Lec.

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. . 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. 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

1. 2. 3. 4. Elicited Sharp Less zone Not affected by body position 5. Easily localized 1. 2. 3. 4. 5.

Irreversible
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. 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. 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. 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 dont 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)
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.