Pathology of the Dental Pulp PDF

Pathology of the Dental Pulp  Introduction  The dental pulp is the part in the center of a tooth made up of living connective tissue and cells called odontoblasts  The pulp contains the blood vessels the nerves and connective tissue inside a tooth and...

Pathology of the Dental Pulp  Introduction  The dental pulp is the part in the center of a tooth made up of living connective tissue and cells called odontoblasts  The pulp contains the blood vessels the nerves and connective tissue inside a tooth and provides the tooth’s blood and nutrients.  Pulpitis is inflammation of the pulpal tissue regardless of the presence of an infectious agent u lp s P es bsc A Etiology: 1- Bacterial “Microbial” injury A. Dental caries Bacteria generally reach the pulp as a result of dental caries including root caries and recurrent caries. B. Marginal leakage C. Cracks in crown D. Periodontal pocket “Perio-endo lesion” Pulpitis may be a complication of advanced periodontal disease as a result of periodontal pocket involving the periapical tissue or communicating with accessory root canal producing a combined periodontal-endodontic lesion. E. Malformed teeth “Invaginated odontome” Dens-in-dente F. Anachoresis “the localization of blood-borne bacteria within already inflamed pulp. Mean circulating bacteria in the blood tend to localize in inflamed areas. 2- Mechanical injury  Traumatic accidents (Fractures, concussion, luxation, avulsion, traumatic occlusion, Bruxism).  Iatrogenic damage (accidental pulp exposure during dental procedures)  Attrition, abrasion 3. Barotrauma (aerodontalgia):  When flying at high altitude in unpressurized aircraft, or rapid decompression in divers.  Attributed to formation of „Nitrogen bubbles’ in pulp tissue or vessels.  Thought not to be a direct cause, but rather an exacerbating cause in presence of caries 4- Thermal injury  Severe thermal stimuli can be transmitted through large un-insulated metallic restorations.  Iatrogenic: traumatic dental procedures as cavity preparation, polishing, & exothermic chemical reactions of dental materials. 5- Chemical injury  Erosion  Inappropriate use of acidic dental materials. e.g. (Zinc Phosphate in deep cavities or Composite without cavity liner). 6- Electrical changes: - Two dissimilar metals (gold & amalgam) + saliva galvanic current pulp irritation  Pathology of Dental Pulp 1. Pulpitis a) Reversible Pulpitis b) Irreversible Pulpitis i. Acute : a) Abnormally responsive to cold b) Abnormally responsive to heat ii. Chronic : c) Asymptomatic with pulp exposure d) Hyperplastic pulpitis e) Internal resorption. 2.Healing of Pulp 3.Secondary dentin 4.Pulp Necrosis 5.Pulp Calcification 6.Age Changes in the Pulp  Reversible pulpitis (Hyperemia) A level of pulpal inflammation in which the tissue is capable of returning to a normal state of health if the noxious stimuli are removed. Clinical features:  A sudden mild-to-moderate pain appears upon stimulation.  Pain resolves within seconds after removal of stimulus.  Pain is provoked by: Cold stimuli (e.g. ice, beverages, cold air). Sweet or sour foods and beverages.  Electric pulp testing: tooth responds at lower levels of current.  No mobility or sensitivity to percussion.  Deep carious lesions as the bacteria are still some distance from the pulp, acid permeating along the dentinal tubules gives rise to hyperemia Histopathological features: 1. Dilatation of blood vessels. 2. Edema fluid collection due to damage of vessles wall & allowing extravasation of RBC or diapedesis of WBC. 3. Slowing of blood flow & hemoconcentration due to transudation can causes thrombosis 4. Reparative or reactionary dentin in adjacent dentinal wall Treatment: It requires either direct or indirect capping treatment. Hyperaemia can be classified histopathologically into: Active hyperaemia (arteries) Passive hyperaemia (veins) Irreversible Pulpitis  Acute irreversible pulpitis It is that form of pulpitis which rapidly develops from the reversible pulpitis if the invading microorganisms are sufficiently virulent or the resistance is lowered. Etiology :  Bacterial invasion through the dental caries (most common).  acute exacerbation of chronic inflammatory process (chronic pulpitis).  Reversible pulpitis may deteriorate into irreversible pulpitis. Clinical features:  Patient has sharp, severe pain upon thermal stimulation.  