site of infection to the
• The polyps fill up the entire sinus cavity and distant part of body via the blood vessels or
these are made up of hyperplastic, granulation lymphatics.
tissue with lymphocytic and sometimes plasma • Spread of “toxins” liberated by the pathogenic
cell infiltrations. microbes to distant organs either via blood
vessels or lymphatics (erythrogenic toxins
TREATMENT

• Removal of primary sources of infection
• Drainage

424 Essentials of Oral Pathology

liberated by beta hemolytic Streptococci 4. Dajani AS, Taubert KA, et al. Prevention of bacterial
produce diffuse, bright skin rashes in scarlet endocarditis: Recommendations by the Americal
fever. Heart Association. J Am Med Assoc 1997; 277(22):
1794-801.
Examples of Various Oral “Foci” of Infections
5. De Leo AA, Schoenknecht FD, Anderson MW,
• Periapical abscess (acute or chronic) Peterson JC. The incidence of bacteremia following
• Pericoronitis oral prophylaxis on pediatric patients. Oral Surg,
• Infected periapical granuloma or cyst 1974;37:36.
• Periodontal abscess
6. Giunta JL. Comparison of erysipelas and odontogenic
• Infected dental pulp or root canals cellulitis. T Endod 1987;13:291-4.
• Infected root fragments of teeth
• Osteomyelitis 7. Gonty AA, Costich ER. Service facial and cervical
• Syphilitic chancre infections associated with gas-producing bacteria
• Infections in the maxillary sinus, nasal sinus, report of two cases. T Oral Surg 1981;39:702-7.

throat and tonsils, etc. 8. Heilelman JF, Dirlam JH. Severe cellulitis of dental
origin with gas-producing bacteria. T Indiana Dent
COMMON CONSEQUENCES OF “FOCAL Assoc 1982;61:11-3.
INFECTIONS” FROM THE OROFACIAL
REGION 9. Kaban LB, McGill T. Orbital cellulitis of dental origin:
differential diagnosis and the use of the computed
Several life-threatening systemic diseases can tomography as a diagnostic aid. T Oral Surg
occur due to either ‘direct spread of infections or 1980;38:682-5.
dissemination of toxins’ liberated by the oral
pathogenic microorganisms into the blood. 10. Lacassin F, Hoen B, et al. Procedures associated with
Following are few examples of these diseases infective endocarditis in adults: a case-control study.
caused by focal infections from the oral and Europ Heart J 1995;16(12):1968-74.
orofacial infective sources:
• Subacute bacterial endocarditis 11. Madden GJ, Smith OP. Lingual cellulitis causing
• Cavernous sinus thrombosis upper airway obstruction. Br T Oral Maxillofac
• Meningitis and brain abscess Surg.1990;28:309-10.
• Subdural empyema
• Suppurative encephalitis 12. Matusow RJ. Acute pulpal-alveolar cellulitis
• Ocular diseases syndrome: V: apical closure of immature teeth by
• Renal diseases infection control: the importance of an endodontic
• Gastrointestinal diseases seal with therapeutic factors: part 2. Oral Surg Oral
• Upper respiratory tract disease Med Oral Pabol. 1991;72:96-100.
• Dermatological lesions
• Bacteremia, septicemia, toxemia and pyemia 13. Matusow RJ. The acute primary endodontic cellulitis
• Rheumatoid arthritis and rheumatic fever. syndrome: etiologic, pathogenic, and therapeutic
factors. Compendium 1988;9:682-4,687-90.
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bacterial endocarditis in the Netherlands. II.

