1-Diseases of the pulp.

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Lec.4
Oral pathology
Diseases of the pulp
Pulp:is delicate fibrous connective tissue containing blood
vessels, lymphatic, nerves and undifferentiated connective tissue
cells.
Pulp is unique in that it is surrounded by:
1. Rigid dentin which prevent the excessive swelling of the tissue in the
hyperemic edematous phases of inflammation.
2. The blood vessels supplying the pulp tissue enter the tooth through
tiny apical foramen which prevent the development of an extensive
collateral blood supply to the inflamed part.
3. Specialized cells of the pulp are the odontoblast cells which line the
outer layer of the pulp and communicate to the D.E.J by long
extension of their cell bodies lying within the dentinal tubule.
-These cells are responsible for sensitivity of teeth and for the formation
of the reparative dentin.
-Inflammation of the pulp is like inflammation of connective tissue any
where else in the body and pulpitis refers to the inflammation of the pulp
tissue.
1. The pulp is totally surrounded by hard dentin which limits the
ability of the pulp to tolerate oedema.
2. The pressure rises in the pulp associated with an inflammatory
exudate which may cause local collapse of the venous part of the
microcirculation , this lead to local tissue hypoxia and anoxia
which in turn lead to pulp necrosis. Also chemical mediator
released from the necrotic tissue leads to further inflammation and
edema.
Pulpitis can be due to:
1. Bacterial cause: the most common cause of pulpitis is by dental
caries in which the bacteria and bacterial toxin spread through the
dentinal tubules and then to the pulp.
-Also invasion of the bacteria to the pulp can be due to fracture of the
teeth that expose the dental pulp to the oral microorganism flora.
-Erosion, attrition and periodontal disease, pulp may be affected in
(P.D.)disease via lateral canals and via the apical foramen in cases of
severe disease
-The importance of bacterial infection in pulpitis get much
experimental support in a germ-free rats in which surgical pulp
exposure were not followed by progressive pulpitis even when we
have much food impaction.
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. 2. Physical causes: Thermal:
Severe thermal change in a tooth can produce pulpitis as in cavity
preparation without adequate cooling, large metallic restoration,
trauma especially to the periodontal anterior teeth can result in
pulpitis.Trauma either from the occlusion or due to an accident.
3.Chemical causes: various chemicals are applied to dentinal tubule in
the form of filling, base and disinfectants.
Unlined composite restoration may cause low grade chronic pulpitis.
The eugenol in the temporary dressing, zinc oxide and eugenol is used
to relief the pain of toothache but is also a pulp irritant.
4.Mechanical causes: This includes : traumatic accident, iatrogenic
damage from dental procedure, attrition and abrasion.
Classification of pulpitis:
In the past, pulpitis has been classified into many classifications
according to clinical : acute and chronic, open and closed, partial and
total, exudative and suppurative , reversible or irreversible .
Those are confused classifications because the inflammation of the
pulp is a continuous process and very difficult to classify it into so
many classifications.
RECENT CLASSIFICATION:
1. Focal reversible pulpitis.
2. Acute pulpitis.
3. Chronic pulpitis.
4. Chronic hyperplastic pulpitis.(pulp polyp).
Focal reversible pulpitis:
It is also called hyperemia which can be regarded as the earliest form of
pulpitis.
Clinical features:
1. The pain is sharp and intense and respond to sudden change in
temperature.
2. Pain remain for 5-10 min. or even 20 min.
3. Sensitivity will disappear as soon as the stimulus is removed.
4. Easily localized to a particular tooth.
5. The tooth may show a deep carious lesion, large restoration or
restoration with defective margin.
Histological features:
1. Dilatation of the pulp vessels.
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2. Oedema may present due to change to the capillaries, and due to
this , there may be extravasation of R.B.C or W.B.C.
3. Thrombosis sometimes is seen due to hemostasis.
Treatment and prognosis:
1. If the irritant is removed before the pulp is severely damaged, then
the condition is reversible.