Cold is especially uncomfortable but heat, sweet or acids can elicit pain.  Pain continues after the stimulus is removed.  Pain can be spontaneous, continuous and exacerbated when lying down.  The patient is unable to identify the offending tooth within the quadrant.  The tooth is not sensitive to percussion in the early stage until the infection reaches the periapical region it becomes sensitive.  In the later stage of acute pulpitis, the pain increases in intensity and become as a throbbing pressure that can keep patients awake at night.  At this point heat increases the pain; however cold may produce relief.  In early stage of acute pulpitis, the tooth may be hyper-reactive to electric stimulation (respond to pulp test at lower levels of recurrent), but when pulp damage increases, sensitivity is reduced (responds to electric pulp testing at higher levels of current) until there is no response is demonstrated (dead tissue) Histopathology  Blood vessel dilatation and inflammatory exudate:  In the early acute partial pulpitis occurs and characterised by continued vascular dilatation and pavementation of PMNLs from the BV into pulp tissue with oedema fluid to attack the infection.  Disintegration of odontoblastic layer: The odontoblasts may disorganise and becomes oedematous and areas of odontoblast destruction may be seen.  Pulp abscess (focal liquefaction necrosis): At this stage area of tissue, liquefaction may occur leading to abscess formation as PMNLs migrates to surrounds the necrotic tissues (Acute pulp abscess)  Total pulpal suppurative necrosis: As a sequela of this inflammatory reaction, the whole pulp may be involved and complete pulp necrosis (Acute suppurative pulpitis) is the end-result. Treatment :It requires root canal treatment.  Chronic irreversible pulpitis It is that form of pulpitis which develops from acute pulpitis or if the irritant is of low virulence. Types: a) Chronic closed pulpitis (very rare) b) Chronic open pulpitis (chronic open ulcerative pulpitis) c) Chronic open hyperplastic pulpitis (pulp polyp). Clinical features:  Pain is not prominent , mild ,dull ache which is intermittent.  Reaction to thermal changes is reduced because of degeneration of nerves.  Response to pulp tester is reduced.  Wide open carious lesion & with exposure of pulp cause relatively little pain Histopathological features: i. It is assumed that most pulp affected with chronic pulpitis will show accumulations of mononuclear leukocytes mainly lymphocytes and plasma cells. ii. As most of the chronic inflammatory process collagen fibres and newly formed capillaries becomes prominent (granulation tissues). iii. These granulation tissues appear on surface of the exposed pulp resemble ulcer surface (open ulcerative form) Treatment: It requires root canal treatment  Chronic hyperplastic pulpitis (Pulp polyp)  It is that form of chronic pulpitis in which the pulp tissue is opening to the oral cavity associated with polyp (small globular tissue mass).  Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding.  Characterized by the development of granulation tissue, covered at times with epithelium and resulting from long standing low grade irritation.  Due to acute caries resulting in crown disintegration & early pulpal involvement where the entire dentinal roof is missing thus pulp is communicating with oral cavity preventing tissue pressure compromising pulpal blood flow. Clinical features:  It appears as a pinkish globular tissue mass protruding from the pulp chamber and often filling the entire cavity.  Teeth with large, open carious lesions  It is usually seen in the children and young adults.  It usually affects the deciduous molars and the first permanent molars.  It is usually painless.  It may bleed easily due to the vascularity degree of it  Pulp is relatively insensitive. Histopathological features:  Hyperplastic tissue is basically granulation tissue consists of collagen fibers, fibroblasts, chronic inflammatory cell infiltration and blood vessels.  Inflammatory cell infiltration (lymphocytes ,plasma cell, PMNLs)  Stratified squamous type epithelial lining resembles oral mucosa with well formed well formed rete pegs Radiography:  Large open cavity with direct access to the pulp chamber. Treatment:  It requires eliminating of the pulp polyp with root canal treatment.  Healing of the pulp  Injured odontoblasts are replaced by new cells from pulp.  