pulpal pahology

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PULPAL PATHOLOGY AND ITS SEQUELAE

PULPAL PATHOLOGY AND ITS SEQUELAEPresenterDr. Ravi AcharyaPG ResidentDept. Of Conservative Dentistry and EndodonticsB.P.Koirala Institute of Health SciencesDharan, Nepal"The pulp lives for the dentin and the dentin lives by the grace of the pulp. Few marriages in nature are marked by a greater affinity." Alfred L. OgilvieCONTENTSResponse of the pulp to dental cariesImmune response in the dental pulpHard tissue response to irritationHistologic changes in acute inflammation Histologic changes in the chronic inflammationHaemodynamic changes in the pulp during cariesNeural changes during pulpal inflammationAntiinflammatory and antinociceptive mechanisms in the dental pulpLess common pulpal responsesFactors limiting the pulps responseIatrogenic effects on the dental pulpSystemic factorsPulpal sequelae to impact trauma

The causes of pulp inflammation, necrosis, and dystrophy are:I. BacterialA. Coronal ingress1. Caries2. Fracturea. Completeb. Incomplete (cracks, infraction)3. Nonfracture trauma4. Anomalous tracta. Dens invaginatus (dens in dente) b. Dens evaginatusc. Radicular lingual groove (palatogingival groove)B. Radicular ingress1. Caries2. Retrogenic infectiona. Periodontal pocketb. Periodontal abscess3. HematogenicII. TraumaticA. Acute1. Coronal fracture2. Radicular fracture3. Vascular stasis4. Luxation5. AvulsionB. Chronic1. Adolescent female bruxism2. Traumatism3. Attrition or abrasion4. ErosionIII. IatralA. Cavity preparation1. Heat of preparation2. Depth of preparation3. Dehydration4. Pulp horn extensions5. Pulp hemorrhage6. Pulp exposure7. Pin insertion8. Impression takingB. Restoration1. Insertion2. Fracturea. Completeb. Incomplete3. Force of cementing4. Heat of polishingC. Intentional extirpation and root canal fillingD. Orthodontic movementE. Periodontal curettageF. ElectrosurgeryG. Laser burnH. Periradicular curettageI. RhinoplastyJ. OsteotomyK. Intubation for general anesthesia

IV. ChemicalA. Restorative materials1. Cements2. Plastics3. Etching agents4. Cavity liners5. Dentin bonding agents6. Tubule blockage agentsB. Disinfectants1. Silver nitrate2. Phenol3. Sodium fluorideC. Desiccants1. Alcohol2. Ether3. OthersV. IdiopathicA. AgingB. Internal resorptionC. External resorptionD.Hereditary hypophosphatemiaE. Sickle cell anemiaF. Herpes zoster infectionG.Human immunodeficiency virus (HIV) andacquired immune deficiency syndrome (AIDS)RESPONSE OF THE PULP TO DENTAL CARIESBacteria are responsible for most pulpal disease.

Kakehashi et al. proved that exposed pulps in gnotobiotic (germ free) rats did not become inflamed while similarly exposed pulps in rats with a full oral flora did.The response of the pulp may vary depending on whether the caries process progresses rapidly (acute caries) or slowly (chronic caries), or is completely inactive (arrested caries).Conditions for growth and availability of nutrients are quite different in enamel caries than in dentinal cariesProducts of bacterial metabolism, notably organic acids and proteolytic enzymes, destroy enamel and dentin.Relatively large bacterial product, bacterial endotoxin, is able to diffuse through dentinal tubules to the pulp chamber .Bacterial antigens diffusing from the lesion to the pulp through the dentinal tubules are captured and processed by APCs, which leads to the activation of the immune system.Deep penetration of dentin by bacteria results in acute inflammation and eventually infection and necrosis of the pulp.The first reaction of odontoblasts to superficial caries lesions in enamel is a marked reduction in the cytoplasm: nucleus ratio, suggesting an altered metabolism.In active lesions, primary odontoblasts are involved in the formation of reactionary dentin.

However, even before the appearance of inflammatory changes, the size and number of odontoblasts decrease, at which time their metabolic activity is reduced while cellular proliferative activity in the cell-free zone of the pulp increases.

Although normally tall columnar cells, odontoblasts adversely affected by caries become flat to cuboidal in shape.

The boundary zone between primary and reparative dentin is atubular and lacks continuity of tubules.Electron microscopic examination of the odontoblasts beneath a superficial caries lesion revealed cellular injury in the form of ballooning degeneration of mitochondria and a reduction in the number and size of other cytoplasmic organelles.Eventually, the primary odontoblasts die, usually followed by proliferation of replacement odontoblasts and reparative dentin formation.