2. If the primary cause is not removed, then extensive pulpitis results
.
Differentiation between reversible and irreversible pulpitis:
Reversible
Irreversible
1.
2.
3.
4.
Elicited
Sharp
Less zone
Not affected by body
position
5. Easily localized
1.
2.
3.
4.
5.
Spontaneous
Dull
More zone
Affected by body position
Difficult to be localized
Acute pulpitis: (severe for short duration)
This extension acute pulpitis may be a sequel of F.R.P. or may occur due
to an acute exacerbation of a chronic inflammatory process.
Clinical features:
1. Usually occur in a tooth with a large carious lesion or a restoration
with defective one or with secondary caries.
2. The involved tooth is sensitive to heat and cold.
3. The pain continues even when the stimulus is removed.
4. The degree of pain correspond with the extent of the infection, as
more of the pulp becomes inflamed, the pain becomes very severe.
5. Pain at night increases due to increased blood pressure.
6. Low pain threshold.
7. Difficulty in localizing the pain due to lack of properioceptive
fibers of the pulp.
Histological features:
Microscopic examination of a tooth with acute pulpitis reveals symptoms
of acute inflammation similar to those attending acute inflammation in
other parts of the body.
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1. Vascular dilatation
2. Oedema in the C.T.
3. Migration of polymorphs, especially beneath the carious
area(lysosomal enzyme when they die)
4. Death of odontoblast.
5. Formation of a pulp abscess ( localized area of pus) which arises
from breakdown of leukocyte, bacteria as well as necrotic tissue.
6. Inflammation spread rapidly to involve the entire pulp lead to
liquefaction and necrosis this is termed as acute suppurative
pulpitis.
Treatment and prognosis:
Pulpatomy can be done if there is only a limited area of tissue involved,
treatment of teeth involved with acute pulpitis is either by R.C.T* or
extraction
Chronic pulpitis:(mild for long duration)
Chronic pulpitis may develop as a result of A.P*,but it can also develop
independently as a slow chronic process.
*R.C.T: Root canal treatment
*A.P: Acute pulpitis
Clinical features:
1. Dull, intermitted pain is indicated.
2. Increased pain threshold due to degeneration of nerve fiber.
3. Last for 1-2 hours.
Treatment: R.C.T or extraction.
Chronic hyperplastic pulpitis (pulp polyp):
This form of chronic pulpitis occurs either as a chronic lesion from the
onset or as a chronic stage of a previously acute pulpitis
Clinical features:
1. Seen particularly in primary molars and sometimes also in newly
erupted permanent molars.
2. We see a polyp in the center of a deep lesion due to excessive
proliferating of chronically inflamed dental tissue.
3. Occur almost in children and young adult .(good blood supply,
large root opening and high tissue resistance).
4. Involve teeth with large, open carious lesions.
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5. A pulp polyp is not sensitive to touch (little nerves in the
hyperplastic tissue), may or may not bleed, this depends on the
degree of vascularity of the tissue .
6. Sometimes, pulp polyp can be confused with hyperplastic gingiva
which extend into the carious defects( by probing we can follow
the origin of the polyp)
Histopathologic features:
1. The polyp is a mass of granulation tissue.
2. Inflammatory cell infiltration, chiefly lymphocyte and plasma cells
sometimes mixed with polymorphs.
3. Pulp polyp appears to be covered with stratified squamous
epithelium as a result of implantation of epithelial cells from the
oral mucous membrane.
Treatment: by R.C.T or extraction.
Gangrenous necrosis of the pulp:
Untreated pulpitis will result in complete necrosis of the pulp tissue, this
is defined as necrosis of the tissue due to ischemia with super imposed
bacterial tissue.
Clinical features:
1. There may be pain which means there is still some vital pulp tissue
left such as another canal.
2. Discoloration of the tooth, because the products of gangrene pass
into the dentinal tubule and show through the translucent enamel
giving the tooth a greenish-black color.