Pulpitis may resolve upon removal of irritant.  It may resolve due to reactionary dentin formation even without removal of caries.  Pulp capping after traumatic pulp exposure or pulpotomy: Ca (OH)2 agents stimulate formation of a calcified barrier.  Secondary Dentin Physiologic Secondary Dentin  Dentin formed after completion of the tooth: regular, organized tubular structure.  Slow, gradual normal (physiologic) process that increases after age 35-40 and leads to smaller pulp chambers and root canals.  Proceeds from crown down through root canals.  More advanced in males; associated with arthritis, gout, renal stones, gallstones, atherosclerosis, and hypertension.  Reduced teeth sensitivity, caries resistance and protection of pulp from trauma.  Localized Secondary Dentin  Reparative Dentin: Irregular or Tertiary Dentin Laid down in areas of focal injury or insult Haphazardly organized; irregular or disorganized tubules Significant traumatic injury can lead to accelerated early pulp obliteration termed calcific metamorphosis (yellow crown) Can occur in response to: Attrition, Fracture, Erosion, Abrasion, Caries, Periodontal disease Mechanical injury from dental procedures, Irritation from dental materials  Pulp necrosis (Pulp gangrene)  May follow pulpitis or trauma to apical blood vessels.  Coagulative necrosis after ischemia.  Liquefactive necrosis after pulpitis may become gangrenous with foul odor upon infection by putrefactive bacteria from caries.  Pulp necrosis in sickling crisis of sickle cell anemia Clinical features:  It is asymptomatic.  It may cause discolored tooth due to degeneration of the dentinal tubules caused by death of the pulp. Histopathological features Pulp Necrosis  It shows either an empty pulp chamber and canal or an isolated empty areas.  Pulp Calcifications  Pulp stones are calcified bodies with an organic matrix and occur most frequently in the coronal pulp, can be seen in radiographs as small opacities  They are common in normal teeth but have an increased frequency in teeth affected by caries, trauma, orthodontic movement and other potential irritants.  True pulp stones contain tubules (albeit few and irregular),and may have an outer layer of predentine and adjacent odontoblasts.  False pulp stones are composed of concentric layers of calcified material with no tubular structure.  stones may be described as free, adherent, or interstitial when they have become surrounded by reactionary dentine. Lamellated (false) pulp stones.  Pulp Calcifications( Pulp stones)  Rounded masses of dentine may form within the pulp and can be seen in radiographs as small opacities. In the past they were thought to cause symptoms but are developmental anomalies. For unknown reasons, they are common in the teeth of patients with Ehlers-Danlos (floppy joint) syndrome, a genetic defect of collagen formation.  Histologically, pulp stones consist of dentine which may show complete or incomplete tubule formation.  A distinction used to be drawn between free and attached pulp stones. However, this is frequently an illusion caused by a plane of section which fails to pass through the connection between the pulp stone and the pulp wall.  Pulp stones. A rounded nodule of calcified tissue in which some irregular tubules may be seen is present in the pulp. Smaller stones and amorphous calcifications surround the main mass (trichrome stain).  Diffuse Calcification  Amorphous dystrophic calcifications may sometimes be seen histologically in the pulp and are thought to be an age-related degenerative change.  Pulp stones and diffuse calcification are of no clinical significance except insofar as they may obstruct endodontic treatment.  Age changes in the pulp  The volume of the pulp gradually decreases with age due to the continued production of secondary dentine. Decreased vascularity, reduction in cellularity, and increase in collagen fiber content have also been reported, and these changes may impair the response of the tissue to injury and its healing potential. The reduction in pulp cell density is accompanied by reduction in the number of odontoblasts throughout adult life to about half their original number by age 70. The reduction is greater in the root than in the crown. It is generally accepted that the prevalence of pulp stones and diffuse calcification increases with age but the evidence for this is inconclusive.