PART I: PHYSICAL INJURIES horizontal in nature and are located in the
middle third of the root. Other fractures of
FRACTURES OF TEETH root usually occur in the apical third area.
Most of the affected teeth become non-vital
Tooth fracture is a common type of injury and it as soon as the fracture occurs. Some may heal
occurs in a variety of situations, e.g. sudden severe by forming reparative dentin. Nonvital teeth
trauma, tooth weakened by a large restoration, show formation of granulation tissue around
non-vital tooth and internal resorptions, etc. the apex with extensive resorption of the
root.
It is important to note that the boys usually
have more tooth fractures in comparison to the CEMENTAL TEAR
girls, and class II malocclusion is associated with
more cases of anterior tooth fractures. Cemental tears are small fractures of the
cementum on the root surface, which usually
Classification of tooth fracture occur as a result of sudden rotational forces.
Cemental tears cause detachment of part of
Class I Simple fracture of the crown that cementum, which remains within the
involves enamel with little or no periodontal ligament. The condition is usually
Class II dentin involvement. asymptomatic.
Class III Fracture involving the enamel and
dentin but not the pulp. TREATMENT
Class IV Extensive fracture involving
Class V considerable dentin and exposing the The fractured vital teeth are easily saved by
Class VI pulp. restoration but in case of fractured nonvital teeth,
Class VII Fracture causing loss of vitality of the root canal treatment (RCT) should be done before
Class VIII affected tooth. any restoration is given.
Class IX Fracture causing complete loss of the
tooth. Post and core crown is built on an existing
Fracture of the root with or without tooth-root, where the crown is lost as a result of
the crown fracture. fracture.
Displacement of the tooth without
any fracture of the crown or the root. Sometimes in cases of a vertical tooth fracture,
Fracture of the crown en mass and the patients often complain of a sharp pain
its replacement. especially during chewing hard foods but the
Fracture involving the deciduous fracture is not detected by radiographs and this
teeth. condition is often known as the “cracked-tooth
syndrome”. It will require extraction of the
ROOT FRACTURE affected tooth.

Root fracture represents a small percentage BRUXISM
of total number of tooth fractures. Most cases
occur due to trauma between the ages of 10 DEFINITION
to 20 years. Most of the root fractures are
Bruxism can be defined as the habitual,
unintentional grinding or clenching of teeth, it

Physical and Chemical Injuries of the Oral Cavity 427

Trauma Causes of premature loss of teeth

• Due to accidents
• Psychotic patients
• Radiation.

Periodontal diseases • Aggressive juvenile periodontitis
• AIDS related periodontal diseases.

Hereditary conditions • Acatalasia
• Chediac-Higashi disease
• Cyclic neutropenia
• Dentin dysplasia-type I (Rootless tooth)
• Hypophosphatesia
• Hypophosphatemia
• Lesch-Nyhan syndrome
• Papillon-Lefevre syndrome
• Down’s syndrome.

Immunocompromised states • HIV/AIDS
• Leukemia
• Chemotherapy.

Neoplasms • Benign and malignant neoplasm of the jaws
• Lymphomas
• Tumor-like conditions.

Miscellaneous factors • Diabetes mellitus
• Histiocytosis–X
• Acrodynia
• Regional odontodysplasia (ghost teeth)
• Osteomyelitis
• Vitamin-C deficiency
• Langerhan’s cell disease.

occurs periodically either during sleep in the Psychological factor
night or during day-time. The person, who has • Emotional upsets due to fear, pain, anger,
the habit of bruxism does grinding or clinching
of teeth at inappropriate moments along with rejection, nervousness or frustrations, etc.
repeated tapping. The act causes considerable • Persons with aggressive, hurried or overly
amount of damage to the teeth and the related
structures. About 10 to 20 percent of the general competitive tendencies.
population is affected by this habit.
Occupational cause: Watchmakers and
CAUSES carpenters are prone to have bruxism (as
they habitually hold the instruments by the
Local factor: Occlusal disturbances. teeth).
Systematic causes: Unrecognized mental tension
due to the following reasons: Habitual cause: Continuous chewing of pan,
• Chronic GI upset tobacco, pencils and finger nails also can cause
• Sleep disorder the defect, etc.
• Heredity
• Physical disability TYPES OF BRUXISM
• Endocrine disorder
There are two types of bruxism:
A. Nocturnal
B. Day-time habit