3. Foul odor when the inflamed pulp are open for R.C.T.
Pulp necrosis:
1. Pulpitis →liquefactive type of N
Gangrenous N
2. Traumatic →injury to the apical blood supply
Coagulative N
Due to ischemia
Internal resorption or idiopathic resorption:
This refers to destruction of the dentin from the pulpal side toward the
out side of the tooth, the cause is unknown; however a history of
trauma may be present.
The dentin is whittled away by giant cell osteoclasts and this process
may continue rapidly or stop spontaneously.
The lesion is a symptomatic and appears on routine radiographs as
ballooning RL expansion of the pulp usually in the root.
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It may occur in the coronal part of the pulp in which case, the pink
tissue of the pulp show through the enamel (pink tooth) which
represents the granulation tissue showing through the remaining tooth
substance.
The treatment is R.C.T., if the resorption perforates the P.D ligament,
the tooth is treated by extraction.
External resorption:
External resorption of the tooth is more common the internal
resorption, it occurs naturally in the shedding of primary teeth.
External resorption refers to the loss of cementum and dentin of a
tooth from the external surface in toward the pulp.Radiographically
appears as irregular loss of root structure.
Known causes are:
1. P.A. inflammation
2. Reimplantation of teeth, the root is resorbed and replaced by bone
causing ankylosis, although sometime, the entire root or roots are
resorbed and the tooth is exfoliated.
3. Tumors and cysts, this is due to pressure on the root by the lesion.
4. Excessive forces during orthodontic movement.
5. Impacted teeth, teeth that are completely embedded in the bone may
undergo resorption of the crown; root or both, there may be resorption
of adjacent tooth without resorption of impacted tooth.
6. Idiopathic resorption.
Calcification of the pulp:
Pulp stones
Round masses of dentine may form within the pulp and can be seen in
radiographs as small opacities.
The cause is unknown; they are also referred to as denticles, because
some of them are composed of dentine, they don’t cause pain and may
interfere with root canal therapy, mostly appear in coronal pulp and
increase in size and number with age.
1. True pulp stone (contain tubule and may have outer layer of
predentin and odontoblast cells)
2. False pulp ( concentric layers of calcified material with no tubule)
According to their location in the pulp:
1. Free
2. Adherent
3. Interstitial, when they are surrounded by reactionary or
secondary dentine.
Barotrauma :(aerodontalgia)
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This occurs in people who are exposed to a high pressure e.g.
divers, or are exposed to a low pressure as airmen. This pain has
been attributed to the formation of nitrogen bubbles in the pulp
tissue or vessels, similar to the decompression syndrome else
where in the body (Caisson disease).
As the pressure is reduced, bubbles of air come out of solution
from the blood and interstitial fluid,O2 and CO2 readily absorbed
and removed while the inert nitrogen remains in the tissue and
cause damage.
Caisson disease:
1. Mild form (pain in one or more large joints)
2. Severe cases (circulatory disturbance and may cause death).
Age changes in the pulp: The size of the pulp decreased
gradually with age due to the continued production of secondary
dentine, decreased elasticity, reduction in the cellularity and
increase in collagen fiber content has also been reported.
These changes may alter the response of the tissue to injury and it
impairs healing potential.
Also the prevalence of pulp stones and diffuses calcification shown
to be increased with age.
There is little correlation between the clinical feature and the type
or extent of the pulp inflammation, histologically ; this is because
an absence of symptom is not indicated that the pulp is normal as
pulp death following pulpitis may occur without any previous
history of pain .
The most difficult thing is the decision clinically whether the
pulpitis is reversible or irreversible which will determine the type
of management of the affected tooth.
This decision depends on many factors:
1. Age of patients
2. Size of the carious lesion
3. Presence or absence of symptoms
4. Pulp vitality tests
5. Radiographic evidence
6. Direct observation.
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