Bacteria infect some tubules long before others are infected.

The distribution of infected tubules is not uniform, as neighboring uninfected tubules are frequently found interspersed among infected tubules.

At the completion of cavity or crown preparation, some infectedtubules may not have been eliminated.Basic reactions that tend to protect the pulp against caries includes:Decrease in the permeability of the dentin due to dentinal sclerosis,Formation of new dentin (tertiary dentin), Effectiveness of inflammatory and immunologic reactions. Dentinal Sclerosis:It develops at the periphery of almost all caries lesions.Most common response to caries.In dentinal sclerosis, the dentinal tubules become partly or completely filled with mineral deposits consisting of both hydroxyapatite and whitlockite crystals.Dentinal sclerosis reduces the permeability of dentin, thus shielding the pulp from irritation.In order for sclerosis to occur, vital odontoblast processes must be present within the tubules.

In highly active caries lesions, odontoblast may die before sclerosis has occurred.Disintegration of odontoblast processes within the tubules results in a dead tract.

Tertiary dentin:There are two types of tertiary dentin based upon the cell type responsible for dentin production:Reactionary DentinReparative Dentin

Compared with primary dentin, reparative dentin is less tubular and less well calcified. At times no tubules are formed; this type of tertiary dentin has been characterized as a form of fibrodentin.If the pulp is inflamed or has undergone degenerative changes, the quality of the dentin is more variable.

An example of a poor quality dentin is Swiss cheese appearance of dentin.The holes represent soft tissue that was trapped in the matrix and subsequently underwent necrosis.Hard tissue response to irritationIrritational dentin

An odontoblast that is mildly stimulated may form dentin that closely resembles normal physiologic dentin.Since odontoblasts are incapable of mitosis, they must be replaced by underlying cells that mature from dividing undifferentiated precursors or by redifferentiation of fibroblasts.

These new cells are atypical, frequently without a process, and thus form an atypical irregular structure called irritation or reparative dentin.

Its formation occurs independently of the presence of inflammation and may form on the walls of an irreversibly damaged pulp.Continued irritation dentin formation may depend on persistent injurious stimuli; such a condition is neither desirable nor reparative.Anything that exposes or contacts dentin has the potential to stimulate formation of underlying irritation dentin.The morphology of irritation dentin has been studied, but little is known of its functions.Some attribute protective properties to this tissue and therefore recommend methods or materials to stimulate its formation.Others doubt its ability to protect the underlying pulp.They have demonstrated its permeability, permitting passage of chemicals and bacteria and other substances.

The presence of irritation dentin delays, but does not prevent, the eventual penetration of caries into the pulp.

BACTERIA AND THEIR BY-PRODUCT CAN REACH THE PULP FROM OTHER SOURCESAnomalous Crown Morphology, Fractures, and Cracks

Fig: Palatogingival GrooveClassification of invaginated teeth

2. Periodontal Disease

Saglie R et al: Scanning electron microscopic depiction of the inside of an ulcerated and infected pocket. Area 1 (right border) is the surface view of lining epithelium. C, epithelial cell. Dotted line demarcates the cut surface of the epithelium (Area 2). The basement lamina (BL) separates the epithelium from connective tissue (Area 3), which contains collagen fibers (CF) and connective tissue cells (CC). Bacteria (top arrow) enter a hole (H) in the epithelium (left by a desquamated cell) and travel through a tunnel to emerge into connective tissue through the hole. Abundant cocci, rods, and filaments are seen alongside the hole on the basement lamina. Filaments and cocci are then seen perforating the basement membrane (double arrow) to penetrate connective tissue and reach blood and/or lymph vessels.3.Blood Stream (Anachoresis)

ANTIGEN RECOGNITION IN THE DENTAL PULPAll three antigen-presenting cell types expressing the type II major histocompatibility complex (MHC) surface proteins, macrophages, dendritic cells, and B lymphocytes, are present and active in the pulp's response to bacteria and toxins.In a normal healthy pulp, macrophages are present in a resting form, as monocytcs. Macrophages require stimulation by bacteria or cytokines before they express type II MHC molecules. At rest they are found predominantly around blood vessels though a few are distributed throughout the tissue.Dendritic cells form a network throughout the pulp concentrating around blood vessels and the odontoblast layer. Some of the dendritic cells in the odontoblast layer extend their processes into the dentinal tubules.They constantly express the MHC molecules on their surface without provocation.The number of dendritic cells increases in the pulp when it becomes inflamed and they accumulate beneath the carious lesion.

B cells have been reported in the normal